A cross-sectional study of the seroprevalence and flock-level factors associated with ovine and caprine brucellosis in southeastern Iran.

This cross-sectional study was conducted to estimate seroprevalence and to identify flock-level factors associated with seropositivity to brucellosis in small ruminants in Kerman province, southeastern Iran. In October-November 2011, serum samples were randomly collected from 1767 sheep and 1233 goats, older than 18 months, from 300 flocks. The sera were initially screened for the presence of anti-Brucella antibodies using the Rose-Bengal test; those found to be positive were then examined by Wright and 2-mercaptoethanol Brucella agglutination tests. A questionnaire was used to collect data on flock-level factors likely associated with the within flock seroprevalence of brucellosis. The associations were statistically evaluated for significance in multivariable logistic models. Sixty three flocks (21.00%; 95% CI: 16.80-26.60) had at least one seropositive animal. The mean within-flock seroprevalence was 3.10% (95% CI: 2.60-3.90). The presence of newly purchased animals (OR=3.42; 95% CI: 1.35-8.65) was significantly associated with seropositivity. Our findings highlight the role of animal movement among flocks in the epidemiology of brucellosis in this region. Thus, a control program for brucellosis in the region is suggested to impose appropriate restrictions on animal trade and improve knowledge of livestock owners about quarantine principles for newly purchased animals.

Investigation of genetic causes of intellectual disability in kerman province, South East of iran.

BACKGROUND: Intellectual disability (ID) has a worldwide prevalence of 1-3% and results from extraordinary heterogeneous. To shed more light on the causes of ID in Kerman Province, in Southeast Iran, we set out in 2008 to perform systematic clinical studies and homozygosity mapping in large Iranian families with ID. METHODS: Fifty seven families with a minimum of two mentally retarded children from Kerman Province were initially tested for metabolic disorders, by Tandem mass spectrometry. Fragile X testing and standard karyotyping were performed for all probands of families. Cases with autosomal recessive (AR) pattern of inheritance and microcephaly were subjected to homozygosity mapping by using several microsatellite markers for known MCPH loci. RESULTS: Three out of seven families with X-linked pattern of inheritance were positive for fragile X syndrome. Chromosome abnormality was not observed in any of dysmorphic patients and all families were negative for metabolic tests. Among the remaining 50 families of AR ID, six were found to be microcephalic, of which 2 linked to two MCPH loci (33.3%). The rest 4 families were not linked to any of the known loci. CONCLUSION: The results of this study showed that ID with microcephaly comprised 12% of ID cases in Kerman Province. In two families with apparent linkage to the MCPH5 and MCPH6 locus, mutation screening was not successful, which might indicate that either the mutation is located in the regulatory sequences of the gene or that there might be another genes present in these regions, which is mutated in such cases.

Effect of Mg-deficiency on endothelial cell allogeneic activation in a model of isolated perfused mouse lung.

Following vascularized organ allotransplantation, an early intragraft inflammatory process is initiated by adhesion molecule-ligand interaction between recipient blood leukocytes and graft endothelial cells (EC). We have previously shown that chronic hypomagnesemia did not induce any inflammatory process in the lung, hence neither EC activation, nor lung remodelling. In the present study we have investigated the effects of allogeneic blood perfusion on lungs from magnesium-deficient mice in our experimental model of isolated mouse lung. After 3h of isogeneic or allogeneic perfusion, no inflammatory process was detected by histochemical examination of lung tissue; the mRNA levels of the adhesion molecules E-selectin, ICAM-1 and VCAM-1, and of the pro-inflammatory cytokines TNF-alpha and IL-2 in lung tissue, determined by reverse transcriptase-polymerase chain reaction (RT-PCR), were similar, and the expression of E-selectin and I-Ab antigen on EC by immunohistochemical staining was undetectable. All of these markers were shown to be dramatically increased after allogeneic perfusion of lung from magnesium-non deficient mice. Our results clearly show that allogeneic perfusion of lungs from magnesium-deficient mice cannot induce EC activation or lung inflammation, indicating that hypomagnesemia in donors does not constitute an additional risk for allograft outcome and might allow to lighten the recipient's immunosuppressive treatment.

Severe Mg-deficiency is not associated with endothelial cell activation in mouse lung.

Several experimental and clinical studies suggest that the lungs are a specific target of Mg-hypomagnesemia, which is a common side effect of cyclosporin A therapy. Due to the possible effect of hypomagnesemia on lung allograft function, the aim of this study was to evaluate endothelial cell (EC) activation and tissue remodelling (apoptosis) in the lungs from mice fed Mg-deficient diets. Immunocytochemical examinations did not reveal any inflammatory process in Mg-deficient mice, infiltration of leukocytes (CD45+ cells), expression of I-Ab class II molecules, E-selectin or ICAM-1 on ECs, and apoptotic cells. Quantification of mRNAs for E-selectin, ICAM-1 and VCAM-1, which are the most pertinent adhesins expressed by ECs, and for the cytokines TNFalpha and IL-2, demonstrated that severe Mg-deficiency does not result in EC activation. The balance between the up-regulation of G-CSF-R and CCL4 genes, and the down-regulation of the OPN gene shown by the cDNA microarray technique might be responsible for the absence of development of an inflammatory response, lung EC activation, and lung remodelling. However, we can hypothesize that severe Mg deficiency results in a latent inflammatory status of the lungs, which might be expressed following immune stresses, like transplantation conditions.

Pulmonary sarcoidosis and the acute respiratory distress syndrome (ARDS).

A 50 year old man presented with 3 weeks of exertional dyspnoea. His chest radiograph on admission revealed diffuse bilateral interstitial infiltrates. He did not respond to antibiotics but subsequently improved on high dose corticosteroids. Bronchoscopic examination with transbronchial biopsy specimens revealed the presence of non-necrotising granulomas. This case demonstrates an unusual clinical presentation of life threatening pulmonary sarcoidosis characterised by the development of acute respiratory distress syndrome (ARDS) with acute respiratory failure.

Generation of a polyclonal antibody against lipid peroxide-modified proteins.

A specific polyclonal antibody against the lipid peroxide (LOOH)-modified rabbit serum albumin (RSA) was generated in rabbits. The antibody selectively recognized the modified protein in a concentration-dependent manner and did not cross react with aldehyde-modified proteins or proteins directly oxidized with the free radical generator 2,2'-azobis (2-amidinopropane) hydrochloride (AAPH). Oxidized low-density lipoprotein (Ox-LDL), but not native LDL, was also recognized by the antibody in a concentration-dependent manner. The antibody also cross reacted with several other proteins modified by LOOH suggesting that the antibody is directed towards a common epitope and not towards the protein sequence. Western blot analysis of normal human plasma showed that at least three different proteins are recognized by the antibody. RAW cells, preincubated with LOOH, were immunostained with the antibody and the antigenic epitopes were present intracellularly, while controls lacking in the primary antibodies failed to show immunoreactivity. Atherosclerotic arteries from cholesterol-fed monkeys and human atherosclerotic lesions were also immunostained by the antibody. The immunoreactivity was co-localized in areas rich in foam cell macrophages. These results suggest that LOOH-modified proteins present an unique antigenic epitope that may represent a primary product of interaction of LOOH with proteins.