Intensified IgA mesangial deposits after administration of sheep anti-type IV collagen serum in mice

Sheep anti-type IV collagen serum was intravenously administered to male mice of the BALB/c, C3H and ddY strains, and their kidneys were morphologically studied monthly for 10 months thereafter. By immunofluorescence, the sheep IgG was seen to have immediately become conjugated to the glomeruli, mainly in a mesangial pattern. Successively, autologous mouse C3 and IgG appeared with the same type of distribution. Within 3 to 4 months after the start of the experiment, mouse IgA also appeared in the mesangium, especially in ddY mice. The intensity and frequency of mesangial IgA deposition and the serum IgA level increased with time in this strain. BALB/c and C3H mice also showed the same tendency of mesangial IgA deposition, although to a lesser degree. In summary, it was concluded that mesangial IgA deposition was due to non-immunological local trapping, on the basis of the results obtained by ELISA analysis of the sera and renal eluate. Although the ddY mouse is known to show spontaneous mesangial IgA deposition associated with a high serum IgA level with aging, these characteristics were much accelerated and intensified by this antiserum treatment. The relation of this observation to the pathogenesis of human IgA nephritis is discussed.     

Epitopic heterogeneity of the CD36 antigen expressed by normal and neoplastic endothelial cells. An immunohistochemical study with a novel monoclonal antibody 8C9.

Phenotypic and functional heterogeneity of endothelial cells (ECs) is being recognized with increasing frequency. Here we report a novel murine monoclonal antibody (MoAb), named 8C9, that detects a unique epitope on the leukocyte differentiation antigen CD36 (platelet glycoprotein IV or IIIb) expressed by both normal and neoplastic ECs. In immunohistochemical and flow-cytometric studies, 8C9-immunoreactivity was detected on capillary ECs, adipocytes, monocytes, platelets and a human monocytoid cell line U-937, which are known to express the CD36 antigen. Blocking experiments using U-937 cells and studies on cryostat sections revealed that a murine MoAb OKM5, which detects the CD36 antigen, blocked the binding of 8C9 to its antigen. Immunoblot analysis showed that 8C9 bound to a 97-kDa membrane protein expressed by U-937 cells treated with phorbol ester. These results indicate that 8C9 detects the CD36 antigen. However, the findings that some OKM5-positive normal ECs in the liver, spleen and lymph nodes as well as neoplastic ECs in a cutaneous angiosarcoma did not react with 8C9, together with the fact that the CD36 antigen does not form a complex or associate with other proteins, suggest epitopic heterogeneity of the CD36 antigen expressed by these tissues.     

Treatable ischemic neuronal damage in the gerbil hippocampus

The Mongolian gerbil is known to develop delayed neuronal death in the hippocampus following brief forebrain ischemia (Brain Res 239: 57-69). Morphological, biochemical, or electrophysiological studies on this neuronal injury have shown that neurons still retain potential reversibility at the earlier period of alteration. To examine this possibility, immediately following 5 min of ischemia in the gerbil, pentobarbital, diazepam, or nizofenone was injected. Seven days following ischemic insult, animals were perfusion fixed and neuronal density in the hippocampal CA1 subfield was counted. Most of the neurons in the CA1 sector survived ischemic insult when a drug was given, whereas most of them were lost without the treatment. The average neuronal density of treated groups showed a statistically significant (p less than 0.01) persistence compared with that of control group. The effective dosage of the drugs were 20-40 mg/kg in pentobarbital, 10-20 mg/kg in diazepam, and 12.5-25 mg/kg in nizofenone. On the other hand, when pentobarbital was injected 1 hr following ischemia, while neurons still remain intact morphologically, it showed no effect. This result indicates that the neuronal damage of "delayed neuronal death" type is reversible if treatment is instituted at an early period of cell change.     

HIV misconceptions among married women in Malawi: the role of household decision-making autonomy

Journal of Public Health - Married women face one of the highest HIV rates in Malawi. Although HIV misconceptions have been identified as a major contributor to HIV infection, we know very little...     

Aktiver Transport der aromatischen Monoamine

Ohne Zusammenfassung     

Morphine-induced metabolic changes in human brain. Studies with positron emission tomography and [fluorine 18]fluorodeoxyglucose

Morphine sulfate effects (30 mg, intramuscularly) on cerebral glucose utilization and subjective self-reports were examined in 12 polydrug abusers by positron emission tomography and [fluorine 18]fluorodeoxyglucose in a double-blind placebo-controlled crossover study. During testing, subjects sat with eyes covered, listening to white noise and "beep" prompts. Morphine significantly reduced glucose utilization by 10% in whole brain and by about 5% to 15% in telencephalic areas and the cerebellar cortex, assuming no contribution of hypercapnia. When the contribution of PaCO2 (45 minutes after morphine was administered) was partialled out, significant morphine-induced reductions persisted in whole brain and six cortical areas. Irrespective of morphine, left-greater-than-right asymmetry occurred in the temporal cortex, and an interaction between hemisphere and drug was noted in the postcentral gyrus. In most cases, effects on glucose utilization were not significantly related to measures of euphoria.