The incidence and clinical features of portopulmonary hypertension (POPH) have not been adequately described and it is currently unknown whether an association exists between the severity of POPH and liver function. Additionally, POPH risk factors are yet to be identified. The aim of this study was to determine the prevalence, describe the clinical features and investigate the potential risk factors of POPH. We conducted a study of 100 cirrhotic patients hospitalized between March 2011 and May 2012 at Tongji Hospital in Shanghai. The clinical characteristics of patients with and without POPH were analyzed. Clinical variables with a possible association with POPH were measured and pulmonary artery systolic pressure (PASP) was determined by cardiac Doppler echocardiography. Of the 100 patients enrolled in this study, 10 were diagnosed with POPH. Seven of the cases were mild, two were moderate and only one was severe; eight were attributed to viral infections. POPH was not detected in patients with schistosomal or alcoholic cirrhosis. Hemoglobin (Hb) levels were lower in patients with POPH compared to those without POPH (P<0.01) and the severity of POPH was not significantly correlated with Child-Pugh grade (R=−0.06, P=0.09). Hb levels, incidence of hepatitis C virus (HCV) infection and portal vein thrombosis differed between the two groups (P<0.05). Hb levels were identified as an independent risk factor associated with POPH and portal vein thrombosis may play an important role during the development of POPH. However, the severity of POPH was not associated with liver function.

Estrogen receptor-α (ERα) is essential for estrogen-dependent growth and its level of expression is a crucial determinant of response to endocrine therapy and prognosis in ERα-positive breast cancer. Breast cancer patients show a wide range of ERα expression levels which change in individual patients during disease progression and in response to systemic therapies. However, little is known concerning how the expression of ERα is regulated in human breast cancer. Recently, several microRNAs (miRNAs) have been identified to regulate ERα expression and to predict ER, progesterone receptor (PR) and human epidermal growth factor 2 (HER2) status. The expression levels of miR-342 and ERα mRNA were analyzed in human breast cancer samples and cell lines by quantitative reverse transcription (RT)-PCR analysis. The correlations between the expression levels of miR-342 and clinicopathological factors were analyzed. Statistically significant associations were observed between miR-342 and ER, HER2 and vascular endothelial growth factor (VEGF) status in the human breast cancer samples and the levels of miR-342 gradually increased as ERα mRNA expression increased. Moreover, ectopic overexpression of miR-342 upregulated the expression levels of the ERα mRNA and significantly sensitized the MCF-7 cells to tamoxifen-induced apoptosis and inhibition of cellular proliferation. These results suggested that miR-342 expression is positively correlated with ERα mRNA expression in human breast cancer and that it may be a significant marker for predicting tamoxifen sensitivity in ERα-positive breast cancer and a potential target for restoring ERα expression and responding to antiestrogen therapy.

Patients with relapsed acute myeloid leukemia (AML) have unfavorable prognosis and require innovative therapeutic approaches. In this study we used fludarabine combined with a middle dose of cytosine arabinoside (Ara-C), mitoxantrone and granulocyte-colony stimulating factor (G-CSF) as a salvage therapy for patients with relapsed AML in China. Forty-five patients with relapsed AML were treated with the Mito-FLAG regimen consisting of mitoxantrone (7 mg/m2, day 1, 3 and 5), fludarabine (30 mg/m2, days 1–5), Ara-C (1 g/m2, over 3 h every 12 h, days 1–5) and G-CSF [5 μg/kg/day subcutaneously from day 0 until the white blood count (WBC) was >20×109/l]. Patients with a partial response (PR) received another course of the same regimen. Patients with a suitable donor and aged <50 years received allogeneic stem cell transplantation (allo-SCT). Twenty-three patients (51%) and 3 patients (7%) achieved complete remission (CR) and PR, respectively, following one or two courses of Mito-FLAG, and the overall response (OR) rate was 58%. Nine patients (20%) received allo-SCT and 4 patients (9%) succumbed early. Hematological toxicity and infections were the most prominent toxicities of this regimen. Other toxicities included nausea, vomiting, bleeding, hyperbilirubinemia, renal toxicity and arrhythmia. The probability of overall survival (OS) at 4 years was 19% (95% CI, 11–26%) and the probability of 4-year disease-free survival (DFS) was 29% for all 23 patients in CR (95% CI, 18–41%). Our data suggest that Mito-FLAG is a highly effective and well-tolerated salvage regimen for relapsed AML.

The aim of this study was to investigate the expression levels of the death-associated protein kinase (DAPK) and E-cadherin in esophageal squamous cell carcinoma (ESCC) and their correlation with clinical and pathological factors. Immunohistochemistry [streptavidin-peroxidase (SP) method], in situ hybridization, immunoblot assays and reverse transcription-PCR (RT-PCR) were used to detect the expression of DAPK and E-cadherin in the carcinomas and the adjacent normal tissues of 76 cases of esophageal squamous carcinomas. The immunoblot assay indicated that the expression levels of DAPK and E-cadherin were decreased significantly in the ESCC tissue (P<0.05) when compared with the adjacent normal tissues. The RT-PCR results showed that the mRNA levels of DAPK and E-cadherin were reduced. The abnormal expression of DAPK was highly correlated with the invasiveness and lymphatic metastasis of the cancer. The abnormal expression of E-cadherin was highly correlated with the differentiation and lymphatic metastasis of the cancer. The decreased expression levels of DAPK and E-cadherin correlated with the development of ESCC. The combined detection of DAPK and E-cadherin proteins may be correlated with the degree of malignancy and metastatic potency of ESCC.

Previous genome-wide association studies (GWAS) have revealed seven single nucleotide polymorphisms (SNPs) that affect lipoprotein-associated phospholipase A2 (Lp-PLA2) activity or levels in American and European individuals. A total of 290 coronary heart disease (CHD) patients, 198 non-CHD patients and 331 unrelated healthy volunteers were recruited for the present case-control study of Han Chinese. Four SNPs (rs964184 of ZNF259, rs7528419 of CELSR2 and rs7756935 and rs1805017 of PLA2G7) were shown to be significantly associated with CHD. The rs964184-G allele of the ZNF259 gene was identified as a risk factor of CHD in females (odds ratio (OR) =1.49, 95% confidence interval (CI) =1.00–2.22, P=0.05). The rs7528419-G allele of the CELSR2 gene was protective against CHD in males (OR=0.48, 95% CI=0.25–0.93, P=0.04). The other two alleles (rs7756935-C and rs1805017-A) of the PLA2G7 gene acted as protective factors against CHD in females (rs7756935-C: OR=0.59, 95% CI=0.35–1.00, P=0.05; rs1805017-A: OR=0.51, 95% CI=0.28–0.93, P=0.03). Moreover, rs1805017 of the PLA2G7 gene was associated with the severity of CHD only in females (r2=0.02, P=0.04). We identified four Lp-PLA2-associated SNPs significantly associated with CHD in a Han Chinese population. Specifically, rs7528419 was protective factor against CHD in males, while the other two SNPs (rs7756935 and rs1805017 of the PLA2G7 gene) were protective factors against CHD in females and rs964184 of the ZNF259 gene was regarded as a risk factor for CHD in females.

To explore the process of pressure ulcer formation, interleukin (IL)-17 expression levels were observed in a mouse model of pressure ulcers. Twenty mice were divided into experimental and control groups (10 mice per group). A mouse model of pressure ulcers was established by inducing ischemia-reperfusion injury on local tissue in the experimental group. Pressure ulcer tissues in the experimental group and normal mouse tissue in the control group were stained using hematoxylin and eosin (H&E) and observed using light microscopy. The protein and mRNA expression levels of IL-17, in mouse pressure ulcer tissues from the experimental group and in the normal tissue from the control group, were determined using real-time PCR and western blot analysis, respectively. The mRNA and protein expression levels of IL-17 were compared between the two groups. H&E staining indicated that striated muscle was arranged orderly and cellular structure was intact in the control group, whilst inflammatory cell infiltration was observed in the muscle tissue of the experimental group. The expression levels of IL-17 mRNA were 0.307±0.058 ng in the experimental group and 0.112±0.042 ng in the control group (P<0.05). The expression levels of the IL-17 protein were 0.434±0.097 ng in the experimental group and 0.181±0.040 ng in the control group (P<0.05). IL-17 expression levels were increased in pressure ulcers, which suggests that IL-17 may be associated with pressure ulcers.

Fibrinogen (Fg) contributes to thrombosis and hemostasis and plays a role in inflammation. Fg is also known to play a significant role in atherosclerosis (AS). P-selectin has been associated with AS. The present study aimed to identify the role of Fg in AS and to examine the possible mechanisms behind the effects of fibrinogen on AS using Sprague-Dawley (SD) rats as a model system. Diet-induced atherosclerotic SD rats were adopted as the experimental models. Fg was transfused into these rats and the degree of atherosclerotic lesion development was compared with that of control rats. Blood was obtained from the common abdominal aorta and then the biochemical characteristics were measured and ELISA assays performed. The aortas were then carefully separated, removed and placed in 10% (w/v) neutral formalin for use at a later stage. The root of the aorta was cut and samples were washed, dehydrated, cleared, dipped in wax, embedded, sliced, coated, grilled and stained with HE. Pathological HE-stained sections were examined by light microscopic analysis and immunohistochemistry was performed for Fg and P-selectin on representative tissue sections. The Fg-transfused, high-fat diet-fed group developed atherosclerotic lesions more readily compared with the control group. Immunohistochemical analysis revealed that Fg expression was higher in the endarterium of the Fg-transfused, high-fat diet-fed rats. P-selectin expression was also found to be correlated with Fg expression. Fg actively promotes atherosclerotic lesion development; one possible mechanism behind this is the ability of Fg to enhance P-selectin expression, which is also able to facilitate the development of atherosclerotic lesions.

The present study aimed to discuss the method and effect of posterior internal fixation of thoracolumbar fractures strengthened by the vertical stress pedicle screw fixation of fractured vertebrae. Patients with single thoracolumbar fractures were examined retrospectively. Fourteen patients (group A) had been treated with vertical stress pedicle screw fixation of a fractured vertebra and sixteen patients (group B) received traditional double-plate fixation, as a control. All patients were diagnosed with fresh fractures with a complete unilateral or bilateral pedicle and no explosion of the inferior half of the vertebral body or inferior endplate. In group A, patients received conventional posterior distraction and lumbar lordosis restoration, as well as pedicle screws in the fractured vertebra in a vertical direction to relieve stress to achieve a local stress balance. All patients were followed up postoperatively for 4–18 months (average, 12.6 months). The vertical stress pedicle screw fixation assisted in the reduction of vertebrae fracture, which reduced the postoperative Cobb’s angle loss. There was a significant difference in the change of Cobb’s angle between the two groups one year after surgery (P<0.01). Conditional application of pedicle screws in a single thoracolumbar fracture enhances the stability of the internal fixation system and is conducive to the correction of kyphosis and maintenance of the corrective effects.

Degenerative lumbar scoliosis (DLS) progresses with aging after 50–60 years. The genetic association of DLS remains largely unclear. In this study, the genetic association between glutamate receptor, ionotropic, N-methyl D-aspartate (NMDA, GRIN) receptor genes and DLS was investigated. A total of 9 coding single nucleotide polymorphisms (cSNPs) in NMDA receptor genes [GRIN2A (rs8049651, Leu425Leu; rs9806806, Tyr730Tyr); GRIN2B (rs7301328, Pro122Pro; rs35025065, Asp447Asp; rs1805522, Ile602Ile; rs1806201, Thr888Thr; rs1805247, His1399His); and GRIN2C (rs689730, Ala33Ala; rs3744215, Arg1209Ser)] were selected and genotyped using direct sequencing in 70 patients with DLS and 141 healthy controls. Multiple logistic models (codominant, dominant and recessive) were calculated for the odds ratio (OR), 95% confidence interval (CI) and corresponding P-values. The SNPStats, SNPAnalyzer and HelixTree programs were used for the evaluation of the genetic data. Among the SNPs examined, no significant associations were observed between the NMDA receptor genes and DLS. When the patients were divided into two groups according to clinical characteristics based on Cobb’s angle (<20° or ≥20°) and lateral listhesis (<6 mm or ≥6 mm), associations were observed between rs689730 of GRIN2C and Cobb’s angle (codominant, P=0.038; dominant, P=0.022) and between rs7301328 of GRIN2B and lateral listhesis (codominant, P=0.003; dominant, P=0.015; recessive, P=0.015). These results indicate that the GRIN2A, GRIN2B and GRIN2C genes do not affect the development of DLS. However, the GRIN2C gene may be associated with Cobb’s angle, while the GRIN2B gene may be associated with lateral listhesis.

Interleukin-8 (IL-8) or CXCL8 is a potent chemotactic factor that is involved in atherogenesis. IL-8 mediates its pre-inflammatory effects through interaction with CXCR1 and CXCR2. In the present study, we investigated the effects of angiotensin II (Ang II) on IL-8 synthesis and CXCR1/CXCR2 expression of THP-1 monocytes. IL-8 was measured in the culture medium using ELISA. Expression of chemokine receptors CXCR1 and CXCR2 was evaluated by flow cytometry. Results demonstrated that the addition of Ang II increased IL-8 production in the THP-1 monocytes. The Ang II type 1 receptor blocker (ARB) losartan significantly blocked Ang II-induced IL-8 production. Notably, losartan blocked LPS-induced IL-8 production by THP-1 monocytes and produced a small but statistically significant reduction of baseline IL-8 production of naïve THP-1 cells. Losartan also produced a statistically significant increase of fluorescence intensity of naïve CXCR1- and CXCR2-positive THP-1 monocytes, probably as a negative feedback effect secondary to IL-8 downregulation. In conclusion, we demonstrated that Ang II increased IL-8 production by THP-1 monocytes. Losartan significantly suppressed the latter effect, suggesting an AT-1 mediated pathway. Moreover, losartan suppressed the IL-8 production of naïve THP-1 monocytes and LPS-treated THP-1 monocytes, suggesting a broader spectrum of pleiotropic effects. Extrapolating this in vitro observation to in vivo pathways, we propose Ang II-induced IL-8 production by monocytes as another pre-atherogenic potential of Ang II that can be effectively blocked by the AT1 receptor blockade.

A rapid, sensitive and specific HPLC-MS/MS method was developed and validated for the quantification of potassium oxonate (Oxo) in human plasma using [13C2,15N3]-Oxo as an internal standard (IS). The target substance was separated from human plasma using the solid-phase extraction method. Chromatography separation was performed on a Waters:Atlantis dC18 column (150×4.6 mm, 5.0 μm) with a mobile phase consisting of H2O with 0.1% formic acid in acetonitrile (90:10, v/v). The mass spectrometer works with electrospray ionization and multiple reaction monitoring in its negative ion mode, using target ions at [M–H]− m/z 111.9 for Oxo and [M–H]− m/z 117.0 for the IS. The mean standard curve was linear (r=0.9991) over the concentration range of 2.0–200.0 ng/ml and had good back-calculated accuracy and precision. The intra- and inter-day precision were <6.33% and the accuracy was >99.38%. The extraction recovery was >60.26%. The lower limit of quantification achieved with this method was 2.0 ng/ml. This assay method was demonstrated to be accurate, sensitive and simple and was successfully applied to a pharmacokinetic study following single oral administration of a 40-mg S-1 capsule in 12 tumor patients.

The aim of the present study was to investigate the effect of Apelin-13 on cardiomyocyte autophagy and to determine the underlying mechanism of this effect. To establish an autophagic model system, the cardiomyocytes of Sprague Dawley rats (postnatal day 3) were cultured and divided into five groups: normal control (Co), glucose deprivation (GD), GD+Apelin-13, GD+Apelin-13 treated with the Akt-specific inhibitor triciribine (GD+Apelin-13+Triciribine) and triciribine alone (Triciribine). The intracellular autophagosomes were then observed using transmission electron microscopy (TEM) and the expression levels of cellular autophagy-related protein microtubule-associated protein 1 light chain 3 (LC3), phosphatidylinositol-3-kinase (PI3K) and mammalian target of rapamycin (mTOR) protein were measured using western blotting. Compared with the Co group, the ratio of LC3-II/LC3-I increased significantly in all treatment groups, with the exception of the Triciribine group (P<0.05). Compared with the GD group, the ratio of LC3-II/LC3-I was significantly decreased, and the PI3K and mTOR expression was significantly enhanced in the GD+Apelin-13 and GD+Apelin-13+Triciribine groups (P<0.05). Compared with the GD+Apelin-13 group, the ratio of LC3-II/LC3-I increased significantly (P<0.05) and the PI3K expression remained unchanged in the GD+Apelin-13+Triciribine group (P>0.05), but mTOR expression was significantly reduced (P<0.05). GD led to increased numbers of autophagosomes and augmented the LC3-II/LC3-I ratio (P<0.05). Apelin-13 pretreatment attenuated GD-induced cardiomyocte injury, decreased the autophagosome number and the ratio of LC3-II/LC3-I (P<0.05), enhanced PI3K activity (P<0.05) and upregulated the phosphorylation levels of the Akt and mTOR proteins (P<0.05). The Akt-specific inhibitor triciribine weakened the protective role of Apelin-13 (P<0.05). To a certain extent, Apelin-13 inhibited GD-induced cardiomyocyte autophagy, which may be related in part to the activation of the PI3K/Akt/mTOR signaling pathway.

This study demonstrates the removal of virus particles from B95-8 host cells that maintain normal activity under optimal osmotic pressure. After infecting B95-8 cells with Epstein-Barr virus (EBV) particles, the cells were treated with isosmotic solution [0.90% NaCl (330 mOsm/kg H2O)], hyposmotic solutions [0.36% NaCl (115 mOsm/kg H2O) and 0.27% NaCl (93 mOsm/kg H2O)] and distilled water. The pumping levels of virus particles were observed by inverse phase contrast microscopy and transmission electron microscopy (TEM). After treatment with the hyposmotic solutions, the following results were observed: firstly, after culturing for 24 and 48 h, the B95-8 cells in the hyposmotic solutions grew as well as the cells cultured in the isosmotic solution. Secondly, the virus particles in the B95-8 host cells overflowed onto the surface of the cells, while the organelle structures remained intact. This phenomenon was repeated in the removal of human immunodeficiency virus (HIV) from leukomonocytes. By optimizing the osmotic pressure, the activity of the B95-8 host cells was retained and the EBV particles were transported from the cells onto the cell surface.

The DNA methylation inhibitor 5-aza-2′-deoxycytidine (5-aza-CdR) is widely used as an anticancer drug for the treatment of leukemia and solid tumors. Gastric cancer (GC) patients who were positive for caudal type homeobox transcription factor 2 (CDX2) expression showed a higher survival rate compared with those who were CDX2 negative, which suggests that CDX2 performs a tumor suppressor role. However, the molecular mechanisms leading to the inactivation of CDX2 remain unclear. In the present study we demonstrated that the expression levels of CDX2 and DNA methyltransferase enzyme 1 (DNMT1) mRNA were significantly higher in GC compared with distal non-cancerous tissue. The expression of CDX2 mRNA was significantly correlated with Lauren classification, TNM stage and lymph node metastasis. DNMT1 mRNA expression was significantly correlated with TNM stage, pathological differentiation and lymph node metastasis. The expression of CDX2 mRNA was inversely correlated with that of DNMT1 mRNA in GC. Hypermethylation of the CDX2 gene promoter region, extremely low expression levels of CDX2 mRNA and no expression of CDX2 protein were the characteristics observed in MKN-45 and SGC-7901 GC cell lines. Following the treatment of MKN-45 cells with 5-aza-CdR, the hypermethylated CDX2 gene promoter region was demethylated and expression of CDX2 was upregulated, while DNMT1 expression was downregulated. Furthermore, a concentration- and time-dependent growth inhibition as well as increased apoptosis were observed. Caspase-3, −8 and −9 activities increased in a concentration-dependent manner following exposure to different concentrations of 5-aza-CdR. Therefore, our data show that the overexpression of DNMT1 and methylation of the CDX2 gene promoter region is likely to be responsible for CDX2 silencing in GC. 5-Aza-CdR may effectively induce re-expression of the CDX2 gene, inhibit cell proliferation and enhance the caspase-independent apoptosis of MKN-45 cells in vitro.

The aim of this study was to investigate the feasibility of establishing dog models of lunatomalacia through liquid nitrogen freezing. Twelve adult crossbred dogs were divided into three groups. Unilateral lunates were peeled off the parenchyma and frozen to result in avascular necrosis. They were observed dynamically through X-ray, computed tomography (CT) and magnetic resonance imaging (MRI). Furthermore, gross and histomorphological observations of samples were performed. Disseminated punctate hyperintense images and abnormal manifestations were detected, respectively. At 12 weeks after surgery, uneven bone density of the lunate and a flattened lunate of irregular shape were detected. A large area of irregular hypointense foci and hyperintensity was observed. Gross sample observation revealed a large area of dead bone. A decrease in the density of the trabecular bones and several vacant bone lacunas were visible. Liquid nitrogen freezing is a successful and reliable method for preparing animal models of lunatomalacia.

The current study aimed to observe the effects of sufentanil and remifentanil combined with propofol in target-controlled infusion (TCI) on perioperative stress reaction in elderly patients. A total of 80 elderly patients requiring general anesthesia were recruited. They were divided into four groups (each n=20) according to different target concentrations of remifentanil and sufentanil. These target concentrations were: 4 ng/ml remifentanil + 0.2 ng/ml sufentanil for group I; 3 ng/ml remifentanil + 0.3 ng/ml sufentanil for group II; 2 ng/ml remifentanil + 0.5 ng/ml sufentanil for anesthesia induction and post-intubation 3 ng/ml remifentanil + 0.2 ng/ml sufentanil for anesthesia maintenance for group III; and 5 ng/ml remifentanil for anesthesia induction and post-intubation 4 ng/ml remifentanil for anesthesia maintenance for group IV. Norepinephrine (NE), epinephrine (E) and angiotensin II (Ang II) levels in plasma were measured prior to the induction of anesthesia, as well as at several different time-points following surgery. The numbers of intraoperative severe hemodynamic fluctuation, postoperative eye-opening and extubation time, and post-extubation restlessness and pain scores were recorded. Group IV had a larger circulation fluctuation control number and higher levels of NE, E and Ang II at 3 h after surgery than any other group (P<0.01). Although group IV had shorter postoperative eye-opening and extubation times compared with the other groups (P<0.05), it also had higher restlessness and pain scores (P<0.01). The combined use of sufentanil and remifentanil stabilizes perioperative hemodynamics and reduces stress hormone levels.

The aim of this study was to evaluate the diagnostic value of 64-multislice spiral computed tomography (64-MSCT) for coronary stenosis compared with selective X-ray coronary angiography (SCA). Patients with chest pain, chest tightness or coronary stenosis received SCA and they acted as the controls. The sensitivity and accuracy of 64-MSCT were analyzed as compared with SCA. Images from 64-MSCT were obtained for 95 patients. For the diagnosis of myocardial bridge, 64-MSCT coronary CT angiography (CTA) is superior to SCA. In cases of mild coronary stenosis, combined with clinical symptoms, patients may choose to receive conservative treatment instead of SCA. However, cases of moderate coronary stenosis should receive SCA to determine the diagnosis. In conclusion, no difference was observed between 64-MSCT coronary CTA and SCA in their ability to exclude true negative diagnoses and diagnosing true positives of coronary disease. The 64-MSCT coronary CTA method produces improved image quality for diagnosis of coronary stenosis and is a non-invasive, reliable and effective method for the diagnosis of the severity of coronary stenosis.

The aim of this study was to obtain geometric data of in vivo patellar ligament (PL) and anterior cruciate ligament (ACL) by MRI and to analyze the correlation of the two with body weight, height and gender. A total of 157 cases with normal sagittal images of bilateral PL and ACL were enrolled. The PL and ACL lengths in the images were measured using the Radworks 5.1 application. The intraclass correlation coefficient for the data measured independently by three doctors was 0.997–1.000. In individuals aged 15–24 years, the values of PL and ACL length and the PL to ACL ratio were 43.95±4.25 mm, 38.45±4.62 mm and 1.15±1.09 in males and 42.03±0.94 mm, 36.00±1.06 mm and 1.18±0.1 in females, respectively. In individuals aged 25–64 years, the values in males were 40.99±4.45 mm, 36.06±3.74 mm and 1.14±0.09 and in females were 39.84±0.64 mm, 36.50±0.81 mm and 1.11±0.02, respectively. In individuals aged ≥65 years, the values in males were 41.43±3.08 mm, 36.62±3.44 mm and 1.15±0.09 and in females were 38.94±0.79 mm, 34.36±0.85 mm and 1.13±0.07, respectively. There was a significant difference between PL and ACL length on the same side (P<0.01). The data obtained was stable and repeatable. The present study established a database of PL and ACL length and the ratio of the two measured by MRI.

The aim of this study was to observe the clinical effects of bilateral decompression via vertebral lamina fenestration for lumbar interbody fusion in the treatment of lower lumbar instability. The 48 patients comprised 27 males and 21 females, aged 47–72 years. Three cases had first and second degree lumbar spondylolisthesis and all received bilateral vertebral lamina fenestration for posterior lumbar interbody fusion (PLIF) using a threaded fusion cage (TFC), which maintains the three-column spinal stability. Attention was given to ensure the correct pre-operative fenestration, complete decompression and the prevention of adhesions. After an average follow-up of 26.4 months, the one year post-operative X-ray radiographs suggested that the successful fusion rate was 88.1%, and this was 100% in the two-year post-operative radiographs. Moreover, the functional recovery rate was 97.9%. Bilateral vertebral lamina fenestration for lumbar interbody fusion is an ideal surgical method for the treatment of lower lumbar instability. The surgical method retains the spinal posterior column and middle column and results in full decompression and reliable fusion by a limited yet effective surgical approach.

To evaluate the encapsulation of VX2 hepatic allografts in rabbits induced by octreotide and celecoxib administration following transcatheter arterial embolisation (TAE), rabbits with hepatic VX2 allografts were divided into four groups: control, TAE, octreotide + celecoxib (O+C) and the multimodality therapy (TAE+O+C). Allograft metastasis, capsule thickness and percentage of clear cells were measured and vascular endothelial growth factor (VEGF) and CD31 were detected by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) analysis. The extrahepatic metastases of each intervention group were significantly fewer than those of the control group, with the TAE+O+C group exhibiting the fewest extrahepatic metastases. The TAE+O+C group had the greatest proportion of clear cells and thickest capsule on day 30. Increased capsule thickness was negatively correlated with tumour metastasis. In addition, VEGF expression levels assessed by immunohistochemistry and RT-PCR in the three intervention groups were significantly lower than those in the control group. Furthermore, the TAE+O+C group had a significantly reduced CD31 count induced by TAE. These results demonstrate that TAE, followed by long-term administration of octreotide and celecoxib, synergistically inhibits VX2 hepatic allograft metastasis by increasing the proportion of clear cells, promoting encapsulation and inhibiting angiogenesis.

The aim of this study was to investigate whether abnormal expression of matrix metalloproteinase (MMP)-9/tissue inhibitors of MMPs (TIMP)-1 and B cell lymphoma 2 (BCL-2)/BCL-2-associated X protein (BAX) are correlated with the characteristic accelerated fibrosis and apoptosis during ageing and in atrial fibrillation (AF). Four groups of dogs were studied: adult dogs in sinus rhythm (SR), aged dogs in SR, adult dogs with AF induced by rapid atrial pacing and aged dogs with AF induced by rapid atrial pacing. The mRNA and protein expression levels of the target gene in the left atrium were measured by quantitative reverse transcription-polymerase chain reaction (RT-PCR) and western blot analysis. Pathohistological and ultrastructural changes were assessed by light and electron microscopy. The apoptotic indices of myocytes were detected by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL). The mRNA and protein expression levels of MMP-9 and BAX and those of TIMP-1 and BCL-2 were significantly upregulated and down-regulated, respectively, in the aged groups compared with the adult groups. Compared with the control groups, the adult and aged groups with AF exhibited significantly increased mRNA and protein expression levels of MMP-9 and BAX and decreased expression levels of TIMP-1 and BCL-2. Samples of atrial tissue demonstrated abnormal pathohistological and ultrastructural changes, accelerated fibrosis and apoptosis. MMP-9/TIMP-1 and BCL-2/BAX hold potential for use as substrates conducive to AF and their abnormal expression plays a major role in structural remodeling of the atrium.

The present study aimed to evaluate the effect of using one-stage posterior C2 and C3 pedicle screw fixation or combined anterior C2-C3 fusion in the treatment of unstable hangman’s fracture. A total of 13 patients with unstable hangman’s fractures underwent C2 and C3 pedicle screw fixation, lamina interbody fusion or combined anterior C2-C3 fusion and imaging examinations to evaluate the fracture fixation and healing condition at three days and three months following surgery. Postoperative X-ray and computed tomography (CT) results showed high fracture reduction, good internal fixation position and reliable fracture fixation. The three-month postoperative CT showed good vertebral fracture healing. C2 and C3 pedicle screw fixation has a good curative effect in the treatment of unstable hangman’s fracture. The direct fixation of the fracture enables early ambulation by the patients.

Propyl gallate (PG) is an antioxidant that has been used as an additive in several foods to protect against oxidation. The present study examined the anti-inflammatory effect of PG on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced inflammation in human THP-1 monocytes. Pretreatment with PG markedly inhibited the TPA-induced expression levels of cyclooxygenase-2 and prostaglandin E2. The application of PG significantly inhibited the nuclear translocation of p65, a subunit of nuclear factor-κB (NF-κB) and phosphorylation of p65 (Ser536) in TPA-treated THP-1 cells. PG also inhibited the phosphorylation of IκB and IκB kinase. These results indicate that PG inhibits the inflammatory response by blocking the NF-κB signaling pathway in TPA-induced THP-1 monocytes. Therefore, PG may be useful as a therapeutic agent in inflammatory diseases.

Ganoderma lucidum is a traditional Oriental medicine that has been widely used as a tonic to promote longevity and health in Korea and other Asian countries. Although a great deal of work has been carried out on the therapeutic potential of this mushroom, the pharmacological mechanisms of its anti-inflammatory actions remain unclear. In this study, we evaluated the inhibitory effects of G. lucidum ethanol extract (EGL) on the production of inflammatory mediators and cytokines in lipopolysaccharide (LPS)-stimulated murine BV2 microglia. We also investigated the effects of EGL on the LPS-induced activation of nuclear factor kappaB (NF-κB) and upregulation of toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88). Elevated levels of nitric oxide (NO), prostaglandin E2 (PGE2) and pro-inflammatory cytokine production were detected in BV2 microglia following LPS stimulation. We identifed that EGL significantly inhibits the excessive production of NO, PGE2 and pro-inflammatory cytokines, including interleukin (IL)-1β and tumor necrosis factor-α in a concentration-dependent manner without causing cytotoxicity. In addition, EGL suppressed NF-κB translocation and transcriptional activity by blocking IκB degradation and inhibiting TLR4 and MyD88 expression in LPS-stimulated BV2 cells. Our results indicate that the inhibitory effects of EGL on LPS-stimulated inflammatory responses in BV2 microglia are associated with the suppression of the NF-κB and TLR signaling pathways. Therefore, EGL may be useful in the treatment of neurodegenerative diseases by inhibiting inflammatory mediator responses in activated microglia.

The present study aimed to evaluate the early effects of interspinous spacers on lumbar degenerative disease. The clinical outcomes of 23 patients with lumbar degenerative disease, treated using interspinous spacer implantation alone or combined with posterior lumbar fusion, were retrospectively studied and assessed with a visual analogue scale (VAS) and the Oswestry Disability Index (ODI). Pre-operative and post-operative interspinous distance, disc space height, foraminal width and height and segmental lordosis were determined. The early effects and complications associated with the interspinous spacers were recorded. The surgical procedures performed with the in-space treatment were easy and minimally invasive. The VAS scores and ODI were improved post-operatively compared with pre-operatively. Significant changes in the interspinous distance, disc space height, foraminal width and height and segmental lordosis were noted. In-space treatment for degenerative lumbar disease is easy and safe, with good early effects. The in-space system provides an alternative treatment for lumbar degenerative disease.