Lipopolysaccharide induces paired immunoglobulin-like receptor B (PirB) expression, synaptic alteration, and learning-memory deficit in rats.

Some typical immune proteins are expressed in the nervous system, among which the paired-immunoglobulin-like receptor B (PirB) is a receptor for major histocompatibility complex class I antigen (MHC-I), but may play a physiological role in the brain for neuronal circuitry stability by inhibiting synaptic plasticity. Chronic neuroinflammation is common to many neurodegenerative diseases and is often associated with neuronal/synaptic damage and dysfunction. Here we examined the expression of PirB in the rat brain following intracerebral application of lipopolysaccharide (LPS), which has been shown to induce proinflammatory changes and cognitive deficits in rodents. One month after unilateral intrahippocampal LPS injection (10 µg in 4 µl phosphate-buffered saline, PBS), increased protein levels and immunoreactivity of PirB were detected in the ipsilateral hippocampal formation and cortex of the experimental group relative to vehicle (PBS) control. The increased PirB labeling was localized to astrocytes and neurons. Reduced synaptophysin protein levels and immunoreactivity were also found in the ipsilateral hippocampal formation and cortex in LPS-treated rats relative to controls. Morris water maze tests indicated that hippocampus-dependent spatial learning and memory were impaired in LPS-treated animals. Our findings add new experimental data for an upregulation of immune proteins in neuronal and glial cells in the brain in a model of endotoxin-induced neuroinflammation, synaptic alteration, and cognitive decline. The results suggest that PirB modulation may be involved in the pathological process under neurodegenerative conditions.

Diagnosis and surgical treatment of carotid body tumors: 25 years' experience in China.

Carotid body tumors (CBT) are rare neoplasms arising from the small chemoreceptor organ in the adventitia of the common carotid bifurcation. A retrospective survey was conducted in 33 patients, treated by curative resection of the neoplasm, from 1980 to 2005, to investigate clinical features, preoperative treatment and surgical approach, and determine the optimum management for CBT. The demographic characteristics, clinical features, surgical approach and complications were documented and analyzed. Accurate diagnosis and effective preoperative training were associated with a good surgical outcome. Carotid arteriography accurately diagnoses and evaluates the brain's collateral circulation in the circle of Willis. Ultrasonography is useful. Carotid blood flow obstruction (Matas' training) is effective. Complete excision of the carotid system without a vascular replacement is possible only after reliable Matas' training and objective observation of the establishment of circulation in the circle of Willis. Correct treatment of the internal and common carotid artery is important to reduce postoperative complications. The continuity of the common and internal carotid artery should be retained if possible, and carotid artery repair is recommended. Minor complications occurred in five (15%) patients and one patient died from a cause not related to the CBT at follow-up.

Effects of estrogen and raloxifene on neuroglia number and morphology in the hippocampus of aged female mice.

Hormone replacement therapy with the gonadal steroid estrogen or synthetic agents such as raloxifene, a selective estrogen receptor modulator, may affect cellular function in brains of postmenopausal women. In vitro studies suggest that 17beta estradiol and raloxifene can alter the microglial and astrocyte expression of immuno-neuronal modulators, such as cytokines, complement factors, chemokines, and other molecules involved in neuroinflammation and neurodegeneration. To directly test whether exogenous 17beta estradiol and raloxifene affect the number of glial cells in brain, C57BL/6NIA female mice aged 20-24 months received bilateral ovariectomy followed by s.c. placement of a 60-day release pellet containing 17beta estradiol (1.7 mg), raloxifene (10 mg), or placebo (cholesterol). After 60 days, numbers of microglia and astrocytes were quantified in dentate gyrus and CA1 regions of the hippocampal formation using immunocytochemistry and design-based stereology. The results show that long-term 17beta estradiol treatment in aged female mice significantly lowered the numbers of astrocytes and microglial cells in dentate gyrus and CA1 regions compared with placebo. After long-term treatment with raloxifene, a similar reduction was observed in numbers of astrocytes and microglial cells in the hippocampal formation. These findings indicate that estrogen and selective estrogen receptor modulators can influence glial-mediated inflammatory pathways and possibly protect against age- and disease-related neuropathology.

[Linear growth retardation and social factors among schoolchildren from the city of Osasco, São Paulo, Brazil] / Retardo do crescimento e condições sociais em escolares de Osasco, São Paulo, Brasil.

Cases and controls were selected for this retrospective investigation of the social determinants of growth retardation, from a Height Census carried out in the 1989 school year,involving children attending the first grade of all public and private schools in Osasco (in the Greater Metropolitan Area of São Paulo, Brazil). The cases, totalling 125 children entering school aged 7-8 years old, were characterized by a height-for-age index below -2 z score of the NCHS/WHO reference. The controls, totalling 139 children entering school at the same age, were characterized by a height-for-age index above -1 z score. Socioeconomíc variables such as family income, head-of-family's level of schooling, mother's schooling, environmental sanitation, and housing conditions were significant factors associated with the stunting process. Risk of linear growth retardation tended to be higher with lower social class (odds ratio = 7.3 for sub-proletariat vs. petit bourgeois; p < 0,001 for overall trend), suggesting the biological impact of Brazil's economic slowdown during the 1980s.