Racial/ethnic and educational inequities in restrictive abortion policy variation and adverse birth outcomes in the United States

Background To examine racial/ethnic and educational inequities in the relationship between state-level restrictive abortion policies and adverse birth outcomes from 2005 to 2015 in the United States. Methods Using a state-level abortion restrictiveness index comprised of 18 restrictive abortion policies, we conducted a retrospective longitudinal analysis examining whether race/ethnicity and education level moderated the relationship between the restrictiveness index and individual-level probabilities of preterm birth (PTB) and low birthweight (LBW). Data were obtained from the 2005–2015 National Center for Health Statistics Period Linked Live Birth-Infant Death Files and analyzed with linear probability models adjusted for individual- and state-level characteristics and state and year fixed-effects. Results Among 2,250,000 live births, 269,253 (12.0%) were PTBs and 182,960 (8.1%) were LBW. On average, states had approximately seven restrictive abortion policies enacted from 2005 to 2015. Black individuals experienced increased probability of PTB with additional exposure to restrictive abortion policies compared to non-Black individuals. Similarly, those with less than a college degree experienced increased probability of LBW with additional exposure to restrictive abortion policies compared to college graduates. For all analyses, inequities worsened as state environments grew increasingly restrictive. Conclusion Findings demonstrate that Black individuals at all educational levels and those with fewer years of education disproportionately experienced adverse birth outcomes associated with restrictive abortion policies. Restrictive abortion policies may compound existing racial/ethnic, socioeconomic, and intersecting racial/ethnic and socioeconomic perinatal and infant health inequities

Absence of PKC-alpha attenuates lithium-induced nephrogenic diabetes insipidus.

Lithium, an effective antipsychotic, induces nephrogenic diabetes insipidus (NDI) in ∼40% of patients. The decreased capacity to concentrate urine is likely due to lithium acutely disrupting the cAMP pathway and chronically reducing urea transporter (UT-A1) and water channel (AQP2) expression in the inner medulla. Targeting an alternative signaling pathway, such as PKC-mediated signaling, may be an effective method of treating lithium-induced polyuria. PKC-alpha null mice (PKCα KO) and strain-matched wild type (WT) controls were treated with lithium for 0, 3 or 5 days. WT mice had increased urine output and lowered urine osmolality after 3 and 5 days of treatment whereas PKCα KO mice had no change in urine output or concentration. Western blot analysis revealed that AQP2 expression in medullary tissues was lowered after 3 and 5 days in WT mice; however, AQP2 was unchanged in PKCα KO. Similar results were observed with UT-A1 expression. Animals were also treated with lithium for 6 weeks. Lithium-treated WT mice had 19-fold increased urine output whereas treated PKCα KO animals had a 4-fold increase in output. AQP2 and UT-A1 expression was lowered in 6 week lithium-treated WT animals whereas in treated PKCα KO mice, AQP2 was only reduced by 2-fold and UT-A1 expression was unaffected. Urinary sodium, potassium and calcium were elevated in lithium-fed WT but not in lithium-fed PKCα KO mice. Our data show that ablation of PKCα preserves AQP2 and UT-A1 protein expression and localization in lithium-induced NDI, and prevents the development of the severe polyuria associated with lithium therapy

Vaginal Cytomegalovirus Shedding Before and After Initiation of Antiretroviral Therapy in Rakai, Uganda.

Vaginal shedding of cytomegalovirus (CMV) DNA was determined longitudinally among 96 women coinfected with human immunodeficiency virus (HIV), herpes simplex virus 2, and CMV starting antiretroviral therapy (ART) during a placebo-controlled trial of HSV-2 suppression with acyclovir in Rakai, Uganda. Vaginal CMV was detected in 75 of 96 women (78.0%) and 379 of 1080 individual visits (35.1%). ART status, higher HIV RNA viral load before ART initiation, and younger age were significantly associated with increased frequency of CMV shedding (P < .01). Compared to pre-ART, CMV shedding peaked from month 2 to month 4 after ART initiation, suggesting possible immune reconstitution inflammatory syndrome. Further studies need to determine the clinical significance of asymptomatic CMV shedding

Vaginal Cytomegalovirus Shedding Before and After Initiation of Antiretroviral Therapy in Rakai, Uganda.

Vaginal shedding of cytomegalovirus (CMV) DNA was determined longitudinally among 96 women coinfected with human immunodeficiency virus (HIV), herpes simplex virus 2, and CMV starting antiretroviral therapy (ART) during a placebo-controlled trial of HSV-2 suppression with acyclovir in Rakai, Uganda. Vaginal CMV was detected in 75 of 96 women (78.0%) and 379 of 1080 individual visits (35.1%). ART status, higher HIV RNA viral load before ART initiation, and younger age were significantly associated with increased frequency of CMV shedding (P < .01). Compared to pre-ART, CMV shedding peaked from month 2 to month 4 after ART initiation, suggesting possible immune reconstitution inflammatory syndrome. Further studies need to determine the clinical significance of asymptomatic CMV shedding

Vaginal Cytomegalovirus Shedding Before and After Initiation of Antiretroviral Therapy in Rakai, Uganda

Vaginal shedding of cytomegalovirus (CMV) DNA was determined longitudinally among 96 women coinfected with human immunodeficiency virus (HIV), herpes simplex virus 2, and CMV starting antiretroviral therapy (ART) during a placebo-controlled trial of HSV-2 suppression with acyclovir in Rakai, Uganda. Vaginal CMV was detected in 75 of 96 women (78.0%) and 379 of 1080 individual visits (35.1%). ART status, higher HIV RNA viral load before ART initiation, and younger age were significantly associated with increased frequency of CMV shedding (P < .01). Compared to pre-ART, CMV shedding peaked from month 2 to month 4 after ART initiation, suggesting possible immune reconstitution inflammatory syndrome. Further studies need to determine the clinical significance of asymptomatic CMV shedding

Elevated cytomegalovirus IgG antibody levels are associated with HIV-1 disease progression and immune activation.

ObjectiveTo assess the association between cytomegalovirus (CMV) IgG antibody levels, HIV disease progression, and immune activation markers.DesignA prospective cohort study was conducted among women enrolled in a trial that was designed to determine the effect of acyclovir on HIV disease progression in Rakai, Uganda.MethodsThe primary endpoints were progression to a CD4 T-cell count less than 250 cells/μl, nontraumatic death, or initiation of antiretroviral therapy (ART). CD4 T-cell counts, HIV viral load, C-reactive protein (CRP), and soluble CD14 levels were assessed biannually for 24 months. CMV IgG antibodies were measured at baseline among all women and annually among a subset of women who initiated ART.ResultsThere were 300 HIV/CMV-coinfected participants who contributed a total of 426.4 person-years with a median follow-up time of 1.81 years. Compared with the lowest CMV IgG tertile group at baseline, the highest CMV IgG tertile group was associated with an increased risk to reach a primary endpoint independent of acyclovir use, age, CD4 T-cell count, and HIV viral load at baseline [adjusted hazard ratio = 1.59; (95% CI = 1.05-2.39); P = 0.027]. Among pre-ART visits (n = 1200), women in the highest baseline CMV IgG tertile had increasing annual rates of soluble CD14 and CRP levels, which was not observed for the low CMV IgG tertile group. Compared with pre-ART visits, CMV IgG antibody levels were higher post-ART initiation, and concurrent levels remained associated with soluble CD14 and CRP during suppressive ART (n = 88 person-visits).ConclusionThe magnitude of the immune response to CMV was associated with HIV disease progression and immune activation in sub-Saharan Africa

AQP2 expression is not changed in short-term lithium-treated PKCα KO mice.

<p>A) IM tissue collected from injected WT and PKCα KO mice was subjected to Western blot analysis and probed for AQP2. Representative blots showing both nonglycosylated (29-kDa) and glycosylated (35- to 50-kDa) AQP2 <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101753#pone.0101753-Terris1" target="_blank">[59]</a>, and the corresponding loading control, β tubulin. Each lane represents one animal. B) Combined densitometry of all forms of AQP2 in the IM normalized to β tubulin. C) OM tissue probed for AQP2 and β tubulin. D) Combined densitometry of all forms of AQP2 in the OM normalized to β tubulin. Data are presented as percent difference in expression from Day 0, untreated mice as mean ± SEM where *  =  p<0.05 vs. WT day 0 and §  =  p<0.05 vs. PKCα KO day 0 is deemed significant. <i>n = 6</i>.</p

UT-A1 expression is not changed in short-term lithium-treated PKCα KO mice.

<p>IM tissue collected from injected WT and PKCα KO mice was subjected to Western blot analysis and probed for UT-A1. A) Representative blots showing the multiple glycosylated forms of UT-A1 that span between 97 and 117 kDa <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101753#pone.0101753-Chen1" target="_blank">[60]</a>, and the corresponding loading control, β tubulin. Each lane represents one animal. B) Combined densitometry of all glycosylated forms of UT-A1 normalized to β tubulin. Data are presented as percent difference in expression from Day 0, untreated mice as mean ± SEM where *  =  p<0.05 vs. WT day 0 and §  =  p<0.05 vs. PKCα KO day 0 is deemed significant. <i>n = 6</i>.</p

Lithium-induced NDI is attenuated in PKCα KO mice.

<p>WT and PKCα KO mice were provided standard chow or chow containing lithium (40 mmol/kg) for 6 weeks. Single animals were subsequently placed in individual metabolic cages to determine 24-h water intake. Urine and serum were also collected at this time point for metabolic determinations. Uprot/Uosm  =  urinary protein/urine osmolality ratio, CrCl/BW  =  creatinine clearance normalized to body weight (29–30 g). Data are presented as mean ± SEM where *  =  p<0.05 vs. WT day 0 and §  =  p<0.05 vs. PKCα KO day 0 is deemed significantly different. <i>n = 5</i>.</p