Do People Live at Sea Level and the Dead Sea Level Have Different Patterns of Anti-Hypertensive Drugs

Background: people live at various areas of sea level may have different patterns of anti-hypertensive drugs. Such a relation has never been reported in Jordan. Study objectives: the current study investigated how the sea level will impact the prevalence of hypertension in these areas, and how will affect the pharmacological properties of such a population. Methodology: a cross-sectional study design was involved to collect data from study participants. A total of 1000 participants were randomly selected from the two study areas. 500 participants from each. Participants were matched for age and gender. Blood pressure were measured for all participants. Blood samples were withdrawn to investigate the level of angiotensin II. Data was collected through organizing a working excel sheet and was further analyzed through using SPSS version 20. Data was presented as means, standard deviations, frequencies and percentages. The relationships between variables were examined using independent T-test. Significance was measured at an alpha < 0.05. Study findings: the main findings of the present study were that the mean of SBP is significantly higher in the Dead Sea (122.42±10.53 mmHg) than the Sea level area (118.07±11.64 mmHg), (p=0.001). Another significant variable was MBP which its mean was 91.64 ± 8.90 mmHg in the Dead Sea and 89.84 ± 8.72 mm Hg. The difference in the mean was statistically significant (p=0.001). The level of angiotensin II was 8.84 ± 4.65pg/ml in the Dead Sea area and 11.21± 6.05pg/ml in the area of the Sea level. The difference in the mean of the two study areas was not statistically significant (p>0.05). Conclusions: although the level of angiotensin II was not significantly varied between the study areas, but its trend was to be higher in the Sea level area. It was surprised to have higher levels of SBP and MBP in the Dead Sea rather than the Seal level area. It can be implied that the therapeutic options of hypertensive drugs follow different patterns independent of angiotensin II pathways

Microglial cannabinoid type 1 receptor regulates brain inflammation in a sex-specific manner

Background: Neuroinflammation is a key feature shared by most, if not all, neuropathologies. It involves complex biological processes that act as a protective mechanism to fight against the injurious stimuli, but it can lead to tissue damage if self-perpetuating. In this context, microglia, the main cellular actor of neuroinflammation in the brain, are seen as a double-edged sword. By phagocyting neuronal debris, these cells can not only provide tissue repair but can also contribute to neuronal damage by releasing harmful substances, including inflammatory cytokines. The mechanisms guiding these apparent opposing actions are poorly known. The endocannabinoid system modulates the release of inflammatory factors such as cytokines and could represent a functional link between microglia and neuroinflammatory processes. According to transcriptomic databases and in vitro studies, microglia, the main source of cytokines in pathological conditions, express the cannabinoid type 1 receptor (CB1R). Methods: We thus developed a conditional mouse model of CB1R deletion specifically in microglia, which was subjected to an immune challenge (peripheral lipopolysaccharide injection). Results: Our results reveal that microglial CB1R differentially controls sickness behavior in males and females. Conclusion: These findings add to the comprehension of neuroinflammatory processes and might be of great interest for future studies aimed at developing therapeutic strategies for brain disorders with higher prevalence in men