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Identification of biomarkers for the novel therapeutics targets of Chronic obstructive pulmonary disease (COPD) is an important area of current research. In this study, the level of inflammatory cytokines was investigated and correlated these levels with erythrocytic antioxidant activities in COPD patients with smokers and without smokers and parameters of severity.Plasma levels of Interleukin (IL)-6, IL-8 and IL-10 concentrations were assayed by means of Enzyme-linked Immunosorbent Assay (ELISA) and erythrocytic glutathione-s-transferase (GST) and glutathione peroxidase (GPx) activities were estimated by spectrophotometric method.Both IL-6 and IL-8 plasma levels showed a statistically significantly higher in COPD patients as compared to healthy controls (p0.05) and GPx activities (r= - 0.080, p>0.05). Similarly IL-8 was also found negative association with GST (r= - 0.260, p>0.05) and GPx activities (r= - 0.268, p>0.05). Whereas, a significant positive association was observed between IL-10 and erythrocytic GST (r= 0.494, p In conclusion, Plasma levels of inflammatory cytokines IL-6 and IL-8 are related with severity of COPD and IL-10 and oxidative stress markers GST and GPx are co-dependent and strongly interrelated processes and may be used as a potential marker for the evaluation of COPD.

Diabetes has emerged as a major threat to human life globally. Genomic studies have found a significant link between the Pro12Ala polymorphism of the PPAR-γ2 gene with incidence as well as occurrence of the risk of metabolic syndrome. The present study was aimed at assessing the PPAR-γ2 variant in an Asian Indian cohort of type 2 diabetes patients and its correlation with metabolic parameters. The present case-control study involved 100 type 2 diabetic patients and 100 asymptomatic healthy volunteers enrolled in random. Assessment of demographic factors and biochemical parameters were done for all enrolled. In addition, genotyping for the Pro12Ala (CCA to GCA) polymorphism was done by polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP) technology. The genotyping study detected the frequency of the CC genotype (Pro12Pro) to be higher in frequency in comparison to the heterozygous CG genotype in both, cases and controls. The homozygous GG genotype (Ala12Ala) was not detected in any of the cases or controls assessed. Biochemical analysis of the levels of malondialdehyde (MDA) detected a significant increase (p

Background: The role of Apolipoprotein-E (APO-E) in lipid metabolism and cholesterol transport is a key component of lipid metabolism which plays a role in diseases like hypercholesterolemia, diabetes, and cardiovascular disease. The aim of this study was to determine the genotypes, allelic frequencies, gene expression and methylation related to apolipoprotein E polymorphism in Coronary Artery Disease (CAD) patients and compare with non-CAD healthy subjects of South Indian population. Methods: The APO-E alleles and genotypes were determined by PCR-RFLP. Gene expression profiles for E3/E3 genotypes were determined using RT-PCR and methylation status was determined using Methyl Specific PCR assay in one hundred patients and an equal number of controls. Results: Four APO-E genotypes (E4/E4, E3/E3, E3/E4, and E2/E3) were identified with different allele frequency. Among these, E3/E3 genotype and E3 allele were found to be significantly higher in cases than controls. The present study showed that the mRNA expression of APO-E was up-regulated in CAD patients with E3/E3 genotype in comparison with controls. Methylation status indicated a significant association of E3/E3 genotypes with the disease. Conclusion: Different populations studied worldwide showed inherent variable frequencies of the APO-E alleles and genotypes, with the most frequent allele being E3. In this study, the APO-E genotypes E2/E3/E4 showed variable response to CAD, further, there was a significant association of E3/E3 genotypes to CAD risk; this genotype can be suggested for the diagnosis of CAD.

Tobacco exposure is the primary leading cause for cancer of the oral cavity, the airways and lung. The carcinogens in cigarette smoke have been linked as an environmental risk factor for causing genetic mutations in tumor suppressor, including TP53 (p53) which has been linked as a causative for occurrence and progression in lung cancer. The aim of the current case-control study is to assess the presence and frequency of chromosomal aberrations between smokers and non-smokers in case and control group. Further, analysis was also extended to include the p53 codon 72 Arg/Pro mutation analysis between the groups of study cohort. In methods, the case-control epidemiological study included a total of 100 cases and controls who were further categorized as smokers and non-smokers for analysis. Chromosomal aberration assay was done on peripheral blood lymphocytes and studied using Geimsa stain, while analysis of the p53 codon 72 Arg/Pro mutation was done by allele-specific polymerase chain reaction assay. The chromosomal aberration assessed include structural abnormalities like breaks, fragment, dysenteric and gaps, as well as numerical aneuploidies. Results showing the number of chromosomal aberrations was higher among smoker cases as compared to controls, and numerical aneuploidy was also detected only among this cohort. The mean of chromosomal aberrations observed between cases and controls and smokers as well as non-smokers was significant at p

Single nucleotide polymorphism (SNP) in the epidermal growth factor receptor (EGFR) plays a crucial role in head and neck cancer (HNC) disease progression and targeted therapies. Hence the present study aims to identify the mutations in EGFR gene (exon 20) in HNC considering their exposure to tobacco and alcohol habits. Mutational analysis was carried out by polymerase chain reaction (PCR) followed by single stranded confirmatory polymorphism (SSCP) techniques on the study group comprising of 129 HNC cases and 150 healthy volunteers. Four different SNP’s (R776H, G779G, Q787Q, and L798H) were observed with the overall mutation rate of 75.19% in HNC cases and 46% in controls. Q787Q was found to be more prevalent (p,0.05) and its genotypes GG, GA, and AA were 24.80%, 61.24%, and 13.95%. The study concluded that EGFR was found to be a polymorphic gene associated with HNC disease, and these SNPs were also prevalent in healthy volunteers with tobacco and alcohol habits. The observed SNPs in healthy volunteers indicated the importance of relative risk to HNC disease. These mutations were known to increase growth factor signaling cascade and confer susceptibility to the inhibitors.

Familial hypercholesterolemia (FH), a well-known lipid disease caused by inherited genetic defects in cholesterol uptake and metabolism is underdiagnosed in many countries including Saudi Arabia. The present study aims to identify the molecular basis of severe clinical manifestations of FH patients from unrelated Saudi consanguineous families. Two Saudi families with multiple FH patients fulfilling the combined FH diagnostic criteria of Simon Broome Register, and the Dutch Lipid Clinic Network (DLCN) were recruited. LipidSeq, a targeted resequencing panel for monogenic dyslipidemias, was used to identify causative pathogenic mutation in these two families and in 92 unrelated FH cases. Twelve FH patients from two unrelated families were sharing a very rare, pathogenic and founder LDLR stop gain mutation i.e., c.2027delG (p.Gly676Alafs*33) in both the homozygous or heterozygous states, but not in unrelated patients. Based on the variant zygosity, a marked phenotypic heterogeneity in terms of LDL-C levels, clinical presentations and resistance to anti-lipid treatment regimen (ACE inhibitors, β-blockers, ezetimibe, statins) of the FH patients was observed. This loss-of-function mutation is predicted to alter the free energy dynamics of the transcribed RNA, leading to its instability. Protein structural mapping has predicted that this non-sense mutation eliminates key functional domains in LDLR, which are essential for the receptor recycling and LDL particle binding. In conclusion, by combining genetics and structural bioinformatics approaches, this study identified and characterized a very rare FH causative LDLR pathogenic variant determining both clinical presentation and resistance to anti-lipid drug treatment.

Background: The cytochrome P-450 2J2 (CYP2J2) is known to be one of the major enzymes of epoxygenase pathway of arachidonic acid in extrahepatic tissues, which produces series of regioisomeric cis-epoxyeicosatrienoic acids (EETs) such as 5,6-, 8,9-, 11,12-, and 14,15-EETs. In the present study, we analyzed the impact of a genetic variant in CYP2J2 on coronary artery disease (CAD) in the Telangana region of Indian population. Material and methods: The case–control study consisted of 100 CAD cases and 110 healthy controls. The deoxyribonucleic acid was extracted using the salting out method. Genotyping and gene expression was performed by polymerase chain reaction (PCR)-restriction fragment length polymorphism and real-time-PCR methods. Results: In the present study, the percentage of smokers, alcoholics, hypertensive patients, and diabetics was high. Increase in fasting glucose, urea, creatinine, fasting triglycerides, total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), total cholesterol/high-density lipoprotein (TC/HDL), LDL/HDL, homocysteine, and C-reactive protein levels were significantly higher in patients with CAD than in controls (p

Antioxidants are involved in the process of cellular damage prevention, which is considered as an avenue for cancer development. Free radicals are produced in the body upon exposure to stress, cigarette smoke, alcohol, toxins found in personal care products, pesticides in foods, radiation from the sun, viruses, germs or fungi etc. CCND1/CyclinD1 protein was found to be overexpressed in Oral squamous cell carcinoma. One hundred patients with oral squamous cell carcinoma were recruited along with hundred controls for this study from MNJ institute of Oncology with the approval of Ethics Committee, 5 ml blood samples were collected from each patient and centrifuged to collect serum for various assays. The antioxidant enzymes like catalase, SOD, GPX and GST were estimated using enzymatic assays. Results were expressed as unit of activity for mg of protein. Insilco analysis is performed using STRING v 11 Protein interaction tool. The patients with oral cancer had significantly reduced activities of SOD, GST and GPX (1.49 ± 0.49, 3.97 ± 0.86 and 10.7 ± 0.73 respectively) compared to healthy controls (4.37 ± 1.43, 6.10 ± 1.12 and 13.8 ± 1.25 respectively) (p

BACKGROUND Xeroderma pigmentosum complementation group C (XPC), a DNA repair protein, plays an important role in the maintenance of genomic integrity and is essential for the nucleotide excision repair pathway. Polymorphisms in the XPC gene may alter DNA repair leading to genetic instability and oncogenesis. The present study aimed to assess the relationship between the XPC Ala499Val (rs2228000 C>T) and Lys939Gln (rs2228001 A>C) non-synonymous polymorphisms and susceptibility to chronic myeloid leukemia (CML) pathogenesis, disease progression and the response to targeted therapeutic regimen, imatinib mesylate. METHODS This case-control study included 212 cases and 212 controls, and the genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism assays. RESULTS Our results showed significant association of variant CT (odds ratio = 1.92, 95% confidence interval = 1.21-3.06, p = 0.003) and TT (odds ratio = 2.84, 95% confidence interval = 1.22-6.71, p = 0.007) genotypes in patients with the XPC Ala499Val polymorphism and CML risk. In addition, these genotypes were associated with CML progression to advanced phases (p = 0.006), splenomegaly (p = 0.017) and abnormal lactate dehydrogenase levels (p = 0.03). XPC Lys939Gln was found to correlate with a poor response to therapy, showing borderline significant association with minor cytogenetic response (p = 0.08) and a poor molecular response (p = 0.06). Significant association of the Ala499Val and Lys939Gln polymorphisms with prognosis was observed (Hasford high risk, p = 0.031 and p = 0.019, respectively). Haplotype analysis showed a strong correlation of variant TC haplotype with poor therapy responses (minor cytogenetic response, p = 0.019; poor molecular response, p

Cardiac Arrhythmias (CA) are responsible for syncope and sudden cardiac death (SCD) in several million cases worldwide. The molecular basis of CA pathogenesis is known, but the underlying mechanisms connecting genotype to phenotype changes in the proteins are not yet fully explored. Hence, in this study, three LQT2-linked missense mutations (Thr613Met, Ser641Phe and Gly648Ser) located in exon-7 region of KCNH2 gene identified in CA patients was assessed for their deleteriousness using diverse computational algorithms. The SIFT and PolyPhen-2 methods, which depends on sequence conservation across species, and protein structure-based information have attributed pathogenicity to these variants. Protein behavior studies at 3D level have identified that these three missense mutations induce biochemically severe amino acid changes that may alters the structure and function of KCNH2. Our molecular docking suggested that mutant KCNH2 protein shows a similar binding interactions to KB-R7943 as compared to the wild type model. These findings could be useful in resorting to alternate therapies for subset of CA patients who show limited therapeutic response to KB-R7943. This study supports that in silico approaches could act as a first-line filters to screen the potential impact of CA linked KCNH2 mutations depending upon the perspective of molecular evolution and phenotype of proteins.

Background Genetic factors play a significant role in pathogenesis of most diseases of heart. The present study was undertaken to correlate coronary artery disease with demographical, biochemical alterations, SNPs, gene expression and chromosomal abnormalities and for further enlightening the investigation in this field. Methods 150 patients taking clopidogrel drug were selected and single nucleotide polymorphism was done by PCR-RFLP techniques. With the same patients cytogenetic analysis was carried out on leukocyte cultures by karyotyping. Gene expression studies for 20 CAD patients and normal controls were done by RT-PCR techniques. Results In this study of patients with coronary artery disease the frequencies of the Extreme Metabolizers, Intermediate Metabolizers in CYP2C19*2 (rs4244285) were present in 90% and 10% but no Poor Metabolizers were found in this allele. The frequencies of Extreme Metabolizer, Intermediate Metabolizer and Poor Metabolizer in CYP2C19*3 (rs4986893) were present in 41%, 50% and 9% respectively. Among 20 CAD samples, 13 of 20 (65%) showed CYP2C19 gene over expression in CAD patients and all controls showed normal expression. Among the 150 CAD patients, 145 had normal karyotype, only five patients showed change in normal karyogram carried out by leukocyte culture. Conclusion Genetic testing of CYP2C19 may help in prescribing a dose according to genetic makeup and represent the initial steps towards the development of diagnostic tests and therapeutic strategies that will substantially improve human health. This study highlights the progress that has been made in using pharmacogenomic and gene expression analysis, cardiovascular genomic research and the potential for applying these findings in clinical medicine.

Recent times have witnessed the emergence of pharmaceuticals and personal care products (PPCPs) in the environment due to their increased utilizations and nondegradable properties. Further their presence and accumulation in the environment seriously affects human health. These PPCPs are a unique group of physiological modulators as their effect can be observed at low doses which increase gradually due to their bioaccumulation. Their alarming increase in the environment impacts all living beings including humans, which is a cause of much concern, as some compounds are known to be endocrine disrupters. Therefore this article reviews the current state-of-knowledge on PPCPs and their chronic or acute toxicities, as determined by a wide array of experimental protocols. The health effects posed by these contaminants are evaluated in the light of its dose-dependent persistence, bioaccumulation, and toxicity criteria. Available literature on the sources, transport, and impact on biological systems of PPCPs are evaluated, followed by a comprehensive review of the reported concentrations of different PPCP groups on human health. The future perspectives for research on PPCPs and their health effects are discussed considering the identified research gaps in current knowledge.

CYP3A4, a "heme" containing isoform, abundantly found in the liver, gastro-intestinal tract, lungs and renal cells, also known as drug metabolising enzyme (DME) may be responsible for the disease progression in cancers such as lung cancer. Hence, we have targeted this protein for improving drug selection and in preventing adverse reactions. The aim of this study was to examine chemotherapeutic drug binding to CYP3A4 and the interactions therein. We have used Schrodinger suite 2014, to perform molecular docking of human CYP3A4, by Induced Fit Docking using gemcitabine, cisplatin, carboplatin, docetaxel and paclitaxel drugs. We evaluated drug-binding affinities using Prime/MMGBSA and using these scores we compared the affinities of combination therapies against CYP3A4. Analysis of the docking results showed gemcitabine>carboplatin>cisplatin as the order of binding affinities, with gemcitabine having the best docking score. Interestingly, docetaxel and paclitaxel did not bind to CYP3A4*1B. The combination drug-binding affinity analysis showed gemcitabine+carboplatin to have the best docking score and hence, efficacy. Our investigation has identified the residue Arg 105 to be more frequently involved in drug binding to CYP3A4. Our results suggest that gemcitabine or combination of gemcitabine+carboplatin could serve as an excellent therapy against CYP3A4 in NSCLC patients. Thus, our study depicts binding of chemotherapeutic drugs to CYP3A4 and has identified the residues that may be targeted for therapy in NSCLC patients.

In individuals with diabetes, a log linear relationship exists between cholesterol levels and cardiovascular disease. Type 2 diabetes (T2D) and Statins, a cholesterol lowering drug, have a complex relationship. Statins are potent modulators of CYP3A4 2 enzyme and endothelial nitric oxide synthase (eNOS) functions in a number of cholesterol-independent, cardio protective actions in T2D. The aim of this study was to evaluate the CYP3A4 2 and eNOS gene mutations in a large number of T2D patients undergoing statin treatments. Blood samples were collected from 386 subjects in which 196 diabetic patients with hyperlipidemia were undergoing statin treatment (108 females and 88 males). The 190 healthy non-diabetic volunteers formed the control group. We investigated single nucleotide polymorphisms in diabetic patients and controls, and found that the statin therapy was not found to be effective in lowering LDL-cholesterol levels. Statistical analysis showed that T2D patients had significantly higher values of not only glucose levels but also a very high value of Triglycerides and cholesterol at the time of presentation. Our results for CYP3A4 2 showed that the genotype TT (wild type) had lower LDL when compared to TC (heterozygous). Similarly, the genotype TC (heterozygous) had lower LDL when compared to CC (homozygous). A similar trend was observed in the GG (wild type) and GT (heterozygous) of eNOS. In conclusion, we have described for the first time a significant correlation of statin treatment and CYP3A4 2 and eNOS gene polymorphisms in T2D, suggesting a new genetic susceptibility factor for insulin resistance and hyperlipidemia in T2D.

Recent times have pointed out that the genetic polymorphism in oncogenes influences the chemotherapeutic responses in cancer treatments. We are aware of the fact that every year thousands of deaths are caused by fatal drug reactions; a few potential causes that can be mentioned includethe fact that there are the severity of the disease being treated, drug interactions, nutritional status, renal and liver functions being affected, and also the inherited differences in drug metabolism and genetic polymorphism [1,2]. This may be due to the difference in DNA sequence among individuals, groups, or populations. Genetic polymorphisms may be the result of chance processes, or may have been induced by external agents (such as, xenobiotics / drugs, viruses, environmental exposures or radiation). Sequence variations (mutations) in the genes encoding enzymes and other proteins result from stochastic genetic processes and may accumulate in the population, depending on selective pressures [3]. One of the major causes of interindividual variation of drug effects is due to genetic variation of drug metabolism. Persidis [4] has very appropriately defined: that “pharmacogenomics approach is a redefinition of what a disease is at the molecular level”. This is the reason why the progress in SNP mapping and characterization is also very important, as it will help pinpoint the genomic variations much sooner and enable the clinically relevant correlations to be made more effectively [5-7].

In this study investigations were made to detect the assocn. of MTHFR C677T and A1298C polymorphisms in breast cancer patients, in the South Indian population. Eighty eight women patients with breast cancer and 95 healthy women as controls were included in the study after their consent to participate in this program. MTHFR gene polymorphisms were detd. by the PCR-RFLP method. The allele frequencies of the MTHFR C677T were 27.84% in the breast cancer subjects and 19.47% in the controls. The allele frequencies of the MTHFR A1298C were 25.56% in the breast cancer subjects and 17.89% in the controls. Frequencies of MTHFR C677C, C677T and T677T were 47.9%, 44.8%, 7.1% in breast cancer patients and 63.2, 34.5 and 4.6% in the controls. Frequencies of MTHFR A1298A, A1298C and C1298C were 54.8, 40.8 and 5.1% in breast cancer patients and 66.9, 30.1 and 2.9% in the controls. When we compared the frequencies of C677T and T677T with C677C, A1298C and C1298C with A1298A, we found less significant assocn. between specific MTHFR variants in breast cancer patients. Our findings suggest that MTHFR C677T and A1298C gene variants do not have a major influence on the susceptibility to breast cancer in south Indian population. [on SciFinder(R)]

Background: Cardiovascular disease (CVD) remains a major cause of morbidity and death not only in developed countries but also in developing countries. The associated risk factors which have been linked to CVD include diabetes, hypertension, and the like and non-modifiable risk factors such as age, sex, and family history. However, one cannot fully explain why some individuals are prone to CAD and others are not. Indians, like the Americans, Europeans, and Japanese also have the highest rate of heart disease, but are associated with high mortality. Objective: The aim of this study was to analyze various demographic and clinical characteristics retrospectively to investigate any unreported parameters. Materials and Methods: It has been examined and statistically analyzed the records of 530 patients with coronary heart disease on angiography and who underwent cardiac evaluation at Mahavir Hospital and Research Centre, Hyderabad, Telangana, India between July 2012 and March 2014. Also, a few routine parameters like TC, HDL, LDL, triglycerides and conventional risk factors, serum electrolytes, blood grouping, pattern, and severity of the disease were included. Result: Among 530 patients 70% were males, 30% were females. Smokers were 320 patients, and very few (10%) were alcoholics. 30.18% patients suffered from hypertension, 40.56% had diabetes mellitus, 47.16% had dyslipidemia, and about 15–20% had family history. The levels of TC, LDL-C and triglycerides were higher in males than females as compared to HDL-C. Angiographic analysis showed 20% patients had single vessel disease (SVD), 24.5% patients had double vessel disease (DVD), and 40.56% had triple vessel disease (TVD). Further 4.33% had left main disease and 10% had normal coronary angiogram. The mean values for serum creatinine, serum potassium, and serum sodium were highly associated (p=0.001). Conclusion: The present study recorded major abnormalities in mean lipid levels as elevated TC and LDL-C levels and low HDL-C in CAD patients. The male preponderance indicted smoking as the major risk factor, while associated complications like diabetes and hypertension were significantly more common. Double and triple vessels disease was most common in this study. One interesting observation was that CVD patients with B blood group were more in numbers in this study followed by O group, then A and very few with AB group. Further most of them were non-alcoholic. These results reinforces in the control of biochemical parameters, improvement of quality of life, in the prevention and management of CAD.

The hypoglycemic effect of the aqueous extract ofAbroma augusta (Family: Steculiceae) was studied in normal as well as alloxan diabetic rats. Treatement of diabetic rats with 4 ml (4gm dry weight) of agueous extract ofA. augusta for 16 weeks resulted in gradual but significant fall in fasting blood glucose and improvement in glucose tolerance. Serum total and LDL cholesterol and triacylglycerol which increased in diabetic rats showed improvement. These results show that the water extract ofA. augusta has both hypoglycemic and hypocholesterolemic effects.

Background: The wide spectrum of clinical features in advanced stages of non-small cell lung cancer (NSCLC) probably contributes to disparities in outcomes because of different prognostic variables significant for stage IIIB/IV patients. Hence the aim of this study was to check for favorable response of patients to various chemotherapeutic combinations with respect to patient survival in stage IIIB and stage IV NSCLC disease. We selected those patients for our study who were receiving treatment with paclitaxel, gemcitabine or etoposide in combination with platinum based drugs. Materials and Methods: Seventy-two patients who visited the hospital from June 2009 to November 2012 with confirmed diagnosis of lung cancer were included, and data were collected for follow up and classified according to treatment received with respect to patients’ regimen and response, and overall survival. This study analyzed tumor variables that were associated with clinical outcome in advanced NSCLC patients who were undergoing first-line chemotherapy for stage IIIB/IV NSCLC. Results: Comparative data on various parameters like age, gender, stage, histology, site of disease, metastatic site and chemo-regimens was analyzed; these parameters predicted variable significant improvement for overall survival (p≥0.05). One and two year survival rates were 20.8% and 15.3% . Conclusions: In this study we found slight improvement in survival rates in NSCLC and clinical outcomes with one combination (carboplatin+paclitaxel). Overall there were only marginal differences in survival rates for other chemo-regimens evaluated in this study.

Leptin plays an important role in mammary tumor formation (Candida N Pereral et al., 2008 1). It is secreted by adipose tissue that acts on the brain to regulate energy expenditure and food intake and has an important role in energy balance, insulin pathway and inflammation. Hence the aim of our investigation has been to study the impact of Lep-2548G/A polymorphism in breast cancer as compared to matched controls. This study mainly focuses on the polymorphism leptin gene for variants by a screening this gene in south Indian obese subjects (n = 154 obese breast cancer cases and n=145 obese controls). We utilized PCR-RFLP based assay to evaluate the association between the Gln2548Arg polymorphism of the leptin gene and breast cancer risk in a case control study. The distributions of all three genotypes GG, GA and AA in breast cancer cases were 18.8%, 44.8%, and 36.4% compared to that of the controls, 33.0%, 29.6%, and 37.4%. We found that postmenopausal breast cancer cases showed statistically significant association with GA genotype when compared with premenopausal women without the disease (p= 0.001). This difference was between the cases and controls in the Gln2548Arg genotypes. Our findings suggest that the LEP Gln2548Arg polymorphism may be a useful biomarker associated with the risk of breast cancer women in Indian population.

In a developing country like India, classification and identification of the species of Anopheline mosquitoes in control operations of mosquito-borne diseases is of paramount importance. The WHO monograph, which describes the taxonomic data in the form of a pictorial key is generally difficult to understand by a non-taxonomist. Utilizing the principles of ID3 algorithm, a novel rule-based system, for the fast identification of unknown species of Indian Anopheline mosquitoes, is developed. The rule-based system is user-friendly, menu-driven and even a novice can make use of it in the identification of the unknown species with little practice. The above software is available on floppy disk and can be obtained with a minimum cost. This program can be ported on 5 1/4" or 3 1/2" floppy disk.

Keeping in view the need for corporate communications in cancer research perspective, which means communications serves as the liaison between an organization and public. This editorial presents a view which is very different from commercial-marketing a product or laisoning with producer companies etc. It is all about developments in cancer research which leads one to understand - what is personalized medicine. As the scientific and medical communities begin to decipher the secrets locked in the human genome code, the way we approach the diagnosis, treatment and prevention of disease will change dramatically. With the detection of human genome, scientists have already created large databases filled with thousands of single nucleotide sequence changes. Some of these single nucleotide polymorphisms (SNPs) could define the genetic basis of what keeps healthy or makes us sick. Currently the most common applications for SNP related research tools are gene-disease association studies, drug-gene interactions and drug target validation. Other popular applications are disease susceptibility studies or diagnostics, pharmacogenomic studies for clinical trials, drug target screening, and new technology development.

Background : CYP1A1 is one of the commonest genes which had been widely investigated to find the risk of various malignancies in different ethnic groups. The polymorphism in these genes with a combination of environmental exposure has been hypothesized to confer a differential risk of cancer for individuals carrying these genetic variants. Based on this model, individuals with higher CYP1A1 activity would be at increased risk of cancer when exposed to high levels of smoke components. The proposed mechanism involves cytochrome P450 1A1 (CYP1A1), a gene that is inducible by xenobiotics to produce genetic susceptibility for malignancies. Patients and procedures : We performed a case–control study in 205 cases with histopathologically confirmed squamous cell carcinoma of head and neck and reported habits of bidi or cigarettes smoking and 245 similar controls to investigate the role of CYP1A1 polymorphisms in the risk of head and neck cancers especially among smokers of Hyderabad Indian population. Venous blood samples (5 ml) were collected from patients and control groups; genomic DNA was extracted and used for polymerase chain reaction (PCR) to determine the genotypes. RFLP assays were designed to detect each of the variant CYP1A1 alleles. Results and discussion : CYP1A1m1/m1 genotype (OR = 8.12, 95% CI: 3.27–21.30) and CYP1A1w1/m1 showed elevated risk when compared with CYP1A1w1/w1. Similarly CYP1A1w2/m2 (OR = 1.58, 95% CI: 0.94–2.67) and CYP1A1m2/m2 (OR = 6.31, 95% CI: 2.74–18.69) genotypes also showed elevated risk when compared with CYP1A1w2/w2 genotype. This data demonstrated that smoking was a risk factor for head and neck cancers. The m2 mutations were in close linkage disequilibrium with the m1 mutations; 53% m1 mutants had the mutation in the m2 site. Conclusion : Those individuals carrying at least one CYP1A1 m1 or m2 variant allele were at a 2-fold elevated risk for head and neck cancer. Our data clearly demonstrates that CYP1A1 is an important determinant in susceptibility to tobacco-induced head and neck carcinogens and there is an association between genetic polymorphism in the CYP1A1 locus and elevated risk of the type of smoking among Indians. This appears to be a new and important prognostic and diagnostic marker for determining the risk of head and neck cancers genetically.

Background: The purpose of this study was to investigate the genotype frequencies of CYP3A4*1B and CYP3A5*3 in lung cancer patients which may be useful in determining the patients' predisposition to platinum based therapies, and may be helpful for individualized drug dosing and improved therapeutics and disease management. Results: We evaluated these two common polymorphisms in south Indian population, based on case-control study of 126 lung cancer cases and 111 controls using a PCR-RFLP-based assay. The investigation of the CYP3A4*1B gene polymorphism revealed, no significant difference in distribution between the lung cancer patients and the controls (p=0.65) . The distribution of CYP3A5*3 homozygous genotypes and heterozygous plus homozygous genotypes were significantly associated (p=0.0004 & p=0.0001) with lung cancer patients, and the *3/*3 genotype had a 4.38 fold increased risk for lung cancer. In our study *1A/*1B heterozygous genotype patients were found to constitute a major percentage of patients receiving Gemcitabine plus carboplatin therapy. Conclusions: In conclusion, the results of our study indicated a relationship between CYP 3A4*1B and CYP3A5*3 polymorphisms and genetic predispositions to lung cancer. Thus detection of CYP3A4*1B/CYP3A4 and CYP3A5*3/CYP3A5 genotype frequencies in Indian population may be important in view of interindividualized drug dosing, improved therapeutics and disease management.

Introduction: Age related hearing impairment (ARHI) is the most common sensory deficit in the elderly population and has become a severe social health problem. Several mechanisms have been described for hearing impairment in elderly people. Probable cause of hearing impairment may result from damage in the inner and outer hair cell, loss of stria vascularis, thickening of basilar membrane, or loss of sensory elements in the basal end of the cochlea. The aim of present study is to identify the protein biomarkers associated with ARHI using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Materials and Methods: Total 96 study subjects (48 experimental and 48 controls) were selected for this study. Serum samples were used for biochemical analysis and one-dimensional electrophoresis. Statistical analysis was done by GraphPad software. Results: Glucose, serum creatinine, and urea levels were in normal range and mean urea and creatinine levels are insignificantly associated with ARHI while mean glucose level is significantly associated with ARHI. Smoking/alcohol consumption did not show any significant association with ARHI. The molecular weight of the differentially expressed protein was 16.2 kDa as calculated by gel image analyzer software. The differentially expressed protein may be cochlin tomoprotein (CTP) of 16 kDa which is an isomer of cochlin protein. CTP contains all the known mutation sites associated with deafness. Conclusion: The expression of differentially expressed protein was consistently observed among experimental subjects as compared to control. This protein may help in the prediagnosis of ARHI due to added advantage of enhanced expression in subjects of ARHI. Results revealed males were more prone to ARHI than female.

Acute lymphocytic leukemia (ALL) is the most common pediatric cancer worldwide, and is particularly more common in the Indian population. Hence, research is increasingly examining the factors involved in disease development. In the present study, we examined the effect of MTHFR (5,10-methylenetetrahydrofolate reductase) C677T and A1298C polymorphisms in ALL. Blood samples of 135 children with ALL and 142 matched controls were analysed. The presence of MTHFR C677T and A1298C polymorphisms were screened using polymerase chain reaction-restriction fragment length polymorphism based approaches. The frequency of MTHFR 677CC, 677CT and 677TT genotypes were 37.77%, 57.03% and 5.18% in cases and 55.63%, 40.84% and 3.52% in controls, respectively. Frequencies of MTHFR 1298AA, 1298AC and 1298CC genotypes were 30.37%, 61.48% and 8.14% in cases and 45.77%, 47.88% and 6.33% in controls, respectively. The present study inidcates that there is an association between MTHFR gene polymorphisms and ALL. MTHFR variants also showed a gender bias. The frequencies of MTHFR 677CC and 677CT genotypes were 33.33% and 65.51% in males and 45.83% and 41.66% in females. Frequencies of MTHFR 1298AA, 1298AC and 1298CC genotypes were 26.43%, 67.81% and 5.74% in males and 37.5%, 50.0% and 12.5% in females, respectively. It is evident that the male children were more susceptible to ALL compared to female children. Associations found in these studies were significant with respect to gender bias; hence, it is possible that MTHFR C677T and A1298C can be good markers for ALL. Moreover, the possibility also exists that these variants may be influenced by the folate uptake of mothers during pregnancy, thereby influencing the enzyme activity and the ethnicity of the cases examined to date. The gender bias of MTHFR polymorphism in ALL is reported for the first time.

A comparative study was made on the effect of povidone-iodine on wound healing in normal, diabetic and steroid depressed states in the excision wound model in rats. Healing was assessed by the rate of contraction of wounds and epithelialization after three weeks of topical application. Normal and diabetic groups were comparable (P < 0.02) concerning the above-mentioned parameters as well as collagen formation. The steroid group showed significant retardation in healing time (P < 0.001), epithelialization (P < 0.001) and collagen formation (P < 0.001) showing that povidone-iodine did not overcome the steroid effect.

Water hyacinth growth is kept under control by the week eating weevils, Neochetina eichhornae (Warner) and N. bruchi (Hustache). Water hyacinth is generally considered an aquatic weed because it clogs waterways, although it has recently been evaluated as a potential biological filter for sewage effluents. Water hyacinth plants are continuously subjected to contamination by mercury and other heavy metals from industrial effluents and fertilizer impurities. Little is known about the interaction of heavy metals/plants/insects. Aminotransferases are generally considered as indices for metabolic disturbances during Hg exposure. These enzymes are key enzymes for transamination, i.e., transfer of amino group from amino acid to keto acids which are ubiquitous in insects. The objective of the present study was to examine the bioaccumulation of mercury through the food chain in Neochetina eichhornae and its impact on protein metabolism.

Oxidative stress has been suggested in the pathogenesis of Chronic Obstructive Pulmonary Disease (COPD) with an additional burden of diabetes, hypertension and cardiovascular disease. In the present study, we investigated erythrocyte antioxidant enzymes activities in correlation to COPD severity and COPD comorbidities. One hundred twenty seven subjects with COPD and 59 healthy controls participated in this study. COPD severity was done based on the Global Initiative for Chronic Obstructive Lung Disease criteria. The erythrocytes enzyme activities of superoxide dismutase (SOD), catalase (CAT), glutathione-s-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GR) and total antioxidant status (TAS) were measured with spectrophotometric method. COPD patients showed significant decrease in TAS (p > 0.05), GST (p