Social media and disordered eating among middle-aged women: Not just an adolescent concern.

Evidence suggests social media use is strongly linked to disordered eating (e.g., binge eating and dietary restraint) among adolescent and young adult women, in part because it promotes engagement in social comparison (the tendency to evaluate one's own standing or ability by comparing it to another's). Yet no study has examined the impact of social media use and comparison on disordered eating among middle-aged women. Participants (N = 347), ages 40-63, completed an online survey about their social media use, social comparison, and disordered eating (bulimic symptoms, dietary restraint, and broad eating pathology). Results indicated that 89 % (n = 310) of middle-aged women used social media in the past year. Most participants (n = 260; 75 %) used Facebook, and at least a quarter used Instagram or Pinterest. Approximately 65 % (n = 225) used social media at least daily. Controlling for age and body mass index, social media-specific social comparison was positively associated with bulimic symptoms, dietary restriction, and broad eating pathology (all ps < 0.001). Multiple regression models evaluating frequency of social media use and social media-specific social comparison together revealed that social comparison explained a significant amount of unique variance in bulimic symptoms, dietary restriction, and broad eating pathology (all ps < 0.001) above and beyond frequency of social media use. Instagram explained a significant proportion of variance of dietary restraint compared to other social media platforms (p = .001). Findings suggest a large percentage of middle-aged women frequently engage with some type of social media. Further, social media-specific social comparison, rather than frequency of social media use, may be driving disordered eating in this age group of women.

Urinalysis for the diagnosis of glomerulonephritis: role of dysmorphic red blood cells.

Background: Dysmorphic red blood cells (dRBCs) on urine microscopy have been associated with glomerulonephritis (GN). We assessed the prevalence and ability of dRBCs to differentiate GN from other kidney diseases. Methods: Adult patients with kidney biopsy performed between 2012 and 2015 at a single center who had a concurrent urinalysis were retrospectively studied. The association of ≥25% dRBCs with the presence of glomerular pathology was assessed. Univariate and multivariate logistic regression were performed on significantly associated variables. Results: The mean age of the 482 eligible subjects was 55 years and 47.7% were female. Overall, 173 (35.9%) had <25% and 76 (15.8%) had ≥25% urine dRBCs. Kidney biopsies revealed glomerular disease in 372 (77.2%) (GN 46% and non-GN 54%). At the dRBC threshold of ≥25% used at our center, a sensitivity of 20.4%, specificity of 96.3% and positive predictive value of 94.6% for glomerular disease were observed. In a logistic regression model, urine RBCs [>10 versus ≤10 (P < 0.001)] but not dRBCs ≥25% (P = 0.3) independently predicted the presence of GN. A scoring system (0-3) based on hematuria and proteinuria levels revealed the risk for biopsy-proven GN was 15% when the score was 0 compared with 83% when it was 3. Conclusions: The presence of ≥25% urine dRBCs is specific but not sensitive for GN. In this cohort, the combined hematuria (>10 RBCs/high-power field) and proteinuria performed just as well as dRBCs plus proteinuria to predict underlying GN. A model based on the degree of hematuria and proteinuria found on urinalysis was able to predict the presence of GN.

Cell-specific temporal infection of the brain in a simian immunodeficiency virus model of human immunodeficiency virus encephalitis.

Increasing evidence supports early brain infection by human immunodeficiency virus (HIV). Definitive temporal studies determining when and within which brain cells viral DNA is present are lacking. This study utilized simian immunodeficiency virus (SIV)-infected macaques sacrificed at days 10, 21, 56, and 84 post inoculation. Laser-microdissection isolated pure perivascular macrophage, parenchymal microglia, and astrocyte populations. Nested polymerase chain reaction (PCR) and sequencing determined the presence and characteristics of SIV V3 and V1 env DNA from each population. At day 10, SIV DNA was detected in perivascular macrophage and astrocytes but not parenchymal microglia. gp41 expression was restricted to perivascular macrophage. At day 21, SIV DNA was not detected in any cell type. At day 56, SIV DNA was detectable in perivascular macrophage from one of two macaques, with no gp41 expression detected. At day 84 (morphologic and clinical encephalitis), SIV DNA was detected in all cell types, gp41 was only detected in perivascular macrophage and parenchymal microglia. The neurovirulent molecular clone, SIV/17E-Fr, was the only genotype identified in the brain cell populations. Early, productive brain SIV infection was transient and restricted to trafficking perivascular macrophage. During the nonencephalitic stage, there was a period of time when no SIV DNA could be detected in the brain cell populations. SIV was then seen to reenter the brain via infected perivascular macrophage, leading to productive infection of brain parenchymal macrophage/microglia with a terminal phase of encephalitis. These data challenge current notions of a HIV reservoir within latently infected, semipermanent brain cells and has significant implications for the timing and design of therapies to prevent HIV encephalitis (HIVE).

Use of laser capture microdissection to detect integrated HIV-1 DNA in macrophages and astrocytes from autopsy brain tissues.

The importance of astrocytes as a reservoir of human immunodeficiency virus type 1 (HIV-1) in the brain remains elusive. By combining immunohistochemistry, laser capture microdissection, and triple-nested Alu-PCR, we demonstrate integrated HIV-1 in astrocytes and macrophages isolated directly from autopsy brain tissues of HIV-1-infected subjects. The ability of HIV-1 to integrate in terminally differentiated astrocytes suggests a permanent reservoir of provirus in brain that will impact the development and likely success of strategies aimed at eradicating HIV-1.

Increased adipocyte apoptosis in lipoatrophy improves within 48 weeks of switching patient therapy from Stavudine to abacavir or zidovudine.

OBJECTIVES: Lipoatrophy is an important manifestation of the lipodystrophy syndrome and is particularly associated with stavudine exposure. Increased apoptosis has been suggested as a possible mechanism of lipoatrophy. We assessed the degree and reversibility of adipocyte apoptosis in patients with lipoatrophy before and 48 weeks after substituting abacavir or zidovudine for stavudine. METHODS: Apoptotic adipocytes were identified using terminal transferase dUTP nick end labeling and quantified using video image analysis. RESULTS: Fat biopsy specimens were obtained from patients before (n = 15) and 48 weeks after (n = 10) switching from stavudine and from 20 HIV-uninfected controls. More apoptotic cells were seen in fat samples from patients with lipoatrophy treated with stavudine than in specimens from controls (P < 0.0001). Forty-eight weeks after switching from stavudine to abacavir or zidovudine, there was a reduction in apoptotic cells per unit area (P = 0.01) and as a proportion of all adipocytes present (P = 0.02) in patient biopsy specimens. Levels of adipocyte apoptosis in the 48-week biopsy specimens were no longer significantly different from those seen in control biopsy specimens (P > 0.1). CONCLUSIONS: Increased apoptosis is present in fat samples from patients with lipoatrophy treated with stavudine. This improves toward normal within 48 weeks of switching from stavudine to abacavir or zidovudine, suggesting a causative role for stavudine in this process.