bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Longitudinal Study of the Effects of ART on Plasma Chemokine Levels in Malaysian HIV Patients
Authors: Chew Constance S. N. , Cherry Catherine L. , Kamarulzaman Adeeba , Yien Tan Hong , Aghafar Zayd , Price Patricia 
Published: June 2013

Objectives: Chemokines influence the migration of leukocytes to secondary lymphoid tissue and sites of inflammation. In HIV patients, they are implicated in inflammatory complications of antiretroviral therapy (ART), notably Immune Reconstitution Disease (IRD) and Sensory Neuropathy (SN). However most chemokines have not been monitored as patients begin ART or correlated with IRD and SN.Methods: Plasma chemokine levels were assessed longitudinally using commercial ELISAs in 69 patients treated in Kuala Lumpur, Malaysia. Plasma was available at baseline and after 6, 12, 24 and 48 weeks on ART. Chemokine genotypes were assessed using allele-specific fluorescent probes. IRD were diagnosed in 15 patients. 30 patients were screened for SN using the ACTG BPNS tool after six months on ART. SN was detected in 8 patients.Results: Plasma CXCL10 levels decreased on ART compared to baseline (p= 0.002–0.0001), but remain higher than healthy controls (p≤ 0.0001). The decline was clearer in patients without IRD. CCL5 levels rose on ART but remained similar to controls. CCL2 levels were higher in patients than controls after week 12. Plasma chemokine levels were not affected by CD4+ T-cell counts or any genotypes tested. Several patients with SN displayed higher CCL5 levels throughout therapy compared to patients without neuropathy. Levels of other chemokines and chemokine genotypes were not associated with SN.Conclusions: Chemokines are differentially affected by ART. CXCL10 and CCL5 may influence IRD and CCL5 warrants further investigation for an effect in SN. These trends are not influenced by chemokine genotypes investigated here.
Gender Differences in Animal Models of Posttraumatic Stress Disorder
Authors: Cohen Hagit , Yehuda Rachel 
Published: June 2013

Epidemiological studies report higher prevalence rates of stress-related disorders such as acute stress disorder and post-traumatic stress disorder (PTSD) in women than in men following exposure to trauma. It is still not clear whether this greater prevalence in woman reflects a greater vulnerability to stress-related psychopathology. A number of individual and trauma-related characteristics have been hypothesized to contribute to these gender differences in physiological and psychological responses to trauma, differences in appraisal, interpretation or experience of threat, coping style or social support. In this context, the use of an animal model for PTSD to analyze some of these gender-related differences may be of particular utility. Animal models of PTSD offer the opportunity to distinguish between biological and socio-cultural factors, which so often enter the discussion about gender differences in PTSD prevalence.In this review, we present and discuss sex-differences in behavioral, neurochemical, neurobiological and pharmacological findings that we have collected from several different animal studies related to both basal conditions and stress responses. These models have used different paradigms and have elicited a range of behavioral and physiological manifestations associated with gender. The overall data presented demonstrate that male animals are significantly more vulnerable to acute and chronic stress, whereas females are far more resilient. The stark contradiction between these findings and contemporary epidemiological data regarding human subjects is worthy of further study. The examination of these gender-related differences can deepen our understanding of the risk or the pathophysiology of stress-related disorders.
Abnormal Expression of Matrix Metalloproteinase-9 (MMP9) Correlates with Clinical Course in Chinese Patients with Endometrial Cancer
Authors: Yu Fang , Jiang Qingping , Zhou Ying , Yang Zhen , Yu Xiaoli , Wang Hao , Liu Zhen , Wang Lijing , Fang Weiyi , Guo Suiqun 
Published: June 2013

Aims and background: The aim of the present study was to analyze the expression of matrix metalloproteinase-9 (MMP9) in endometrial cancer and its correlation with clinicopathologic features in Chinese patients, including the survival of patients with endometrial cancer.Methods: Using immunohistochemistry analysis, we analyzed MMP9 protein expression in clinicopathologically characterized 128 endometrial cancer (EC) cases with age ranging from 30 to 85 years (median=51.6 years) and 30 endometrial atypical hyperplasia (EAH) and 30 normal endometrium (NE). Cases with greater than or equal to 6 and less than 6 with the score value of cytoplasmic MMP9 immunostaining were regarded as high expression and low expression, respectively. The relationship between the expression levels of MMP9 and clinical features was analyzed in EC cases.Results: Immunohistochemical analysis revealed that the protein expression of MMP9 detected in EC tissues was higher than that in the EAH tissues and NE tissues (P=0.006). In addition, high levels of MMP9 protein were positively correlated with the status of lymph node metastasis (P=0.044) and the histopathological grade (P<0.05) of EC patients. Patients with higher MMP9 expression did not correlate with EC patients' clinical outcome in China. Multivariate analysis suggested that status of lymph node metastasis and depth of myometrial invasion, but not MMP9 expression level, were significantly correlated with patients' survival.Conclusion: MMP9 is highly expressed in ECs and correlates with the progression of ECs, but not be helpful in predicting the prognosis of EC patients.
Soluble Mesothelin-Related Peptides Levels in Patients with Malignant Mesothelioma
Authors: Franko Alenka , Dolzan Vita , Kovac Viljem , Arneric Niko , Dodic-Fikfak Metoda 
Published: June 2013

Soluble mesothelin-related peptides (SMRP) are a potential tumor marker for malignant mesothelioma. The aim of this study was to determine the differences in SMRP levels in patients with malignant mesothelioma before treatment and in various responses to treatment and to investigate whether SMRP level could be useful in evaluating tumor response to treatment. The study included patients with malignant mesothelioma treated at the Institute of Oncology Ljubljana between March 2007 and December 2009. Blood samples were collected before treatment and/or in various responses to treatment. SMRP levels were determined using ELISA assay based upon a combination of two monoclonal antibodies. Mann-Whitney test was used to determine the differences in SMRP levels in various responses to treatment.Median SMRP was 2.80 nmol/L (range 0.00–34.80) before treatment, 0.00 nmol/L (range 0.00–0.00) in complete response, 0.48 nmol/L (range 0.00–4.40) in partial response, 1.65 nmol/L (range 0.00–20.71) in stable disease and 7.15 nmol/L (range 0.44–31.56) in progressive disease. Pre-treatment SMRP levels were significantly higher than in stable disease, partial response and complete response (p=0.006), as were SMRP levels in progressive disease compared to stable disease, partial response and complete response (p= 0.006), as were SMRP levels in progressive disease compared to stable disease, partial response and complete response (p< 0.001).Our findings suggest that SMRP may be a useful tumor marker for detecting the progression of malignant mesothelioma and evaluating tumor response to treatment.
Circulating Levels of High Molecular Weight (HMW) Adiponectin and Total Adiponectin in Relation to Fat Distribution, Oxidative Stress and Inflammation in Asian Indians
Authors: Indulekha K. , Surendar J. , Anjana R.M. , Gokulakrishnan K. , Balasubramanyam M. , Aravindhan V. , Mohan V. 
Published: June 2013

Aim: To look at the association of total and high molecular weight (HMW) adiponectin with markers of fat distribution, oxidative stress and inflammation in Asian Indians.Methods: A total of 120 subjects were chosen randomly from Chennai Urban Rural Epidemiological Study. Fasting HMW adiponectin levels, TNF-alpha and oxidized LDL were measured using ELISA. High sensitivity C reactive protein (hsCRP) was measured by a high sensitive nephelometric assay. Lipid peroxidation was measured by Tbars assay and protein carbonyl content was assessed by DNPH assay. Visceral and subcutaneous fat areas were assessed by computed tomography (CT) scan.When stratified based on the tertiles of visceral fat, the levels of total (p= 0.03) and HMW adiponectin (p= 0.007) were highest in the first tertile followed by tertiles 2 and 3 whereas in tertiles of subcutaneous fat, there was no such trend. With increasing tertiles of Tbars, the levels of total (p= 0.03) and HMW adiponectin decreased (p= 0.002). The levels of HMW (p< 0.001) but not total adiponectin was also found to decrease with increasing tertiles of Protein carbonyl content. The levels of Total (p= 0.02) and HMW adiponectin (p= 0.004) were highest in the first tertile of oxidized LDL followed by tertile 2 and tertile 3. With increasing tertiles of TNF-alpha total (p= 0.01) and HMW adiponectin (p= 0.004) was found to decrease. With increasing tertiles of hs-CRP, Total (p= 0.005) and HMWadiponectin (p= 0.007)was found to decrease.Conclusion: Oxidative stress markers, visceral but not subcutaneous fat and inflammation are associated with total and HMW adiponectin levles in Asian Indians.
Poly Thymidine Polymorphism and Cystic Fibrosis in a Non-Caucasian Population
Authors: Tabaripour Reza , Niaki Haleh Akhavan , Douki Mohammad Reza Esmaeeli , Bazzaz Javad Tavakkoly , Larijani Bagher , Yaghmaei Parichehr 
Published: June 2013

Background:Cystic fibrosis is a monogenic recessive disorder found predominantly in Caucasian population. This disease arises from mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. In this study we consider poly T polymorphism c.1210-12T[5], c.1210-12T[7], c.1210-12T[9] (T5, T7, T9) in the intron 8 of CFTR gene in normal individuals and cystic fibrosis patients in the north of Iran.Material and methods:40 CF patients and 40 normal individuals were screened for poly T polymorphism in intron 8 of CFTR gene using Reverse Dot Blot method which was also used to detect p.Phe508del among CF patients.Results:T7allele is the most prevalent in both normal and CF patients. Its abundance is approximately 75%. T9and T5represent approximately 20% and 5% of alleles respectively. T7/ T7genotype is the most present in both normal and CF patients with 72.5% and 60% prevalence respectively. p.Phe508del was present in 13 CFTR alleles belonging to 7 patients with either homozygote T9/ T9, T7/ T7or compound heterozygote T7/ T9genotypes.Conclusion:Contrary to the Caucasians, T7allele is more frequent in Northern Iranian CF patients. The presence of p.Phe508del and T7allele in the same framework is reported for the first time in this part of the world. Further investigations of other populations will help to understand whether p.Phe508del arose by selection pressure in this part of the world or was imported from European countries. The abundance of T5, T7, T9alleles indicates that this polymorphism can be used as one of the informative markers for detection of normal and mutant alleles in prenatal diagnosis or carrier assessment in families with previous history of the disease in regions with high degree of CFTR mutation heterogeneity.
Cord Blood Levels of IL-6, IL-8 and IL-10 May Be Early Predictors of Bronchopulmonary Dysplasia in Preterm Newborns Small for Gestational Age
Authors: Rocha Gustavo , Proença Elisa , Guedes Ana , Carvalho Carmen , Areias Augusta , Ramos João Pedro , Rodrigues Teresa , Guimarães Hercília 
Published: June 2013

Introduction: Various cytokines have been associated to the occurrence of bronchopulmonary dysplasia (BPD) in preterm neonates.AIM: To establish an association between cord blood cytokines and BPD, so that they could be used, in clinical practice, as early markers of BPD.Material and methods: Preterms less than 30 weeks gestational age, were analysed by ELISA microassay for venous cord blood IL-1β, IL-6, IL-8, TNF-αand IL-10, and compared between the BPD and non-BPD groups.Results: One hundred and fifty neonates completed the study; 31 (21%) small for gestational age (SGA); 16 were deceased before 28 days of life; 36 developed mild BPD and 20 developed moderate/severe BPD. Elevated cord blood IL-8 was associated with death or moderate/severe BPD. SGA patients with moderate/severe BPD presented higher cord blood values of IL-8, lower IL-6 and IL-10 when compared with SGA without moderate/severe BPD; and higher IL-8 levels when compared with patients without moderate/severe BPD.Conclusion: These results support an association between cord blood IL-8 and moderate/severe BPD, independently of the intra-uterine growth; and the association of cord blood IL-6 and IL-10 and moderate/severe BPD in SGA preterm newborns.
eNOS Gene Variants and the Risk of Premature Myocardial Infarction
Authors: Zigra Aggeliki-Maria , Rallidis Loukianos S. , Anastasiou Georgia , Merkouri Efrossyni , Gialeraki Argyri 
Published: June 2013

BACKGROUND: Endothelial nitric oxide synthase (eNOS) as well as nitric oxide play an important role in the regulation of cardiovascular function. There are limited and controversial data regarding the impact of polymorphisms of eNOS gene that is implicated in the vasoconstrictive properties of the endothelium in the pathogenesis of premature myocardial infarction (MI).OBJECTIVE: We examined whether two common polymorphisms of eNOS gene (G894T and T786C) are associated with the development of premature MI.METHODS: We recruited 107 patients with premature MI and compared them to 103 age- and sex- matched controls. All patients underwent coronary angiogram and were classified into the subgroup of patients with ‘normal’ or ‘near normal’ coronary arteries and the subgroup of patients with significant coronary artery disease (≥ 50% stenosis in lumen diameter of coronary arteries). The genetic polymorphisms of eNOS gene were assayed with polymerase chain reaction and reverse hybridization.RESULTS: Nineteen patients (17.8%) had ‘normal’ or ‘near normal’ coronary arteries. A significantly higher frequency of homozygosity for the 786C (32%) and the 894T (21%) alleles of the eNOS gene in patients who develop early MI in the setting of angiographically 'normal' or 'near normal' coronary arteries were found.CONCLUSIONS: Our data suggest that the T786C and the G894T genetic polymorphisms are associated with the development of MI in very young individuals, whose coronary arteries are characterized by very small atheromatic burden.
The Search for a Genetic Factor Associating with Immune Restoration Disease in HIV Patients Co-Infected withMycobacterium tuberculosis
Authors: Affandi Jacquita S. , Kumar Manoj , Agarwal Upasna , Singh Sarman , Price Patricia 
Published: June 2013

BACKGROUND: Up to 43% of HIV-infected patients co-infected withMycobacterium tuberculosisexperience exacerbations of tuberculosis (TB) after commencing antiretroviral therapy (ART). These are termed immune restoration disease (IRD). It is unclear why individual susceptibility varies.OBJECTIVE: We investigate if single nucleotide polymorphisms (SNP) in genes encoding cytokines, chemokines and their receptors associate with development of an IRD event in patients of two different ethnicities.METHODS: DNA samples were available from small well-characterised groups of HIV patients treated in Cambodia (TB-IRD,n= 17; HIV+TB+controls, n = 55) and India (TB-IRD,n= 19; HIV+TB+controls,n= 43). HIV patients with a TB diagnosis but no evidence of IRD were included to control for susceptibility to TB per se. Sixteen SNP implicated in inflammation or mycobacterial disease were genotyped.RESULTS: Susceptibility to TB-IRD associated with carriage of TNFA-1031*T (rs1799964;P=0.05) and SLC11A1 D543N*G (rs17235409;P=0.04) in Cambodian patients and carriage of IL18-607*G (rs1946518;P=0.02) and VDR FokI (F/f)*T (rs10735810;P=0.05) in Indian patients.CONCLUSIONS: Associations between polymorphisms in immune-related genes and TB-IRD were found, but none were common across two ethnicities.
HER1R497K andHER2I655V Polymorphisms Are Linked to Development of Breast Cancer
Authors: AbdRaboh Naglaa R. , Shehata Hanan H. , Ahmed Manal B. , Bayoumi Fatehia A. 
Published: June 2013

BACKGROUND: Polymorphism of the genes of Human Epidermal growth factor receptor1 (HER1) and receptor2 (HER2) have been reported to be linked to pathogenesis of several malignant tumors but still there is contradiction regarding their association with breast cancer.OBJECTIVE: In this case control study we aimed to analyze the frequency ofHER1R497K (rs 11543848) andHER2I655V (rs 1136201) Polymorphisms in breast cancer.SUBJECT AND METHOD: The frequency ofHER1Arg(R) 497Lys (K) andHER2Ile (I) 655Val (V) polymorphisms were tested in 64 breast cancer patients and 86 normal control by polymerase chain reaction followed by restriction fragment polymorphism detection. Immunohistochemical analysis was done for HER2 protein on the available 18 malignant tissue samples.RESULTS:HER1497K andHER2655V variant had significantly increased breast cancer risk (OR=2.6, 95% CI 1.6–4.2, OR=2.2, 95% CI 1.2–4.1, p< 0.05) respectively. Moreover, combinedHER1K497 andHER2V655 variant was detected in 26.6% malignant in comparison to 8.14% of control group (OR=4.1, 95% CI 1.58–10.57), but, no significant association was noticed between both Polymorphisms and clinicopathological features of the disease. As regard HER2 immunohistochemical expression no significant correlation was revealed with HER2 655V polymorphism.CONCLUSIONS: Our findings suggest thatHER1497K andHER2655V polymorphisms are potential risk factor for development of breast cancer.
MTHFRGene C677T Mutation andACEGene I/D Polymorphism in Turkish Patients with Osteoarthritis
Authors: Inanir Ahmet , Yigit Serbulent , Tural Sengul , Cecen Osman , Yildirim Eren 
Published: June 2013

Osteoarthritis is a degenerative joint disorder resulting in destruction of articular cartilage, osteophyte formation, and subchondral bone sclerosis. In recent years, numerous genetic factors have been identified and implicated in osteoarthritis. The aim of the current study was to examine the influence of methylenetetrahydrofolate reductase (MTHFR) gene C677T mutation and angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) variations on the risk of osteoarthritis.Genomic DNA is obtained from 421 persons (221 patients with osteoarthritis and 200 healthy controls).ACEgene I/D polymorphism genotypes were determined using polymerase chain reaction using I and D allele-specific primers. TheMTHFRC677T mutation was analyzed by polymerase chain reaction (PCR) based restriction fragment length polymorphism (RFLP) methods. We found significant difference between the groups with respect to bothACEandMTHFRgenotype distributions (p< 0.001,p< 0.001 respectively). Our study suggests thatACEgene DD genotype andMTHFRgene CC genotype could be used as genetic markers in osteoarthritis in Turkish study populations.
Biomarkers Associated with Vascular and Valvular Calcification in Chronic Hemodialysis Patients
Authors: Lee Chien-Te , Chua Sarah , Hsu Chung-Yao , Tsai Yu-Che , Ng Hwee-Yeong , Kuo Chien-Chun , Wu Chien-Hsing , Chen Te-Chun , Chiu Terry Ting-Yu , Lee Yueh-Ting 
Published: June 2013

Background: Cardiovascular calcification, including arterial intimal and medial calcification (AIC and AMC) and valvular calcification (VC) are important predictors of outcome in chronic dialysis patients. We aimed to compare their prevalence and analyze respective risk factors in hemodialysis (HD) patients.Methods: A total of 81 HD patients were enrolled. Vascular calcification was assessed by plain film radiography of the pelvis and VC was diagnosed by echocardiography. Demographic data was reviewed and serum levels of calcification-relevant biomarkers were determined. Patients with and without calcification were then compared.Results: The prevalence study indicated that 36 patients had AIC (44.4%), 17 had AMC (21%) and 60 (74.1%) had VC. Patients with vascular calcification were older, and had a higher prevalence of diabetes. Their IL-6, osteoprotegerin, and uric acid levels were higher. Serum fetuin-A was lower in patients with VC. Logistic regression analysis revealed age, uric acid and diabetes to be independently associated with AIC; uric acid, diabetes and osteoprotegerin with AMC. Fetuin-A was the sole associate of VC.Conclusions: It is concluded that the prevalence of cardiovascular calcification in chronic HD patients was high with cardiac valve involvement more frequent. Factors associated with different type of calcification were not identical. Changes in biomarkers may represent clinical clues for assessment of cardiovascular calcification in HD patients.
AURKA Governs Self-Renewal Capacity in Glioma-Initiating Cells via Stabilization/Activation of β-catenin/Wnt Signaling
Authors: Xia Zhibo , Wei Ping , Zhang Heng , Ding Zhiming , Yang Lixuan , Huang Zhengsong , Zhang Nu 
Published: June 2013

Abstract
Glioma-initiating cells (GIC), which are characterized by their self-renewal capacity and tumorigenicity, were recently identified as a highly tumorigenic subpopulation of glioblastoma multiforme and are considered responsible for glioblastoma recurrence and chemo/radiation resistance. Previously, it was revealed that Wnt signaling activation is critical to the self-renewal of GICs. However, the molecular mechanism underlying the high expression of β-catenin, the key transcription factor of the Wnt signaling pathway, remains elusive. In this investigation, it was determined that aurora kinase A (AURKA) regulates the self-renewal and tumorigenicity of GICs by stabilizing β-catenin. In GICs, AURKA directly interacts with AXIN and disrupts the AXIN/GSK3β/β-catenin destruction complex and stabilizes β-catenin, thereby activating Wnt signaling to promote self-renewal. Stable knockdown of AURKA destabilizes β-catenin by increasing phosphorylated β-catenin bound to AXIN and suppresses Wnt signaling, which inhibits the ability of GICs to self-renew. This effect is rescued by expression of an AURKA kinase dead mutant, D274A, which lacks the ability to phosphorylate GSK3β, indicating that stabilization of β-catenin by AURKA in GICs is independent from phosphorylation of GSK3β. Functional experiments confirm that inhibition of AUKRA in GICs could suppress their “stemness,” self-renewal ability, and tumorigenicity both in vitro and in vivo, and these effects could be rescued by stabilized β-catenin mutant. These findings indicate that AURKA competes away the binding of AXIN from β-catenin, induces β-catenin stabilization, and activates Wnt signaling in GICs.
Implications: AURKA kinase inhibition could effectively attenuate Wnt signaling, thereby inhibiting the self-renewal and tumorigenicity of GICs, and may be a novel target for glioblastoma treatment strategies. Mol Cancer Res; 11(9); 1101–11. ©2013 AACR.