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1.  Effect of Chromium Dinicocysteinate Supplementation on Circulating Levels of Insulin, TNF-α, Oxidative Stress and Insulin Resistance in Type 2 Diabetic Patients: Randomized, Double-Blind, Placebo-Controlled Study 
Molecular nutrition & food research  2012;56(8):1333-1341.
Background and Aims
Chromium and cysteine supplementation have been shown to improve glucose metabolism in animal studies. This study examined the hypothesis that chromium dinicocysteinate (CDNC), a complex of chromium and L-cysteine, is beneficial in lowering oxidative stress, vascular inflammation and glycemia in type 2 diabetic patients.
Methods
Type 2 diabetic patients enrolled in this study were given placebo for one month for stabilization and then randomized into one of three groups: placebo (P), chromium picolinate (CP) or CDNC, after which they received daily oral supplementation for 3 months. Of the 100 patients enrolled in the study, 74 patients completed it. There were 25 patients in the P supplemented group, 25 in the CP supplemented and 24 in the CDNC supplemented group who completed the study. Blood markers of glycemia, vascular inflammation, HOMA insulin resistance and oxidative stress were determined at randomization and after 3 months of supplementation with P, CP or CDNC.
Results
There was a significant decrease at 3 months in insulin resistance (p=0.02) and in the levels of protein oxidation (p=0.02) and TNF-α (p=0.01) in the CDNC supplemented cohort compared to baseline. However, there was no statistically significant change in these markers in the CP supplemented group compared to baseline. Insulin levels significantly decreased(p=0.01) for subjects receiving CDNC but not CP. There was no significant impact of supplementation on HbA1c or glucose levels in either of the groups.
Conclusions
CDNC supplementation lowers insulin resistance by reducing blood levels of TNF-α, insulin, and oxidative stress in type 2 diabetic patients. Therefore, CDNC supplementation has potential as an adjunct therapy for individuals with type 2 diabetes.
doi:10.1002/mnfr.201100719
PMCID: PMC4077620  PMID: 22674882
Chromium; L-cysteine; oxidative stress; insulin resistance; diabetes
2.  Recombinant AAV9-TLK1B Administration Ameliorates Fractionated Radiation-Induced Xerostomia 
Human Gene Therapy  2013;24(6):604-612.
Abstract
Salivary glands are highly susceptible to radiation, and patients with head and neck cancer treated with radiotherapy invariably suffer from its distressing side effect, salivary hypofunction. The reduction in saliva disrupts oral functions, and significantly impairs oral health. Previously, we demonstrated that adenoviral-mediated expression of Tousled-like kinase 1B (TLK1B) in rat submandibular glands preserves salivary function after single-dose ionizing radiation. To achieve long-term transgene expression for protection of salivary gland function against fractionated radiation, this study examines the usefulness of recombinant adeno-associated viral vector for TLK1B delivery. Lactated Ringers or AAV2/9 with either TLK1B or GFP expression cassette were retroductally delivered to rat submandibular salivary glands (1011 vg/gland), and animals were exposed, or not, to 20 Gy in eight fractions of 2.5 Gy/day. AAV2/9 transduced predominantly the ductal cells, including the convoluted granular tubules of the submandibular glands. Transgene expression after virus delivery could be detected within 5 weeks, and stable gene expression was observed till the end of study. Pilocarpine-stimulated saliva output measured at 8 weeks after completion of radiation demonstrated >10-fold reduction in salivary flow in saline- and AAV2/9-GFP-treated animals compared with the respective nonirradiated groups (90.8% and 92.5% reduction in salivary flow, respectively). Importantly, there was no decrease in stimulated salivary output after irradiation in animals that were pretreated with AAV2/9-TLK1B (121.5% increase in salivary flow; p<0.01). Salivary gland histology was better preserved after irradiation in TLK1B-treated group, though not significantly, compared with control groups. Single preemptive delivery of AAV2/9-TLK1B averts salivary dysfunction resulting from fractionated radiation. Although AAV2/9 transduces mostly the ductal cells of the gland, their protection against radiation assists in preserving submandibular gland function. AAV2/9-TLK1B treatment could prove beneficial in attenuating xerostomia in patients with head and neck cancer undergoing radiotherapy.
Shanmugam and colleagues demonstrate that a single instillation of recombinant AAV9 encoding Tousled-like kinase 1B (TLK1B) in rat submandibular glands leads to a complete amelioration of salivary dysfunction caused by fractionated radiation. They suggest that this treatment modality may be beneficial in attenuating xerostomia in headand-neck cancer patients undergoing radiotherapy.
doi:10.1089/hum.2012.235
PMCID: PMC3689188  PMID: 23614651
3.  Inhibition of glutathione synthesis in brain endothelial cells lengthens S-phase transit time in the cell cycle: Implications for proliferation in recovery from oxidative stress and endothelial cell damage 
Redox biology  2013;1(1):131-139.
Oxidative stress-induced decrease in tissue or systemic glutathione (GSH) and damage to the vascular endothelium of the blood-brain barrier such as occurs in diabetes or stroke will have important implications for brain homeostasis. Endothelial proliferation or repair is crucial to preserving barrier function. Cell proliferation has been associated with increased intracellular GSH, but the kinetic and distribution of GSH during cell cycle is poorly understood. Here, we determined the influence of cellular GSH status on the early dynamics of nuclear-to-cytosol (N-to-C) GSH distribution (6-h interval) during proliferation in a human brain microvascular endothelial cell line (IHEC). Control IHECs exhibited two peak S-phases of the cell cycle at 48 and 60 h post seeding that temporally corresponded to peak nuclear GSH levels and expression of cdk1, the S-to-G2-to-M checkpoint controller, suggesting a link between cell cycle progression and nuclear GSH. Sustained inhibition of GSH synthesis delayed S-to-G2/M cell transition; cell arrest in the S-phase was correlated with decreased total nuclear GSH and increased nuclear expressions of chk2/phospho-chk2 and GADPH. The temporal correspondence of nuclear chk2 activation and GAPDH expression with S-phase prolongation is consistent with enhanced DNA damage response and extended time for DNA repair. Strikingly, when GSH synthesis was restored, cell transit time through S-phase remained delayed. Significantly, total nuclear GSH remained depressed, indicating a time lag between restored cellular GSH synthetic capacity and recovery of the nuclear GSH status. Interestingly, despite a delay in cell cycle recovery, nuclear expressions of chk2/phospho-chk2 and GAPDH resembled those of control cells. This means that restoration of nuclear DNA integrity preceded normalization of the cell cycle. The current results provide important insights into GSH control of endothelial proliferation with implications for cell repair or wound healing in recovery post-oxidative damage.
doi:10.1016/j.redox.2013.01.003
PMCID: PMC3652486  PMID: 23682351
nuclear-to-cytosolic GSH distribution; GSH and endothelial proliferation; GSH and cell cycle; DNA damage response; brain microvascular endothelial cells
5.  Pleural ultrasonography versus chest radiography for the diagnosis of pneumothorax: review of the literature and meta-analysis 
Critical Care  2013;17(5):R208.
Introduction
Ultrasonography is being increasingly utilized in acute care settings with expanding applications. Pneumothorax evaluation by ultrasonography is a fast, safe, easy and inexpensive alternative to chest radiographs. In this review, we provide a comprehensive analysis of the current literature comparing ultrasonography and chest radiography for the diagnosis of pneumothorax.
Methods
We searched English-language articles in MEDLINE, EMBASE and Cochrane Library dealing with both ultrasonography and chest radiography for diagnosis of pneumothorax. In eligible studies that met strict inclusion criteria, we conducted a meta-analysis to evaluate the diagnostic accuracy of pleural ultrasonography in comparison with chest radiography for the diagnosis of pneumothorax.
Results
We reviewed 601 articles and selected 25 original research articles for detailed review. Only 13 articles met all of our inclusion criteria and were included in the final analysis. One study used lung sliding sign alone, 12 studies used lung sliding and comet tail signs, and 6 studies searched for lung point in addition to the other two signs. Ultrasonography had a pooled sensitivity of 78.6% (95% CI, 68.1 to 98.1) and a specificity of 98.4% (95% CI, 97.3 to 99.5). Chest radiography had a pooled sensitivity of 39.8% (95% CI, 29.4 to 50.3) and a specificity of 99.3% (95% CI, 98.4 to 100). Our meta-regression and subgroup analyses indicate that consecutive sampling of patients compared to convenience sampling provided higher sensitivity results for both ultrasonography and chest radiography. Consecutive versus nonconsecutive sampling and trauma versus nontrauma settings were significant sources of heterogeneity. In addition, subgroup analysis showed significant variations related to operator and type of probe used.
Conclusions
Our study indicates that ultrasonography is more accurate than chest radiography for detection of pneumothorax. The results support the previous investigations in this field, add new valuable information obtained from subgroup analysis, and provide accurate estimates for the performance parameters of both bedside ultrasonography and chest radiography for pneumothorax evaluation.
doi:10.1186/cc13016
PMCID: PMC4057340  PMID: 24060427
6.  Elevated acetoacetate and MCP-1 levels in cord blood of infants of diabetic mothers 
Neonatology  2012;102(3):163-168.
Background
Infants of diabetic mothers (IDM) are at increased risk for metabolic complications. Type 1 and some type 2 diabetic patients have elevated levels of ketone bodies acetoacetate (AA) and β-hydroxybutyrate (BHB).
Objective
The aim of this study is to examine how hyperketonemia in diabetic mothers affects markers of inflammation and oxidative stress in their offspring.
Methods
Blood was obtained from 23 diabetic mothers and 13 healthy mothers, and their infants’ umbilical cords at the delivery. IL-8, MCP-1 and protein carbonyl (protein oxidation) levels were determined by ELISA. U937 human monocyte cell culture was used to examine the effect of AA and BHB on secretion of MCP-1.
Results
There was a significant increase in the levels of AA in cord blood of diabetic mothers compared with cord blood of healthy mothers. A significant increase in the levels of protein oxidation (p<0.05) and MCP-1 levels (p<0.05) were observed in the cord blood of IDMs. The level of MCP-1 significantly correlated (r=0.51, p=0.01) with the concentration of AA in the IDM. In further experiments with cultured monocytes treated with exogenous AA (0-4 mM), a significant increase in MCP-1 secretion was observed with AA but not in BHB-treated monocytes.
Conclusion
Blood levels of AA and MCP-1 are elevated in IDM, which may contribute to the development of the metabolic complications seen in IDM.
doi:10.1159/000339286
PMCID: PMC3557819  PMID: 22776897
Infant of diabetic mother; Oxidative stress; MCP-1; acetoacetate; Hyperketonemia
7.  The prevalence of platelet activating factor acetylhydrolase single nucleotide polymorphisms in relationship to necrotizing enterocolitis in Northwest Louisiana infants 
SpringerPlus  2013;2:294.
Purpose
Studies documented that platelet activating factor (PAF) and the enzyme platelet activating factor acetylhydrolase (PAFAH) play a very important role in the pathogenesis of neonatal necrotizing enterocolitis (NEC). In this retrospective, case-controlled pilot study, the authors investigated the prevalence of single nucleotide polymorphisms (Ile198Thr and Ala379Val) of the PAFAH gene.
Subjects and methods
We screened 570 blood samples from both Caucasian and African-American preterm infants in the Northwest Louisiana population for the above mentioned PAFAH gene polymorphisms. Out of 570 infants, 36 had stage I or II NEC based on diagnostic coding, the International Classification of Diseases, 9th revision, Clinical Modification, 2009 (ICD-9-CM). The remaining infants without an ICD-9-CM diagnosis of NEC were recruited as control population. The DNA was isolated and restriction fragment length polymorphism microplate polymerase chain reaction assay was performed.
Results
Variants of the PAFAH gene polymorphism (Ile198Thr and Ala379Val) frequencies were not significantly different between the infants with NEC and the control group (P value of 0.26 by either multiple logistic regression analysis or the Cochran-Mantel-Haenszel test).
Conclusions
This is the first study of its kind in exploring the relationship between NEC and single nucleotide polymorphisms in the coding genes of the enzyme PAFAH. Our preliminary data demonstrated that adjusted for the effect of race, PAFAH polymorphisms (Ile198Thr and Ala379Val) have no significant effect on NEC.
doi:10.1186/2193-1801-2-294
PMCID: PMC3710407  PMID: 23888267
Necrotizing enterocolitis; Neonates; Preterm; Single nucleotide polymorphisms; Platelet activating factor; PAF; PAF acetylhydrolase; PAFAH
8.  Inhibition of glutathione synthesis in brain endothelial cells lengthens S-phase transit time in the cell cycle: Implications for proliferation in recovery from oxidative stress and endothelial cell damage☆ 
Redox Biology  2013;1(1):131-139.
Oxidative stress-induced decrease in tissue or systemic glutathione (GSH) and damage to the vascular endothelium of the blood-brain barrier such as occurs in diabetes or stroke will have important implications for brain homeostasis. Endothelial proliferation or repair is crucial to preserving barrier function. Cell proliferation has been associated with increased intracellular GSH, but the kinetic and distribution of GSH during cell cycle is poorly understood. Here, we determined the influence of cellular GSH status on the early dynamics of nuclear-to-cytosol (N-to-C) GSH distribution (6-h interval) during proliferation in a human brain microvascular endothelial cell line (IHEC). Control IHECs exhibited two peak S-phases of the cell cycle at 48 and 60 h post seeding that temporally corresponded to peak nuclear GSH levels and expression of cdk1, the S-to-G2-to-M checkpoint controller, suggesting a link between cell cycle progression and nuclear GSH. Sustained inhibition of GSH synthesis delayed S-to-G2/M cell transition; cell arrest in the S-phase was correlated with decreased total nuclear GSH and increased nuclear expressions of chk2/phospho-chk2 and GADPH. The temporal correspondence of nuclear chk2 activation and GAPDH expression with S-phase prolongation is consistent with enhanced DNA damage response and extended time for DNA repair. Strikingly, when GSH synthesis was restored, cell transit time through S-phase remained delayed. Significantly, total nuclear GSH remained depressed, indicating a time lag between restored cellular GSH synthetic capacity and recovery of the nuclear GSH status. Interestingly, despite a delay in cell cycle recovery, nuclear expressions of chk2/phospho-chk2 and GAPDH resembled those of control cells. This means that restoration of nuclear DNA integrity preceded normalization of the cell cycle. The current results provide important insights into GSH control of endothelial proliferation with implications for cell repair or wound healing in recovery post-oxidative damage.
Graphical abstract
Highlights
► Increased nuclear-to-cytosol GSH was associated with brain endothelial cell (IHEC) cell cycle progression. ► Inhibition of GSH synthesis decreased nuclear GSH and delayed S-to-G2 transition. ► S-phase prolongation was linked to elevated DNA damage response. ► Recovery of nuclear GSH and normal cell cycle lagged behind the restoration of GSH synthesis.
doi:10.1016/j.redox.2013.01.003
PMCID: PMC3652486  PMID: 23682351
GSH, glutathione; GSSG, glutathione disulfide; H1, histone H1; cdk1, cyclin dependent kinase 1; ATM, ataxia telangiectasia mutated; chk2, checkpoint kinase 2; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; Nuclear-to-cytosolic GSH distribution; GSH and endothelial proliferation; GSH and cell cycle; DNA damage response; Brain microvascular endothelial cells
10.  Efficacy and Comparative Effectiveness of Sirolimus (Rapamune) as an Anticancer Drug 
The Laryngoscope  2011;121(5):978-982.
Objectives/Hypothesis
To evaluate antitumor efficacy of the generic mTOR inhibitor sirolimus in preclinical animal models of head and neck squamous cell carcinoma (HNSCC) and compare its effects with those of the patented analog Temsirolimus.
Study Design
In vivo study.
Methods
To develop xenograft established tumor model (ETM) of HNSCC, FaDu cells were injected subcutaneously into nude mice. When tumors reached 50–60mm3 mice were randomized into 5 groups and treated daily i.p. with sirolimus at various doses for 5 days a week for 3 weeks. Tumor volumes were measured. The results were compared with historical data on Temsirolimus effects. In the minimal residual disease (MRD) model surgical wounds were created and FaDu cells implanted. After 72h, animals were randomized into two groups and were injected i.p. with 0 or 5 mg/kg sirolimus for 5 days a week for one month.
Results
In the ETM, sirolimus significantly inhibited tumor growth (p<0.01) although there was no overall significant difference in tumor growth inhibition between sirolimus and Temsirolimus. In the MRD model, sirolimus significantly suppressed growth of tumors (p<0.001) and improved survival compared with controls (p<0.01). There was a significant decrease in pS6 expression, indicating mTOR inhibition.
Conclusion
In this study we demonstrate that the generic mTOR inhibitor sirolimus shows potent antitumor activity in HNSCC and produces comparable effects to the patent drug Temsirolimus. Sirolimus has the potential of serving as an economic and comparative targeted agent to Temsirolimus in the treatment of HNSCC.
Level of Evidence
1b Individual randomized controlled trial.
doi:10.1002/lary.21724
PMCID: PMC3085006  PMID: 21520111
sirolimus; Temsirolimus; head and neck squamous cell carcinoma
11.  When Is Posterolateral Orbitotomy Useful in a Pterional Craniotomy? A Morphometric Study 
Skull Base  2011;21(3):147-152.
Adding posterolateral orbitotomy to pterional craniotomy allows greater exposure of the anterolateral skull base. However, there is a paucity of literature quantifying the relative benefit of adding posterolateral orbitotomy for various surgical targets. Our study is a step to address this issue. We performed dissections of five cadaveric heads (10 sides). The anterior communicating artery (A-Com) complex, posterior chiasm (anterior third ventricular region), ipsilateral optic canal, and ipsilateral supraclinoid internal carotid artery (ICA) bifurcation were chosen as targets. A pterional craniotomy was performed and the targets were morphometrically analyzed. Subsequently, posterolateral orbitotomy was done and analysis repeated. The field of view and measurements quantifying the angle of attack were compared. Addition of orbitotomy to pterional craniotomy increased the angle of exposure to ICA bifurcation, anterior third ventricular region, and A-Com complex by average of 15%, 29%, and 50%, respectively. Our study shows the addition of a posterolateral orbitotomy to the pterional craniotomy improves the angle of attack to the anterior third ventricular region and the A-Com complex, thus supporting the use of orbitopterional craniotomy for suprasellar lesions extending into anteroinferior third ventricle and A-Com aneurysms that point superiorly/posteriorly.
doi:10.1055/s-0031-1275242
PMCID: PMC3312105  PMID: 22451817
Pterional craniotomy; posterolateral orbitotomy; Morphometric; study
13.  High Sensitivity C - Reactive Protein is Associated with Diastolic Dysfunction in Young African Americans without Clinically Evident Cardiac Disease 
Background:
Diastolic dysfunction (DD) is associated with myocardial fibrosis mediated by inflammation. Higher levels of inflammation found in African Americans (AAs) may predict DD among asymptomatic individuals. We tested the hypothesis that high sensitivity C-reactive protein (hs-CRP), a biomarker of inflammation, is associated with DD in asymptomatic AAs.
Methods:
We prospectively recruited 107 asymptomatic AAs without any history of cardiac, renal or inflammatory diseases or alcoholism. We measured hs-CRP and B-type Natriuretic peptide (BNP) levels and estimated left ventricular end diastolic pressure (LVEDP), mass and systolic function with echocardiography. Multivariate logistic regression analysis was used to define whether hs-CRP is an independent predictor of LVEDP.
Results:
Among 107 subjects: the mean age was 48±10 yrs, 58 (54%) were men, 59 (55%) had diabetes (DM), 48 (45%) had hypertension (HTN), the mean BMI was 30.5±4.8 and the mean ejection fraction was 63.1±5.8%. DD was present in 56(52%) subjects, 38 (36%) of whom also had a high LVEDP. On multivariate analysis, hs-CRP was independently associated with DD [odds ratio 3.36 (95% CI= 1.07 - 10.5, p = 0.04]. There was a 61% and 133% increase in the prevalence of any DD and DD with high LVEDP, respectively, between the lowest and the highest hs-CRP quartiles.
Conclusion:
Diastolic dysfunction is prevalent among asymptomatic African Americans and it is independently associated with elevated level of hs-CRP, an inflammation marker.
doi:10.2174/1874192401105010188
PMCID: PMC3170931  PMID: 21915224
Diastolic dysfunction; Inflammation; High sensitivity C-reactive protein; Biomarkers.
14.  Comparison of Radiosensitizing Effects of the mTOR Inhibitor CCI-779 to Cisplatin in Experimental Models of Head and Neck Squamous Cell Carcinoma 
Molecular cancer therapeutics  2009;8(8):2255-2265.
Purpose
To determine if the mTOR inhibitor CCI-779 can sensitize head and neck squamous cell carcinoma (HNSCC) to radiotherapy (XRT) and compare the radiosensitizing effects to cisplatin with its known considerable toxicity.
Experimental Design
Radiosensitizing effects of CCI-779 were assayed on HNSCC cell lines in vitro. CCI-779 (5mg/kg), cisplatin (1 mg/kg) and XRT (2 Gy) alone and in combination were evaluated for antitumor activity in mice bearing FaDu and SCC40 xenografts. Effects of CCI-779 on radiation-induced activation of the Akt/mTOR pathway were analyzed.
Results
Although CCI-779 did not sensitize HNSCC cells to ionizing radiation in vitro, combination of CCI-779 and XRT significantly augmented the in vivo tumor growth inhibitory effects of XRT and CCI-779 (P<0.05). In addition CCI-779+XRT suppressed tumor growth more effectively than cisplatin+XRT (P<0.05). CCI-779+XRT significantly improved survival compared to XRT alone in both cisplatin-sensitive FaDu (P<0.01) and cisplatin-resistant SCC40 xenograft mice (P<0.05). There were no additional benefits of adding cisplatin to CCI-779+XRT. CCI-779 significantly attenuated irradiation-induced upregulation of the mTOR pathway, increased apoptosis and displayed potent antiangiogenic activity in FaDu xenografts that was further enhanced by its combination with radiotherapy (P<0.05) which may explain the mechanism of its selective radiosensitizing effects in vivo and not in vitro.
Conclusions
Antitumor activity of radiotherapy was enhanced when combined with CCI-779 in HNSCC xenograft model. CCI-779+XRT showed antitumor activity superior to conventional chemoradiotherapy with cisplatin. These results pave the way for clinical trials utilizing molecular targeted therapy with CCI-779 in combination with radiotherapy for HNSCC treatment.
doi:10.1158/1535-7163.MCT-08-1184
PMCID: PMC2758817  PMID: 19625495
rapamycin analogues; temsirolimus; mTOR; in vivo; apoptosis
15.  Quantification of the Advantages of the Extended Frontal Approach to Skull Base 
Skull Base  2004;14(3):133-142.
ABSTRACT
This anatomic study evaluated the extent that a fronto-orbital osteotomy (FOO) added to a bilateral frontal craniotomy widened the exposure to the midline compartment of the anterior, middle, and posterior cranial fossae. The goal was to determine if osteotomy would significantly increase angles for two targets: the foramen magnum (FM) and anterior clinoid process (ACP). Stepwise dissections were performed on five cadaveric heads. A bilateral frontal craniotomy was made, followed by FOO. After the ethmoids were removed, the planum sphenoidale was drilled to enter the sphenoid sinus. Further drilling exposed the anterior clivus, which was drilled down to FM. Excellent exposure of the basilar artery, vertebral artery, and brain stem was achieved. With and without FOO, angles of exposure were measured for two targets: the ACP and FM. The angle of exposure after FOO increased markedly with an average gain of 76% for the ACP and of 80% for FM. Compared with a conventional bifrontal craniotomy, the addition of FOO increased the surgical exposure and minimized frontal lobe retraction for accessing lesions of the anterior, middle, and posterior cranial fossae.
doi:10.1055/s-2004-832253
PMCID: PMC1151683  PMID: 16145596
Brain tumor; extended frontal approach; operative approach; skull base; skull base tumor
16.  Comparison of Hepatitis C Viral Loads in Patients with or without Human Immunodeficiency Virus 
A better understanding of how human immunodeficiency virus (HIV) coinfection affects the course of hepatitis C virus (HCV) infection is required to select patients with HIV who would benefit from current HCV therapy. Between June 1996 and March 2000, HCV RNA levels were quantified for 1,279 patients at the Louisiana State University Health Sciences Center; 28 of these patients were coinfected with HIV. HCV loads were quantified by the Bayer branched-DNA assay with a lower limit of detection of 0.2 Meq/ml. We compared the median HCV RNA levels of for patients coinfected with HIV and HCV and patients infected only with HCV who were in the same age range (23 to 55 years). The median HCV load for the 28 patients coinfected with HCV and HIV (17.8 Meq/ml) was significantly greater (P < 0.05) than that for similarly aged patients infected only with HCV (6.1 Meq/ml). The HCV load did not correlate with age or sex for either group of patients. A significant (R = −0.4; P < 0.05) negative correlation was observed between HCV load and CD4 count in the coinfected group, for whom the CD4 counts at the time of HCV load analysis ranged from 6 to 1,773/mm3. The increased HCV load in patients coinfected with HCV and HIV compared to that in patients infected only with HCV and the inverse relationship of the HCV load to the CD4 count indicate that immunosuppression results in decreased control of HCV replication. In addition, we report significantly higher HCV loads among coinfected African Americans than Caucasians.
doi:10.1128/CDLI.8.4.690-694.2001
PMCID: PMC96128  PMID: 11427412

Results 1-16 (16)