Stress among medical students of Gorgan (South East of Caspian Sea), Iran

Objective: This study aims to estimate the prevalence of psychological stress and association between the levels of stress and study variables among Gorgan medical students. Materials and methods: All three year medical students (129 basic sciences students) in Gorgan Faculty of Medicine, Golestan University of medical Sciences, were asked to complete the Kessler 10 questionnaire. Results: The findings showed mild, moderate and severe stress among 26.22%, 20.50% and 14.75% study subjects. 39.35% of medical students had no stress. There was statistically significant association between year of study and stress levels (p= 0.040). Conclusion: The results indicate that there is a decrease in the psychological health of first year medical students. Provided that stress management courses are organised by medical schools, when the students arrive, they will cope up with the stress in coming years. These courses may reduce the negative effects of stress on medical students. By providing such courses and reducing stress level, medical students may improve their medical education

Prevalence of Cryptosporidium spp. infection in renal transplant and hemodialysis patients

Transplanted and hemodialysis patients are frequently affected by parasitic diseases such as cryptosporidiosis. Cryptosporidium is a parasite causing self-limited diarrhea and enteritis in healthy individuals. The presence of Cryptosporidium infection was studied in three groups including 87 renal transplant patients, 103 hemodialysis patients, and 60 healthy individuals as the control group. Two stool specimens were obtained from each case. The specimens were concentrated by the formalin-ether method and two smears were prepared from each. The smears were stained by modified acid-fast method and were observed under a light microscope. Ten (11.5) renal transplant and 4 (3.88) hemodialysis patients were positive for Cryptosporidium infection. No positive results were obtained in the control group. The results showed a statistically significant difference between renal transplant and control groups (P=0.02), but the difference between hemodialysis and control groups was not significant (P=0.2). The results also showed that the rate of Cryptosporidium infection in renal transplant patients was much higher than hemodialysis patients. The susceptibility of renal transplant patients to Cryptosporidium infection is much more than other studied groups and this could be due to immunosuppressive therapy in these patients

Phenotypic expansion of DGKE-associated diseases.

Atypical hemolytic uremic syndrome (aHUS) is usually characterized by uncontrolled complement activation. The recent discovery of loss-of-function mutations in DGKE in patients with aHUS and normal complement levels challenged this observation. DGKE, encoding diacylglycerol kinase-ε, has not been implicated in the complement cascade but hypothetically leads to a prothrombotic state. The discovery of this novel mechanism has potential implications for the treatment of infants with aHUS, who are increasingly treated with complement blocking agents. In this study, we used homozygosity mapping and whole-exome sequencing to identify a novel truncating mutation in DGKE (p.K101X) in a consanguineous family with patients affected by thrombotic microangiopathy characterized by significant serum complement activation and consumption of the complement fraction C3. Aggressive plasma infusion therapy controlled systemic symptoms and prevented renal failure, suggesting that this treatment can significantly affect the natural history of this aggressive disease. Our study expands the clinical phenotypes associated with mutations in DGKE and challenges the benefits of complement blockade treatment in such patients. Mechanistic studies of DGKE and aHUS are, therefore, essential to the design of appropriate therapeutic strategies in patients with DGKE mutations

Molecular and Serological Techniques to Determine the Acute and Chronic Phase of Toxoplasmosis in HIV Patients

BACKGROUND AND OBJECTIVE: Toxoplasma gondii is associated with several complications including neurological problems, ocular damage and encephalitis in immunodeficiency individuals. Early diagnosis of this infection can lead to better management of this disease. Therefore, this study was conducted to determine the presence of Toxoplasma gondii with two serologic and molecular methods in HIV-infected individuals. METHODS: In this cross-sectional study, 102 male patients with HIV with a mean age of 40 ± 9.2 years were examined. The serum sample was used for ELISA to determine the acute and chronic phase and cellular samples using Real Time-PCR for determining the acute phase of the disease. The relationship between age groups and the HIV transmission pathway, as well as the age group, was compared with the results of the Toxoplasma gondii test. FINDINGS: Out of 102 samples tested for IgM anti-Toxoplasma gondii antigen by ELFA, all (100%) samples were negative, but for anti-IgG anti-parasite, 44 samples (43.1%) were positive and 58 Sample (56.9%) was negative. Out of 102 samples tested by RT-PCR, all (100%) samples were negative for Toxoplasma DNA. There was a statistically significant relationship between age groups and transmission pathways (p<0.001), as well as between age groups with anti-Toxoplasma gondii IgG levels (p<0.001). CONCLUSION: According to the results of this study, the use of IgM-ELFA and PCR-RT methods for the diagnosis of acute phase and IgG-ELFA in the chronic phase of the disease is important. With the diagnosis of chronic form of toxoplasmosis, preventive treatments can be used in HIV + patients

Localization of a gene for nonsyndromic renal hypodysplasia to chromosome 1p32-33.

Nonsyndromic defects in the urinary tract are the most common cause of end-stage renal failure in children and account for a significant proportion of adult nephropathy. The genetic basis of these disorders is not fully understood. We studied seven multiplex kindreds ascertained via an index case with a nonsyndromic solitary kidney or renal hypodysplasia. Systematic ultrasonographic screening revealed that many family members harbor malformations, such as solitary kidneys, hypodysplasia, or ureteric abnormalities (in a total of 29 affected individuals). A genomewide scan identified significant linkage to a 6.9-Mb segment on chromosome 1p32-33 under an autosomal dominant model with reduced penetrance (peak LOD score 3.5 at D1S2652 in the largest kindred). Altogether, three of the seven families showed positive LOD scores at this interval, demonstrating heterogeneity of the trait (peak HLOD 3.9, with 45% of families linked). The chromosome 1p32-33 interval contains 52 transcription units, and at least 23 of these are expressed at stage E12.5 in the murine ureteric bud and/or metanephric mesenchyme. These data show that autosomal dominant nonsyndromic renal hypodysplasia and associated urinary tract malformations are genetically heterogeneous and identify a locus for this common cause of human kidney failure

A guided tour of asynchronous cellular automata

Research on asynchronous cellular automata has received a great amount of attention these last years and has turned to a thriving field. We survey the recent research that has been carried out on this topic and present a wide state of the art where computing and modelling issues are both represented.Comment: To appear in the Journal of Cellular Automat

Prevalence of anti-toxoplasma gondii antibodies in young Iranians: The Caspian III study

Background: Toxoplasmosis is a worldwide neglected tropical and sub-tropical infection caused by Toxoplasma gondii (T. gondii). Most of the previous studies on the seroprevalence of T. gondii in Iran have been done at provincial level and on specific populations, including pregnant females. Socioeconomic parameters are associated with the prevalence of this disease. In this study, the authors evaluated the presence of anti-T. gondii antibodies and the related risk factors in Iranian adolescents. Methods: This was a cross-sectional study on serum samples from the third Iranian national school-based survey (the CASPIAN III study), which included 10- to 18-year-old students. Participants were selected by multistage sampling from 27 Iranian provinces. In this study, serum samples of 882 adolescents from 16 provinces were randomly selected and examined for IgG and IgM antibodies against T. gondiiby theEnzymeLinked Fluorescent Assay (ELFA).Demographicandsocioeconomic factors related to T. gondii infection were gathered using the global school-based health survey (GSHS) questionnaire. Results: The overall T. gondii IgGandIgMseropositivitywas56.3 (95 CI: 53.4 to 59.2)and3.7 (95CI: 2.7 to 4.9), respectively. In multivariate logistic regression model, family size was statistically associated with seroprevalence of anti T. gondii IgG. Living in crowded households (households with more than 4 people vs. households with less than 4 people) increased the risk of seropositivity of T. gondii (OR: 1.40, 95 CI: 1.10 to 1.99). Conclusions: The results of this study indicate that about 40 of Iranian adolescents have not had contact with the T. gondii, thus the risk of congenital toxoplasmosis might be high in young females. Also, household size was the main factor associated with T. gondii infection. Preventive strategies and health education in Iranian adolescents are recommended. © 2017, Pediartric Infections Research Center

Mutations in DSTYK and dominant urinary tract malformations.

ABSTRACT Introduction Congenital abnormalities of the kidney of the urinary tract are the most common cause of pediatric kidney failure. These disorders are highly heterogeneous, and their etiology is poorly understood. Methods We performed genome-wide linkage analysis and whole-exome sequencing in a family with autosomal dominant congenital abnormalities of the kidney of the urinary tract (7 affected family members). We also performed sequence analysis in 311 unrelated patients, as well as histologic and functional studies. Results Linkage analysis identified five regions of the genome that were shared among all affected family members. Exome sequencing identified a single rare deleterious variant within these linkage intervals, a heterozygous splice-site mutation in dual serine/threonine and tyrosine protein kinase (DSTYK). This variant, which resulted in aberrant gene product splicing, was present in all affected family members. Additional independent DSTYK mutations, including nonsense and splice-site mutations, were detected among 7/311 unrelated patients. DSTYK is highly expressed in the maturing epithelia of all major organs, localizing to cell membranes. Knockdown in zebrafish resulted in multi-organ developmental defects, resembling loss of fibroblast growth factor (FGF) signaling. Consistent with this finding, DSTYK colocalizes with FGF receptors in the ureteric bud and metanephric mesenchyme. Finally, DSTYK knockdown in human embryonic kidney cells inhibited FGF-stimulated ERK-phosphorylation, the principal signal downstream of receptor tyrosine kinases. Conclusions We detected DSTYK mutations in 2.2% of patients with congenital abnormalities of the kidney and urinary tract whom we studied, suggesting that DSTYK is a major determinant of human urinary tract development, downstream of FGF signaling

Genetic studies of IgA nephropathy: past, present, and future

Immunoglobulin A nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide and an important cause of kidney disease in young adults. Highly variable clinical presentation and outcome of IgAN suggest that this diagnosis may encompass multiple subsets of disease that are not distinguishable by currently available clinical tools. Marked differences in disease prevalence between individuals of European, Asian, and African ancestry suggest the existence of susceptibility genes that are present at variable frequencies in these populations. Familial forms of IgAN have also been reported throughout the world but are probably underrecognized because associated urinary abnormalities are often intermittent in affected family members. Of the many pathogenic mechanisms reported, defects in IgA1 glycosylation that lead to formation of immune complexes have been consistently demonstrated. Recent data indicates that these IgA1 glycosylation defects are inherited and constitute a heritable risk factor for IgAN. Because of the complex genetic architecture of IgAN, the efforts to map disease susceptibility genes have been difficult, and no causative mutations have yet been identified. Linkage-based approaches have been hindered by disease heterogeneity and lack of a reliable noninvasive diagnostic test for screening family members at risk of IgAN. Many candidate-gene association studies have been published, but most suffer from small sample size and methodological problems, and none of the results have been convincingly validated. New genomic approaches, including genome-wide association studies currently under way, offer promising tools for elucidating the genetic basis of IgAN