Human Immunodeficiency Virus and Homelessness Among U.S.-Born and Foreign-Born Tuberculosis Cases in Georgia

According to the Centers for Disease Control and Prevention, tuberculosis (TB) is an infectious disease caused by bacteria and can easily spread in the U.S. and worldwide. TB infections in the U.S. have been much lower compared to other countries around the world in the last 40 years, but with the recent increase in an immigrant foreign-born population, there is a serious risk of the spread of TB. The goal of the study was to look into U.S.-born vs. foreign-born populations among TB/HIV/homeless cases in the state of GA from 2014 to 2018. The quantitative study was performed using secondary data from the CDC Online Tuberculosis Information System. Univariate Chi-square and multivariate regression analyses were done while using the social ecological model as theoretical framework. Findings show no evidence of the association between origin of birth, the odds of being foreign-born TB case in GA and HIV status, rather U.S.-born to be more HIV positive and homeless. There was no significant association related to sex and being foreign-born among HIV positive TB cases, and no significant association related to age groups in homeless TB cases. The study contributes to positive social change by improving treatment plans to eliminate TB in GA refuting the assumption that foreign born persons are more likely than U.S.-born persons to be HIV positive and homeless, thus reducing the stigma among the foreign-born population. These findings will benefit society and will result in immigrant friendly and less biased society for all

Contractile force is enhanced in Aortas from pendrin null mice due to stimulation of angiotensin II-dependent signaling.

Pendrin is a Cl-/HCO3- exchanger expressed in the apical regions of renal intercalated cells. Following pendrin gene ablation, blood pressure falls, in part, from reduced renal NaCl absorption. We asked if pendrin is expressed in vascular tissue and if the lower blood pressure observed in pendrin null mice is accompanied by reduced vascular reactivity. Thus, the contractile responses to KCl and phenylephrine (PE) were examined in isometrically mounted thoracic aortas from wild-type and pendrin null mice. Although pendrin expression was not detected in the aorta, pendrin gene ablation changed contractile protein abundance and increased the maximal contractile response to PE when normalized to cross sectional area (CSA). However, the contractile sensitivity to this agent was unchanged. The increase in contractile force/cross sectional area observed in pendrin null mice was due to reduced cross sectional area of the aorta and not from increased contractile force per vessel. The pendrin-dependent increase in maximal contractile response was endothelium- and nitric oxide-independent and did not occur from changes in Ca2+ sensitivity or chronic changes in catecholamine production. However, application of 100 nM angiotensin II increased force/CSA more in aortas from pendrin null than from wild type mice. Moreover, angiotensin type 1 receptor inhibitor (candesartan) treatment in vivo eliminated the pendrin-dependent changes contractile protein abundance and changes in the contractile force/cross sectional area in response to PE. In conclusion, pendrin gene ablation increases aorta contractile force per cross sectional area in response to angiotensin II and PE due to stimulation of angiotensin type 1 receptor-dependent signaling. The angiotensin type 1 receptor-dependent increase in vascular reactivity may mitigate the fall in blood pressure observed with pendrin gene ablation

Force/CSA in response to Angiotensin II in isolated mouse thoracic aorta from wild type and pendrin null mice.

<p>Force/CSA was measured in response to angiotensin II (100 nM) in thoracic aortas from pendrin null (KO) and wild type (WT) mice (Panel A). Panel B shows Force/CSA in response to 100 nM angiotensin II when expressed as the percentage of force/CSA observed in response to phenylephrine (10 µM). n = 7 in each group. *p<0.05.</p

Pendrin gene ablation does not increase aortic contractile force through changes in Ca²⁺ sensitivity.

<p>Rings from wild type and pendrin null mice were Ca²⁺ depleted by incubating in the presence of the Ca²⁺ chelator, EGTA, and then depolarized with 50 mM KCl. Vascular contractility was measured following the addition of calcium to the bath in increments of 0.2 mM <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0105101#pone.0105101-McMahon2" target="_blank">[22]</a>, n = 5–6.</p

<i>Slc26a4</i> mRNA levels in wild-type aorta and kidneys.

<p><i>Slc26a4</i> mRNA levels in wild-type aorta and kidneys.</p

Inhibition of the angiotensin type 1 receptor equalizes aortic contractile force and cross sectional area in pendrin null and wild type mice.

<p>Aortic rings from candesartan-treated wild type and pendrin null mice were isometrically mounted and maximum force generated/cross sectional area was measured in response to the cumulative addition of KCl (Panel A) and PE (Panel B) (n = 5–6). Cross sectional area of the aorta wall was measured in each of the vessels studied (Panel C). Aorta thickness (intima and media, Panel D) was measured by morphometry in separate candesartan-treated wild type (n = 6) and pendrin null (n = 6) mice. Body weights for the aorta thickness measurements were the following: wild type 24.4±0.9 g versus 21.4±1.0 g for pendrin null mice.</p

Pendrin gene ablation does not affect steady state catecholamine production.

<p>24 hour urinary epinephrine and norepinephrine excretion of pendrin null and wild type mice are shown.</p