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1.  Correlation of Serum CA-125 and Progesterone Levels with Ultrasound Markers in The Prediction of Pregnancy Outcome in Threatened Miscarriage 
Background
The aim of this study was to evaluate the relationship between ultrasonographic findings and serum progesterone and cancer antigen-125 (CA-125) levels in threatened miscarriage and to predict pregnancy outcome.
Materials and Methods
In a prospective comparative case-control study, serum CA-125 and progesterone levels were measured for 100 pregnant women with threatened miscarriage who attended the outpatient clinic or the causality department of Obstetrics and Gynecology at Kasr El-Aini Hospital, Giza, Egypt, during the period from March 2013 to October 2013. Ultrasound was performed for fetal viability, crown-rump length (CRL), gestational sac diameter (GSD) and fetal heart rate (FHR). The patients were followed up and divided into two groups based on the outcome: 20 women who miscarried (group 1), and 80 women who continued pregnancy (group 2). The sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and overall accuracy were tested for CA-125 and progesterone levels in prediction of the pregnancy outcome. Correlation of these chemical markers with the ultrasound markers was also examined.
Results
In the group that miscarried, CA-125 level was significantly higher (P<0.001) and serum progesterone level was significantly lower (P<0.001). For prediction of the outcome of pregnancy, the cut-off limit of 31.2 IU/ml for CA-125 level yielded sensitivity, specificity and an overall accuracy of 96.2, 100 and 99.4% respectively. The cut-off limit of 11.5 ng/ml for progesterone level yielded sensitivity, specificity and an overall accuracy of 97.5, 100 and 99.8% respectively. CA-125 level had a negative correlation with progesterone level and FHR levels (r=-0.716, P<0.001) and (r=-0.414, P<0.001) respectively. Serum progesterone level correlated with GSD (r=0.521, P<0.001) and with CRL (r=0.407, P<0.001) and FHR (r=0.363, P<0.001). CA-125 level was significantly higher in the group that showed hematoma as compared with the group without hematoma (P<0.001). Also, serum progesterone level was significantly lower in the group that showed hematoma as compared with the group without hematoma (P=0.017).
Conclusion
Serum CA-125 and progesterone levels are valid early predictors of the outcome of pregnancy in women with threatened miscarriage. They are correlated with some ultrasonographic markers (GSD, CRL, and FHR).
PMCID: PMC4793171  PMID: 26985338
First Trimester; Ultrasound; CA-125; Progesterone; Threatened Miscarriage
2.  Evaluation of HE4, CA-125, Risk of Ovarian Malignancy Algorithm (ROMA) and Risk of Malignancy Index (RMI) in the Preoperative Assessment of Patients with Adnexal Mass 
Oman Medical Journal  2016;31(5):336-344.
Objectives
To evaluate the validity and compare the performance of cancer antigen-125 (CA-125), human epididymis protein 4 (HE4), the risk of malignancy index (RMI), and the risk of ovarian malignancy algorithm (ROMA) in the diagnosis of ovarian cancer in patients with ovarian lesions discovered during their preoperative work-up investigations.
Methods
This prospective, cross-sectional study looked at patients who attended the gynecology department at the Royal Hospital, Muscat, from 1 March 2014 to 30 April 2015, for the evaluation of an ovarian lesion. The inclusion criteria included women who underwent surgical intervention and who had a preoperative pelvic ultrasound with laboratory investigation for CA-125 and HE4. The study validated the diagnostic performance of CA-125, RMI, HE4, and ROMA using histopathological diagnosis as the gold standard.
Results
The study population had a total of 213 cases of various types of benign (77%) and malignant (23%) ovarian tumors. CA-125 showed the highest sensitivity (79%) when looking at the total patient population. When divided by age, the sensitivity was 67% in premenopausal women. In postmenopausal women, CA-125 had lower sensitivity (89%) compared to RMI, HE4, and ROMA (93% each). A high specificity of 90% was found for HE4 in the total patient population, 93% in premenopausal women and 75% in postmenopausal women. CA-125 had the highest specificity (79%) in postmenopausal women. Both CA-125 and RMI were frequently elevated in benign gynecological conditions particularly in endometriosis when compared to HE4 and ROMA. We also studied modifications of the optimal cut-offs for the four parameters. Both CA-125 and RMI showed a significant increase in their specificity if the cut-off was increased to ≥ 60 U/mL for CA-125 and to ≥ 250 for RMI. For HE4, we noted an improvement in its specificity in postmenopausal women when its cut-off was increased to140 pmol/L.
Conclusions
HE4 and ROMA showed a very high specificity, but were less sensitive than CA-125 and RMI in premenopausal women. However, they were of comparable sensitivity in postmenopausal women and were valuable in distinguishing benign ovarian tumors or endometriosis from ovarian cancer. Modifying the cut-off values of the different markers resulted in a higher accuracy compared to the standard cut-offs, but at the expense of reduced sensitivity.
doi:10.5001/omj.2016.68
PMCID: PMC4996955  PMID: 27602187
CA-125 Antigen; Human Epididymis-specific Protein E4; Risk of Malignancy Index (RMI); Risk of Ovarian Malignancy Algorithm (ROMA); Ovarian Neoplasms.
3.  The Daily Profiles of Circulating AMH and INSL3 in Men are Distinct from the Other Testicular Hormones, Inhibin B and Testosterone 
PLoS ONE  2015;10(7):e0133637.
The testes secrete four hormones (anti-Müllerian hormone, insulin-like peptide 3, Inhibin B and testosterone) from two endocrine cell types. It is unknown whether anti-Müllerian hormone and insulin-like peptide 3 levels have a diurnal variation, and if so, whether they covary during the day with testosterone and InhB. Sera were obtained from 13 men at 00:00, 06:00, 09:00, 12:00, 14:00, 17:00 and 19:00 hours and the levels of their testicular hormones measured by ELISA. A second cohort of 20 men was similarly examined with blood drawn at 19:00 and the following 06:00. Anti-Müllerian hormone levels exhibited a subtle diurnal pattern with a 19:00 peak that was 4.9% higher on average than the 06:00 nadir (p = 0.004). The decrease in anti-Müllerian hormone coincided with a rise in testosterone and InhB, but there was no association between the person-to-person variation in the diurnal patterns of anti-Müllerian hormone and testosterone or Inhibin B. Insulin-like peptide 3 had no diurnal pattern, with only minor sporadic variation between time points being observed in some men. In conclusion, the diurnal and sporadic variation of each testicular hormone is distinct, indicating that the major regulation is at the level of the hormone rather than at the endocrine cell type. Consequently, the balance of the hormones being released by the testes has complex variation during the day. The physiological significance of this will vary depending on which combinations of testicular hormones that the target cells respond to.
doi:10.1371/journal.pone.0133637
PMCID: PMC4507845  PMID: 26192622
4.  Serum anti-Müllerian hormone predicts ovarian response and cycle outcome in IVF patients 
Purpose
This prospective study was designed to investigate whether anti-Müllerian hormone (AMH) levels at basal and ovulation triggering day are associated with ovarian response and pregnancy outcome for in vitro fertilization (IVF).
Method
60 infertility women undergoing IVF were prospectively studied. On day 3 of the menstrual cycle (D3), measurements of AMH, inhibin B, FSH, LH, and E2 and ultrasound evaluation of antral follicle count (AFC) were performed. Serum AMH and inhibin B levels were remeasured on the day of hCG administration (DhCG). The outcome measures were the number of retrieved oocytes and clinical pregnancy.
Results
Number of retrieved oocytes was statistically significant and correlated with D3 AMH, AFC, DhCG AMH, DhCG inhibin B, FSH, and age (r = 0.885, 0.874, 0.742, 0.732, −0.521, −0.385, respectively). Statistically significant differences were found between pregnant and non-pregnant women regarding D3 AMH and AFC. Multiple regression analysis for prediction of pregnancy showed D3 AMH to be a good predictor of clinical pregnancy.
Conclusion
AMH correlates better than age, FSH, and inhibin B with the number of retrieved oocytes. Serum basal AMH may offer a better prognostic value for clinical pregnancy than other currently available markers of IVF outcome in our preliminary study.
doi:10.1007/s10815-009-9332-8
PMCID: PMC2758947  PMID: 19768530
Anti-Müllerian hormone; IVF; Ovarian reserve; Pregnancy
5.  The Immunoexpressions and Prognostic Significance of Inhibin Alpha and Beta Human Chorionic Gonadotrophins (hCG) in Breast Carcinomas 
Purpose
Pregnancy and hCG treatments are considered essential for inhibiting breast cancer. The effect of hCG is accompanied by the synthesis of inhibin, a transforming growth factor involved in cell differentiation and proliferation. Inhibin is considered a tumor suppressor, but its role in the breast is unclear. The aim of this study was to determine the frequency and tissue distribution of the expressions of inhibin-α and β-hCG in breast cancer, and their prognostic relevance with other biological parameters.
Materials and Methods
334 of formalin-fixed, paraffin embedded tissue blocks were selected, and then immunostained for inhibin-α and β-hCG. The inhibin-α expression was compared with those of β-hCG, ER, PR and HER-2/neu, as well as the tumor characteristics and recurrences.
Results
Inhibin-α and β-hCG were expressed in 87 (26.0%) and 44 cases (13.2%), respectively. Inhibin-α was found in 25.1% of infiltrating ductal carcinomas (67/267), 26.7% of intraductal carcinomas (8/30), 33.3% of lobular tumors (3/9), 80.0% of apocrine carcinomas (4/5) and 21.7% of the other types (5/23). Inhibin-α was correlated with β-hCG (p<0.0001), PR (p=0.010) and HER-2/neu (p=0.021). HCG was focally expressed in the cytoplasm of the conventional types, but the apocrine type displayed diffusely intense cytoplasmic staining, which correlated with histological tumor types (p<0.001).
Conclusion
Inhibin was significantly correlated with the expressions of hCG, PR and HER-2/neu. Therefore, it might be a useful marker in the prevention and hormonal treatment of breast cancer, such as hCG and progesterone. HCG was expressed significantly higher in the apocrine type than the conventional types, suggesting it can be a useful adjunct in differentiating other cancer types.
doi:10.4143/crt.2005.37.4.241
PMCID: PMC2785916  PMID: 19956521
Breast neoplasms; Human chorionic gonadotrophin (hCG); Inhibins
6.  Male Central Precocious Puberty: Serum Profile of Anti-Müllerian Hormone and Inhibin B before, during, and after Treatment with GnRH Analogue 
We aimed to describe the functional changes of Sertoli cells, based on the measurement of serum anti-Müllerian hormone (AMH) and inhibin B during treatment with GnRHa and after its withdrawal in boys with central precocious puberty. Six boys aged 0.8 to 5.5 yr were included. AMH was low at diagnosis in patients >1 yr but within the normal range in younger patients. AMH increased to normal prepubertal levels during treatment. After GnRHa withdrawal, AMH declined concomitantly with the rise in serum testosterone. At diagnosis, inhibin B was elevated and decreased throughout therapy, remaining in the upper normal prepubertal range. In patients with testicular volume above 4 mL AMH remained higher in spite of suppressed FSH. After treatment withdrawal, inhibin B rose towards normal pubertal levels. In conclusion, AMH did not decrease in patients <1 yr reflecting the lack of androgen receptor expression in Sertoli cells in early infancy. Serum inhibin B might result from the contribution of two sources: the mass of Sertoli cells and the stimulation exerted by FSH. Sertoli cell markers might provide additional tools for the diagnosis and treatment followup of boys with central precocious puberty.
doi:10.1155/2013/823064
PMCID: PMC3845850  PMID: 24324495
7.  Immunohistochemistry Study of P53 and C-erbB-2 Expression in Trophoblastic Tissue and Their Predictive Values in Diagnosing Malignant Progression of Simple Molar Pregnancy 
Background
Finding a tumor marker to predict the aggressive behavior of molar pregnancy in early stages has yet been a topic for studies.
Objectives
In this survey we planned to study patients with molar pregnancy to 1) assess the p53 and c-erbB-2 expression in trophoblastic tissue, 2) to study the relationship between their expression intensity and progression of a molar pregnancy to gestational trophoblastic neoplasia, and 3) to determine a cut off value for the amount of p53 and c-erbB-2 expression which might correlate with aggressive behavior of molar pregnancy.
Patients and Methods
In a prospective cross sectional study by using a high accuracy technique EnVision Tm system for immunohistochemistry staining of molar pregnancy samples, we evaluated p53 and c-erbB-2 expression in cytotrophoblast and syncytiotrophoblast and the correlation of their expression with progression of molar pregnancy to gestational trophoblastic neoplasia (GTN). Normal prostatic tissue and Breast cancer tissue were used as positive controls.
Results
We studied 28 patients with simple molar pregnancy (SMP) and 30 with GTN. Cytotrophobalst had significantly higher expression of p53 and c-erbB-2 and syncytiotrophoblast had greater expression of p53 in GTN group as compared to SMP group. The cut off values for percentage of p53 positive immunostained cytotrophoblast and syncytiotrophoblast were 5.5% and 2.5%. In c-erbB-2 positive membranous stained cytotrophoblast the cut off was 12.5%.
Conclusions
Our data suggests that over expression of p53 and c-erbB-2 is associated with malignant progression of molar pregnancy. We encountered that high expression of p53 and c-erbB-2 in trophoblastic cells could predict gestational trophoblastic neoplasia during the early stages.
doi:10.17795/ijcp-4115
PMCID: PMC5038832  PMID: 27703642
Complete Hydatiform Mole; P53; C-erbB-2; Prognosis
8.  Changes in Circulating ProAMH and Total AMH during Healthy Pregnancy and Post-Partum: A Longitudinal Study 
PLoS ONE  2016;11(9):e0162509.
Circulating Anti-Müllerian hormone (AMH) is derived from the gonads, and is a mixture of the prohormone (proAMH), which does not bind to AMH receptors, and receptor-competent AMH. The functions of a hormone are partially defined by the factors that control its levels. Ovarian reserve accounts for 55~75% of the woman-to-woman variation in AMH level, leaving over 25% of the biological variation to be explained. Pregnancy has been reported to decrease circulating AMH levels, but the observations are inconsistent, with the effect of pregnancy on the bioactivity of AMH being unknown. We have therefore undertaken a longitudinal study of circulating proAMH and total AMH during pregnancy. Serum samples were drawn at 6–8 gestational time-points (first trimester to post-partum) from 25 healthy women with prior uneventful pregnancies. The total AMH and proAMH levels were measured at each time-point using ELISA. The level of circulating total AMH progressively decreased during pregnancy, in all women (p<0.001). On average, the percentage decline between the first trimester and 36–39 weeks’ gestation was 61.5%, with a standard deviation of 13.0% (range 30.4–81.2%). The percentage decline in total AMH levels associated with maternal age (R = -0.53, p = 0.024), but not with the women’s first trimester AMH level. The postpartum total AMH levels showed no consistent relationship to the woman’s first trimester values (range 31–273%). This raises the possibility that a fundamental determinant of circulating AMH levels is reset during pregnancy. The ratio of proAMH to total AMH levels exhibited little or no variation during pregnancy, indicating that the control of the cleavage/activation of AMH is distinct from the mechanisms that control the total level of AMH.
doi:10.1371/journal.pone.0162509
PMCID: PMC5017784  PMID: 27612037
9.  Abstracts from the 3rd International Genomic Medicine Conference (3rd IGMC 2015) 
Shay, Jerry W. | Homma, Noriko | Zhou, Ruyun | Naseer, Muhammad Imran | Chaudhary, Adeel G. | Al-Qahtani, Mohammed | Hirokawa, Nobutaka | Goudarzi, Maryam | Fornace, Albert J. | Baeesa, Saleh | Hussain, Deema | Bangash, Mohammed | Alghamdi, Fahad | Schulten, Hans-Juergen | Carracedo, Angel | Khan, Ishaq | Qashqari, Hanadi | Madkhali, Nawal | Saka, Mohamad | Saini, Kulvinder S. | Jamal, Awatif | Al-Maghrabi, Jaudah | Abuzenadah, Adel | Chaudhary, Adeel | Al Qahtani, Mohammed | Damanhouri, Ghazi | Alkhatabi, Heba | Goodeve, Anne | Crookes, Laura | Niksic, Nikolas | Beauchamp, Nicholas | Abuzenadah, Adel M. | Vaught, Jim | Budowle, Bruce | Assidi, Mourad | Buhmeida, Abdelbaset | Al-Maghrabi, Jaudah | Buhmeida, Abdelbaset | Assidi, Mourad | Merdad, Leena | Kumar, Sudhir | Miura, Sayaka | Gomez, Karen | Carracedo, Angel | Rasool, Mahmood | Rebai, Ahmed | Karim, Sajjad | Eldin, Hend F. Nour | Abusamra, Heba | Alhathli, Elham M. | Salem, Nada | Al-Qahtani, Mohammed H. | Kumar, Sudhir | Faheem, Hossam | Agarwa, Ashok | Nieschlag, Eberhard | Wistuba, Joachim | Damm, Oliver S. | Beg, Mohd A. | Abdel-Meguid, Taha A. | Mosli, Hisham A. | Bajouh, Osama S. | Abuzenadah, Adel M. | Al-Qahtani, Mohammed H. | Coskun, Serdar | Abu-Elmagd, Muhammad | Buhmeida, Abdelbaset | Dallol, Ashraf | Al-Maghrabi, Jaudah | Hakamy, Sahar | Al-Qahtani, Wejdan | Al-Harbi, Asia | Hussain, Shireen | Assidi, Mourad | Al-Qahtani, Mohammed | Abuzenadah, Adel | Ozkosem, Burak | DuBois, Rick | Messaoudi, Safia S. | Dandana, Maryam T. | Mahjoub, Touhami | Almawi, Wassim Y. | Abdalla, S. | Al-Aama, M. Nabil | Elzawahry, Asmaa | Takahashi, Tsuyoshi | Mimaki, Sachiyo | Furukawa, Eisaku | Nakatsuka, Rie | Kurosaka, Isao | Nishigaki, Takahiko | Nakamura, Hiromi | Serada, Satoshi | Naka, Tetsuji | Hirota, Seiichi | Shibata, Tatsuhiro | Tsuchihara, Katsuya | Nishida, Toshirou | Kato, Mamoru | Mehmood, Sajid | Ashraf, Naeem Mahmood | Asif, Awais | Bilal, Muhammad | Mehmood, Malik Siddique | Hussain, Aadil | Jamal, Qazi Mohammad Sajid | Siddiqui, Mughees Uddin | Alzohairy, Mohammad A. | Al Karaawi, Mohammad A. | Nedjadi, Taoufik | Al-Maghrabi, Jaudah | Assidi, Mourad | Al-Khattabi, Heba | Al-Ammari, Adel | Al-Sayyad, Ahmed | Buhmeida, Abdelbaset | Al-Qahtani, Mohammed | Zitouni, Hédia | Raguema, Nozha | Ali, Marwa Ben | Malah, Wided | Lfalah, Raja | Almawi, Wassim | Mahjoub, Touhami | Elanbari, Mohammed | Ptitsyn, Andrey | Mahjoub, Sana | El Ghali, Rabeb | Achour, Bechir | Amor, Nidhal Ben | Assidi, Mourad | N’siri, Brahim | Morjani, Hamid | Nedjadi, Taoufik | Al-Ammari, Adel | Al-Sayyad, Ahmed | Salem, Nada | Azhar, Esam | Al-Maghrabi, Jaudah | Chayeb, Vera | Dendena, Maryam | Zitouni, Hedia | Zouari-Limayem, Khedija | Mahjoub, Touhami | Refaat, Bassem | Ashshi, Ahmed M. | Batwa, Sarah A. | Ramadan, Hazem | Awad, Amal | Ateya, Ahmed | El-Shemi, Adel Galal Ahmed | Ashshi, Ahmad | Basalamah, Mohammed | Na, Youjin | Yun, Chae-Ok | El-Shemi, Adel Galal Ahmed | Ashshi, Ahmad | Basalamah, Mohammed | Na, Youjin | Yun, Chae-Ok | El-Shemi, Adel Galal | Refaat, Bassem | Kensara, Osama | Abdelfattah, Amr | Dheeb, Batol Imran | Al-Halbosiy, Mohammed M. F. | Al lihabi, Rghad Kadhim | Khashman, Basim Mohammed | Laiche, Djouhri | Adeel, Chaudhary | Taoufik, Nedjadi | Al-Afghani, Hani | Łastowska, Maria | Al-Balool, Haya H. | Sheth, Harsh | Mercer, Emma | Coxhead, Jonathan M. | Redfern, Chris P. F. | Peters, Heiko | Burt, Alastair D. | Santibanez-Koref, Mauro | Bacon, Chris M. | Chesler, Louis | Rust, Alistair G. | Adams, David J. | Williamson, Daniel | Clifford, Steven C. | Jackson, Michael S. | Singh, Mala | Mansuri, Mohmmad Shoab | Jadeja, Shahnawaz D. | Patel, Hima | Marfatia, Yogesh S. | Begum, Rasheedunnisa | Mohamed, Amal M. | Kamel, Alaa K. | Helmy, Nivin A. | Hammad, Sayda A. | Kayed, Hesham F. | Shehab, Marwa I. | El Gerzawy, Assad | Ead, Maha M. | Ead, Ola M. | Mekkawy, Mona | Mazen, Innas | El-Ruby, Mona | Shahid, S. M. A. | Jamal, Qazi Mohammad Sajid | Arif, J. M. | Lohani, Mohtashim | Imen, Moumni | Leila, Chaouch | Houyem, Ouragini | Kais, Douzi | Fethi, Chaouachi Dorra Mellouli | Mohamed, Bejaoui | Salem, Abbes | Faggad, Areeg | Gebreslasie, Amanuel T. | Zaki, Hani Y. | Abdalla, Badreldin E. | AlShammari, Maha S. | Al-Ali, Rhaya | Al-Balawi, Nader | Al-Enazi, Mansour | Al-Muraikhi, Ali | Busaleh, Fadi | Al-Sahwan, Ali | Borgio, Francis | Sayyed, Abdulazeez | Al-Ali, Amein | Acharya, Sadananda | Zaki, Maha S. | El-Bassyouni, Hala T. | Shehab, Marwa I. | Elshal, Mohammed F. | M., Kaleemuddin | Aldahlawi, Alia M. | Saadah, Omar | McCoy, J. Philip | El-Tarras, Adel E. | Awad, Nabil S. | Alharthi, Abdulla A. | Ibrahim, Mohamed M. M. | Alsehli, Haneen S. | Dallol, Ashraf | Gari, Abdullah M. | Abbas, Mohammed M. | Kadam, Roaa A. | Gari, Mazen M. | Alkaff, Mohmmed H. | Abuzenadah, Adel M. | Gari, Mamdooh A. | Abusamra, Heba | Karim, Sajjad | eldin, Hend F. Nour | Alhathli, Elham M. | Salem, Nada | Kumar, Sudhir | Al-Qahtani, Mohammed H. | Moradi, Fatima A. | Rashidi, Omran M. | Awan, Zuhier A. | Kaya, Ibrahim Hamza | Al-Harazi, Olfat | Colak, Dilek | Alkousi, Nabila A. | Athanasopoulos, Takis | Bahmaid, Afnan O. | Alhwait, Etimad A. | Gari, Mamdooh A. | Alsehli, Haneen S. | Abbas, Mohammed M. | Alkaf, Mohammed H. | Kadam, Roaa | Dallol, Ashraf | Kalamegam, Gauthaman | Eldin, Hend F. Nour | Karim, Sajjad | Abusamra, Heba | Alhathli, Elham | Salem, Nada | Al-Qahtani, Mohammed H. | Kumar, Sudhir | Alsayed, Salma N. | Aljohani, Fawziah H. | Habeeb, Samaher M. | Almashali, Rawan A. | Basit, Sulman | Ahmed, Samia M. | Sharma, Rakesh | Agarwal, Ashok | Durairajanayagam, Damayanthi | Samanta, Luna | Abu-Elmagd, Muhammad | Abuzenadah, Adel M. | Sabanegh, Edmund S. | Assidi, Mourad | Al-Qahtani, Mohammed | Agarwal, Ashok | Sharma, Rakesh | Samanta, Luna | Durairajanayagam, Damayanthi | Assidi, Mourad | Abu-Elmagd, Muhammad | Al-Qahtani, Mohammed | Abuzenadah, Adel M. | Sabanegh, Edmund S. | Samanta, Luna | Agarwal, Ashok | Sharma, Rakesh | Cui, Zhihong | Assidi, Mourad | Abuzenadah, Adel M. | Abu-Elmagd, Muhammad | Al-Qahtani, Mohammed | Alboogmi, Alaa A. | Alansari, Nuha A. | Al-Quaiti, Maha M. | Ashgan, Fai T. | Bandah, Afnan | Jamal, Hasan S. | Rozi, Abdullraheem | Mirza, Zeenat | Abuzenadah, Adel M. | Karim, Sajjad | Al-Qahtani, Mohammed H. | Karim, Sajjad | Schulten, Hans-Juergen | Al Sayyad, Ahmad J. | Farsi, Hasan M. A. | Al-Maghrabi, Jaudah A. | Mirza, Zeenat | Alotibi, Reem | Al-Ahmadi, Alaa | Alansari, Nuha A. | Albogmi, Alaa A. | Al-Quaiti, Maha M. | Ashgan, Fai T. | Bandah, Afnan | Al-Qahtani, Mohammed H. | Ebiya, Rasha A. | Darwish, Samia M. | Montaser, Metwally M. | Abusamra, Heba | Bajic, Vladimir B. | Al-Maghrabi, Jaudah | Gomaa, Wafaey | Hanbazazh, Mehenaz | Al-Ahwal, Mahmoud | Al-Harbi, Asia | Al-Qahtani, Wejdan | Hakamy, Saher | Baba, Ghali | Buhmeida, Abdelbaset | Al-Qahtani, Mohammed | Al-Maghrabi, Jaudah | Al-Harbi, Abdullah | Al-Ahwal, Mahmoud | Al-Harbi, Asia | Al-Qahtani, Wejdan | Hakamy, Sahar | Baba, Ghalia | Buhmeida, Abdelbaset | Al-Qahtani, Mohammed | Alhathli, Elham M. | Karim, Sajjad | Salem, Nada | Eldin, Hend Nour | Abusamra, Heba | Kumar, Sudhir | Al-Qahtani, Mohammed H. | Alyamani, Aisha A. | Kalamegam, Gauthaman | Alhwait, Etimad A. | Gari, Mamdooh A. | Abbas, Mohammed M. | Alkaf, Mohammed H. | Alsehli, Haneen S. | Kadam, Roaa A. | Al-Qahtani, Mohammed | Gadi, Rawan | Buhmeida, Abdelbaset | Assidi, Mourad | Chaudhary, Adeel | Merdad, Leena | Alfakeeh, Saadiah M. | Alhwait, Etimad A. | Gari, Mamdooh A. | Abbas, Mohammed M. | Alkaf, Mohammed H. | Alsehli, Haneen S. | Kadam, Roaa | Kalamegam, Gauthaman | Ghazala, Rubi | Mathew, Shilu | Hamed, M. Haroon | Assidi, Mourad | Al-Qahtani, Mohammed | Qadri, Ishtiaq | Mathew, Shilu | Mira, Lobna | Shaabad, Manal | Hussain, Shireen | Assidi, Mourad | Abu-Elmagd, Muhammad | Al-Qahtani, Mohammed | Mathew, Shilu | Shaabad, Manal | Mira, Lobna | Hussain, Shireen | Assidi, Mourad | Abu-Elmagd, Muhammad | Al-Qahtani, Mohammed | Rebai, Ahmed | Assidi, Mourad | Buhmeida, Abdelbaset | Abu-Elmagd, Muhammad | Dallol, Ashraf | Shay, Jerry W. | Almutairi, Mikhlid H. | Ambers, Angie | Churchill, Jennifer | King, Jonathan | Stoljarova, Monika | Gill-King, Harrell | Assidi, Mourad | Abu-Elmagd, Muhammad | Buhmeida, Abdelbaset | Al-Qatani, Muhammad | Budowle, Bruce | Abu-Elmagd, Muhammad | Ahmed, Farid | Dallol, Ashraf | Assidi, Mourad | Almagd, Taha Abo | Hakamy, Sahar | Agarwal, Ashok | Al-Qahtani, Muhammad | Abuzenadah, Adel | Karim, Sajjad | Schulten, Hans-Juergen | Al Sayyad, Ahmad J. | Farsi, Hasan M. A. | Al-Maghrabi, Jaudah A. | Buhmaida, Abdelbaset | Mirza, Zeenat | Alotibi, Reem | Al-Ahmadi, Alaa | Alansari, Nuha A. | Albogmi, Alaa A. | Al-Quaiti, Maha M. | Ashgan, Fai T. | Bandah, Afnan | Al-Qahtani, Mohammed H. | Satar, Rukhsana | Rasool, Mahmood | Ahmad, Waseem | Nazam, Nazia | Lone, Mohamad I. | Naseer, Muhammad I. | Jamal, Mohammad S. | Zaidi, Syed K. | Pushparaj, Peter N. | Jafri, Mohammad A. | Ansari, Shakeel A. | Alqahtani, Mohammed H. | Bashier, Hanan | Al Qahtani, Abrar | Mathew, Shilu | Nour, Amal M. | Alkhatabi, Heba | Zenadah, Adel M. Abu | Buhmeida, Abdelbaset | Assidi, Mourad | Al Qahtani, Muhammed | Faheem, Muhammad | Mathew, Shilu | Mathew, Shiny | Pushparaj, Peter Natesan | Al-Qahtani, Mohammad H. | Alhadrami, Hani A. | Dallol, Ashraf | Abuzenadah, Adel | Hussein, Ibtessam R. | Chaudhary, Adeel G. | Bader, Rima S. | Bassiouni, Randa | Alquaiti, Maha | Ashgan, Fai | Schulten, Hans | Alama, Mohamed Nabil | Al Qahtani, Mohammad H. | Lone, Mohammad I. | Nizam, Nazia | Ahmad, Waseem | Jafri, Mohammad A. | Rasool, Mahmood | Ansari, Shakeel A. | Al-Qahtani, Muhammed H. | Alshihri, Eradah | Abu-Elmagd, Muhammad | Alharbi, Lina | Assidi, Mourad | Al-Qahtani, Mohammed | Mathew, Shilu | Natesan, Peter Pushparaj | Al Qahtani, Muhammed | Kalamegam, Gauthaman | Pushparaj, Peter Natesan | Khan, Fazal | Kadam, Roaa | Ahmed, Farid | Assidi, Mourad | Sait, Khalid Hussain Wali | Anfinan, Nisreen | Al Qahtani, Mohammed | Naseer, Muhammad I. | Chaudhary, Adeel G. | Jamal, Mohammad S. | Mathew, Shilu | Mira, Lobna S. | Pushparaj, Peter N. | Ansari, Shakeel A. | Rasool, Mahmood | AlQahtani, Mohammed H. | Naseer, Muhammad I. | Chaudhary, Adeel G. | Mathew, Shilu | Mira, Lobna S. | Jamal, Mohammad S. | Sogaty, Sameera | Bassiouni, Randa I. | Rasool, Mahmood | AlQahtani, Mohammed H. | Rasool, Mahmood | Ansari, Shakeel A. | Jamal, Mohammad S. | Pushparaj, Peter N. | Sibiani, Abdulrahman M. S. | Ahmad, Waseem | Buhmeida, Abdelbaset | Jafri, Mohammad A. | Warsi, Mohiuddin K. | Naseer, Muhammad I. | Al-Qahtani, Mohammed H. | Rubi | Kumar, Kundan | Naqvi, Ahmad A. T. | Ahmad, Faizan | Hassan, Md I. | Jamal, Mohammad S. | Rasool, Mahmood | AlQahtani, Mohammed H. | Ali, Ashraf | Jarullah, Jummanah | Rasool, Mahmood | Buhmeida, Abdelbasit | Khan, Shahida | Abdussami, Ghufrana | Mahfooz, Maryam | Kamal, Mohammad A. | Damanhouri, Ghazi A. | Jamal, Mohammad S. | Jarullah, Bushra | Jarullah, Jummanah | Jarullah, Mohammad S. S. | Ali, Ashraf | Rasool, Mahmood | Jamal, Mohammad S. | Assidi, Mourad | Abu-Elmagd, Muhammad | Bajouh, Osama | Pushparaj, Peter Natesan | Al-Qahtani, Mohammed | Abuzenadah, Adel | Jamal, Mohammad S. | Jarullah, Jummanah | Mathkoor, Abdulah E. A. | Alsalmi, Hashim M. A. | Oun, Anas M. M. | Damanhauri, Ghazi A. | Rasool, Mahmood | AlQahtani, Mohammed H. | Naseer, Muhammad I. | Rasool, Mahmood | Sogaty, Sameera | Chudhary, Adeel G. | Abutalib, Yousif A. | Merico, Daniele | Walker, Susan | Marshall, Christian R. | Zarrei, Mehdi | Scherer, Stephen W. | Al-Qahtani, Mohammad H. | Naseer, Muhammad I. | Faheem, Muhammad | Chaudhary, Adeel G. | Rasool, Mahmood | Kalamegam, Gauthaman | Ashgan, Fai Talal | Assidi, Mourad | Ahmed, Farid | Zaidi, Syed Kashif | Jan, Mohammed M. | Al-Qahtani, Mohammad H. | Al-Zahrani, Maryam | Lary, Sahira | Hakamy, Sahar | Dallol, Ashraf | Al-Ahwal, Mahmoud | Al-Maghrabi, Jaudah | Dermitzakis, Emmanuel | Abuzenadah, Adel | Buhmeida, Abdelbaset | Al-Qahtani, Mohammed | Al-refai, Abeer A. | Saleh, Mona | Yassien, Rehab I. | Kamel, Mahmmoud | Habeb, Rabab M. | Filimban, Najlaa | Dallol, Ashraf | Ghannam, Nadia | Al-Qahtani, Mohammed | Abuzenadah, Adel Mohammed | Bibi, Fehmida | Akhtar, Sana | Azhar, Esam I. | Yasir, Muhammad | Nasser, Muhammad I. | Jiman-Fatani, Asif A. | Sawan, Ali | Lahzah, Ruaa A. | Ali, Asho | Hassan, Syed A. | Hasnain, Seyed E. | Tayubi, Iftikhar A. | Abujabal, Hamza A. | Magrabi, Alaa O. | Khan, Fazal | Kalamegam, Gauthaman | Pushparaj, Peter Natesan | Abuzenada, Adel | Kumosani, Taha Abduallah | Barbour, Elie | Al-Qahtani, Mohammed | Shabaad, Manal | Mathew, Shilu | Dallol, Ashraf | Merdad, Adnan | Buhmeida, Abdelbaset | Al-Qahtani, Mohammed | Assidi, Mourad | Abu-Elmagd, Muhammad | Gauthaman, Kalamegam | Gari, Mamdooh | Chaudhary, Adeel | Abuzenadah, Adel | Pushparaj, Peter Natesan | Al-Qahtani, Mohammed | Hassan, Syed A. | Tayubi, Iftikhar A. | Aljahdali, Hani M. A. | Al Nono, Reham | Gari, Mamdooh | Alsehli, Haneen | Ahmed, Farid | Abbas, Mohammed | Kalamegam, Gauthaman | Al-Qahtani, Mohammed | Mathew, Shilu | Khan, Fazal | Rasool, Mahmood | Jamal, Mohammed Sarwar | Naseer, Muhammad Imran | Mirza, Zeenat | Karim, Sajjad | Ansari, Shakeel | Assidi, Mourad | Kalamegam, Gauthaman | Gari, Mamdooh | Chaudhary, Adeel | Abuzenadah, Adel | Pushparaj, Peter Natesan | Al-Qahtani, Mohammed | Abu-Elmagd, Muhammad | Kalamegam, Gauthaman | Kadam, Roaa | Alghamdi, Mansour A. | Shamy, Magdy | Costa, Max | Khoder, Mamdouh I. | Assidi, Mourad | Pushparaj, Peter Natesan | Gari, Mamdooh | Al-Qahtani, Mohammed | Kharrat, Najla | Belmabrouk, Sabrine | Abdelhedi, Rania | Benmarzoug, Riadh | Assidi, Mourad | Al Qahtani, Mohammed H. | Rebai, Ahmed | Dhamanhouri, Ghazi | Pushparaj, Peter Natesan | Noorwali, Abdelwahab | Alwasiyah, Mohammad Khalid | Bahamaid, Afnan | Alfakeeh, Saadiah | Alyamani, Aisha | Alsehli, Haneen | Abbas, Mohammed | Gari, Mamdooh | Mobasheri, Ali | Kalamegam, Gauthaman | Al-Qahtani, Mohammed | Faheem, Muhammad | Mathew, Shilu | Pushparaj, Peter Natesan | Al-Qahtani, Mohammad H. | Mathew, Shilu | Faheem, Muhammad | Mathew, Shiny | Pushparaj, Peter Natesan | Al-Qahtani, Mohammad H. | Jamal, Mohammad Sarwar | Zaidi, Syed Kashif | Khan, Raziuddin | Bhatia, Kanchan | Al-Qahtani, Mohammed H. | Ahmad, Saif | AslamTayubi, Iftikhar | Tripathi, Manish | Hassan, Syed Asif | Shrivastava, Rahul | Tayubi, Iftikhar A. | Hassan, Syed | Abujabal, Hamza A. S. | Shah, Ishani | Jarullah, Bushra | Jamal, Mohammad S. | Jarullah, Jummanah | Sheikh, Ishfaq A. | Ahmad, Ejaz | Jamal, Mohammad S. | Rehan, Mohd | Abu-Elmagd, Muhammad | Tayubi, Iftikhar A. | AlBasri, Samera F. | Bajouh, Osama S. | Turki, Rola F. | Abuzenadah, Adel M. | Damanhouri, Ghazi A. | Beg, Mohd A. | Al-Qahtani, Mohammed | Hammoudah, Sahar A. F. | AlHarbi, Khalid M. | El-Attar, Lama M. | Darwish, Ahmed M. Z. | Ibrahim, Sara M. | Dallol, Ashraf | Choudhry, Hani | Abuzenadah, Adel | Awlia, Jalaludden | Chaudhary, Adeel | Ahmed, Farid | Al-Qahtani, Mohammed | Jafri, Mohammad A. | Abu-Elmagd, Muhammad | Assidi, Mourad | Al-Qahtani, Mohammed | khan, Imran | Yasir, Muhammad | Azhar, Esam I. | Al-basri, Sameera | Barbour, Elie | Kumosani, Taha | Khan, Fazal | Kalamegam, Gauthaman | Pushparaj, Peter Natesan | Abuzenada, Adel | Kumosani, Taha Abduallah | Barbour, Elie | EL Sayed, Heba M. | Hafez, Eman A. | Schulten, Hans-Juergen | Elaimi, Aisha Hassan | Hussein, Ibtessam R. | Bassiouni, Randa Ibrahim | Alwasiyah, Mohammad Khalid | Wintle, Richard F. | Chaudhary, Adeel | Scherer, Stephen W. | Al-Qahtani, Mohammed | Mirza, Zeenat | Pillai, Vikram Gopalakrishna | Karim, Sajjad | Sharma, Sujata | Kaur, Punit | Srinivasan, Alagiri | Singh, Tej P. | Al-Qahtani, Mohammed | Alotibi, Reem | Al-Ahmadi, Alaa | Al-Adwani, Fatima | Hussein, Deema | Karim, Sajjad | Al-Sharif, Mona | Jamal, Awatif | Al-Ghamdi, Fahad | Al-Maghrabi, Jaudah | Baeesa, Saleh S. | Bangash, Mohammed | Chaudhary, Adeel | Schulten, Hans-Juergen | Al-Qahtani, Mohammed | Faheem, Muhammad | Pushparaj, Peter Natesan | Mathew, Shilu | Kumosani, Taha Abdullah | Kalamegam, Gauthaman | Al-Qahtani, Mohammed | Al-Allaf, Faisal A. | Abduljaleel, Zainularifeen | Alashwal, Abdullah | Taher, Mohiuddin M. | Bouazzaoui, Abdellatif | Abalkhail, Halah | Ba-Hammam, Faisal A. | Athar, Mohammad | Kalamegam, Gauthaman | Pushparaj, Peter Natesan | Abu-Elmagd, Muhammad | Ahmed, Farid | Sait, Khalid HussainWali | Anfinan, Nisreen | Gari, Mamdooh | Chaudhary, Adeel | Abuzenadah, Adel | Assidi, Mourad | Al-Qahtani, Mohammed | Mami, Naira Ben | Haffani, Yosr Z. | Medhioub, Mouna | Hamzaoui, Lamine | Cherif, Ameur | Azouz, Msadok | Kalamegam, Gauthaman | Khan, Fazal | Mathew, Shilu | Nasser, Mohammed Imran | Rasool, Mahmood | Ahmed, Farid | Pushparaj, Peter Natesan | Al-Qahtani, Mohammed | Turkistany, Shereen A. | Al-harbi, Lina M. | Dallol, Ashraf | Sabir, Jamal | Chaudhary, Adeel | Abuzenadah, Adel | Al-Madoudi, Basmah | Al-Aslani, Bayan | Al-Harbi, Khulud | Al-Jahdali, Rwan | Qudaih, Hanadi | Al Hamzy, Emad | Assidi, Mourad | Al Qahtani, Mohammed | Ilyas, Asad M. | Ahmed, Youssri | Gari, Mamdooh | Ahmed, Farid | Alqahtani, Mohammed | Salem, Nada | Karim, Sajjad | Alhathli, Elham M. | Abusamra, Heba | Eldin, Hend F. Nour | Al-Qahtani, Mohammed H. | Kumar, Sudhir | Al-Adwani, Fatima | Hussein, Deema | Al-Sharif, Mona | Jamal, Awatif | Al-Ghamdi, Fahad | Al-Maghrabi, Jaudah | Baeesa, Saleh S. | Bangash, Mohammed | Chaudhary, Adeel | Al-Qahtani, Mohammed | Schulten, Hans-Juergen | Alamandi, Alaa | Alotibi, Reem | Hussein, Deema | Karim, Sajjad | Al-Maghrabi, Jaudah | Al-Ghamdi, Fahad | Jamal, Awatif | Baeesa, Saleh S. | Bangash, Mohammed | Chaudhary, Adeel | Schulten, Hans-Juergen | Al-Qahtani, Mohammed | Subhi, Ohoud | Bagatian, Nadia | Karim, Sajjad | Al-Johari, Adel | Al-Hamour, Osman Abdel | Al-Aradati, Hosam | Al-Mutawa, Abdulmonem | Al-Mashat, Faisal | Al-Maghrabi, Jaudah | Schulten, Hans-Juergen | Al-Qahtani, Mohammad | Bagatian, Nadia | Subhi, Ohoud | Karim, Sajjad | Al-Johari, Adel | Al-Hamour, Osman Abdel | Al-Mutawa, Abdulmonem | Al-Aradati, Hosam | Al-Mashat, Faisal | Al-Qahtani, Mohammad | Schulten, Hans-Juergen | Al-Maghrabi, Jaudah | shah, Muhammad W. | Yasir, Muhammad | Azhar, Esam I | Al-Masoodi, Saad | Haffani, Yosr Z. | Azouz, Msadok | Khamla, Emna | Jlassi, Chaima | Masmoudi, Ahmed S. | Cherif, Ameur | Belbahri, Lassaad | Al-Khayyat, Shadi | Attas, Roba | Abu-Sanad, Atlal | Abuzinadah, Mohammed | Merdad, Adnan | Dallol, Ashraf | Chaudhary, Adeel | Al-Qahtani, Mohammed | Abuzenadah, Adel | Bouazzi, Habib | Trujillo, Carlos | Alwasiyah, Mohammad Khalid | Al-Qahtani, Mohammed | Alotaibi, Maha | Nassir, Rami | Sheikh, Ishfaq A. | Kamal, Mohammad A. | Jiffri, Essam H. | Ashraf, Ghulam M. | Beg, Mohd A. | Aziz, Mohammad A. | Ali, Rizwan | Rasool, Mahmood | Jamal, Mohammad S. | Samman, Nusaibah | Abdussami, Ghufrana | Periyasamy, Sathish | Warsi, Mohiuddin K. | Aldress, Mohammed | Al Otaibi, Majed | Al Yousef, Zeyad | Boudjelal, Mohamed | Buhmeida, Abdelbasit | Al-Qahtani, Mohammed H. | AlAbdulkarim, Ibrahim | Ghazala, Rubi | Mathew, Shilu | Hamed, M. Haroon | Assidi, Mourad | Al-Qahtani, Mohammed | Qadri, Ishtiaq | Sheikh, Ishfaq A. | Abu-Elmagd, Muhammad | Turki, Rola F. | Damanhouri, Ghazi A. | Beg, Mohd A. | Suhail, Mohd | Qureshi, Abid | Jamal, Adil | Pushparaj, Peter Natesan | Al-Qahtani, Mohammad | Qadri, Ishtiaq | El-Readi, Mahmoud Z. | Eid, Safaa Y. | Wink, Michael | Isa, Ahmed M. | Alnuaim, Lulu | Almutawa, Johara | Abu-Rafae, Basim | Alasiri, Saleh | Binsaleh, Saleh | Nazam, Nazia | Lone, Mohamad I. | Ahmad, Waseem | Ansari, Shakeel A. | Alqahtani, Mohamed H.
BMC Genomics  2016;17(Suppl 6):487.
Table of contents
O1 Regulation of genes by telomere length over long distances
Jerry W. Shay
O2 The microtubule destabilizer KIF2A regulates the postnatal establishment of neuronal circuits in addition to prenatal cell survival, cell migration, and axon elongation, and its loss leading to malformation of cortical development and severe epilepsy
Noriko Homma, Ruyun Zhou, Muhammad Imran Naseer, Adeel G. Chaudhary, Mohammed Al-Qahtani, Nobutaka Hirokawa
O3 Integration of metagenomics and metabolomics in gut microbiome research
Maryam Goudarzi, Albert J. Fornace Jr.
O4 A unique integrated system to discern pathogenesis of central nervous system tumors
Saleh Baeesa, Deema Hussain, Mohammed Bangash, Fahad Alghamdi, Hans-Juergen Schulten, Angel Carracedo, Ishaq Khan, Hanadi Qashqari, Nawal Madkhali, Mohamad Saka, Kulvinder S. Saini, Awatif Jamal, Jaudah Al-Maghrabi, Adel Abuzenadah, Adeel Chaudhary, Mohammed Al Qahtani, Ghazi Damanhouri
O5 RPL27A is a target of miR-595 and deficiency contributes to ribosomal dysgenesis
Heba Alkhatabi
O6 Next generation DNA sequencing panels for haemostatic and platelet disorders and for Fanconi anaemia in routine diagnostic service
Anne Goodeve, Laura Crookes, Nikolas Niksic, Nicholas Beauchamp
O7 Targeted sequencing panels and their utilization in personalized medicine
Adel M. Abuzenadah
O8 International biobanking in the era of precision medicine
Jim Vaught
O9 Biobank and biodata for clinical and forensic applications
Bruce Budowle, Mourad Assidi, Abdelbaset Buhmeida
O10 Tissue microarray technique: a powerful adjunct tool for molecular profiling of solid tumors
Jaudah Al-Maghrabi
O11 The CEGMR biobanking unit: achievements, challenges and future plans
Abdelbaset Buhmeida, Mourad Assidi, Leena Merdad
O12 Phylomedicine of tumors
Sudhir Kumar, Sayaka Miura, Karen Gomez
O13 Clinical implementation of pharmacogenomics for colorectal cancer treatment
Angel Carracedo, Mahmood Rasool
O14 From association to causality: translation of GWAS findings for genomic medicine
Ahmed Rebai
O15 E-GRASP: an interactive database and web application for efficient analysis of disease-associated genetic information
Sajjad Karim, Hend F Nour Eldin, Heba Abusamra, Elham M Alhathli, Nada Salem, Mohammed H Al-Qahtani, Sudhir Kumar
O16 The supercomputer facility “AZIZ” at KAU: utility and future prospects
Hossam Faheem
O17 New research into the causes of male infertility
Ashok Agarwa
O18 The Klinefelter syndrome: recent progress in pathophysiology and management
Eberhard Nieschlag, Joachim Wistuba, Oliver S. Damm, Mohd A. Beg, Taha A. Abdel-Meguid, Hisham A. Mosli, Osama S. Bajouh, Adel M. Abuzenadah, Mohammed H. Al-Qahtani
O19 A new look to reproductive medicine in the era of genomics
Serdar Coskun
P1 Wnt signalling receptors expression in Saudi breast cancer patients
Muhammad Abu-Elmagd, Abdelbaset Buhmeida, Ashraf Dallol, Jaudah Al-Maghrabi, Sahar Hakamy, Wejdan Al-Qahtani, Asia Al-Harbi, Shireen Hussain, Mourad Assidi, Mohammed Al-Qahtani, Adel Abuzenadah
P2 Analysis of oxidative stress interactome during spermatogenesis: a systems biology approach to reproduction
Burak Ozkosem, Rick DuBois
P3 Interleukin-18 gene variants are strongly associated with idiopathic recurrent pregnancy loss.
Safia S Messaoudi, Maryam T Dandana, Touhami Mahjoub, Wassim Y Almawi
P4 Effect of environmental factors on gene-gene and gene-environment reactions: model and theoretical study applied to environmental interventions using genotype
S. Abdalla, M. Nabil Al-Aama
P5 Genomics and transcriptomic analysis of imatinib resistance in gastrointestinal stromal tumor
Asmaa Elzawahry, Tsuyoshi Takahashi, Sachiyo Mimaki, Eisaku Furukawa, Rie Nakatsuka, Isao Kurosaka, Takahiko Nishigaki, Hiromi Nakamura, Satoshi Serada, Tetsuji Naka, Seiichi Hirota, Tatsuhiro Shibata, Katsuya Tsuchihara, Toshirou Nishida, Mamoru Kato
P6 In-Silico analysis of putative HCV epitopes against Pakistani human leukocyte antigen background: an approach towards development of future vaccines for Pakistani population
Sajid Mehmood, Naeem Mahmood Ashraf, Awais Asif, Muhammad Bilal, Malik Siddique Mehmood, Aadil Hussain
P7 Inhibition of AChE and BuChE with the natural compounds of Bacopa monerri for the treatment of Alzheimer’s disease: a bioinformatics approach
Qazi Mohammad Sajid Jamal, Mughees Uddin Siddiqui, Mohammad A. Alzohairy, Mohammad A. Al Karaawi
P8 Her2 expression in urothelial cell carcinoma of the bladder in Saudi Arabia
Taoufik Nedjadi, Jaudah Al-Maghrabi, Mourad Assidi, Heba Al-Khattabi, Adel Al-Ammari, Ahmed Al-Sayyad, Abdelbaset Buhmeida, Mohammed Al-Qahtani
P9 Association of angiotensinogen single nucleotide polymorphisms with Preeclampsia in patients from North Africa
Hédia Zitouni, Nozha Raguema, Marwa Ben Ali, Wided Malah, Raja Lfalah, Wassim Almawi, Touhami Mahjoub
P10 Systems biology analysis reveals relations between normal skin, benign nevi and malignant melanoma
Mohammed Elanbari, Andrey Ptitsyn
P11 The apoptotic effect of thymoquinone in Jurkat cells
Sana Mahjoub, Rabeb El Ghali, Bechir Achour, Nidhal Ben Amor, Mourad Assidi, Brahim N'siri, Hamid Morjani
P12 Sonic hedgehog contributes in bladder cancer invasion in Saudi Arabia
Taoufik Nedjadi, Adel Al-Ammari, Ahmed Al-Sayyad, Nada Salem, Esam Azhar, Jaudah Al-Maghrabi
P13 Association of Interleukin 18 gene promoter polymorphisms - 607A/C and -137 G/C with colorectal cancer onset in a sample of Tunisian population
Vera Chayeb, Maryam Dendena, Hedia Zitouni, Khedija Zouari-Limayem, Touhami Mahjoub
P14 Pathological expression of interleukin-6, -11, leukemia inhibitory factor and their receptors in tubal gestation with and without tubal cytomegalovirus infection
Bassem Refaat, Ahmed M Ashshi, Sarah A Batwa
P15 Phenotypic and genetic profiling of avian pathogenic and human diarrhegenic Escherichia coli in Egypt
Hazem Ramadan, Amal Awad, Ahmed Ateya
P16 Cancer-targeting dual gene virotherapy as a promising therapeutic strategy for treatment of hepatocellular carcinoma
Adel Galal Ahmed El-Shemi, Ahmad Ashshi, Mohammed Basalamah, Youjin Na, Chae-Ok YUN
P17 Cancer dual gene therapy with oncolytic adenoviruses expressing TRAIL and IL-12 transgenes markedly eradicated human hepatocellular carcinoma both in vitro and in vivo
Adel Galal Ahmed El-Shemi, Ahmad Ashshi, Mohammed Basalamah, Youjin Na, Chae-Ok Yun
P18 Therapy with paricalcitol attenuates tumor growth and augments tumoricidal and anti-oncogenic effects of 5-fluorouracil on animal model of colon cancer
Adel Galal El-Shemi, Bassem Refaat, Osama Kensara, Amr Abdelfattah
P19 The effects of Rubus idaeus extract on normal human lymphocytes and cancer cell line
Batol Imran Dheeb, Mohammed M. F. Al-Halbosiy, Rghad Kadhim Al lihabi, Basim Mohammed Khashman
P20 Etanercept, a TNF-alpha inhibitor, alleviates mechanical hypersensitivity and spontaneous pain in a rat model of chemotherapy-induced neuropathic pain
Djouhri, Laiche, Chaudhary Adeel, Nedjadi, Taoufik
P21 Sleeping beauty mutagenesis system identified genes and neuronal transcription factor network involved in pediatric solid tumour (medulloblastoma)
Hani Al-Afghani, Maria Łastowska, Haya H Al-Balool, Harsh Sheth, Emma Mercer, Jonathan M Coxhead, Chris PF Redfern, Heiko Peters, Alastair D Burt, Mauro Santibanez-Koref, Chris M Bacon, Louis Chesler, Alistair G Rust, David J Adams, Daniel Williamson, Steven C Clifford, Michael S Jackson
P22 Involvement of interleukin-1 in vitiligo pathogenesis
Mala Singh, Mohmmad Shoab Mansuri, Shahnawaz D. Jadeja, Hima Patel, Yogesh S. Marfatia, Rasheedunnisa Begum
P23 Cytogenetics abnormalities in 12,884 referred population for chromosomal analysis and the role of FISH in refining the diagnosis (cytogenetic experience 2004-2013)
Amal M Mohamed, Alaa K Kamel, Nivin A Helmy, Sayda A Hammad, Hesham F Kayed, Marwa I Shehab, Assad El Gerzawy, Maha M. Ead, Ola M Ead, Mona Mekkawy, Innas Mazen, Mona El-Ruby
P24 Analysis of binding properties of angiotensin-converting enzyme 2 through in silico method
S. M. A. Shahid, Qazi Mohammad Sajid Jamal, J. M. Arif, Mohtashim Lohani
P25 Relationship of genetics markers cis and trans to the β-S globin gene with fetal hemoglobin expression in Tunisian sickle cell patients
Moumni Imen, Chaouch Leila, Ouragini Houyem, Douzi Kais, Chaouachi Dorra Mellouli Fethi, Bejaoui Mohamed, Abbes Salem
P26 Analysis of estrogen receptor alpha gene polymorphisms in breast cancer: link to genetic predisposition in Sudanese women
Areeg Faggad, Amanuel T Gebreslasie, Hani Y Zaki, Badreldin E Abdalla
P27 KCNQI gene polymorphism and its association with CVD and T2DM in the Saudi population
Maha S AlShammari, Rhaya Al-Ali, Nader Al-Balawi , Mansour Al-Enazi, Ali Al-Muraikhi, Fadi Busaleh, Ali Al-Sahwan, Francis Borgio, Abdulazeez Sayyed, Amein Al-Ali, Sadananda Acharya
P28 Clinical, neuroimaging and cytogenetic study of a patient with microcephaly capillary malformation syndrome
Maha S. Zaki, Hala T. El-Bassyouni, Marwa I. Shehab
P29 Altered expression of CD200R1 on dendritic cells of patients with inflammatory bowel diseases: in silico investigations and clinical evaluations
Mohammed F. Elshal, Kaleemuddin M., Alia M. Aldahlawi, Omar Saadah,
J. Philip McCoy
P30 Development of real time PCR diagnostic protocol specific for the Saudi Arabian H1N1 viral strains
Adel E El-Tarras, Nabil S Awad, Abdulla A Alharthi, Mohamed M M Ibrahim
P31 Identification of novel genetic variations affecting Osteoarthritis patients
Haneen S Alsehli, Ashraf Dallol, Abdullah M Gari, Mohammed M Abbas, Roaa A Kadam, Mazen M. Gari, Mohmmed H Alkaff, Adel M Abuzenadah, Mamdooh A Gari
P32 An integrated database of GWAS SNVs and their evolutionary properties
Heba Abusamra, Sajjad Karim, Hend F Nour eldin, Elham M Alhathli, Nada Salem, Sudhir Kumar, Mohammed H Al-Qahtani
P33 Familial hypercholesterolemia in Saudi Arabia: prime time for a national registry and genetic analysis
Fatima A. Moradi, Omran M. Rashidi, Zuhier A. Awan
P34 Comparative genomics and network-based analyses of early hepatocellular carcinoma
Ibrahim Hamza Kaya, Olfat Al-Harazi, Dilek Colak
P35 A TALEN-based oncolytic viral vector approach to knock out ABCB1 gene mediated chemoresistance in cancer stem cells
Nabila A Alkousi, Takis Athanasopoulos
P36 Cartilage differentiation and gene expression of synovial fluid mesenchymal stem cells derived from osteoarthritis patients
Afnan O Bahmaid, Etimad A Alhwait, Mamdooh A Gari, Haneen S Alsehli, Mohammed M Abbas, Mohammed H Alkaf, Roaa Kadam, Ashraf Dallol, Gauthaman Kalamegam
P37 E-GRASP: Adding an evolutionary component to the genome-wide repository of associations (GRASP) resource
Hend F Nour Eldin, Sajjad Karim, Heba Abusamra, Elham Alhathli, Nada Salem, Mohammed H Al-Qahtani, Sudhir Kumar
P38 Screening of AGL gene mutation in Saudi family with glycogen storage disease Type III
Salma N Alsayed, Fawziah H Aljohani, Samaher M Habeeb, Rawan A Almashali, Sulman Basit, Samia M Ahmed
P39 High throughput proteomic data suggest modulation of cAMP dependent protein kinase A and mitochondrial function in infertile patients with varicocele
Rakesh Sharma, Ashok Agarwal, Damayanthi Durairajanayagam, Luna Samanta, Muhammad Abu-Elmagd, Adel M. Abuzenadah, Edmund S. Sabanegh, Mourad Assidi, Mohammed Al-Qahtani
P40 Significant protein profile alterations in men with primary and secondary infertility
Ashok Agarwal, Rakesh Sharma, Luna Samanta, Damayanthi Durairajanayagam, Mourad Assidi, Muhammad Abu-Elmagd, Mohammed Al-Qahtani, Adel M. Abuzenadah, Edmund S. Sabanegh
P41 Spermatozoa maturation in infertile patients involves compromised expression of heat shock proteins
Luna Samanta, Ashok Agarwal, Rakesh Sharma, Zhihong Cui, Mourad Assidi, Adel M. Abuzenadah, Muhammad Abu-Elmagd, Mohammed Al-Qahtani
P42 Array comparative genomic hybridization approach to search genomic answers for spontaneous recurrent abortion in Saudi Arabia
Alaa A Alboogmi, Nuha A Alansari, Maha M Al-Quaiti, Fai T Ashgan, Afnan Bandah, Hasan S Jamal, Abdullraheem Rozi, Zeenat Mirza, Adel M Abuzenadah, Sajjad Karim, Mohammed H Al-Qahtani
P43 Global gene expression profiling of Saudi kidney cancer patients
Sajjad Karim, Hans-Juergen Schulten, Ahmad J Al Sayyad, Hasan MA Farsi, Jaudah A Al-Maghrabi, Zeenat Mirza, Reem Alotibi, Alaa Al-Ahmadi, Nuha A Alansari, Alaa A Albogmi, Maha M Al-Quaiti, Fai T Ashgan, Afnan Bandah, Mohammed H Al-Qahtani
P44 Downregulated StAR gene and male reproductive dysfunction caused by nifedipine and ethosuximide
Rasha A Ebiya, Samia M Darwish, Metwally M. Montaser
P45 Clustering based gene expression feature selection method: A computational approach to enrich the classifier efficiency of differentially expressed genes
Heba Abusamra, Vladimir B. Bajic
P46 Prognostic significance of Osteopontin expression profile in colorectal carcinoma
Jaudah Al-Maghrabi, Wafaey Gomaa, Mehenaz Hanbazazh, Mahmoud Al-Ahwal, Asia Al-Harbi, Wejdan Al-Qahtani, Saher Hakamy, Ghali Baba, Abdelbaset Buhmeida, Mohammed Al-Qahtani
P47 High Glypican-3 expression pattern predicts longer disease-specific survival in colorectal carcinoma
Jaudah Al-Maghrabi, Abdullah Al-Harbi, Mahmoud Al-Ahwal, Asia Al-Harbi, Wejdan Al-Qahtani, Sahar Hakamy, Ghalia Baba, Abdelbaset Buhmeida, Mohammed Al-Qahtani
P48 An evolutionary re-assessment of GWAS single nucleotide variants implicated in the Cholesterol traits
Elham M Alhathli, Sajjad Karim, Nada Salem, Hend Nour Eldin, Heba Abusamra, Sudhir Kumar, Mohammed H Al-Qahtani
P49 Derivation and characterization of human Wharton’s jelly stem cells (hWJSCs) in vitro for future therapeutic applications
Aisha A Alyamani, Gauthaman Kalamegam, Etimad A Alhwait, Mamdooh A Gari, Mohammed M Abbas, Mohammed H Alkaf, Haneen S Alsehli, Roaa A Kadam, Mohammed Al-Qahtani
P50 Attitudes of healthcare students toward biomedical research in the post-genomic era
Rawan Gadi, Abdelbaset Buhmeida, Mourad Assidi , Adeel Chaudhary, Leena Merdad
P51 Evaluation of the immunomodulatory effects of thymoquinone on human bone marrow mesenchymal stem cells (BM-MSCs) from osteoarthritic patients
Saadiah M Alfakeeh, Etimad A Alhwait, Mamdooh A Gari, Mohammed M Abbas, Mohammed H Alkaf, Haneen S Alsehli, Roaa Kadam, Gauthaman Kalamegam
P52 Implication of IL-10 and IL-28 polymorphism with successful anti-HCV therapy and viral clearance
Rubi Ghazala, Shilu Mathew, M.Haroon Hamed, Mourad Assidi, Mohammed Al-Qahtani, Ishtiaq Qadri
P53 Selection of flavonoids against obesity protein (FTO) using in silico and in vitro approaches
Shilu Mathew, Lobna Mira, Manal Shaabad, Shireen Hussain, Mourad Assidi, Muhammad Abu-Elmagd, Mohammed Al-Qahtani
P54 Computational selection and in vitro validation of flavonoids as new antidepressant agents
Shilu Mathew, Manal Shaabad, Lobna Mira, Shireen Hussain, Mourad Assidi, Muhammad Abu-Elmagd, Mohammed Al-Qahtani
P55 In Silico prediction and prioritization of aging candidate genes associated with
progressive telomere shortening
Ahmed Rebai, Mourad Assidi, Abdelbaset Buhmeida, Muhammad Abu-Elmagd, Ashraf Dallol, Jerry W Shay
P56 Identification of new cancer testis antigen genes in diverse types of malignant human tumour cells
Mikhlid H Almutairi
P57 More comprehensive forensic genetic marker analyses for accurate human remains identification using massively parallel sequencing (MPS)
Angie Ambers, Jennifer Churchill, Jonathan King, Monika Stoljarova, Harrell Gill-King, Mourad Assidi, Muhammad Abu-Elmagd, Abdelbaset Buhmeida, Muhammad Al-Qatani, Bruce Budowle
P58 Flow cytometry approach towards treatment men infertility in Saudi Arabia
Muhammad Abu-Elmagd, Farid Ahmed, Ashraf Dallol, Mourad Assidi, Taha Abo Almagd, Sahar Hakamy, Ashok Agarwal, Muhammad Al-Qahtani, Adel Abuzenadah
P59 Tissue microarray based validation of CyclinD1 expression in renal cell carcinoma of Saudi kidney patients
Sajjad Karim, Hans-Juergen Schulten, Ahmad J Al Sayyad, Hasan MA Farsi, Jaudah A Al-Maghrabi, Abdelbaset Buhmaida, Zeenat Mirza, Reem Alotibi, Alaa Al-Ahmadi, Nuha A Alansari, Alaa A Albogmi, Maha M Al-Quaiti, Fai T Ashgan, Afnan Bandah, Mohammed H Al-Qahtani
P60 Assessment of gold nanoparticles in molecular diagnostics and DNA damage studies
Rukhsana Satar, Mahmood Rasool, Waseem Ahmad, Nazia Nazam, Mohamad I Lone, Muhammad I Naseer, Mohammad S Jamal, Syed K Zaidi, Peter N Pushparaj, Mohammad A Jafri, Shakeel A Ansari, Mohammed H Alqahtani
P61 Surfing the biospecimen management and processing workflow at CEGMR Biobank
Hanan Bashier, Abrar Al Qahtani, Shilu Mathew, Amal M. Nour, Heba Alkhatabi, Adel M. Abu Zenadah, Abdelbaset Buhmeida, Mourad Assidi, Muhammed Al Qahtani
P62 Autism Spectrum Disorder: knowledge, attitude and awareness in Jeddah, Kingdom of Saudi Arabia
Muhammad Faheem, Shilu Mathew, Shiny Mathew, Peter Natesan Pushparaj, Mohammad H. Al-Qahtani
P63 Simultaneous genetic screening of the coagulation pathway genes using the Thromboscan targeted sequencing panel
Hani A. Alhadrami, Ashraf Dallol, Adel Abuzenadah
P64 Genome wide array comparative genomic hybridization analysis in patients with syndromic congenital heart defects
Ibtessam R. Hussein, Adeel G. Chaudhary, Rima S Bader, Randa Bassiouni, Maha Alquaiti, Fai Ashgan, Hans Schulten, Mohamed Nabil Alama, Mohammad H. Al Qahtani
P65 Toxocogenetic evaluation of 1, 2-Dichloroethane in bone marrow, blood and cells of immune system using conventional, molecular and flowcytometric approaches
Mohammad I Lone, Nazia Nizam, Waseem Ahmad, Mohammad A Jafri, Mahmood Rasool, Shakeel A Ansari, Muhammed H Al-Qahtani
P66 Molecular cytogenetic diagnosis of sexual development disorders in newborn: A case of ambiguous genitalia
Eradah Alshihri, Muhammad Abu-Elmagd, Lina Alharbi, Mourad Assidi, Mohammed Al-Qahtani
P67 Identification of disease specific gene expression clusters and pathways in hepatocellular carcinoma using In Silico methodologies
Shilu Mathew, Peter Pushparaj Natesan, Muhammed Al Qahtani
P68 Human Wharton’s Jelly stem cell conditioned medium inhibits primary ovarian cancer cells in vitro: Identification of probable targets and mechanisms using systems biology
Gauthaman Kalamegam, Peter Natesan Pushparaj, Fazal Khan, Roaa Kadam, Farid Ahmed, Mourad Assidi, Khalid Hussain Wali Sait, Nisreen Anfinan, Mohammed Al Qahtani
P69 Mutation spectrum of ASPM (Abnormal Spindle-like, Microcephaly-associated) gene in Saudi Arabian population
Muhammad I Naseer, Adeel G Chaudhary, Mohammad S Jamal, Shilu Mathew, Lobna S Mira, Peter N Pushparaj, Shakeel A Ansari, Mahmood Rasool, Mohammed H AlQahtani
P70 Identification and characterization of novel genes and mutations of primary microcephaly in Saudi Arabian population
Muhammad I Naseer, Adeel G Chaudhary, Shilu Mathew, Lobna S Mira, Mohammad S Jamal, Sameera Sogaty, Randa I Bassiouni, Mahmood Rasool, Mohammed H AlQahtani
P71 Molecular genetic analysis of hereditary nonpolyposis colorectal cancer (Lynch Syndrome) in Saudi Arabian population
Mahmood Rasool, Shakeel A Ansari, Mohammad S Jamal, Peter N Pushparaj, Abdulrahman MS Sibiani, Waseem Ahmad, Abdelbaset Buhmeida, Mohammad A Jafri, Mohiuddin K Warsi, Muhammad I Naseer, Mohammed H Al-Qahtani
P72 Function predication of hypothetical proteins from genome database of chlamydia trachomatis
Rubi, Kundan Kumar, Ahmad AT Naqvi, Faizan Ahmad, Md I Hassan, Mohammad S Jamal, Mahmood Rasool, Mohammed H AlQahtani
P73 Transcription factors as novel molecular targets for skin cancer
Ashraf Ali, Jummanah Jarullah, Mahmood Rasool, Abdelbasit Buhmeida, Shahida Khan, Ghufrana Abdussami, Maryam Mahfooz, Mohammad A Kamal, Ghazi A Damanhouri, Mohammad S Jamal
P74 An In Silico analysis of Plumbagin binding to apoptosis executioner: Caspase-3 and Caspase-7
Bushra Jarullah, Jummanah Jarullah, Mohammad SS Jarullah, Ashraf Ali, Mahmood Rasool, Mohammad S Jamal
P75 Single cell genomics applications for preimplantation genetic screening optimization: Comparative analysis of whole genome amplification technologies
Mourad Assidi, Muhammad Abu-Elmagd, Osama Bajouh, Peter Natesan Pushparaj, Mohammed Al-Qahtani, Adel Abuzenadah
P76 ZFP36 regulates miRs-34a in anti-IgM triggered immature B cells
Mohammad S Jamal, Jummanah Jarullah, Abdulah EA Mathkoor, Hashim MA Alsalmi, Anas MM Oun, Ghazi A Damanhauri, Mahmood Rasool, Mohammed H AlQahtani
P77 Identification of a novel mutation in the STAMBP gene in a family with microcephaly-capillary malformation syndrome
Muhammad I. Naseer, Mahmood Rasool, Sameera Sogaty, Adeel G. Chudhary, Yousif A. Abutalib, Daniele Merico, Susan Walker, Christian R. Marshall, Mehdi Zarrei, Stephen W. Scherer, Mohammad H. Al-Qahtani
P78 Copy number variations in Saudi patients with intellectual disability and epilepsy
Muhammad I. Naseer, Muhammad Faheem, Adeel G. Chaudhary, Mahmood Rasool, Gauthaman Kalamegam, Fai Talal Ashgan, Mourad Assidi, Farid Ahmed, Syed Kashif Zaidi, Mohammed M. Jan, Mohammad H. Al-Qahtani
P79 Prognostic significance of CD44 expression profile in colorectal carcinoma
Maryam Al-Zahrani, Sahira Lary, Sahar Hakamy, Ashraf Dallol, Mahmoud Al-Ahwal, Jaudah Al-Maghrabi, Emmanuel Dermitzakis, Adel Abuzenadah, Abdelbaset Buhmeida, Mohammed Al-Qahtani
P80 Association of the endothelial nitric oxide synthase (eNOS) gene G894T polymorphism with hypertension risk and complications
Abeer A Al-refai, Mona Saleh, Rehab I Yassien, Mahmmoud Kamel, Rabab M Habeb
P81 SNPs array to screen genetic variation among diabetic patients
Najlaa Filimban, Ashraf Dallol, Nadia Ghannam, Mohammed Al-Qahtani, Adel Mohammed Abuzenadah
P82 Detection and genotyping of Helicobacter pylori among gastric cancer patients from Saudi Arabian population
Fehmida Bibi, Sana Akhtar, Esam I. Azhar, Muhammad Yasir, Muhammad I. Nasser, Asif A. Jiman-Fatani, Ali Sawan
P83 Antimicrobial drug resistance and molecular detection of susceptibility to Fluoroquinolones among clinical isolates of Salmonella species from Jeddah-Saudi Arabia
Ruaa A Lahzah, Asho Ali
P84 Identification of the toxic and virulence nature of MAP1138c protein of Mycobacterium avium subsp. paratuberculosis
Syed A Hassan, Seyed E Hasnain, Iftikhar A Tayubi, Hamza A Abujabal, Alaa O Magrabi
P85 In vitro and in silico evaluation of miR137 in human breast cancer
Fazal Khan, Gauthaman Kalamegam, Peter Natesan Pushparaj, Adel Abuzenada, Taha Abduallah Kumosani, Elie Barbour, Mohammed Al-Qahtani
P86 Auruka gene is over-expressed in Saudi breast cancer
Manal Shabaad, Shilu Mathew, Ashraf Dallol, Adnan Merdad, Abdelbaset Buhmeida, Mohammed Al-Qahtani
P87 The potential of immunogenomics in personalized healthcare
Mourad Assidi, Muhammad Abu-Elmagd, Kalamegam Gauthaman, Mamdooh Gari, Adeel Chaudhary, Adel Abuzenadah, Peter Natesan Pushparaj, Mohammed Al-Qahtani
P88 In Silico physiochemical and structural characterization of a putative ORF MAP0591 and its implication in the pathogenesis of Mycobacterium paratuberculosis in ruminants and humans
Syed A Hassan, Iftikhar A Tayubi, Hani MA Aljahdali
P89 Effects of heat shock on human bone marrow mesenchymal stem cells (BM-MSCs): Implications in regenerative medicine
Reham Al Nono, Mamdooh Gari, Haneen Alsehli, Farid Ahmed, Mohammed Abbas, Gauthaman Kalamegam, Mohammed Al-Qahtani
P90 In Silico analyses of the molecular targets of Resveratrol unravels its importance in mast cell mediated allergic responses
Shilu Mathew, Fazal Khan, Mahmood Rasool, Mohammed Sarwar Jamal, Muhammad Imran Naseer, Zeenat Mirza, Sajjad Karim, Shakeel Ansari, Mourad Assidi, Gauthaman Kalamegam, Mamdooh Gari, Adeel Chaudhary, Adel Abuzenadah, Peter Natesan Pushparaj, Mohammed Al-Qahtani
P91 Effects of environmental particulate matter on bone-marrow mesenchymal stem cells
Muhammad Abu-Elmagd, Gauthaman Kalamegam, Roaa Kadam, Mansour A Alghamdi, Magdy Shamy, Max Costa, Mamdouh I Khoder, Mourad Assidi, Peter Natesan Pushparaj, Mamdooh Gari, Mohammed Al-Qahtani
P92 Distinctive charge clusters in human virus proteomes
Najla Kharrat, Sabrine Belmabrouk, Rania Abdelhedi, Riadh Benmarzoug, Mourad Assidi, Mohammed H. Al Qahtani, Ahmed Rebai
P93 In vitro experimental model and approach in identification of new biomarkers of inflammatory forms of arthritis
Ghazi Dhamanhouri, Peter Natesan Pushparaj, Abdelwahab Noorwali, Mohammad Khalid Alwasiyah, Afnan Bahamaid, Saadiah Alfakeeh, Aisha Alyamani, Haneen Alsehli, Mohammed Abbas, Mamdooh Gari, Ali Mobasheri, Gauthaman Kalamegam, Mohammed Al-Qahtani
P94 Molecular docking of GABAA receptor subunit γ-2 with novel anti-epileptic compounds
Muhammad Faheem, Shilu Mathew, Peter Natesan Pushparaj, Mohammad H. Al-Qahtani
P95 Breast cancer knowledge, awareness, and practices among Saudi females residing in Jeddah
Shilu Mathew, Muhammad Faheem, Shiny Mathew, Peter Natesan Pushparaj, Mohammad H. Al-Qahtani
P96 Anti-inflammatory role of Sesamin by Attenuation of Iba1/TNF-α/ICAM-1/iNOS signaling in Diabetic Retinopathy
Mohammad Sarwar Jamal, Syed Kashif Zaidi, Raziuddin Khan, Kanchan Bhatia, Mohammed H. Al-Qahtani, Saif Ahmad
P97 Identification of drug lead molecule against vp35 protein of Ebola virus: An In-Silico approach
Iftikhar AslamTayubi, Manish Tripathi, Syed Asif Hassan, Rahul Shrivastava
P98 An approach to personalized medicine from SNP-calling through disease analysis using whole exome-sequencing of three sub-continental populations
Iftikhar A Tayubi, Syed Hassan, Hamza A.S Abujabal
P99 Low versus high frequency of Glucose –6 – Phosphate Dehydrogenase (G6PD) deficiency in urban against tribal population of Gujarat – A signal to natural selection
Ishani Shah, Bushra Jarullah, Mohammad S Jamal, Jummanah Jarullah
P100 Spontaneous preterm birth and single nucleotide gene polymorphisms: a recent update
Ishfaq A Sheikh, Ejaz Ahmad, Mohammad S Jamal, Mohd Rehan, Muhammad Abu-Elmagd, Iftikhar A Tayubi, Samera F AlBasri, Osama S Bajouh, Rola F Turki, Adel M Abuzenadah, Ghazi A Damanhouri, Mohd A Beg, Mohammed Al-Qahtani
P101 Prevalence of congenital heart diseases among Down syndrome cases in Saudi Arabia: role of molecular genetics in the pathogenesis
Sahar AF Hammoudah, Khalid M AlHarbi, Lama M El-Attar, Ahmed MZ Darwish
P102 Combinatorial efficacy of specific pathway inhibitors in breast cancer cells
Sara M Ibrahim, Ashraf Dallol, Hani Choudhry, Adel Abuzenadah, Jalaludden Awlia, Adeel Chaudhary, Farid Ahmed, Mohammed Al-Qahtani
P103 MiR-143 and miR-145 cluster as potential replacement medicine for the treatment of cancer
Mohammad A Jafri, Muhammad Abu-Elmagd, Mourad Assidi, Mohammed Al-Qahtani
P104 Metagenomic profile of gut microbiota during pregnancy in Saudi population
Imran khan, Muhammad Yasir, Esam I. Azhar, Sameera Al-basri, Elie Barbour, Taha Kumosani
P105 Exploration of anticancer targets of selected metabolites of Phoenix dactylifera L. using systems biological approaches
Fazal Khan, Gauthaman Kalamegam, Peter Natesan Pushparaj, Adel Abuzenada, Taha Abduallah Kumosani, Elie Barbour
P106 CD226 and CD40 gene polymorphism in susceptibility to Juvenile rheumatoid arthritis in Egyptian patients
Heba M. EL Sayed, Eman A. Hafez
P107 Paediatric exome sequencing in autism spectrum disorder ascertained in Saudi families
Hans-Juergen Schulten, Aisha Hassan Elaimi, Ibtessam R Hussein, Randa Ibrahim Bassiouni, Mohammad Khalid Alwasiyah, Richard F Wintle, Adeel Chaudhary, Stephen W Scherer, Mohammed Al-Qahtani
P108 Crystal structure of the complex formed between Phospholipase A2 and the central core hydrophobic fragment of Alzheimer’s β- amyloid peptide: a reductionist approach
Zeenat Mirza, Vikram Gopalakrishna Pillai, Sajjad Karim, Sujata Sharma, Punit Kaur, Alagiri Srinivasan, Tej P Singh, Mohammed Al-Qahtani
P109 Differential expression profiling between meningiomas from female and male patients
Reem Alotibi, Alaa Al-Ahmadi, Fatima Al-Adwani, Deema Hussein, Sajjad Karim, Mona Al-Sharif, Awatif Jamal, Fahad Al-Ghamdi, Jaudah Al-Maghrabi, Saleh S Baeesa, Mohammed Bangash, Adeel Chaudhary, Hans-Juergen Schulten, Mohammed Al-Qahtani
P110 Neurospheres as models of early brain development and therapeutics
Muhammad Faheem, Peter Natesan Pushparaj, Shilu Mathew, Taha Abdullah Kumosani, Gauthaman Kalamegam, Mohammed Al-Qahtani
P111 Identification of a recurrent causative missense mutation p.(W577C) at the LDLR exon 12 in familial hypercholesterolemia affected Saudi families
Faisal A Al-Allaf, Zainularifeen Abduljaleel, Abdullah Alashwal, Mohiuddin M. Taher, Abdellatif Bouazzaoui, Halah Abalkhail, Faisal A. Ba-Hammam, Mohammad Athar
P112 Epithelial ovarian carcinoma (EOC): Systems oncological approach to identify diagnostic, prognostic and therapeutic biomarkers
Gauthaman Kalamegam, Peter Natesan Pushparaj, Muhammad Abu-Elmagd, Farid Ahmed Khalid HussainWali Sait, Nisreen Anfinan, Mamdooh Gari, Adeel Chaudhary, Adel Abuzenadah, Mourad Assidi, Mohammed Al-Qahtani
P113 Crohn’s disease phenotype in northern Tunisian population
Naira Ben Mami, Yosr Z Haffani, Mouna Medhioub, Lamine Hamzaoui, Ameur Cherif, Msadok Azouz
P114 Establishment of In Silico approaches to decipher the potential toxicity and mechanism of action of drug candidates and environmental agents
Gauthaman Kalamegam, Fazal Khan, Shilu Mathew, Mohammed Imran Nasser, Mahmood Rasool, Farid Ahmed, Peter Natesan Pushparaj, Mohammed Al-Qahtani
P115 1q Gain predicts poor prognosis marker for young breast cancer patients
Shereen A Turkistany, Lina M Al-harbi, Ashraf Dallol, Jamal Sabir, Adeel Chaudhary, Adel Abuzenadah
P116 Disorders of sex chromosomes in a diagnostic genomic medicine unit in Saudi Arabia: Prevalence, diagnosis and future guidelines
Basmah Al-Madoudi, Bayan Al-Aslani, Khulud Al-Harbi, Rwan Al-Jahdali, Hanadi Qudaih, Emad Al Hamzy, Mourad Assidi, Mohammed Al Qahtani
P117 Combination of WYE354 and Sunitinib demonstrate synergistic inhibition of acute myeloid leukemia in vitro
Asad M Ilyas, Youssri Ahmed, Mamdooh Gari, Farid Ahmed, Mohammed Alqahtani
P118 Integrated use of evolutionary information in GWAS reveals important SNPs in Asthma
Nada Salem, Sajjad Karim, Elham M Alhathli, Heba Abusamra, Hend F Nour Eldin, Mohammed H Al-Qahtani, Sudhir Kumar
P119 Assessment of BRAF, IDH1, IDH2, and EGFR mutations in a series of primary brain tumors
Fatima Al-Adwani, Deema Hussein, Mona Al-Sharif, Awatif Jamal, Fahad Al-Ghamdi, Jaudah Al-Maghrabi, Saleh S Baeesa, Mohammed Bangash, Adeel Chaudhary, Mohammed Al-Qahtani, Hans-Juergen Schulten
P120 Expression profiles distinguish oligodendrogliomas from glioblastoma multiformes with or without oligodendroglioma component
Alaa Alamandi, Reem Alotibi, Deema Hussein, Sajjad Karim, Jaudah Al-Maghrabi, Fahad Al-Ghamdi, Awatif Jamal, Saleh S Baeesa, Mohammed Bangash, Adeel Chaudhary, Hans-Juergen Schulten, Mohammed Al-Qahtani
P121 Hierarchical clustering in thyroid goiters and hyperplastic lesions
Ohoud Subhi, Nadia Bagatian, Sajjad Karim, Adel Al-Johari, Osman Abdel Al-Hamour, Hosam Al-Aradati, Abdulmonem Al-Mutawa, Faisal Al-Mashat, Jaudah Al-Maghrabi, Hans-Juergen Schulten, Mohammad Al-Qahtani
P122 Differential expression analysis in thyroiditis and papillary thyroid carcinomas with or without coexisting thyroiditis
Nadia Bagatian, Ohoud Subhi, Sajjad Karim, Adel Al-Johari, Osman Abdel Al-Hamour, Abdulmonem Al-Mutawa, Hosam Al-Aradati, Faisal Al-Mashat, Mohammad Al-Qahtani, Hans-Juergen Schulten, Jaudah Al-Maghrabi
P123 Metagenomic analysis of waste water microbiome in Sausdi Arabia
Muhammad W shah, Muhammad Yasir, Esam I Azhar, Saad Al-Masoodi
P124 Molecular characterization of Helicobacter pylori from faecal samples of Tunisian patients with gastric cancer
Yosr Z Haffani, Msadok Azouz, Emna Khamla, Chaima Jlassi, Ahmed S. Masmoudi, Ameur Cherif, Lassaad Belbahri
P125 Diagnostic application of the oncoscan© panel for the identification of hereditary cancer syndrome
Shadi Al-Khayyat, Roba Attas, Atlal Abu-Sanad, Mohammed Abuzinadah, Adnan MerdadAshraf Dallol, Adeel Chaudhary, Mohammed Al-Qahtani, Adel Abuzenadah
P126 Characterization of clinical and neurocognitive features in a family with a novel OGT gene missense mutation c. 1193G > A/ (p. Ala319Thr)
Habib Bouazzi, Carlos Trujillo, Mohammad Khalid Alwasiyah, Mohammed Al-Qahtani
P127 Case report: a rare homozygous deletion mutation of TMEM70 gene associated with 3-Methylglutaconic Aciduria and cataract in a Saudi patient
Maha Alotaibi, Rami Nassir
P128 Isolation and purification of antimicrobial milk proteins
Ishfaq A Sheikh, Mohammad A Kamal, Essam H Jiffri, Ghulam M Ashraf, Mohd A Beg
P129 Integrated analysis reveals association of ATP8B1 gene with colorectal cancer
Mohammad A Aziz, Rizwan Ali, Mahmood Rasool, Mohammad S Jamal, Nusaibah samman, Ghufrana Abdussami, Sathish Periyasamy, Mohiuddin K Warsi, Mohammed Aldress, Majed Al Otaibi, Zeyad Al Yousef, Mohamed Boudjelal, Abdelbasit Buhmeida, Mohammed H Al-Qahtani, Ibrahim AlAbdulkarim
P130 Implication of IL-10 and IL-28 polymorphism with successful anti-HCV therapy and viral clearance
Rubi Ghazala, Shilu Mathew, M. Haroon Hamed, Mourad Assidi, Mohammed Al-Qahtani, Ishtiaq Qadri
P131 Interactions of endocrine disruptor di-(2-ethylhexyl) phthalate (DEHP) and its metabolite mono-2-ethylhexyl phthalate (MEHP) with progesterone receptor
Ishfaq A Sheikh, Muhammad Abu-Elmagd, Rola F Turki, Ghazi A Damanhouri, Mohd A. Beg
P132 Association of HCV nucleotide polymorphism in the development of hepatocellular carcinoma
Mohd Suhail, Abid Qureshi, Adil Jamal, Peter Natesan Pushparaj, Mohammad Al-Qahtani, Ishtiaq Qadri
P133 Gene expression profiling by DNA microarrays in colon cancer treated with chelidonine alkaloid
Mahmoud Z El-Readi, Safaa Y Eid, Michael Wink
P134 Successful in vitro fertilization after eight failed trials
Ahmed M. Isa, Lulu Alnuaim, Johara Almutawa, Basim Abu-Rafae, Saleh Alasiri, Saleh Binsaleh
P135 Genetic sensitivity analysis using SCGE, cell cycle and mitochondrial membrane potential in OPs stressed leukocytes in Rattus norvegicus through flow cytometric input
Nazia Nazam, Mohamad I Lone, Waseem Ahmad, Shakeel A Ansari, Mohamed H Alqahtani
doi:10.1186/s12864-016-2858-0
PMCID: PMC4959372  PMID: 27454254
10.  Urinary gonadotropin fragment (UGF) measurements in the diagnosis and management of ovarian cancer. 
UGF is a small peptide present in the urines and tissues of patients with gynecologic cancers. Published research (which, at present, mainly comes from our laboratory) on the general application of UGF as a tumor marker, and on its use in the diagnosis of ovarian cancer, is reviewed, and new studies on its use, alone and with CA125, in the management of patients with ovarian cancer, are presented. In 234 healthy women, 89 with benign disease, and 79 with ovarian cancer, UGF levels were above 3 fmol/ml (low cut-off) in 12 percent, 7 percent, and 82 percent, respectively, and above 8 fmol/ml (high cut-off) in 1.7 percent, less than 1.1 percent, and 59 percent, respectively. Similarly, 11 percent, 14 percent, and 70 percent, respectively, had CA125 levels above 35 U/ml (low cut-off), and less than 1.9 percent, 1.2 percent, and 49 percent had levels above a 200 U/ml (high cut-off). Ideally, the higher UGF and CA125 cut-offs should be used for diagnostic applications, like differentiation of a benign from a malignant pelvic mass (false-positive rate: UGF, less than 1.1 percent; CA125, 1.2 percent), but raising the cut-offs diminishes sensitivities for malignancy (UGF, 59 percent; CA125, 49 percent). The populations detected by the two markers only partially overlap, however, so that, together, UGF or CA125 can identify 75 percent of malignant pelvic masses. Levels of UGF (cut-off, greater than 3 fmol/ml) and CA125 (35 U/ml) were also monitored in 30 women undergoing therapy for ovarian cancer. Clinical observations were reflected at each clinic visit by UGF alone in 67 percent, by CA125 alone in 57 percent, and by UGF and CA125 together in 87 percent of cases. While separately UGF and CA125 levels predicted 71 percent and 57 percent, together they forecast 86 percent of recurrent cancers prior to clinical manifestations. UGF and CA125 should be used together in the detection and management of ovarian cancers.
PMCID: PMC2589077  PMID: 2596125
11.  Gestational Age-specific Cut-off Values Are Needed for Diagnosis of Subclinical Hypothyroidism in Early Pregnancy 
Journal of Korean Medical Science  2015;30(9):1308-1312.
During the first trimester of pregnancy, thyroid-stimulating hormone (TSH) >2.5 mIU/L has been suggested as the universal criterion for subclinical hypothyroidism. However, TSH levels change continuously during pregnancy, even in the first trimester. Therefore the use of a fixed cut-off value for TSH may result in a different diagnosis rate of subclinical hypothyroidism according to gestational age. The objective of this study was to obtain the normal reference range of TSH during the first trimester in Korean gravida and to determine the diagnosis rate of subclinical hypothyroidism using the fixed cut-off value (TSH >2.5 mIU/L). The study population consisted of pregnant women who were measured for TSH during the first trimester of pregnancy (n=492) and nonpregnant women (n=984). Median concentration of TSH in pregnant women was lower than in non-pregnant women. There was a continuous decrease of median TSH concentration during the first trimester of pregnancy (median TSH concentration: 1.82 mIU/L for 3+0 to 6+6 weeks; 1.53 mIU/L for 7+0 to 7+6 weeks; and 1.05 mIU/L for 8+0 to 13+6 weeks). Using the fixed cut-off value of TSH >2.5 mIU/L, the diagnosis rate of subclinical hypothyroidism decreased significantly according to the gestational age (GA) at TSH (25% in 3+0 to 6+6 weeks, 13% in 7+0 to 7+6 weeks, and 9% for 8+0 to 13+6 weeks, P<0.001), whereas the diagnosis rate was 5% in all GA with the use of a GA-specific cut-off value (P=0.995). Therefore, GA-specific criteria might be more appropriate for the diagnosis of subclinical hypothyroidism.
doi:10.3346/jkms.2015.30.9.1308
PMCID: PMC4553679  PMID: 26339172
Hypothyroidism; Pregnancy Trimester, First; Thyrotropin; Reference Values
12.  Prediction of Postchemotherapy Ovarian Function Using Markers of Ovarian Reserve 
The Oncologist  2013;19(1):68-74.
Chemotherapy results in transient or permanent ovarian failure in the majority of women. Prechemotherapy assessment of serum anti-Müllerian hormone may be useful for predicting postchemotherapy ovarian function. This finding has implications for decision making about adjuvant endocrine therapy in premenopausal women treated with chemotherapy.
Learning Objectives
Explain the association between clinical factors and postchemotherapy ovarian function.Explain the association between biochemical markers and postchemotherapy ovarian function.Discuss the role that age and anti-Müllerian hormone may play in prediction of postchemotherapy ovarian function status.
Background.
Reproductive-aged women frequently receive both chemotherapy and endocrine therapy as part of their treatment regimen for early stage hormone receptor-positive breast cancer. Chemotherapy results in transient or permanent ovarian failure in the majority of women. The difficulty in determining which patients will recover ovarian function has implications for adjuvant endocrine therapy decision making. We hypothesized that pretreatment serum anti-Müllerian hormone (AMH) and inhibin B concentrations would predict for ovarian function following chemotherapy.
Methods.
Pre- and perimenopausal women aged 25–50 years with newly diagnosed breast cancer were enrolled. Subjects underwent phlebotomy for assessment of serum AMH, inhibin B, follicle-stimulating hormone, and estradiol prior to chemotherapy and 1 month and 1 year following completion of treatment. Associations among hormone concentrations, clinical factors, and biochemically assessed ovarian function were assessed.
Results.
Twenty-seven subjects were evaluable for the primary endpoint. Median age was 41. Twenty subjects (74.1%) experienced recovery of ovarian function within 18 months. Of the 26 evaluable subjects assessed prior to chemotherapy, 19 (73.1%) had detectable serum concentrations of AMH. The positive predictive value of a detectable baseline serum AMH concentration for recovery of ovarian function was 94.7%, and the negative predictive value was 85.7%. On univariate analysis, younger age and detectable serum AMH concentration at chemotherapy initiation were predictive of increased likelihood of recovery of ovarian function.
Conclusion.
Prechemotherapy assessment of serum AMH may be useful for predicting postchemotherapy ovarian function. This finding has implications for decision making about adjuvant endocrine therapy in premenopausal women treated with chemotherapy.
doi:10.1634/theoncologist.2013-0145
PMCID: PMC3903057  PMID: 24319018
Breast cancer; Chemotherapy; Ovarian function; Anti-Müllerian hormone
13.  Serum anti-Müllerian hormone and antral follicle count as predictive markers of OHSS in ART cycles 
Objective
To evaluate predictive role of day–3 serum anti-Müllerian hormone (AMH) levels and antral follicle count (AFC) in ovarian hyperstimulation syndrome (OHSS) in patients undergoing IVF/ICSI cycles.
Materials and methods
Forty-one women with moderate/severe OHSS and 41 age matched women without OHSS were compared to evaluate the predictive value of certain risk factors for OHSS. AFC, and E2, FSH, LH, AMH, inhibin-B levels measured on day 3 of the menstrual cycle before controlled ovarian hyperstimulation.
Results
Mean FSH was significantly lower (p < 0.0001); and mean LH, AFC and AMH were significantly higher in women with OHSS compared to women without OHSS (p = 0.049, p < 0.0001 and p < 0.0001, respectively). There was no significant difference in inhibin B (p = 0.112) and estradiol (p = 0.706) between the groups. The ROC area under curve (AUC) for AMH presented the largest AUC among the listed risk factors. AMH (AUC = 0.87) and AFC (AUC = 0.74) had moderate accuracy for predicting OHSS while Inhibin B (AUC = 0.58) and LH (AUC = 0.61) had low accuracy. The cut-off value for AMH 3.3 ng/mL provided the highest sensitivity (90%) and specificity (71%) for predicting OHSS. It’s positive (PPV) and negative predictive values (NPV) were 61% and 94%, respectively. The cut-off value for AFC was 8 with 78% sensitivity, 65% specificity, 52% PPV and 86% NPV.
Conclusion
Measurement of basal serum AMH and AFC can be used to determine the women with high risk for OHSS.
doi:10.1007/s10815-011-9627-4
PMCID: PMC3241835  PMID: 21882017
Antimullerian hormone; Ovarian hyperstimulation syndrome; Antral follicle count
14.  Novel Family of Gynecologic Cancer Antigens Detected by Anti-HIV Antibody 
Objective: The reactivity of gynecologic cancer proteins with monoclonal antibody (MAb) directed against the human immunodeficiency virus I (HIV-I) was tested.
Methods: Cytoplasmic and nuclear proteins, extracted from a broad range of gynecologic cancers obtained during standard surgical procedures, were tested in Western blotting with MAb 5023 developed against the amino acid sequences 308–322 of the envelope protein gp120 of HIV-I.
Results: Three cell membrane proteins, Mrl20,000 (p120), Mr41,000 (p41), and Mr24,000 (p24), and one chromatin protein, Mr24,000 (p24), were detected by MAb 5023 in invasive, poorly differentiated cervical squamous-cell carcinoma; ovarian serous cystadenocarcinoma; poorly and well-differentiated endometrial carcinoma; vulvar squamous-cell carcinoma; and malignant mixed müllerian tumor. The same antigens were identified in cervical carcinoma cell line SiHa. Neither p120 nor p24 was recognized by other MAbs directed against the variable loop of gp120. Antigens p120 and p41 were undetectable in normal ovarian tissue and in biopsy samples of normal vaginal and rectal mucosa. Rectosigmoid cancer as well as colon carcinoma, lung carcinoma, and melanoma cell lines all tested negative.
Conclusions: The identified antigens may represent either the products of human genes (proto-onc-ogenes) or, more likely, the products of an unknown virus specifically expressed in female cancer.
doi:10.1155/S1064744994000608
PMCID: PMC2364385  PMID: 18475387
15.  Functional Maintenance of Differentiated Embryoid Bodies in Microfluidic Systems: A Platform for Personalized Medicine 
The utility and advantage of a microfluidic chip culture system to enhance the development of personalized, on-demand, treatment modules using embryoid bodies (EBs) is demonstrated. Under microfluidic conditions, differentiated steroidogenic EBs continued to secrete estradiol and progesterone at physiologically relevant concentrations. These results present a platform for the development of a new therapeutic system for personalized medicine.
Hormone replacement therapies have become important for treating diseases such as premature ovarian failure or menopausal complications. The clinical use of bioidentical hormones might significantly reduce some of the potential risks reportedly associated with the use of synthetic hormones. In the present study, we demonstrate the utility and advantage of a microfluidic chip culture system to enhance the development of personalized, on-demand, treatment modules using embryoid bodies (EBs). Functional EBs cultured on microfluidic chips represent a platform for personalized, patient-specific treatment cassettes that can be cryopreserved until required for treatment. We assessed the viability, differentiation, and functionality of EBs cultured and cryopreserved in this system. During extended microfluidic culture, estradiol, progesterone, testosterone, and anti-müllerian hormone levels were measured, and the expression of differentiated steroidogenic cells was confirmed by immunocytochemistry assay for the ovarian tissue markers anti-müllerian hormone receptor type II, follicle-stimulating hormone receptor, and inhibin β-A and the estrogen biosynthesis enzyme aromatase. Our studies showed that under microfluidic conditions, differentiated steroidogenic EBs continued to secrete estradiol and progesterone at physiologically relevant concentrations (30–120 pg/ml and 150–450 pg/ml, respectively) for up to 21 days. Collectively, we have demonstrated for the first time the feasibility of using a microfluidic chip system with continuous flow for the differentiation and extended culture of functional steroidogenic stem cell-derived EBs, the differentiation of EBs into cells expressing ovarian antigens in a microfluidic system, and the ability to cryopreserve this system with restoration of growth and functionality on thawing. These results present a platform for the development of a new therapeutic system for personalized medicine.
doi:10.5966/sctm.2014-0119
PMCID: PMC4339847  PMID: 25666845
Stem cells; Cryopreservation; Microenvironment; Microphysiological systems; Hormone secretion; Reproductive medicine
16.  A Pilot Study of Predictive Markers of Chemotherapy-Related Amenorrhea Among Premenopausal Women with Early Stage Breast Cancer 
Cancer investigation  2008;26(3):286-295.
Background
Premenopausal women treated for early stage breast cancer (ESBC) are at risk for chemotherapy-related amenorrhea (CRA). Prospectively-validated, predictive markers of CRA are needed.
Patients and Methods
Premenopausal women with ESBC and planned chemotherapy (≥ 25% risk of amenorrhea) were evaluated. Follicle stimulating hormone (FSH), estradiol, Inhibin A and B, anti-Müllerian hormone (AMH), and quality of life (QOL) were prospectively evaluated pre-, post-, 6 months and 1 year post-chemotherapy and correlated with age and menstrual status. CRA was defined as absence of menses 1 year post-chemotherapy.
Results
Forty-four women were evaluated at the time of analysis. Median age at diagnosis and FSH 1 year post-chemotherapy were higher among women with CRA (44 yrs [33–51] vs. 40 yrs [31–43]; p = 0.03; 39.8 vs. 5.0 mLU/mL, p = 0.0058, respectively). Median estradiol 1 year post-chemotherapy was higher among women who resumed menses (108.3 vs. 41.3 pg/mL, p = 0.01). Pre-chemotherapy median Inhibin B and AMH were lower among women with CRA (33.2 vs. 108.8 pg/mL; p = 0.03; 0.16 vs. 1.09 ng/mL, p = 0.02, respectively). The risk of CRA was increased among women with lower pre-chemotherapy Inhibin B (RR = 1.67, p = 0.15) and AMH (RR = 1.83, p = 0.05). Amongst women whose pre-chemotherapy Inhibin B and AMH values were below the median, the incidence of CRA was 87.5%.
Conclusions
Results indicate that pre-chemotherapy Inhibin B and AMH are lower among women experiencing CRA and may be predictive of CRA among premenopausal women facing chemotherapy for ESBC.
doi:10.1080/07357900701829777
PMCID: PMC2883164  PMID: 18317970
Amenorrhea; Breast cancer; Chemotherapy; Premenopausal; Quality of life
17.  Anti-Mullerian-hormone levels during pregnancy and postpartum 
Background
The number of unintentionally childless couples is increasing as more couples seek to conceive for the first time in the third or fourth decade of the woman’s life. Determination of ovarian reserve is an essential component of infertility assessment. The Anti-Müllerian-Hormone (AMH) seems to be the most reliable predictor of ovarian reserve. In this study we analyzed AMH in a cohort of pregnant women without fertility impairment to determine age-dependent decline and possible AMH fluctuations during pregnancy and postpartum.
Methods
A total of 554 healthy women aged 16 to 47 years without history of infertility or previous surgery on the ovaries were enrolled in the study between 1995 and 2012. In 450 women, a single measurement of AMH was taken during pregnancy, allowing for cross sectional analysis of trimester- and age-related differences in AMH levels. For another 15 women longitudinal data on AMH levels for all trimesters was recorded. In addition, for 69 women AMH was measured at the time just before and after delivery, and for another 20 AMH was measured just before delivery and once on each of the first four days after delivery. We used AMH-Gen-II ELISA (Beckman Coulter, Immunotech, Webster, USA) for the assessment of AMH levels. Non-parametric statistical tests were used to compare AMH levels between age groups, trimesters and postpartum.
Results
Comparison between the trimesters revealed a significant difference in AMH values at each trimester (first trimester: 1.69 ng/ml (IQR 0.71–3.10), second trimester: 0.8 ng/ml (IQR 0.48–1.41), third trimester: 0.5 ng/ml (IQR 0.18–1.00)). AMH significantly dropped during the course of pregnancy and immediately after delivery, whereas an increase was observed over the first four days postpartum. Women, greater than or equal to 35 years, showed significant lower AMH levels than those <35 years across all trimesters.
Conclusions
AMH levels decrease during pregnancy. The decline in AMH levels during pregnancy indicates ovarian suppression. AMH levels recover quickly after delivery. AMH levels assessed in pregnant women are not an accurate indicator of ovarian reserve, since AMH levels during pregnancy seem not to be independent of gestational age.
doi:10.1186/1477-7827-11-60
PMCID: PMC3724719  PMID: 23844593
Anti-mullerian hormone; Pregnancy; Postpartum; Ovarian suppression; Ovarian reserve
18.  Mechanism and preclinical prevention of increased breast cancer risk caused by pregnancy 
eLife  2013;2:e00996.
While a first pregnancy before age 22 lowers breast cancer risk, a pregnancy after age 35 significantly increases life-long breast cancer risk. Pregnancy causes several changes to the normal breast that raise barriers to transformation, but how pregnancy can also increase cancer risk remains unclear. We show in mice that pregnancy has different effects on the few early lesions that have already developed in the otherwise normal breast—it causes apoptosis evasion and accelerated progression to cancer. The apoptosis evasion is due to the normally tightly controlled STAT5 signaling going astray—these precancerous cells activate STAT5 in response to pregnancy/lactation hormones and maintain STAT5 activation even during involution, thus preventing the apoptosis normally initiated by oncoprotein and involution. Short-term anti-STAT5 treatment of lactation-completed mice bearing early lesions eliminates the increased risk after a pregnancy. This chemoprevention strategy has important implications for preventing increased human breast cancer risk caused by pregnancy.
DOI: http://dx.doi.org/10.7554/eLife.00996.001
eLife digest
Pregnancy changes the probability that a woman will later develop breast cancer. If a woman’s first pregnancy occurs before her 22nd birthday, the chances of developing breast cancer are reduced. However, if the first pregnancy occurs after her 35th birthday, there is an increased risk of breast cancer. It is not clear why this age-related difference exists, but as more women wait until their 30s to start a family, there is greater urgency to understand this difference.
Breasts undergo extensive changes during pregnancy. This remodeling makes their cells less likely to multiply, and also less likely to develop tumors, which could explain the protective effect of pregnancy for younger women. But why would older women not reap the same benefits? One hypothesis is that older first-time mothers are more likely than younger first-time mothers to already have breast tissue with cells carrying cancer-causing mutations, or to have clusters of abnormal precancerous cells.
Now, Haricharan et al. have tested this hypothesis by inserting two cancer-causing genes into female mice. Half of the mice were then made pregnant and allowed to nurse their young, whilst the other half were never mated. Although, both groups of mice later developed tumors, the mice that had been pregnant developed more tumors and did so faster.
The increased cancer levels in the mice that had been pregnant were not due to them having more precancerous cells at the early stages of pregnancy than the unmated mice of the same age. Further, the precancerous cells in the impregnated mice did not proliferate faster than those in the mice that were never pregnant. Instead, pregnancy weakened the protective process that culls pre-existing precancerous cells. These cells evaded destruction by activating a signaling pathway called the STAT5 pathway in response to pregnancy hormones.
Haricharan et al. also examined tissue samples from women with a very early form of breast cancer and found elevated levels of STAT5 in tumors from women who had been pregnant compared to those who had not been pregnant.
The good news is that precancerous cells do not always become cancerous. However, for those women with a high risk of developing breast cancer, Haricharan et al. suggest that temporarily reducing STAT5 activity after pregnancy with medication might reduce this risk. Treating mice with anti-STAT5 drugs for a few weeks after they finished nursing their young lessened the elevated cancer risk, and so the next challenge is to see if this approach will also be effective in human clinical trials.
DOI: http://dx.doi.org/10.7554/eLife.00996.002
doi:10.7554/eLife.00996
PMCID: PMC3874103  PMID: 24381245
STAT5; pregnancy; breast cancer; chemoprevention; Human; Mouse
19.  GATA-3 EXPRESSION IN TROPHOBLASTIC TISSUES: An Immunohistochemical Study of 445 Cases, Including Diagnostic Utility 
Immunohistochemical expression of GATA-3 is seen predominantly in non-neoplastic bladder and breast epithelium and their respective carcinomas; however, data on expression in normal and lesional trophoblastic tissues are limited. Immunohistochemical staining for GATA-3 was assessed in a range of normal/lesional trophoblastic tissues and tumors in the differential diagnosis (n=445), including non-molar products of conceptions/2nd and 3rd trimester placentas/ ectopic pregnancies, hydatidiform moles, placental site nodules, normal/exaggerated implantation sites, choriocarcinomas, epithelioid trophoblastic tumors, placental site trophoblastic tumors, atypical smooth muscle tumors (including leiomyosarcoma), and cervical and pulmonary squamous cell carcinomas. The extent of expression (0 to 4+) and intensity (weak to strong) were recorded. All cases with developing trophoblast/non-neoplastic trophoblastic proliferations and 81% of trophoblastic neoplasms were positive. Of all non-neoplastic trophoblast cell types, expression was observed in cytotrophoblast in 89% of cases, syncytiotrophoblast in 50%, intermediate trophoblast in 100%, and villous trophoblastic columns in 100%. Increasing gestational age was associated with a decrease in extent/intensity of expression in non-neoplastic cytotrophoblast and syncytiotrophoblast while intermediate trophoblast maintained diffuse and strong expression from early to late gestation (p<0.0001). Eighty-nine percent of normal/exaggerated implantation sites showed 3+ or 4+ expression while staining in 55% of placental site nodules was 1+ or 2+. Staining for GATA-3 was present in 78% of choriocarcinomas, 95% of epithelioid trophoblastic tumors, and 71% of placental site trophoblastic tumors. While the number of choriocarcinomas and placental site trophoblastic tumors that showed a spectrum of expression ranging from negative to diffuse was relatively evenly distributed, 81% of epithelioid trophoblastic tumors had 3+ or 4+ staining. None of the atypical smooth muscle tumors and 3% of squamous cell carcinomas were positive, all of which exhibited weak staining. We conclude that GATA-3 is frequently expressed in normal and lesional trophoblastic tissues. It is also differentially expressed in intermediate trophoblast and cytotrophoblast/syncytiotrophoblast, which varies according to time during pregnancy. This study expands the spectrum of neoplasms known to express GATA-3. Thus, recognition of expression in trophoblastic tumors is important because it can present a diagnostic pitfall in the assessment of suspected metastatic bladder or breast carcinomas involving the gynecologic tract. In the evaluation of diagnostically problematic tumors for which trophoblastic neoplasms are in the differential diagnosis, such as leiomyosarcoma and squamous cell carcinoma, GATA-3 can be included as part of an immunohistochemical panel particularly when other trophoblastic markers are either not available or yield ambiguous results.
doi:10.1097/PAS.0000000000000315
PMCID: PMC4268033  PMID: 25188865
GATA-3; trophoblast; choriocarcinoma; leiomyosarcoma; squamous cell carcinoma
20.  Neutrophil elastase in amniotic fluid as a predictor of preterm birth after emergent cervical cerclage 
Abstract
Introduction
The aim of this study was to investigate neutrophil elastase (NE) in amniotic fluid as a potential marker for predicting pregnancy continuation.
Material and methods
We enrolled 34 pregnant women with bulging fetal membrane during the second trimester who underwent emergent cerclage after confirming the absence of intrauterine infection (amniotic fluid glucose ≥15 mg/dL). Amniotic fluid NE levels were compared between women who completed and did not complete 30, 34, and 36 weeks of gestation, and the optimal cut‐off value for predicting pregnancy continuation was estimated. Moreover, the differences in the duration of continued pregnancy were compared between women with NE levels above and below the optimal cut‐off value.
Results
The optimal cut‐off value for NE in amniotic fluid that predicted pregnancy continuation beyond 30, 34, and 36 weeks of gestation was 180 ng/mL; this cut‐off value had a sensitivity, specificity, positive predictive value, and negative predictive value of 84.0, 77.8, 91.3, and 63.7% beyond 30 weeks of gestation; 87.5, 80.0, 91.5, and 72.3% beyond 34 weeks of gestation; and 85.0, 71.4, 80.9, and 76.9% beyond 36 weeks of gestation, respectively. The duration of continued pregnancy from emergent cerclage to delivery was significantly longer in women with amniotic fluid NE <180 ng/mL (95.1 ± 5.4 days) than in women with amniotic fluid NE ≥180 ng/mL (44.8 ± 14.3 days).
Conclusion
The NE levels in amniotic fluid may serve as a useful marker for predicting the duration of continued pregnancy after cervical cerclage.
doi:10.1111/aogs.12928
PMCID: PMC5094512  PMID: 27216361
Amniotic fluid; cervical cerclage; glucose; neutrophil elastase; pregnancy; premature birth
21.  Anti-Müllerian Hormone and Inhibin B Variability during Normal Menstrual Cycles 
Fertility and sterility  2009;94(4):1482-1486.
Objective
Describe anti-Müllerian hormone (AMH) variation across normal menstrual cycles.
Design
Cohort study
Setting
Academic environment
Patients
Twenty regularly-menstruating women
Interventions
Serum AMH and inhibin B assayed daily during one normal menstrual cycle
Main Outcome Measures
Intracycle variability of AMH and inhibin B
Results
Data was classified into quartiles of AMH area-under-the-curve (AUCs). Mean AMH AUC was 15.7 ng/ml for Quartile 1 vs. 43.5, 80.9 and 144.9 ng/ml for Quartiles 2, 3 and 4. Mean AMH levels (ng/ml) were 0.67, 1.71, 3.02, and 5.33, respectively. There was no variation in Quartile 1 AMH rate of change from stochastic modeling, but in Quartiles 2–4, there were increased rates of change in days 2–7. Women in Quartile 1 had the lowest mean inhibin B (24.2 pg/ml vs. 44.3, 43.2, and 42.2 pg/ml) and had shorter menstrual cycles (24.6 days) than women in Quartiles 3 and 4 (28.2 and 28.4 days).
Conclusions
There were two menstrual cycle patterns of AMH. The “aging ovary” pattern included low AMH levels with little variation, lower inhibin B and shorter cycle lengths. The “younger ovary” pattern included higher AMH levels with significant variation days 2–7, suggesting that for women with AMH >1 ng/ml, the interpretation of AMH levels is contingent upon the day of the menstrual cycle on which specimen is obtained.
doi:10.1016/j.fertnstert.2009.07.1674
PMCID: PMC2891288  PMID: 19969291
AMH; menstrual cycle variability; ovarian aging; reproductive aging; ovarian reserve
22.  Comparing Seminal Plasma Biomarkers between Normospermic and Azoospermic Men 
Introduction
Azoospermia affects more than 10% - 15% of infertile male subjects attending infertilty clinics. At present, testicular biopsy is the golden standard procedure for evaluating spermatogenesis status in men with azoospermia. Semen collection and analysis is a non-invasive method and has proven to be valuable in the evaluation of spermatogenesis. Identification of seminal plasma markers with testicular or extra-testicular origins have a great value in predicting the prescence of sperm in testicular tissue and presumptive cause of azoospermia. The aim of this study was to find such markers by comparing the content of seminal plasma using different methods in normospermic and azoospermic men.
Materials and Methods
Semen samples were collected from 200 men attending Avicenna Infertility Clinic (AIC) in Tehran, Iran. Semen samples were analysed according to WHO guidlines. The subjects were divided into two groups: normospermic (n = 100; group one) and azoospermic men (n = 100; group two) according to semen analysis results. Seminal plasma was separated by high speed centrifuagation and stored in -20° C. Four markers including fructose, neutral alpha glucosidase (NαG), inhibin B and anti-Müllerian hormone (AMH) were measured in seminal plasma. Fructose and NαG were evaluated by spectrophotometry, while inhibin B and AMH were assessed by ELISA method. The spermatogenesis status in the azoospermic group was evaluated by histopathological method following testicular biopsy.
Results
Fructose concentration showed no difference between the two groups. However, it was significantly correlated with sperm count (p < 0.01, r = -0.408). Seminal plasma inhibin B (OR: 1.01; 95%: CI: 1.005 - 1.016), AMH (OR: 1.63; 95% CI: 1.17 - 2.28) and NαG, (OR: 1.07; 95% CI: 1.04 - 1.1) levels were higher in normospermic subjects compared to azoospermic men. There were significant differences in inhibin B and AMH concentrations between the two groups based on the presence or absence of mature sperm in testicular biopsies (p < 0.01). Inhibin B concentration was positively correlated with sperm count in the normospermic group, however, NαG concentration correlated with sperm count of normospermic men (p < 0.01, r = 0.345) and the subjects' age in both groups.
Conclusion
Inhibin B and AMH were correlated with the presence of sperm in testicular tissue samples. According to non-specific changes in inhibin B and AMH concentrations, identification of more specific molecular markers in seminal plasma to definitely evaluate the status of spermatogenesis is recommended.
PMCID: PMC3719273  PMID: 23926479
Anti-Mullerian Hormone; Azoospermia; Fructose; Inhibin B; Male infertility; Neutral alpha glucosidase; Seminal plasma; Spermatogenesis
23.  Anti-Müllerian Hormone and Inhibin-A, but not Inhibin-B or Insulin-Like Peptide-3, may be Used as Surrogates in the Diagnosis of Polycystic Ovary Syndrome in Adolescents: Preliminary Results 
Objective:
Polycystic ovary syndrome (PCOS) is a common endocrine problem in adolescents with an increasing prevalence of 30%. Pursuing new biomarkers with high specificity and sensitivity in the diagnosis of PCOS in adolescents is currently an active area of research. We aimed to investigate the diagnostic value of anti-Müllerian hormone (AMH), insulin-like peptide-3 (INSL3), inhibin-A (INH-A), and inhibin-B (INH-B) in adolescents with PCOS and also to determine the association, if any, between these hormones and clinical/laboratory findings related with hyperandrogenism.
Methods:
The study group comprised 53 adolescent girls aged between 14.5 and 20 years who were admitted to our outpatient clinic with symptoms of hirsutism and/or irregular menses and diagnosed as having PCOS in accordance with the Rotterdam criteria. Twenty-six healthy peers, eumenorrheic for at least two years and body mass index-matched, constituted the controls. Fasting blood samples for hormones [luteinizing hormone (LH), follicle-stimulating hormone (FSH), dehydroepiandrosterone-sulfate (DHEAS), androstenedione (D4-A), total/free testosterone (T/fT), sex hormone binding globulin (SHBG), AMH, INSL3, INH-A, INH-B] were drawn after an overnight fast.
Results:
In the PCOS group, 83% of the subjects were oligomenorrheic/amenorrheic and 87% had hirsutism. The LH, LH/FSH ratio, total T, fT, free androgen-index (FAI), DHEAS levels were significantly higher (p=0.005, p=0.042, p=0.047, p<0.001, p=0.007, p=0.014, respectively) and SHBG was significantly lower (p=0.004) in PCOS patients as compared to the controls. Although the INSL-3 and INH-B levels showed no difference between the groups (p>0.05), AMH and INH-A levels were found to be significantly higher in the PCOS group compared to the controls (p<0.001, p<0.001, respectively). In multiple linear regression analysis, WC SDS (p=0.028), logD4-A (p=0.033), logSHBG (p=0.031), and total ovarian volume (p=0.045) had significant effects on AMH levels, and LH (p=0.003) on INH-A levels. In receiver-operating characteristic analysis, the cut-off values for AMH and INH-A were 6.1 ng/mL (sensitivity 81.1%) and 12.8 pg/mL (sensitivity 86.8%), respectively, to diagnose PCOS. When AMH and INH-A were used in combination, the sensitivity (96.2%) increased.
Conclusion:
INSL3 and INH-B were not found to have diagnostic value in adolescents with PCOS. On the other hand, it was shown that INH-A could be used as a new diagnostic biomarker in addition to AMH.
doi:10.4274/jcrpe.3253
PMCID: PMC5096492  PMID: 27125339
adolescent; anti-Müllerian hormone; inhibin-A; inhibin-B; insulin-like peptide-3; Polycystic ovary syndrome
24.  Feasibility of nephrinuria as a screening tool for the risk of pre-eclampsia: prospective observational study 
BMJ Open  2016;6(8):e011229.
Objectives
To investigate the possibility of nephrinuria as a screening tool for the risk of pre-eclampsia (PE).
Design
Prospective observational study.
Setting
A single university hospital. Changes in urinary nephrin:creatinine ratio (NCR, ng/mg) and protein:creatinine ratio (PCR, mg/mg) in pregnancy were determined. Significant proteinuria in pregnancy (SPIP) was defined as PCR>0.27. PE was diagnosed in women with both SPIP and hypertension.
Participants
89 pregnant women in whom neither hypertension nor SPIP was present at enrolment, providing 31, 125 and 93 random urine samples during first, second and third trimesters, respectively.
Results
PE developed in 14 of the 89 women. NCR increased with increasing PCR in 14 women with PE (correlation coefficient, 0.862; p<0.0001). In contrast, NCR did not change significantly despite significant increases in PCR in 75 women with normotensive pregnancies defined as neither SPIP nor hypertension, indicating that there was little increase in nephrinuria over the physiological range of proteinuria in pregnancy. Relative risk of later development of PE among asymptomatic second and third trimester women with NCR (ng/mg) >122 (95th centile value for 75 women with normotensive pregnancies) was 5.93 (95% CI 2.59 to 13.6; 60% (6/10) vs 10% (8/79)) and 13.5 (95% CI 3.31 to 55.0; 75% (6/8) vs 5.5% (2/36)), respectively, compared with women with NCR≤122 at that time.
Conclusions
Nephrinuria was unlikely to increase in normal pregnancy. A certain NCR cut-off may efficiently differentiate women at higher risk of PE.
doi:10.1136/bmjopen-2016-011229
PMCID: PMC4985984  PMID: 27486123
nephrin; podocyte injury; preeclampsia; proteinuric diseases; urine test
25.  Relation between single serum progesterone assay and viability of the first trimester pregnancy 
SpringerPlus  2012;1(1):80.
This study was designed to detect the relation between serum progesterone and viability of pregnancy during the first trimester. Prospective study carried out in Al-Rashid Maternity and Ahmadi Kuwait oil company hospitals, over three years from February 2009 to February 2012. Two hundred and Sixty (260) pregnant women were hospitalized due to vaginal bleeding and/or abdominal pain during the first trimester of their pregnancies and were included in this study. Women included in this study were; sure of dates, conceived spontaneously with no history of infertility and had a positive serum pregnancy test. 2 ml blood samples were taken for women included in this study for serum progesterone assay. Women included in this study were followed by ultrasound for the viability of the pregnancy till the end of first trimester and the outcome of their pregnancy were recorded, while women with exogenous progesterone support or multiple pregnancies or suspected ectopic pregnancy or Hydatiform mole were excluded from this study. Data were collected and statistically analyzed to detect the relationship between serum progesterone level and viability of pregnancy during the first trimester. The mean age of the studied population was 32.7 ± 5.1 years, the mean gestational age at progesterone assay was 9.7 ± 0.5 week and by the end of the first trimester, women included in this study were classified according to the viability of their pregnancies into; viable pregnancy group 178 (68.5%) cases and non-viable pregnancy group (ended by miscarriage) 82 (31.5%) cases. The mean serum progesterone of the studied population was significantly high in viable pregnancy group (46.5 ± 7.4 ng/ml) compared to non-viable pregnancy group (9.9 ± 4.8 ng/ml), (p <0.05). In this study; 6.7% of viable pregnancies had serum progesterone level <10 ng/ ml, while 20.7% of non-viable pregnancies had serum progesterone level >10 ng/ml, the serum progesterone at cut off level 10 ng/ml was 79.3% sensitive to diagnose non-viable pregnancy and was 93.3% specific to diagnose viable pregnancy. Also, in this study; 1.1% of viable pregnancies had serum progesterone level <20 ng/ ml, while 4.8% of non-viable pregnancies had serum progesterone level >20 ng/ml, the serum progesterone at cut off level 20 ng/ml was 95.1% sensitive to diagnose non-viable pregnancy and was 98.9% specific to diagnose viable pregnancy. Serum progesterone is a reliable marker for early pregnancy failure and single assay of its serum level can differentiate between viable and non-viable pregnancies.
doi:10.1186/2193-1801-1-80
PMCID: PMC3568470  PMID: 23420141
Serum progesterone; Viability; First trimester pregnancy

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