Prevalence of hypertension and possible risk factors of hypertension unawareness among individuals aged 30-75 years from two Panamanian provinces: Results from population-based cross-sectional studies, 2010 and 2019.

BACKGROUND: Recent estimates of hypertension in Panama remain unknown. We aim to describe the variation in prevalence and unawareness of hypertension in two Panamanian provinces using two different cross-sectional population-based studies and to investigate risk factors associated with hypertension unawareness. METHODS: Data were derived from a sub-national study conducted in the provinces of Panama and Colon (PREFREC-2010 [2,733 participants]) and from a nationally representative study (ENSPA-2019), in which we restricted our analyses to the same provinces (4,653 participants). Individuals aged 30-75 years who had (a) self-reported history of hypertension or (b) blood pressure (BP) ≥140/90mmHg or (c) a combination or both were classified as hypertensive. Participants with BP≥140/90mmHg who denied a history of hypertension were considered unaware of the condition. Multivariable logistic regression models were used to estimate the association between risk factors and unawareness, expressed as odds ratios (OR) and 95% confidence interval (CI). FINDINGS: In 2010, the prevalence and unawareness of hypertension in men were 51.6% (95% CI: 45.7-57.5) and 32.3% (25.4-40.1), respectively, and in women 46.0% (42.1-49.9) and 16.1% (12.6-20.4), respectively. In 2019, the prevalence and unawareness of hypertension in men were 46.5% (42.1-51.0) and 52.3% (45.9-58.6), and in women 42.1% (39.6-44.7) and 33.3% (29.8-37.0). Men (2010 and 2019), age <50 years (2010 and 2019), having no/primary education (2010), and living in a non-urban region (2019) were positively associated with hypertension unawareness, whereas obesity (2010), physical inactivity (2010), family history of hypertension (2019), and BP assessment in the year before study enrollment (2010 and 2019) were inversely associated with hypertension unawareness. INTERPRETATION: Benefits of a decrease in the prevalence of hypertension are being undermined by an increase in hypertension unawareness. Actions should be encouraged to strengthen the implementation of the existing healthcare program for cardiovascular risk factor control.

Aquatic environmental effects monitoring guidance for environmental assessment practitioners.

The Canadian Environmental Assessment Act (CEAA) defines the federal environmental assessment (EA) process for evaluating the likelihood that development projects (e.g., roads, buildings, factories) will have impacts on the environment. Environmental effects monitoring (EEM) programs for mining and pulp and paper mills under the Federal Fisheries Act, define the process that is to be used to evaluate existing effects caused by liquid effluents discharged by operating facilities. The EA process occurs before a project is approved, and involves predicting whether the project is going to cause significant environmental impacts. The EEM process occurs after a project is operational, and involves determining whether an existing project has had or is continuing to have significant impacts on the environment. Ideally, the processes are complimentary, with the EA process identifying environmental attributes considered important, and the EEM process demonstrating whether predicted or unpredicted impacts occurred. The two processes are usually done in isolation so potential synergies are lost. The point of this manuscript is to justify bridging the two processes. We use the aquatic environment as the example, and briefly describe the EEM process, aquatic environment indicators, experimental designs, and typical environmental thresholds, to illustrate how the EEM and EA processes link.

Mouse hepatocyte response to peroxisome proliferators: dependency on hepatic nonparenchymal cells and peroxisome proliferator activated receptor alpha (PPARalpha).

Peroxisome proliferators (PPs) are rodent nongenotoxic hepatocarcinogens that induce peroxisome proliferation and DNA synthesis, and suppress apoptosis in rodent hepatocytes. PPs act through the PP-activated receptor alpha (PPARalpha); tumour necrosis factor alpha (TNFalpha) and hepatic nonparenchymal cells (NPCs), the major source of TNF alpha in the liver, have also been implicated in mediating the rodent hepatic response to PPs. Here we investigate the interaction between PPARalpha and NPCs in regulating the response to PPs. Using normal hepatocyte cultures containing around 20% NPCs, the PP nafenopin (50 microM) induced DNA synthesis and suppressed transforming growth factor beta1-induced apoptosis. However, when the NPCs were removed by differential centrifugation, nafenopin did not induce DNA synthesis or suppress apoptosis in the pure hepatocytes. Reconstitution of the normal hepatocyte cultures by mixing together the pure hepatocytes and the previously separated NPCs in the same proportions as the original cell preparation (17.7+/-8.7% NPCs) restored the response to nafenopin. Interestingly, nafenopin was still able to induce beta-oxidation in the pure hepatocyte cultures, consistent with NPCs being required for PP-induced growth but not for peroxisome proliferation. Next, we evaluated the role of PPARalpha in the hepatocyte dependency upon NPCs. Interestingly, NPCs isolated from PPARalpha-null mice, like those isolated from the wild-type NPCs, restored the hepatocyte response to nafenopin. However, as expected, PPARalpha-null hepatocytes remained non-responsive to PPs, irrespective of the genotype of the added NPCs. These data support a role for NPCs in facilitating a response of hepatocytes to PPs that is ultimately dependent on the presence of PPARalpha in the hepatocyte.

Reactive arthritis-associated bacteria can stimulate lymphocyte proliferation in non-exposed individuals and newborns.

In reactive arthritis (ReA) a specific T cell response to the triggering bacterial antigen is present in the synovial fluid, while in paired peripheral blood T cells the response is markedly reduced. The proliferative response to ReA-associated bacteria in the peripheral blood of ReA patients was compared with that seen in the blood of healthy adults, who denied exposure to these microbes, and in the umbilical cord blood of newborns, who have clearly not been exposed to bacterial antigen. Peripheral blood mononuclear cells (PBMC) from non-exposed adults and those from umbilical cord blood proliferated to ReA-associated bacteria, whilst little response was seen in ReA PBMC. The response was MHC class II-restricted, required processing of the bacterial antigen, was seen in both CD45RO+ and CD45RA+ subsets, and was not oligoclonal. These T cell responses are similar to those previously demonstrated in non-exposed individuals to malaria, leishmania and trypanosoma antigen, and may reflect the existence of 'natural' T cell immunity to ReA-associated bacteria. The lack of such responses in ReA peripheral blood may suggest that such 'natural' responses may restrict the dissemination or progression of infection.

Problems with clinical trials in general practice--a double-blind comparison of cream containing miconazole and hydrocortisone with hydrocortisone alone in the treatment of intertrigo.

A double-blind comparative study between 1% hydrocortisone cream and a combination of 1% hydrocortisone cream and 2% miconazole cream has highlighted some of the problems with this type of research in general practice. The collection of adequate patient numbers within a predefined time scale proved a major problem. However, the study demonstrated the safety and efficacy of both these preparations in the treatment of intertrigo.