[Significance of CMV-seropositivity in the alterations of CD4[+] T- cell subsets and expression of their phenotyping markers in B-cell chronic lymphocytic leukemia]

B-cell chronic lymphocytic leukemia [B-CLL] is a B-cell malignancy which has been associated with a variety of abnormalities in non-malignant T cells. Viral antigens are able to produce profound alterations in T-cell and cytomegalovirus [CMV] has been involved in T-cell abnormalities in healthy elderly individuals. Therefore, the relationship between these changes and CMV was studied in CLL patients. This was a cross sectional study and included 79 B-CLL patients [41 CMV seropositive and 38 CMV seronegative]. The cell counting was done by Coulter cell counter. The T-cell subgroups and cell phenotype were studied by monoclonal antibodies and flow cytometry. The secretion of cytokine was detected by intracellular cytokine staining post stimulation and short time culture. CD8[+] and CD4[+]CD8[dim] T cell subgroups were significantly more in CMV[+] patients than CMV negatives [P<0.01]. IFN-gamma producing T cells were significantly more in CMV [+] patients, whereas IL-2 producing T cells were more in CMV[-] patients [P<0.05 and P<0.01, respectively]. A prominent decrease was seen in the expression of CD27, CD28, CD45RA and CCR7 in CMV[+] patients, whereas CD45RO and CD57 showed significant rise [P<0.05 and P<0.001, respectively]. CMV seropositivity causes broad alterations in T-cells and expression of terminally differentiated phenotype in B-CLL patients. Therefore, such profile in B-CLL is highly related to CMV seropositivity

[Effect of medicinal smokes on some nosocomial infection factors]

Bacterial resistance to antibiotics is a main problem in the treatment of infectious diseases. Thus, searching for alternative drug is essential in Iran and particularly Chaharmahal va bakhtiari province. People use medicinal smokes such as donkey dung and Peganum harmala seed smokes for treatment of infectious diseases. Therefore, this study was aimed to evaluate the antimicrobial property of donkey dung and Peganum harmala seed smokes on Staphylococcus aureus and Pseudomonas aeroginosa. In this interventional and laboratory study, groups of Peganum harmala seed smoke and donkey dung were considered as case groups and antibiotic disks as positive control group. Pseudomonas aeroginosa and Staphylococcus aureus were cultured in suitable medium [Blood Agar, EMB and Mueller-Hinton agar]. Antibiogram blank disks were fumigated separately with Peganum harmala seed and female donkey dung smoke then placed on microbial plate with sterile methods. Following 48 hours incubation at 37°C, the zone of growth inhibition evaluated by measuring the zone around the disks. Fumigation process was done in special chest that designed for this research. We repeated fumigation each 20 minutes for 24 times. Data about measuring the zone of growth inhibition were analyzed by using and mean statistic exam. Staphylococcus aureus was sensitive to Peganum harmala seed, and fdonkey dung smokes and Pseudomonas aeroginosa was sensitive to female donkey dung smoke. Staphylococcus aureus was resistant to cloxacilllin and Pseudomonas aeroginosa was sensitive only to erythromycin and ciprofloxacin. The increasing time of fumigation in sensitive cases enhanced antimicrobial effects and the zone of growth inhibition. Antimicrobial effects of donkey dung smokes on resistance pathogens such as Pseudomonas aeroginosa, Staphylococcus aureus revealed the necessity of performing expanded research about composition and property of this smoke

[Study of LDL receptor gene mutations in patients with familial hypercholesterolemia in Chaharmahal va Bakhtiari province]

Familial hypercholesterolemia is an autosomal dominant inherited disorder, characterized by increased level of low-density lipoprotein cholesterol and lipid accumulation in tendons and arteries. It can cause premature atherosclerosis and increased risk of coronary heart disease [CHD]. Familial hypercholesterolemia is caused mainly by mutations in low-density lipoprotein receptor [LDLR] gene. The aim of this study was to analyze the LDLR gene mutations in a group of patients from Chaharmahal va Bakhtiari province. In this descriptive-lab based study, 57 suspected FH patients were screened for mutations in promoter and exons 1,3,5,11,13,15,16,17 and 18 of LDLR gene using PCR-SSCP strategy. Two different LDLR gene variations, including heterozygote mutation 283T>A and polymorphism 1959T>C, were identified in 1 and 9 FH Families studied, respectively. We conclude that LDLR gene mutation may not be the major cause of FH in the population studied and the cause of FH in Chaharmahal va Bakhtiari province remains to be detected in other loci or genes

[DFNB59 gene mutations screening in non syndromic deaf subjects in Chaharmahal va Bakhtiari province]

The incidence of pre-lingual deafness is about 1 in 1000 neonates from which more than 60% of cases are inherited. Deafness is a heterogeneous disorder and may be due to genetic or environmental cause or both. Mutations in the DFNB59 gene encoding pejvakin protein has been very recently shown to cause neural deafness. In the present study, we have conducted type and frequency of the DFNB59 gene mutations in a cohort of 100 non syndromic deaf subjects in Chaharmahal va Bakhtiari province. In this descriptive-lab based study we investigated the frequency of DFNB59 gene mutations in the entire coding exons of the gene. DNA was extracted from the peripheral blood samples following the standard phenol chloroform procedure. DFNB59 gene mutations were investigated using PCR-SSCP/ Heteroduplex Analysis [HA]. The results of PCRSSCP/HA were confirmed by sequencing of exon 7, nested PCR and PCR-RFLP of 3 known DFNB59 mutations. Altogether 3 different gene polymorphisms [793C>G, 793C>T and 874G>A] and one mutation [988delG] were detected in 7, 5, 2 and 1 subjects respectively. Based on our data from the present study and previous study, we conclude that DFNB59 gene mutations have a very low contribution to deafness in patients in Chaharmahal va Bakhtiari province and are not of great clinical importance in this region

Detection of mutations in exons 5-8 of the P53 gene in gastric cancer samples using PCR-SSCP in Chaharmahal va Bakhtiari province, 2006-2007

Gastric cancer is the second cause of cancer death world wide. Genetic factors including oncogens and tumor suppressor genes are always contributed in progression of this cancer. The P53 tumor suppressor gene has a broad role in the cell such as programmed cell death and stop cell replicating damaged DNA. Mutations in the P53 gene, which are frequently seen in human gastric cancer, impair its tumor suppression function. The aim of this study was to determine the P53 gene mutations in gastric cancer specimens in Chaharmahal va Bakhtiari Province. In this descriptive-lab based study, we investigated the P53 gene mutations in exons 5-8 in 38 paraffin embedded gastric cancer specimens. DNA was extracted following the standard phenol chloroform protocol. The P53 gene mutations were determined using PCR-SSCP procedure. Band shifts were detected in all positive controls examined. However, no shifted band was detected in samples from gastric cancer patients tested. The results of this study demonstrated that association between P53 gene mutations and gastric cancer is very low in Chaharmahal va Bakhtiari province. However, we have examined a limited number of 38 gastric samples and more samples are needed to be investigated to unravel the contribution of P53 gene mutations leading to gastric cancer in this province

Molecular pathology of 6 novel GJB2 allelic variants detected in familial and sporadic Iranian non syndromic hearing loss cases

Mutations of GJB2 gene encoding connexion 26 are the most common cause of hearing loss in many populations. A very wide spectrum of GJB2 gene mutations associated with hearing loss have been detected but pathogenic role has been tested only for a part of them. In this study, we have provided genetic evidence on the pathogenicity of our previously reported novel GJB2 allelic variants. The pathogenic role of GJB2 allelic variants were assessed using co segregation of each allelic variant with hearing loss in family members, absence of the allelic variants in control populations, coexistence with a second GJB2 mutation, nature of the amino acid substitution and evolutionary conservation of the appropriate amino acid. The GJB2 allelic variants including 363delC, 327delGGinsA, H16R and G200R have been co segregated with autosomal recessive non syndromic hearing loss in five families and are not found in control subjects. The G130V and K102Q were found in heterozygous state in two deaf individuals. G130V results in an exchange a residue highly conserved among all the connexins but was found with a rate of 1% in control subjects and K102Q results in an exchange a residue not conserved among all the connexins and not identified in control subjects. We conclude that, 363delC, 327delGGinsA, H16R and G200R may be pathogenic. However, the pathogenicity and inheritance of K102Q and G130V can not be assessed clearly and remains to be identified