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Municipal commonages surround many small towns throughout South Africa, and are an integral component of the national land reform programme. But little is known about their extent, use or value, and most appear to have limited or no management or investment. This paper reports on a survey of randomly selected households in three small towns in the Eastern Cape to ascertain the extent and purpose of use of municipal commonages. Between 27% and 70% of urban households used commonage depending on site. Key resources used were fuelwood, medicinal plants, and grazing of livestock. Typically, commonage using households were poorer and less educated than other urban residents, although the profile of users is unique for each town. Given the extensive use of commonage resources, and their contribution to the livelihoods of the poor, local municipalities need to develop and implement sound management strategies that account for all users of commonages, rather than the oft encountered focus on livestock owners and production.

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We report a case of recurrent listeriosis for which molecular subtyping by automated ribotyping and pulsed-field gel electrophoresis confirmed either relapse of infection or reinfection due to a common source almost 9 months after initial infection due to a unique Listeria monocytogenes strain in a patient with colorectal cancer. This case report illustrates the potential use of molecular subtyping to further understand the pathogenesis and epidemiology of listeriosis and the potential for relapse of Listeria infections in humans.

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OBJECTIVES: This study determined the validity of self-reported data on selected health insurance characteristics. METHODS: We obtained telephone survey data on the presence of health insurance, source of insurance, length of time insured, and type of insurance (managed care or fee-for-service) from a random sample of 351 adults in 3 Wisconsin counties and compared findings with data from respondents' health insurers. RESULTS: More than 97% of the respondents correctly reported that they were currently insured. For source of insurance among persons aged 18 to 64 years, sensitivity was high for those covered through private health insurance (93.8%) but low for those covered through public insurance (6.7%). Only 33.1% of the respondents accurately categorized length of enrollment in their current plan. Overall estimates for managed care enrollment were similar for the 2 sources, but individual validity was low: 84.2% of those in fee-for-service believed that they were in managed care. CONCLUSIONS: Information obtained from the general population about whether they have health insurance is valid, but self-reported data on source of insurance, length of time insured, and type of insurance are suspect and should be used cautiously.

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BACKGROUND: Barotrauma in the flight environment is a significant cause of incidents and mishaps. Upper respiratory infections and allergic rhinitis are considered to increase the risk of barotrauma in the changing pressure environment. In an attempt to identify antecedent conditions as predictors of barotrauma, all adverse outcomes which occurred in a Navy altitude chamber during 1993-94 were investigated. METHODS: A retrospective study of chamber logs, pre-chamber screening questionnaires, and a medical waiver database was conducted on altitude chamber trainees at the Naval Aerospace and Operational Medical Institute. Barotrauma cases were confirmed by reviewing ENT consultation records. Chamber screening questionnaires and medical waiver status were compared between barotrauma cases and a control group from the same chamber runs. RESULTS: Of 5851 trainees, 193 (3.3%) experienced adverse events during this period, with an additional 9 events occurring to inside observers. Barotrauma, with 160 cases, accounted for the greatest number of these events. Upper respiratory symptoms were present in 12 (7.7%) of the barotrauma cases and 15 (4.8%) of the controls. Waivers for upper respiratory conditions such as allergic rhinitis were present in 9 (6.1%) of the barotrauma cases and 17 (5.7%) of the controls. Under-reporting of upper respiratory conditions on pre-chamber screening was found however, with only 7 of 28 cases with recent cold symptoms reporting this prior to chamber training. CONCLUSIONS: No significant differences were found in predictors for barotrauma between cases and controls in this study group.

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This study examined the effect of a self-instructional program on nurses' knowledge of and attitudes and behavioral intentions toward patients with borderline personality disorder. The sample consisted of registered nurses working on inpatient psychiatric units of general hospitals: 19 in the experimental group and 13 in the control group. The Questionnaire on Borderline Personality Disorder was administered before and after nurses completed the program. Significant postintervention differences in knowledge of and attitudes toward patients with the disorder were found between the experimental group and the control group. Self-instruction may improve nurses' care of patients with borderline personality disorder.

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Sudden release of platelet-activating factor (PAF) into the circulation can cause hypotension, tachycardia, and circulatory collapse. To further examine this response, we performed detailed studies of cardiovascular function after PAF administration to young domestic pigs and newborn piglets. Our results indicate that circulatory dysfunction after PAF reflects severe constriction of pulmonary resistance vessels and consequent acute right ventricular failure. Although PAF-induced coronary artery constriction and contractile depression may be complicating problems, left ventricular underperfusion and dysfunction after PAF are mainly the result of systemic arterial hypotension and diminished left ventricular filling. The adverse hemodynamic effects of PAF are accompanied by substantial release of thromboxane A2 (TxA2). These effects are mimicked by the TxA2 agonist U-46619 and partially blocked by specific and nonspecific inhibitors of TxA2 synthesis (OKY-046 and indomethacin). Even more potent blockade of PAF action is exerted by the TxA2 receptor blocker, SQ 29,548. Taken together, these findings indicate that severe pulmonary vascular constriction and hemodynamic collapse soon after intravenous PAF are at least partially mediated by PAF-induced TxA2 release. Tachyphylaxis to PAF influence has been observed in studies of leukocyte and platelet function. We hypothesized that tachyphylaxis to PAF might also occur in our studies of constrictor responses in pulmonary vessels. Recently, we have examined the capacity of PAF to produce sustained pulmonary vasoconstriction in open-chested, anesthetized newborn piglets. Infusions sufficient to produce 100% increase in mean pulmonary artery pressure after 3 min showed no loss of efficacy when sustained for 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)

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Platelet-activating factor (PAF), a likely mediator of endotoxin action, causes thromboxane A2 (TXA2) release and pulmonary hypertension in pigs. We examined the effect of selective TXA2 synthase inhibition with OKY-046 on cyclooxygenase metabolites during PAF-induced pulmonary hypertension. Six closed-chest pigs received PAF in escalating doses (0.1, 0.3, 1.0, and 3.0 nmol intravenously, i.v.) before and after (E)-3[4-(1-imidazolyl methyl) phenyl]-Z-propenoic acid hydrochloride monohydrate OKY-046, 10-mg/kg i.v. bolus plus 20-mg/kg/h infusion. Plasma samples at peak PAF effect had radioimmunoassay (RIA) for the stable metabolites of TXA2 (TXB2) and prostacyclin (6-keto-PGF1 alpha). Tachyphylaxis was not noted in 5 control pigs given sequential repeats of the PAF dosing series. Pulmonary vascular resistance (PVR) was 240 +/- 30 (SE) dyne s cm-5 at baseline and increased to 3,100 +/- 1,300 after 1.0 nmol PAF (p less than 0.05). When the same amount of PAF was given after OKY-046, PVR increased only to 820 +/- 280 dynes/s/cm-5. TXB2 was 34 +/- 7 pg/0.1 ml at baseline and increased to 70 +/- 4 pg/0.1 ml with PAF 1.0 nmol (p less than 0.001). TXB2 levels were unchanged from 34 +/- 4 pg/0.1 ml when PAF 1.0 nmol was administered after OKY-046 (NS vs. pre-OKY-046). In contrast, 6-keto-PGF1 alpha, 6 +/- 2 pg/0.1 ml at baseline, increased to 24 +/- 4 pg/0.1 ml after PAF 1.0 nmol and increased further to 50 +/- 8 pg/0.1 ml when PAF 1.0 nmol was given after OKY-046 (p less than 0.05 vs. pre-OKY-046).(ABSTRACT TRUNCATED AT 250 WORDS)

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Platelet-activating factor (PAF) is a phospholipid mediator that induces cardiovascular collapse and release of the secondary mediator thromboxane A2 (TxA2). To clarify mechanisms involved in this collapse and, specifically, the relative contribution of left ventricular and right ventricular dysfunction, we studied 12 open-chest pigs. PAF infusion (0.04-0.28 nmol.kg-1.min-1) induced a 5- to 120-fold increase in pulmonary vascular resistance, a 75-98% fall in cardiac output, and systemic arterial hypotension. Right ventricular failure was indicated by chamber enlargement, decreased shortening, and increased right atrial pressures. In contrast, left ventricular dysfunction was accompanied by decreases in chamber dimensions and filling pressures that were unresponsive to volume expansion. U 46619 (a stable TxA2 analogue) and mechanical pulmonary artery constriction induced changes similar to PAF. In 11 additional closed-chest pigs, TxA2 blockade with indomethacin attenuated the PAF-induced rise in pulmonary vascular resistance, right ventricular dysfunction, and systemic hypotension. A specific TxA2 synthase inhibitor, OKY-046, also diminished hemodynamic effects of PAF in six other pigs. Tachyphylaxis was not observed in five pigs repeatedly given PAF. We conclude that acute right ventricular failure as the result of severe increase in pulmonary vascular resistance is the primary mechanism early in the course of PAF-induced shock in the pig. PAF-induced release of TxA2 may contribute significantly to these events.

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After coronary occlusion, myocardium originally supplied by the occluded vessel ultimately separates into infarct and surviving muscle. To clarify this process, evolution of collateral blood flow to infarct and to surviving myocardium was retrospectively analyzed after permanent left anterior descending occlusion in 24 closed chest dogs. Microspheres were injected before occlusion and 5 and 20 minutes and 4 hours after occlusion. Ten minutes after occlusion, dogs received either verapamil, 0.4 mg/kg, followed by 0.6 mg/kg per hour for 6 hours (n = 10) or equivalent saline solution (n = 14). These dogs were sacrificed 3 days later, the distribution of the occluded artery was defined by dye perfusion and infarcted myocardium was determined by triphenyltetrazolium staining of heart slices. Surviving muscle within the distribution of the occluded artery was divided into medial regions adjacent to the infarct (medial adjacent) and remote from the infarct (medial remote) and lateral regions adjacent to infarct (lateral adjacent) and remote from the infarct (lateral remote). In both control and verapamil groups, collateral flows in all regions increased significantly by 140 to 400% over 4 hours. However, the relative magnitude of collateral flow to different regions showed a consistent order: infarct less than medial adjacent less than medial remote less than lateral remote. There were no significant differences in regionally matched flows or size of infarction between control and verapamil-treated groups. Collateral perfusion begins to show distinctive patterns of change in infarct and surviving muscle very soon after coronary occlusion. Collateral flow within subdivisions of the occluded coronary artery bed increases as distance from the infarct increases, with lateral segments having higher flows than medial segments. This relation persists during the first 4 hours after occlusion. In this study, verapamil neither increased collateral flow to the occluded bed nor altered minimal flow requirements for myocardial survival.

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