Mechanism of neuroinvasion of Venezuelan equine encephalitis virus in the mouse.

Venezuelan equine encephalitis virus (VEE) causes a biphasic disease in mice following subcutaneous inoculation in the footpad. In the initial phase, virus replicates primarily in the lymphoid tissues and induces a high titer viremia. Subsequently, the virus invades the central nervous system (CNS) from the circulation, and an encephalitis ensues. At the earliest times that VEE specific in situ hybridization signal was observed in the CNS, it was in areas of the brain involved in olfaction, leading to the hypothesis that virus may invade the brain from the circulation through the olfactory system. The results presented in this paper define the route of CNS invasion in experimental murine VEE disease initiated by subcutaneous inoculation. Virus circulating in the blood appears to seed specific areas of the peripheral nervous system during the viremic lymphoid phase of the illness. Virus replication within olfactory and dental tissues is followed by centripetal spread of virus along neural pathways. Virus enters the brain in a pattern reflecting the proximity of the peripheral invasion site to the CNS. Specifically, virus is first found in the brain within the structures of the olfactory system, followed by areas innervated by the trigeminal nerve. Virus later disseminates along fiber tracts and connected circuits within the brain, resulting in a disseminated meningoencephalitis. Surgical or chemical interruption of the olfactory system at the level of the olfactory neuroepithelium or the main olfactory bulb inhibited entry of VEE into the CNS through the olfactory nerve. However, the olfactory route is not absolutely required for CNS invasion, as virus invaded the CNS of olfactory ablated animals through the trigeminal nerve. These observations are consistent with a model of hematogenous seeding of the peripheral nervous system, followed by invasion of the CNS by direct neural spread.

Factors influencing the development of area health education centers with Texas-Mexico border populations.

Area Health Education Centers (AHECs) have been viewed as an appropriate vehicle for implementing new initiatives for training health professionals who will work along the U.S.-Mexico border. Perceptions about this program in Texas were evaluated from July 1988 to June 1989 to identify problems and formulate suggestions that might be of use to academic health science centers (HSCs)--and in particular medical schools--working with Hispanic populations. Interviews were conducted with 116 people: the presidents and/or deans of all eight Texas HSCs and/or medical schools, other deans and faculty, community leaders in five border counties, and state officials. The school and community perspectives about past and present AHEC activities were compared. Some of the barriers were: insufficient components of the health care delivery system to support medical education in severely underserved areas; differing school and community priorities; cultural differences between the school faculty and the community; and feeling among community physicians and dentists that AHECs were a source of competition. The school and community respondents agreed that the AHEC program needs more cooperative planning and training that emphasizes public health education for future AHEC-like activities with border populations.

Hypothyroidism in diabetes treated with the sulphonylurea chlorpropamide - abstract

The study was undertaken to determine the effects of the sulphonylurea, chlorpropamide (Diabin) on thyroid function in diabetics. One hundred and twenty-five diabetic attending the Diabetic Clinic at the University of the West Indies were studied. They were divided into three groups, a control group of 46 patients on diet alone (11) or insulin (35), a second group of 46 patients on 250 mg chlorpropamide daily and a third group of 33 patients receiving 375 mg or more chlorpropamide daily. The three groups were matched for age, sex and duration of diabetes. No patient had been on other drugs known to affect thyroid function and they all had blood urea values within normal limits. A serum thyroxine estimation was done on each subject and all those values of less than 4.5 ug/100 ml were subjected to R.A.I. uptake studies before and after a single dose of T.S.H. In the control group 1 patient was found to have Hashimoto's disease. In each of the other two groups on chlorpropamide there were 3 hypothyroid patients. They all had low serum T4, low R.A.I. uptakes and good response to T.S.H. In three of these six patients the sulphonyl-urea was discontinued and the thyroxine levels rose to normal after varying intervals. It is concluded from this series that hypothyroidism occurs in 7.5 percent of patients on chlorpropamide and that this reversible on discontinuation of the drug (AU)