The aim of this study was to determine the effect of vitamin E deficiency and supplementation on body weight and body composition in intact and ovariectomized growing female rats. One hundred and twenty female Wistar rats aged 3 months were ovariectomized (OVX) or left intact (sham-operated). The intact and OVX rats were divided into 6 groups and given different dietary treatments, i.e. vitamin E deficient diets (VED, 75%VED, 50%VED, 25%VED), normal rat chow diet (RC) and rat chow with oral supplementation of 30mg/kg body weight of -tocopherol (RC+ATF). Body weight of intact and OVX rats in the RC and the RC+ATF groups showed increased significantly after 15 weeks of dietary treatment. Intact and ovariectomized rats fed with VED, 75%VED, 50%VED and 25%VED did not gain weight after 15 weeks. OVX rats had significantly higher body weight than intact rats in the 50%VED, 25%VED, RC and RC+ATF groups. Fat mass of intact rats was increased only in the RC and RC+ATF groups. For OVX rats, fat mass was increased in the VED, 50%VED, RC and RC+ATF groups. OVX groups had significantly higher fat mass when compared with intact groups, however, the significance was greater for the RC and RC+ATF groups. Other parameters of body composition were not significantly affected. In conclusion, vitamin E played an important role in the weight gain of female rats and the gain was primarily due to the increase in fat mass, irrespective of the effect of ovariectomy. Alpha-Tocopherol supplementation conferred little benefit compared to giving RC diet alone in both the intact and ovariectomized female rats. The results also indicate that excessive vitamin E intake might contribute towards obesity in female rats.

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Although several retrospective studies have shown a strong correlation between lipoproteins and atherosclerotic heart disease, the correlation is unclear in cases with coronary vasospasm. This study sought to examine dyslipidemia including lipoprotein(a) [Lp(a)] and Apo(a) phenotypes in coronary artery disease.
One hundred and fifteen patients with mean age of 58.7±13 years suffering from coronary artery disease were selected. They were divided into groups with stable angina pectoris (SA), unstable angina (USA), acute myocardial infarction (AMI). Control group consisted of 40 age and sex matched apparently healthy individuals. The lipids and lipoproteins including Lp(a) were measured using standard methods. Apo(a) phenotypes were evaluated by SDS-PAGE electrophoresis followed by immunoblotting.
In patients with coronary artery disease, high-density lipoprotein cholesterol (HDL-C) levels were significantly lower than those in control (p<0.01), but in SA its level was higher than those of USA and AMI (p<0.05). The levels of triglyceride and very low-density lipoprotein cholesterol (VLDL-C) were higher in SA and no significant differences were noticed in those of total cholesterol, but the concentrations of low-density lipoprotein cholesterol (LDL-C) in USA and AMI were significantly higher than those of SA and control groups. The ApoB concentration was markedly higher in USA group (p<0.002). The mean ± SD levels of total Lp(a) in USA and AMI groups were higher than those of SA and control groups (p<0.001). Comparing the frequencies of low molecular weight (LMW) and high molecular weight (HMW) Apo(a) phenotypes of patients with control group, high frequencies of LMW Apo(a) and high levels of Lp(a) were noticed in USA and AMI groups (p<0.01 in both cases).
Low serum HDL-C and high serum LDL-C and Lp(a) levels were characteristic in patients with USA and AMI. Comparing the frequencies of Apo(a) phenotypes in SA, USA and AMI with those of control it was concluded that Apo(a) phenotyping along with serum levels of Lp(a), HDL-C and LDL-C could be a useful risk predictors for the development of acute coronary syndromes and may be used in discrimination of different types of the coronary artery diseases.

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HESA-A, which contains biologically active compounds of marine origin, has selective toxicity against cancer cells. The present work reports the results of studies investigating the acute and sub-acute oral toxicity of this drug in mice and rats. In acute toxicity study, doses of HESA-A up to 13.7 g/kg and in sub-acute study, oral doses of 1250, 2500 and 5000 mg/kg for 30 consecutive days did not cause any morbidity or mortality. Data analysis of body weight gain, gross observations, blood biochemistry, hematology and histopathological findings did not show significant differences between control and treated groups. An oral dose of 5000 mg/kg of HESA-A can be defined as no-observed-adverse-effectlevel (NOAEL) for mice and rats used under the experimental conditions.

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This study was conducted on pregnant women admitted to various hospitals of Faisalabad for delivery. They were randomly divided into 3 socio-economic groups (low, middle and high) and each group was further subdivided into 3 age groups of < 25, 2632 and >33 years of patients. The study revealed an overall higher (p<0.05) birth weight of newborn of those born to women of middle socio-economic groups than low and high. Overall mean RBC (106/L), PCV (Packed Cell Volume) (%), Hb (g/dL), TLC (Thin Layer Chromatography) (103/L), iron (g/dL), MCV (fL), MCH (pg) and MCHC (g/dL) were 4.00, 34.49, 9.69, 8.9, 212.02, 90.23, 25.63 and 28.80 before delivery, while 4.10, 34.45, 8.73, 10.36, 173.36, 89.77, 22.96 and 25.93, after delivery, respectively. Overall RBC count and PCV showed non-significant difference pre-and post delivery among socio-economic groups and age groups. After delivery overall TLC was significantly higher (p<0.05) but before delivery it was significantly higher (p<0.05) in women of middle than high socio-economic group. Before delivery, overall, Hb, MCH and MCHC were significantly higher (p<0.05) in women of each socio-economic group. Overall, serum iron was higher and RBC showed positive correlation with birth weight (r=0.28, p<0.005) before delivery.

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Secondary hyperparathyroidism is listed among the possible reasons for intensifying the anemia and causing it to be resistant to erythropoietin therapy in hemodialysis patients. Although its exact mechanism is not entirely clarified, shift of bone marrow cells to adipocytes, bone marrow fibrosis and lowered calcitriol can be the cause. However, the role of secondary hyperparathyroidism in severe anemia and resistance to erythropoietin treatment in comparison to other factors like inflammation and iron deficiency is minor. In this study we evaluated the role of secondary hyperparathyroidism in severity of anemia in hemodialysis patients.
This is an analytical study carried on 36 hemodialysis patients of Hajar Medical Educational and Therapeutic Center in Shahrekord. Hgb, Hct, calcium, phosphorus, alkaline phosphatase, intact PTH (iPTH), serum iron, total iron binding capacity, transferrin saturation in percent, ferritin, and also dialysis adequacy by Urea Reduction Rate (URR) in per cent were measured.
All data were analyzed with SPSS software and categorized into mean ± SD, correlations were carried out using Pearson Co-efficient Test.
Total number of patients were 36 of whom 55.5% were male of latter 66.1% were over 40 years of age. Mean ± SD of iPTH were 439.4 ± 433 pg/mL, Hgb were 9 ± 1.9 g/dL and Hct were 28.8 ± 6.3 percent respectively.
This study showed that there were reverse correlations between intact PTH with hematocrit and hemoglobin; and between alkaline phosphatase and Hgb, Hct (p<0.05 for all correlations).
Secondary hyperparathyroidism by itself can intensify anemia encountered in hemodialysis patients. This conclusion needs further attention to control hyperphosphatemia and parathormone hypersecretion for better management of anemia in hemodialysis patients.

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