Should it be the law in Wisconsin that all motorcyclists are required to wear helmets?

Motorcycle crashes are associated with a high incidence of head injuries and fatalities. Helmets have been shown to decrease the risk and occurrence of both head injuries and fatalities in motorcycle crashes, along with a decrease in hospitalizations and healthcare costs. Many states have laws in place requiring all motorcyclists to wear helmets and have shown that laws directly affect these outcomes. Wisconsin is a state in which there is a law regarding helmet use; however, there are contingents. It is required only in those who are younger than 18 years and those with an instructional permit.     

Inhibition of lymphocyte proliferation by fluid-phase C3b as influenced by macrophages

The effect of fluid-phase C3b on mitogen-induced lymphocyte proliferation in the presence and absence of macrophages was studied. In general, C3b inhibited the proliferation of lymphocytes when monocytes (macrophages) were present. The degree of inhibition by C3b was different for B and T lymphocytes and varied for different subpopulations of lymphocyte classes. In the absence of monocytes (macrophages), there was insignificant inhibition by C3b of lymphocyte proliferation, and thus the observed inhibition appeared to be due to the effect of C3b on the monocytes/macrophages present in the mixed lymphocyte preparations.     

MECHANISMS OF CAPTOPRIL-INDUCED POTENTIATION OF THE DEPRESSOR RESPONSES TO ARACHIDONIC ACID IN RATS

The mechanisms underlying potentiation by captopril of the depressor responses to arachidonic acid were studied in chloralose-anaesthetized rats. Captopril, in a dose (0.5 mg/kg, i.v.) which inhibited the pressor responses to angiotensin I (0.03-1 microgram/kg, i.v.), enhanced the depressor responses to bradykinin (3-300 micrograms/kg, i.v.) and potentiated the hypotensive action of arachidonic acid (3 mg/kg, intravenously). This phenomenon was observed not only when captopril and arachidonic acid were administered intravenously, but also when these compounds were injected directly into the aortic arch. The enhancement of arachidonic acid-induced hypotension by captopril was not significantly affected by pretreatment with a low dose of aprotinin (3 mg/kg, i.v.), but was abolished by bilateral nephrectomy or by pretreatment with a higher dose of aprotinin (6 mg/kg, i.v.). It is suggested that captopril augments the depressor responses to arachidonic acid by inhibiting angiotensin converting enzyme. This results in accumulation of bradykinin which in turn increases release of vasodilator prostaglandins, originating most probably, from the kidneys. The possibility that blockade of angiotensin II formation by captopril may leave the vasodilator action of prostaglandin unopposed cannot be excluded.     

B-cell lymphoproliferative disorders in children after bone marrow transplantation: radiologic manifestations

The radiographic findings in five pediatric patients in whom unregulated B-cell lymphoproliferative disorders developed following bone marrow transplantation are described. Four patients received T-cell-depleted bone marrow from mismatched donors and one received nondepleted marrow from a matched sibling donor. These disorders are similar to B-cell lymphoproliferative disorders that have been described in other immunosuppressed hosts. They are associated with Epstein-Barr virus and range from polyclonal proliferation without cytogenetic abnormalities to monoclonal lymphoma with clonal cytogenetic changes. Unlike other postallograft lymphoproliferative processes, B-cell lymphoproliferative disorders in these patients have not responded to antiviral therapy, immunologic therapy, or chemotherapy. The radiographic patterns of disease include diffuse or focal hepatic involvement; gallbladder wall thickening; and pulmonary, soft-tissue, and basal-ganglion masses. These radiologic findings are not specific and evaluation of tissue histology is required for diagnosis.     

Gender-specific differences in family practice graduates

In 1979 the American Academy of Family Physicians (AAFP) conducted a study of family practice residency graduates to develop a database of personal and professional characteristics. Questionnaires were sent to 4,295 physicians, and results were based on a total of 3,021 respondents. Female physicians made up 7.1 percent of this sample; however, analysis of the data at that time did not distinguish between men and women. The current study is a reanalysis of the data collected by the AAFP to include comparisons of male and female respondents and to determine whether gender differences that have been reported in the literature continue to persist. Results indicate that gender differences did persist in four of six areas studied; however, these differences were not so large as described in earlier studies. Areas in which differences were found are demographics, family structure, practice arrangements, and salary. Notable differences were not found in the areas of career choice development and professional activities. Now that the number of female physicians approaches 20 percent of all new family physicians, further data collection efforts are needed to determine their impact on family practice as a specialty.     

苦楝化学成份的研究

从苦楝(Melia azedarach L.)果中分得苦楝新醇(Ⅰ),苦楝醇(Ⅱ)、苦楝酮(Ⅲ)、苦楝二醇(Ⅳ)、香草醛(Ⅴ)和香草酸(Ⅵ)。根据波谱(IR,MS,¹HNMR,¹³CNMR)分析和理化常数测定,确定了它们的结构。其中苦楝新醇(Ⅰ)为新化合物,对菜青小虫有一定的拒食活性。     

Cholinoceptor blockers protect against ethanol-induced gastric mucosal damage in rats.

The role of the cholinergic nervous system in ethanol-induced gastric mucosal damage has been examined in rats. Oral administration of 50 or 80% ethanol produced haemorrhagic lesions which were reduced by atropine pretreatment (0.65, 2.5, 5 or 10 mg/kg injected i.p.); there was lesser protection against the higher dose of ethanol. Pirenzepine (a specific M1 receptor antagonist) pretreatment (0.1, 0.2, 1 or 2 mg/kg, injected s.c.) also protected against ethanol-induced gastric injury to a similar extent; it also increased the amount of adherent mucus on the glandular mucosa. This action may, therefore, account for the protective action of the ganglion blocker. It is concluded that ethanol may stimulate the stomach wall ganglionic nicotinic receptors to activate the postganglionic fibres and subsequently the muscarinic receptors which would then trigger off some of the ulcerogenic mechanisms in the stomach. However, ethanol could also produce gastric damage via the non-cholinergic mechanisms; this action becomes more prominent in gastric injury produced by high doses of ethanol.