Modulation of immune response in asthmatic patients by using inhaled tuberculin

Bronchial asthma is a chronic immuno inflammatory reversible lung disease with airway responsiveness to various stimuli which relived by proper therapy using inhaled steroids or the highly expensive recombinant interferon gamma [IFN-gamma]. This study undertaken to investigate for the first time a novel treatment method using inhaled tuberculin [PPD] to determine whether PPD inhalation could be safely and effectively delivered into the airways of bronchial asthmatic patients in attempt to bring immune deviation away from atopy via inhaling an economic dose of tuberculin. Sixty patients suffering from mild atopic bronchial asthma along with twenty healthy volunteers were included in our study. Patients were randomly categorized into three equally-sized groups received 2, 5 and 10 PPD units respectively. Treatment doses taken every 72 hours for two weeks. Respiratory function tests were examined before and after treatment regime. Interleukin 2 [IL-2], IL-4 and immunoglobulin E [IgE] were measured by ELISA technique in serum and bronchoalveolar lavage fluid [BALF] samples before and after treatment regime. Eosinophil count in BALF was also examined. The results showed that PPD treatment doses caused a significant increase in lung function standards [FEV1 and FEV1/FVC ratio] as compared with before treatment values. Also, the different doses of PPD resulted in a highly significant increase in the levels of serum and BALF IL-2 with a concomitant significant decrease in BALF IL-4 levels when compared with before treatment values. A highly significant decrease in serum and BALF IgE along with eosinophil count was obtained with PPD inhaled doses as compared with before treatment values. To conclude, PPD treatment could be safely, economically and effectively used as a potential therapeutic drug for patients with atopic bronchial asthma. A marked improvement in our laboratory results was observed with 5 and 10 units of PPD

Hepatic antioxidant, oxidative stress and histopathological changes induced by nicotine in a gender based study in adult rats

Nicotine is generally regarded to be a primary risk factor in the development of hepatic, cardiovascular and pulmonary disorders. Therefore, the current study was designed to compare the extent of the oxidative stress induced by nicotine upon the liver of adult male and female rats. Nicotine toxicity was induced by intraperitoneal injection of 0.5 mg base/Kg body weight for 2 months. Cellular damage of liver was assessed by measuring the activity of serum transaminases. Antioxidant status was assessed in liver by measuring the levels of malondialdehyde [MDA], superoxide dismutase [SOD], glutathione peroxidase [GPX], glutathione-S-transferase [GST] and reduced glutathione [GSH]. Histopathological liver changes were examined. The results showed a significant elevation in serum ALT and AST in nicotine-treated rats versus control groups. In comparison with the control findings of male and female rats, nicotine-treated male and female rats showed significant increase in MDA content by 57.3 and 41.8% respectively and a significant reduction in GSH levels by 60.1 and 30.7% respectively with observed significant inhibition in GPX activity by 56.5 and 28.6% respectively and a concomitant significant inhibition in GST activity by 71.2 and 51.2% respectively. Also, significant inhibition in SOD activity was achieved in nicotine-treated male and female rats by 66 and 51.6% versus control groups respectively. Male rats appeared to be more susceptible to nicotine toxicity than females. Histological examination of liver tissues in nicotine-treated male and female rats significantly revealed marked tissue damage and changes versus control counterparts. These changes included focal and confluent necrosis, portal tract inflammation and steatosis. These changes being more obvious and severe in male rats. In conclusion, the results showed the existence of significant sex dependent difference between male and female rats towards nicotine toxicity. Further studies are required to elucidate the precise gonadal hormones mechanism upon the sex dependent difference

Interest of cystatin C as a marker for early impairment of renal function in Egyptian thyroid patients

A randomize prospective study include thirty-two patients [age:30-77 years] of clinical hypo- and hyperthyroidism was planned to evaluate the changes which produced in serum cystatin C compared to creatinine as a sensitive test for early detection of renal failure in patients with thyroid disorders and to determine if significant thyroid hormones disturbance affect cystatin C concentrations. The assays were proposed again when the patients become euthyroid state after treatment. Patients with hyperthyroidism showed significant decrease of cystatin C from 1.0 +/- 0.31 mg/L at time of diagnosis to 0.71 +/- 0.32 mg/L after treatment and significant increase of creatinine from 79.5+26.51 micromol/L to 97.2+26.7 micromol/L in euthyroid state [p<0.001]. In hypothyroid group, it was showed a significant increase in serum cystatin from 0.76 +/- 0.27mg/L to 1.0 +/- 0.21 mg/L in euthyroid state while serum creatinine exhibited significant decrease from 88.4 +/- 26.5micromol/L at time of diagnosis to 70.7 +/- 26.0 micromol/L in euthyroid state [p<0.001]. Our results showed that significant changes in thyroid hormones alternate serum cystatin C concentration so cystatin C should be considered as a sensitive marker for the early prediction of glomerular filtration rate disturbance after thyroid hormones investigations

Biochemical effects of lead pollution in male albino rats

Lead pollution is considered as one of the major risk factors for pregnant women and children. In addition to its dangerous effect on growing youth, lead can accumulate in different organs in the human body. The biological effects of lead exposure in drinking water at different lead doses on male albino rats were investigated. Lead was given to rats in drinking water at 100, 500 and 1000 ppm for 7 weeks. It was observed that lead content was increased in kidneys, liver, brain, RBC's and serum by 26.7, 9.2, 10.7, 12.3 and 5.4-folds respectively at 1000 ppm lead dose compared with control group. It was observed that kidney accumulated very high concentration of lead as compared with other organs with a concomitant increase in serum creatinine in all lead exposed groups with the possibility of producing chronic renal failure. AST, ALT and creatinine were significantly increased by increasing the lead exposure dose. Also, the activity of delta-aminolevulinic acid dehydratase [delta ALAD] was significantly decreased by increasing lead exposure with a concomitant significant decrease in hemoglobin and hematocrite levels but with non-significant decrease in iron indicating the possibility that chronic lead exposure could produce anemia