Despite the increase in obesity among women of reproductive ages, few studies have considered maternal obesity as a risk factor for breast‐feeding success. We tested the hypothesis that women who are obese (BMI = 30–34.9) and very obese (BMI ≥35) before pregnancy are less likely to initiate and maintain breast‐feeding than are their normal‐weight counterparts (BMI = 18.5–24.9) among white and black women. Data from 2000 to 2005 South Carolina Pregnancy Risk Assessment Monitoring System (PRAMS) were used. The overall response rate was 71.0%; there were 3,517 white and 2,846 black respondents. Black women were less likely to initiate breast‐feeding and breast‐fed their babies for a shorter duration than white women. Compared to normal‐weight white women, very obese white women were less likely to initiate breast‐feeding (odds ratio: 0.63; 95% confidence interval (CI) = 0.42, 0.94) and more likely to discontinue breast‐feeding within the first 6 months (hazard ratio (HR) = 1.89; 95% CI: 1.39, 2.58). Among black women, prepregnancy BMI was neither associated with breast‐feeding initiation nor with breast‐feeding continuation within the first 6 months. Because very obese white women are less likely to initiate or continue breast‐feeding than other white women, health professionals should be aware that very obese white women need additional breast‐feeding support. Lower rates of breast‐feeding among black women suggest that they should continue to be the focus of the programs and policies aimed at breast‐feeding promotion in the United States.

A parkinsonian syndrome can be produced in nonhuman primates by administration of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Parkinsonian-like symptoms induced acutely by MPTP were ameliorated after treatment with GM1 ganglioside, a substance shown to have neurotrophic effects on the damaged dopamine system in rodents. Treatment with GM1 ganglioside also increased striatal dopamine and metabolite levels and enhanced the dopaminergic innervation of the striatum as demonstrated by tyrosine hydroxylase immunohistochemistry. These results suggest that GM1 ganglioside may hold promise as a therapeutic agent for the treatment of Parkinson's disease.

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The microglial cell, after many years of neglect, has become recognized as the sole representative cell of the immune system that resides in the normal central nervous system. While normally dormant, microglia can be activated by secretory substances or signals associated with disease or injury, and becomes a phagocytic cell, which also produces its own injurious molecules. In the activating process, its morphology is changed from a resting process-bearing cell, into a rounded amoebic form, and displays new or increased amounts of functional markers, such as receptors and Class I and Class II MHC molecules. Microglia prepared from newborn mice or rats for tissue culture are already activated, and can be used for studies of their phagocytic properties. Although they can phagocytize foreign substances, their uptake and metabolism of myelin are emphasized here, in keeping with their role in demyelinating diseases. A number of receptors have been implicated and appear to be important in the attachment to, and ingestion of, myelin particles in vitro, including the Fc, complement, macrophage scavenger, and the Galectin-3/MAC-2 receptors, although the alpha2-macroglobulin/low-density lipoprotein receptor and mannose receptors have also been suggested as participants in myelin phagocytosis. Certain cytokines and adhesion molecules also regulate the phagocytic activity of microglia. Comparative in vitro studies of phagocytosis by peritoneal macrophages and microglia have shown that the two kinds of cells respond differently to regulatory molecules, and it is concluded that they have different innate properties. The role of microglia in the demyelinative diseases experimental autoimmune encephalomyelitis and multiple sclerosis is emphasized here, and the possible means of intervention in the process leading to myelin destruction is discussed. Published 2001 Wiley-Liss, Inc.