Nutritional status of schoolgirls in Isfahan,Iran: Anthropometric and hematological measurements

Weights, heights and other anthropometric measurements are presented for seven year old schoolgirls belonging to different socioeconomic groups in Iran. It was found that measurements of the children of professional people were indistinguishable from internationally accepted standards. The measurements of girls in the lower socioeconomic strata were lower. Hematological measurements indicated lack of anemia in any of the children. Possible reasons for these findings are discussed in relation to previously published reports of nutritional problems in Iran.     

Association of Plasminogen Activator Inhibitor-1 Gene Polymorphism with Inflammatory Bowel Disease in Iranian Azeri Turkish Patients

Background/Aim:

Previous studies have shown the association of some genetic factors, such as Plasminogen activator inhibitor type-1 (PAI-1) 4G/5G polymorphism, with the development of inflammatory bowel disease (IBD). We aimed to study this polymorphism as a risk factor in IBD patients in this cohort.

Patients and Methods:

One hundred and fifteen IBD patients and 95 healthy controls were selected from Iranian Azeri Turks and -6754G/5G polymorphism of PAI-1 gene was tested by polymerase chain reaction using allele-specific primers confirmed by sequencing.

Results:

There was no significant difference of PAI-1 polymorphism between IBD patients and the control group (P > 0.05). Furthermore, these data showed no significant difference between Crohn''s disease and ulcerative colitis patients. However, 4G/4G homozygotes have reduced probability to progression of loss of appetite, whereas 5G/5G genotypes have increased risk for development of chronic diarrhea without blood, nausea, and loss of appetite.

Conclusions:

Although our study showed no significant association of PAI-1 polymorphism between patients and control group, the carriers of 4G/4G genotype and 4G allele had reduced risk for the progression of IBD features in this cohort.     

Accuracy of somatosensory evoked potentials in diagnosis of mild idiopathic carpal tunnel syndrome

OBJECTIVE: Concerning prevalence of carpal tunnel syndrome (CTS) and the difficulties with electromyography (EMG) and nerve conduction studies (NCS), this study was designed to evaluate the power of somatosensory evoked potential (SSEP) in CTS diagnosis among Iranian patients. PATIENTS AND METHODS: SSEP was performed on 100 asymptomatic hands of 50 healthy participants (40 female, age range 38-59 years) and on 61 hands of 46 patients (39 female, age range 34-58 years). Mean difference between N(20) latency of the middle finger and the wrist (median nerve innervation) as well as N(20) latency of the third finger and the fifth finger (ulnar nerve innervation) were measured. Using receiver operating characteristic (ROC) curve analysis, the upper limits of these variables were defined as 6.0 and 1.5 ms, respectively. Higher amounts in either of these variables were considered as positive SSEP for diagnosis of CTS. Measures of accuracy for SSEP were measured getting clinical diagnosis by two separate neurologists as the reference standard. In the patients' group who underwent both techniques of SSEP and EMG-NCS, kappa statistic as the agreement coefficient between two procedures was calculated. RESULTS: Sensitivity, specificity, and likelihood ratios for positive and negative results of SSEP in diagnosis of CTS were 70.4%, 91.0%, 7.83 and 0.32, respectively. Sensitivity of EMG-NCS in diagnosis of CTS was measured as 81.9%. Measure of agreement between two procedures (kappa) was calculated as 0.42. CONCLUSION: This study showed that positive results of SSEP might have a role in diagnosis of CTS. However, larger studies to demonstrate diagnostic power of SSEP in comparison with EMG-NCS seem necessary.     

Effects of subacute lead acetate administration on nitric oxide and cyclooxygenase pathways in rat isolated aortic ring.

Low level exposure to lead increases blood pressure in human and rats. In this study, we investigated the contribution of the nitric oxide (NO) and cyclooxygenase pathways of aortic rings of 28-day lead-treated and control rats, to the responsiveness to phenylephrine and acetylcholine. There were no differences in phenylephrine contractions between the two groups. N(omega)-nitro-L-Arginine-methyl ester (L-NAME), a NO synthase inhibitor, caused attenuation in contraction response to phenylephrine in the aortic rings of the lead-treated rats, while endothelium-denudation caused attenuation in those of controls. This may be due to either endothelium-derived vasoconstrictor(s) (such as reactive oxygen species or endothelins) or a source of NO in smooth muscle cells. There is a left-shift in acetylcholine relaxation response. Indomethacin incubation caused a left-shift in relaxation response to acetylcholine in controls but without any effect on lead-treated ones. Indomethacin incubation caused attenuation in contraction to phenylephrine in both groups. The relaxation response to sodium nitroprusside is not different between the two groups, suggesting that smooth muscle relaxation component is intact. However, the relaxation response to glyceryl trinitrate is impaired in aortic rings of lead-treated rats. It can be concluded that NO and cyclooxygenase pathways are altered in aortic rings of lead-treated rats, with possible involvement of endothelium-derived vasoconstrictors.     

The atrophy and changes in the cellular compositions of the thymus and spleen observed in mice subjected to short-term exposure to perfluorooctanesulfonate are high-dose phenomena mediated in part by peroxisome proliferator-activated receptor-alpha (PPARα)

We have previously shown that short-term, high-dose exposure of mice to the environmentally persistent perfluorooctanoate (PFOA) results in thymic and splenic atrophy and the attenuation of specific humoral immune responses. Here we characterize the effects of a 10-day treatment with different dietary doses (1–0.001%, w/w) of perfluorooctanesulfonate (PFOS), a similar fluorochemical, on the immune system of male C57BL/6 mice. At doses greater than 0.02%, PFOS induced clinical signs of toxicity in the animals, whereas at the concentration of 0.02%, this compound caused weight loss, hepatomegaly and atrophy of the thymus, spleen and adipose tissue without toxicity. With this latter dose, histopathological and flow-cytometric analysis revealed that (i) the thymic cortex was virtually depleted of cells; (ii) the total numbers of thymocytes and splenocytes were reduced by 84 and 43%, respectively; (iii) although all populations of thymocytes and splenocytes were smaller, the thymic CD4⁺CD8⁺ cells and the splenic B-lymphocytes were most decreased. These alterations resembled those evoked by analogous exposure to PFOA, but were less pronounced. At lower doses (less than 0.02%), PFOS induced hepatomegaly without affecting the thymus or spleen. Finally, comparison of male wild-type 129/Sv mice and the corresponding knock-outs lacking peroxisome proliferator-activated receptor-alpha (PPARα) indicated that these effects of PFOS are not strain-dependent. More importantly, hepatomegaly is independent of PPARα, the thymic changes are partially dependent on this receptor, and splenic responses are largely eliminated in its absence. Thus, immunomodulation caused by PFOS is a high-dose phenomenon partially dependent on PPARα.     

Protein-G binding material from synovial fluid of rhematoid arthritis patients induces unorthodox autoantibodies (IgG1 rheumatoid factor) in NZB,NZW and (NZB x NZW)F1 mice

Our previous studies have demonstrated that injection of rheumatoid arthritis (RA) synovial fluid (SF) induces a marked increase mainly of IgG1 antibody-producing cells in autoimmune disease prone (NZB X NZW)F1 mice but not in CBA mice. In the present study, the in vivo effect of RA-SF on autoantibody production was tested in different strains of mice. Injection of RA-SF induced the production of unorthodox autoantibodies (IgG1 rheumatoid factor, RF) in young (NZB X NZW)F1 mice as well as in their parental strains NZB and NZW, but not in normal mice (CBA) or in mice with severe combined immunodeficiency, indicating that the response is not caused by a conventional immune response against RA-SF material. IgG1 RF production was rapidly induced and reached high levels already on day 7 and lasted for more than 90 days. The induction of IgG1 RF was not the result of polyclonal activation, since RA-SF did not stimulate the production of other antibodies, such as autoantibodies against double-stranded DNA, bromelain-treated mouse red blood cells, myosin, transferrin, cytochrome c, thyroglobulin or myoglobin or antibodies reactive with the hapten TNP. To elucidate the identity of the active substance in RA-SF, responsible for IgG1 RF production, bound and unbound material of RA-SF, eluted from a protein-G column was injected into (NZB X NZW)F1 mice. Only the protein-G binding material was active, indicating that the effect is mediated by autoantibodies or immune complexes in the synovial fluid. Further studies demonstrated that identical concentrations of protein obtained from a pool of normal human IgG or SF from seronegative RA and non-RA arthritides patients did not contain the same activity.     

Traumatic Coronary Artery Fistula Closure with Stent Graft

We present a rare case of a symptomatic acquired large coronary fistula and aneurysm secondary to chest trauma that was successfully closed using stent graft. This case is followed by review of the literature.