Immunomodulatory Effects of γ-HCH (Lindane) in Mice

Mice were fed for 24 weeks with three different subtoxic dosages of γ-HCH (0.012, 0.12 and 1.2 mg/kg) mixed in powdered feed. The immunological profile was assessed at an interval of one month during the entire exposure period. Both the cell mediated and humoral components of immunity showed a biphasic response characterized initially by stimulation followed by suppression in a dose dependent manner. However, γ-HCH did not affect the functional properties of peritoneal macrophages. Histological changes in lymphoid organs were in accordance with the biphasic immunomodulatory effects of γ -HCH.     

Chronic ethanol intake may delay the onset of gossypol-induced infertility in the male rat

Summary. Parameters were obtained from the reproductive organs of ethanol-fed, gossypol-treated Sprague Dawley rats. The experimental animals were fed either on a normal (15.17%) or low protein (8.00%) diet. Measurements included reproductive organ weights, seminal characteristics, serum concentration of testosterone and histological, stereological and histomorphometric evaluation of the testis. The testis size, length and diameter of the seminiferous tubule had the least values in the protein-malnourished, gossy-pol-treated rats (3.01±0.26 g, 0.56 ± 0.03 m, 281.34±11.30 μn), in comparison to corresponding animals which had received ethanol simultaneously with gossypol (3.40 ± 0.25, 0.71±0.06m, 314.42 ± 11.61 μn). As gossypol and ethanol are both associated with reduced reproductive capacity, this unexpected but interesting finding lends support to the hypothesis that either a normal dietary protein or ethanol consumption may modify the action of gossypol on body tissues, including the testis. This effect, presumably mediated through changes caused to the bioavailability of gossypol, modifies its antifertility activity. The present observation further highlights the need to consider the concurrent administration of other drugs, such as alcohol, and the nutritional status in the evaluation of gossypol for various potential uses.     

Inhibition of spontaneous testicular Leydig cell tumor development in F-344 rats by dehydroepiandrosterone.

The incidence of spontaneous Leydig cell tumors of testis is very high in old F-344 rats. We have examined the effect of dehydroepiandrosterone (DHEA), a steroid hormone with antimitotic and anticarcinogenic properties, on spontaneous Leydig cell tumorigenesis. Fifteen-week-old male F-344 rats were fed a diet containing DHEA (0.45% w/w) for 84 weeks. At the termination of experiment none of the 13 rats had Leydig cell hyperplasia or Leydig cell tumors. All the eight control rats of comparable age had Leydig cell tumors. These findings suggest that DHEA is a potent inhibitor of spontaneous Leydig cell tumors of testis in aged rats.     

Dengue fever presenting with acute colitis.

Gastrointestinal manifestations of dengue fever are mainly in the form of bleeding or liver function abnormalities. Dengue fever presenting as acute colitis-like picture is not reported to date. We report a 50-year-old man with dengue fever presenting with lower gastrointestinal bleeding and colonoscopic features of acute inflammatory colitis.     

Benign synovioma causing internal derangement of the knee. A report of nine cases

Nine pedunculated benign synoviomata causing mechanical symptoms similar to those of a torn meniscus are described. The average age of the patients was 34.4 years. During the period of study, 2254 meniscal lesions causing mechanical symptoms were identified, giving an incidence of one benign synovioma for every 250 meniscal lesions. All the lesions were removed arthroscopically with relief of symptoms.     

Long-term effects of physiologic concentrations of dexamethasone on human bone-derived cells

Bone cells derived from human trabecular explants display osteoblastic features. We examined the modulation of alkaline phosphatase activity and cAMP production as the result of exposing trabecular explants to physiologic concentrations of dexamethasone for 4 weeks during cellular outgrowth and subculture. Cells treated with dexamethasone were observed to grow generally more slowly than control cells. Cells appeared larger and more polygonal, and staining for alkaline phosphatase was more intense in the dexamethasone-exposed cultures. There was a progressive increase in cellular PTH responsiveness with increasing duration of exposure of cells to dexamethasone. Cells grown for 6 weeks in 3 x 10(-8) M dexamethasone had a 10-fold increase in PTH-stimulated cyclic AMP accumulation. Dexamethasone-treated cells also had a significantly increased alkaline phosphatase activity. 1,25-(OH)2D3-stimulated alkaline phosphatase activity was increased approximately 20-fold. cAMP responses were significantly increased to PTH (21.7-fold), PGE1 (2.67-fold), and forskolin (4.81-fold), but not to cholera toxin. Dexamethasone-treated cells also had a mean decrease in 1,25-(OH)2D3-stimulated osteocalcin production to 26.2% of control values (p less than 0.001). Hydrocortisone treatment gave rise to similar effects but of smaller magnitude than those of dexamethasone. Testosterone did not have a significant effect on alkaline phosphatase activity or cAMP production. Skin fibroblasts showed a significant enhancement of alkaline phosphatase activity in response to dexamethasone, but of a much smaller magnitude than in bone cells. The phenotypic changes induced by long-term culture in dexamethasone are consistent with the promotion of a more differentiated osteoblastic phenotype.     

Magnetic resonance imaging in full-term infants with repetitive focal seizures.

We report two full-term infants who developed repetitive focal seizures within the first 48 hours of life. Neither infant had predisposing factors and there were no abnormalities on a computed tomography (CT) scan performed on day 2 of life. Magnetic resonance imaging (MRI) performed during the second week of life showed a focal hemorrhagic infarction in both patients. We conclude that either an MRI or a contrast-enhanced CT scan should be obtained within 1 week in patients in whom the initial imaging technique failed to reveal a focal lesion, at which time a cerebral infarction can be diagnosed with greater sensitivity.