(C) 2012 Elsevier Ltd. All rights reserved.”
“Social stress has been linked to several neuropsychiatric diseases, including depression, which is a debilitating disease that has genetic, environmental, and epigenetic underpinnings.

This study examined the effects of repeated social defeat on both depressive-like behaviors and histone acetylation in the hippocampus, amygdala, and dorsal prefrontal cortex of male Sprague-Dawley rats.

Subjects were exposed to four consecutive social defeats. Depressive-like behaviors were assayed in the sucrose preference, forced swim, contextual fear, and social Belinostat approach and avoidance tests. Histone H3 and H4 acetylation in the hippocampus, amygdala, and

prefrontal cortex were examined by Western blots under basal conditions and at several time points. We also investigated the potential involvement of N-methyl-d-aspartic acid (NMDA) receptors and glucocorticoid receptors (GR) by injecting respective antagonists prior to each social

defeat and examining their effect on histone acetylation in the hippocampus.

Social defeat resulted in behavioral changes in the forced swim, social avoidance, and contextual fear tests nearly 6 weeks after defeat, with no change in sucrose preference. Additionally, histone H3 acetylation was increased in the hippocampus 30 min following the last defeat and was not blocked by antagonism of either NMDA or GR receptors. There were no changes in histone H4 acetylation.

These results indicate that social defeat

induces several long-lasting depressive-like behaviors in rats and induces a significant, short-lived enough increase in H3 acetylation in GSK2879552 price the hippocampus, although the underlying mechanism behind this change warrants further investigation.”
“beta-Catenin is a unique intracellular protein functioning as an integral component of the cell-cell adherens complex and a principal signaling protein mediating canonical Wnt signaling. Little is known about its function in adult kidneys in the normal physiologic state or after acute kidney injury (AKI). To study this, we generated conditional knockout mice in which the beta-catenin gene was specifically disrupted in renal tubules (Ksp-beta-cat-/-). These mice were phenotypically normal with no appreciable defects in kidney morphology and function. In the absence of beta-catenin, gamma-catenin functionally substituted for it in E-cadherin binding, thereby sustaining the integrity of epithelial adherens junctions in the kidneys. In AKI induced by ischemia reperfusion or folic acid, the loss of tubular beta-catenin substantially aggravated renal lesions. Compared with controls, Ksp-beta-cat-/- mice displayed higher mortality, elevated serum creatinine, and more severe morphologic injury. Consistently, apoptosis was more prevalent in kidneys of the knockout mice, which was accompanied by increased expression of p53 and Bax, and decreased phosphorylated Akt and survivin.

3mg/dl or >= 50% within 48 h after surgery. Fifty-nine patients in each group were analyzed on an intention-to-treat basis. Acute kidney injury occurred in 12 remote ischemic preconditioned and 28 control patients, reflecting an absolute risk reduction of 0.27 and a significantly reduced relative

risk due to preconditioning of 0.43. Hence, remote ischemic preconditioning prevents acute kidney injury in patients undergoing cardiopulmonary bypass-assisted cardiac surgery. Kidney International (2011) 80, 861-867; doi:10.1038/ki.2011.156; published online 15 www.selleckchem.com/products/stattic.html June 2011″
“In animals, blocking of glutamate signaling at the N-methyl-D-aspartate (NMDA) receptor reduces the neuroendocrine counterregulation to hypoglycemia. Hence, it has been proposed that increased excitatory glutamatergic input to

the hypothalamus signals enforced central nervous see more energy demand under conditions of reduced supply. We examined the effect of the NMDA receptor antagonist memantine on hypoglycemia counterregulation in healthy humans. Hypoglycemic clamp experiments were performed in 10 healthy men after oral administration of 20 mg memantine and placebo. Counterregulatory hormones were measured during baseline and a clamp period of 120 min with hypoglycemia of 2.4 mmol/l lasting for 50 min. In addition, symptoms related to glycemic changes were assessed. Unexpectedly, the counterregulatory responses to hypoglycemia of adrenocorticotropin, cortisol and epinephrine were not decreased but tended to be increased by memantine, while norepinephrine and growth hormone were not affected. Glucagon levels were increased by memantine

treatment during baseline and throughout the Etomoxir hypoglycemic period. After memantine administration, subjects also experienced more neuroglycopenic symptoms during hypoglycemia, whereas differences in autonomic symptoms did not reach significance. Contrasting with findings in animals, blocking the NMDA receptor does not decrease the counterregulatory responses to hypoglycemia in humans. Our data do not support the view that in humans, enhanced glutamate signaling during hypoglycemia supports the satisfaction of increased central nervous energy demands by enforcing hormonal counterregulation. (c) 2008 Elsevier Ltd. All rights reserved.”
“This NIH-funded multicenter randomized study of focal segmental glomerulosclerosis (FSGS) treatment compared the efficacy of a 12-month course of cyclosporine to a combination of oral pulse dexamethasone and mycophenolate mofetil in children and adults with steroid-resistant primary FSGS. Of the 192 patients enrolled, 138 were randomized to cyclosporine (72) or to mycophenolate/dexamethasone (66). The primary analysis compared the levels of an ordinal variable measuring remission during the first year. The odds ratio (0.

Assays for determining SNPs can detect efficiently nucleotide substitutions and can thus be adapted to identify CPV types. In the present study, CPV typing was performed by single nucleotide extension using the mini-sequencing technique. A mini-sequencing signature was established for all the four CPV types (CPV2, 2a, 2b and 2c) and feline panleukopenia

virus. The CPV typing using the mini-sequencing reaction was performed for 13 CPV field isolates and the two vaccine strains available in our repository. All the isolates had been typed earlier by full-length sequencing of the VP2 gene. The typing results obtained from mini-sequencing matched completely with that of sequencing. Typing could be achieved with less than

100 copies of standard plasmid DNA constructs or <= 10(1) FAID(50) of virus by mini-sequencing selleckchem technique. The technique was also efficient for Danusertib datasheet detecting multiple types in mixed infections. (C) 2012 Elsevier B.V. All rights reserved.”
“Aims: Alterations of plasma amyloid-beta (A beta) peptides have been related to a high risk for cognitive impairment and dementia. The present study aimed to measure plasma A beta peptides (A beta 40, A beta 42) and the A beta 40/A beta 42 ratio in a sample of drug-resistant bipolar depressed patients, as well as to explore the possible correlation between biological parameters and clinical changes along an electroconvulsive therapy (ECT) course. Methods: A beta 40 and A beta 42 were measured by means of an ELISA assay in 25 drug-resistant bipolar depressed patients before (T0) and 1 week after (T1) the end of ECT. The patients were clinically evaluated by means of the Hamilton Rating Scale for Depression, 21-item (HRSD-21), the Mini-Mental State Examination, and the Clinical Global Impressions-Severity of Illness Scale. Results: Plasma A beta levels and the A beta 40/A beta 42 ratio were similar at T0 and T1. The A beta 40/A beta 42 ratio correlated positively with the HRSD total score at both T0 and T1. At

T0, a negative correlation Tacrolimus (FK506) was found between the A beta 40/A beta 42 ratio and the improvement of depressive and cognitive symptoms. Moreover, remitters (n = 9; HRSD <= 10) showed a significantly lower A beta 40/A beta 42 ratio at T0 than nonremitters. Conclusion: The present data suggest that a low A beta 40/A beta 42 ratio might characterize a subgroup of depressed patients who respond to ECT, while higher values of this parameter seem to be typical of more severe cases of patients with cognitive impairment. Copyright (c) 2013 S. Karger AG, Basel”
“Cigarette smoking has been linked to a number of personality characteristics, including impulsivity. Smokers tend to endorse high levels of impulsivity, and more impulsive smokers have greater difficulty quitting, but little is known about potential explanatory mechanisms.

In this study, we investigated the ability of NAN-190 to potentiate the circadian rhythm response to light as measured by phase of behavioral activity rhythms. NAN-190 (5 mg/kg, selleckchem i.p.) was able to significantly potentiate the response to light both in dark-adapted and entrained hamsters. Furthermore, NAN-190 was effective even when administered up to 6 h after light onset. Response to a light pulse was both greater in magnitude and involved fewer unstable transient cycles. Finally, NAN-190 was able to speed re-entrainment to a 6 h advance of the light/dark cycle by an average of 6 days when compared with vehicle-treated animals. This work suggests that compounds like

NAN-190 may hold great potential as a pharmaceutical treatment for jetlag, shift

work, and other circadian disorders. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Mismatching for human leukocyte antigen (HLA)-DPB1 in unrelated donor hematopoietic stem cell transplantation (URD-SCT) has been associated with a decreased Citarinostat in vivo risk of disease relapse, indicating that HLA-DP may represent a target for graft-versus-leukemia (GVL) reactivity in HLA class II-expressing hematological malignancies. To investigate whether HLA-DP-specific T cells could mediate GVL reactivity following HLA-DPB1-mismatched URD-SCT and donor lymphocyte infusion (DLI), we analyzed the immune response in a patient with leukemic lymphoplasmacytic lymphoma Ulixertinib supplier responding to DLI without graft-versus-host disease. The emergence of leukemia-reactive CD4+ T cells during the clinical immune response was demonstrated by interferon-gamma (IFN-gamma) enzyme-linked immunosorbent spot (ELISPOT) analysis. Following clonal isolation of these leukemia-reactive CD4+ T cells, blocking studies, panel studies and retroviral transduction experiments of both mismatched HLA-DPB1 alleles identified HLA-DPB1*0201 and HLA-DPB1* 0301 as the targets of this immune response. The HLA-DPB1-specific CD4+ T-cell clones were capable of recognizing and lysing several HLA-DP-expressing myeloid

and lymphoid hematological malignant cells. Since HLA-DP expression is mainly restricted to hematopoietic cells, HLA-DP may be used as a specific target for immunotherapy following T-cell-depleted URD-SCT. Therefore, in patients with HLA class II-expressing hematological malignancies HLA-DP-mismatched SCT may be preferable over fully matched SCT allowing DLI to induce a GVL effect.”
“The orbitofrontal cortex (OFC) plays a critical role in learning a reversal of stimulus-reward contingencies. Dopamine (DA) neurons probably support reversal learning by emitting prediction error signals that indicate the discrepancy between the actually received reward and its prediction. However, the role of DA receptor-mediated signaling in the OFC to adapt behavior to changing stimulus-reward contingencies is largely unknown.

This

article reviews the current literature for each of these classes of drugs, with a focus on efficacy and place in the therapeutic scheme. Levodopa is no longer considered to be toxic and, thus, its early use is not only appropriate but recommended. Ergot agonists are no longer in use, and new agents administered in patch form or subcutaneous injections have been approved. The COMT inhibitor tolcapone, with its significant efficacy, has been reintroduced, and two new MAO inhibitors have been approved. Selected safety issues are discussed, including the incidence of melanoma in relation to LD; pathological gambling and DA agonists; hepatic toxicity of tolcapone; and the tyramine selleck compound or so-called cheese reaction with MAO B inhibitors. The article closes with a discussion of future directions and new drugs under development.”
“Innate immune responses against viral infection, especially the induction of type I interferon, are critical for limiting the replication of the virus. Although it has been shown that DNA can induce type I interferon, to learn more date no natural DNA ligand of a virus that induces type I interferon has been described. Here we screened the genome of murine gammaherpesvirus 68 with mutations at various genomic

locations to map the region of DNA that induces type I interferon. A repetitive region termed the 100-base-pair repeat region is a ligand that is both necessary and sufficient for the viral genomic DNA to induce type I interferon. A region colinear buy IPI-549 with this ligand in the genome of Kaposi’s sarcoma-associated herpesvirus also induces type I interferon. We have thus defined a repetitive region of the genomes of gammaherpesviruses as the first natural DNA virus ligand that induces type I interferon.”
“Huntington disease (HD) is a progressive heredoneurodegenerative disease manifested by chorea and other hyperkinetic (dystonia, myoclonus, tics) and hypokinetic (parkinsonism) movement disorders. In addition, a variety

of psychiatric and behavioral symptoms, along with cognitive decline, contribute significantly to the patient’s disability. Because there are no effective neuroprotective therapies that delay the progression of the disease, symptomatic treatment remains the cornerstone of medical management.. Several classes of medications have been used to ameliorate the various symptoms of HD, including typical and atypical neuroleptics, dopamine depleters, antidepressants, antiglutamatergic drugs, GABA agonists, antiepileptic medications, acetylcholinesterase inhibitors, and botulinum toxin. Recently, surgical approaches including pallidotomy, deep brain stimulation, and fetal cell transplants have been used for the symptomatic treatment of HD. The selected therapy must be customized to the needs of each patient, minimizing the potential adverse effects.

03).

Conclusions: The level of vascular endothelial growth factor expression in tumors was not

a successful predictor of survival in patients with resected stage 3-deazaneplanocin A I non-small cell lung carcinoma. A high microvessel density based on CD105 is a strong predictor of prognosis in these patients. (J Thorac Cardiovasc Surg 2010;140:996-1000)”
“In 2009, we reported an online brain atlas of the common marmoset (Callithrix jacchus) at http://marmoset-brain.org:2008. Here we report new digital images of the primate spinal cord sections added to the website. We prepared histological sections of every segment of the spinal cord of the common marmoset, rhesus monkey and Japanese monkey with various staining techniques. The sections were scanned with Carl Zeiss MIRAX SCAN at light microscopic resolution. Obtained digital data were processed and converted into multi-resolutionary images with Adobe Photoshop and Zoomify Design. These images

of the primate spinal cords are now available LGK-974 research buy on the web via the Internet. (C) 2011 Published by Elsevier Ireland Ltd.”
“Objectives: Thoracic endovascular aneurysm repair (TEVAR) was introduced in 2005 to treat descending thoracic aortic aneurysms. Little is known about TEVAR’s nationwide effect on patient outcomes. We evaluated nationwide data regarding the short-term outcomes of TEVAR and open aortic repair (OAR) procedures performed in the United States during a 2-year period.

Methods: From the Nationwide Inpatient Sample data, we identified

patients who had undergone surgery for an isolated descending thoracic aortic aneurysm from 2006 to 2007. Patients with aneurysm rupture, aortic dissection, vasculitis, connective tissue disorders, or learn more concomitant aneurysms in other aortic segments were excluded. Of the remaining 11,669 patients, 9106 had undergone conventional OAR and 2563 had undergone TEVAR. Hierarchic regression analysis was used to assess the effect of TEVAR versus OAR after adjusting for confounding factors. The primary outcomes were mortality and the hospital length of stay (LOS). The secondary outcomes were the discharge status, morbidity, and hospital charges.

Results: The patients who had undergone TEVAR were older (69.5 +/- 12.7 vs 60.2 +/- 14.2 years; P < .001) and had higher Deyo comorbidity scores (4.6 +/- 1.8 vs 3.3 +/- 1.8; P < .001). The unadjusted LOS was shorter for the TEVAR patients (7.7 +/- 11 vs 8.8 +/- 7.9 days), but the unadjusted mortality was similar (TEVAR 2.3% vs OAR 2.3%; P = 1.0). The proportion of nonelective interventions was similar between the 2 groups (TEVAR 15.9% vs OAR 15.8%; P = .9). The TEVAR and OAR techniques produced similar risk-adjusted mortality rates; however, the TEVAR patients had 60% fewer complications overall (odds ratio, 0.39; P < .001) and a shorter LOS (by 1.3 days). The TEVAR patients’ hospital charges were greater by $6713 (95% confidence interval $1869 to $11,556; P < .001).

Notably, in age-matched old animals that had been raised in total darkness and then experienced monocular deprivation, the distribution and numbers of c-Fos-expressing cells in visual cortex exhibited the same alterations as found in young animals during the sensitive period. These findings suggest click here that the present activity mapping method using c-Fos as a molecular marker is useful for examining the activity-dependent regulation of cortical plasticity, and provides an alternative method to conventional electrophysiological recording. This method is particularly powerful when applied to knockout or transgenic mice in which sampling biases

in electrophysiological recording have been considered inevitable. Furthermore, these findings suggest that c-Fos is involved in OD plasticity as an IEG that transfers

neuronal activity to late gene expression. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Rationale Marijuana use in adolescents is a highly social activity, and interacting endocannabinoid Semaxanib cell line and opioid systems may modulate social reward. However, cannabinoid exposure has been reported to reduce social behavior.

Objectives The aim of this study was to elucidate the mechanisms underlying the paradoxical relationship between cannabinoid exposure and sociability.

Materials and methods We investigated the effect of cannabinoid agonists with a different mechanism of action on social play behavior in adolescent rats. In addition, we examined whether endocannabinoid neurotransmission interacts with opioid and dopaminergic neurotransmission in the modulation of social play behavior.

Results The direct CB1 cannabinoid receptor agonist WIN55,212-2 reduced social play. However, the indirect cannabinoid agonist URB597, which inhibits the hydrolysis of the endocannabinoid anandamide, enhanced social play. This effect of URB597 depended upon stimulation of opioid and dopamine receptors. The well-known stimulatory for effect of morphine on social play was attenuated by the CB1 cannabinoid receptor antagonist SR141716A,

but independent of dopamine receptor stimulation. Combined treatment with ineffective doses of URB597 and morphine increased social play.

Conclusions Cannabinoid neurotransmission can both enhance and inhibit social interaction in adolescent rats depending on how the endocannabinoid system is stimulated. Activation of cannabinoid receptors throughout the brain, which occurs during cannabis use, inhibits sociability. In contrast, on-demand release of endocannabinoids facilitates social interaction, which is magnified by indirect cannabinoid agonists through an interaction with opioid and dopaminergic neurotransmission. These results shed light on the paradoxical relationship between cannabis exposure and sociability and suggest that endocannabinoid degradation inhibitors hold promise for the treatment of social dysfunctions.

“
“A Caucasian girl, the product of a non-consanguineous union, was delivered after a full-term uneventful pregnancy with a birth weight of 4.1 kg. At 15 months, she presented to the emergency room with signs of a respiratory illness and was found to weigh 6.14 kg, below the 3rd percentile for age. She had no history of fevers,

click here dehydration, or photophobia and there was no family history of renal or other medical disease. The patient had one elder sister who had no medical complaints. Physical examination revealed a fair-haired blue-eyed child with pale complexion. Details of her ethnic ancestry were unknown. Blood pressure was normal and the remainder of the physical examination was also unremarkable. Laboratory investigations

at 15 months revealed blood urea nitrogen 9 mg per 100 ml (normal range (N) = 8-25), serum creatinine 0.6 mg per 100 ml (estimated MDV3100 price creatinine clearance < 60 ml min(-1)), serum sodium 133 mmol l(-1) (N = 136-145), potassium 3 mmol l(-1) (N = 3.5-5.5), chloride 105 mmol l(-1) (N = 96-106 mEq l(-1)), total carbon dioxide (CO2) 18.7 mEql(-1) (N = 22-30), serum calcium 10.6 mg per 100 ml (N 8.5-10.6 mg per 100 ml), and phosphate 3.4 mg per 100 ml (N = 2.5-4.6). Arterial blood gas was not drawn. Urinalysis revealed specific gravity < 1.005, no protein or cells, and trace glycosuria. However, there was no evidence of phosphaturia (24 h urinary phosphorous excretion 0.2 mmol, N = 0.4-1.3), hypercalciuria, selleckchem or increased urinary organic acid excretion. Measurement of urinary amino acids was not performed. Hematologic

parameters and thyroid function tests, including thyroid stimulating hormone, T4, and free T4, were within normal limits. Based on the finding of hypokalemia, an investigation for possible Bartter’s syndrome was undertaken. These tests revealed markedly elevated plasma levels of renin (119 853 ng per 100 ml per h, N = 171-115) and aldosterone (715 ng per 100 ml, N = 3-35) that, together with the findings of normal blood pressure, hypokalemia, and hyponatremia, suggested a diagnosis of acquired Bartter’s syndrome.

The patient was treated for the next two and a half years with indomethacin and electrolyte replacement, including potassium chloride and calcium carbonate. During this time, she gained weight and normalization of blood electrolytes. However, at 4 years of age, she was noted to have worsening renal insufficiency (serum creatinine 1.2-1.4 mg per 100 ml) and 4+ proteinuria on dipstick. At this time, an elevated thyroid stimulating hormone was noted (17.27 IU ml(-1), N = 0.3-5.0), indicating hypothyroidism, and thyroid replacement therapy was commenced. Indomethacin was discontinued but renal function and proteinuria continued to deteriorate over the following year. At age 5 years, serum creatinine was 2.

To do so, rats underwent stereotaxic surgery for unilateral delivery of the adenoassociated virus (AAV)-alpha-synuclein into the substantia nigra. This was followed 13 weeks later by delivery of rotenone into the same site.

The effect of the genetic and environmental insults alone or in combination on lateralised motor performance (Corridor, Stepping, and Whisker Tests), nigrostriatal integrity (tyrosine hydroxylase immunohistochemistry), and alpha-synucleinopathy (alpha-synuclein immunohistochemistry) was assessed. We found that rats treated with either AAV-alpha-synuclein or rotenone developed significant motor dysfunction with underlying nigrostriatal neurodegeneration. DAPT in vitro However, when the genetic and environmental insults were sequentially administered, the detrimental impact of the combined

insults on motor performance and nigrostriatal integrity was significantly greater than the impact of either insult alone. This indicates that sequential exposure to relevant genetic and environmental insults is a valid approach to modeling human Parkinson’s disease in the rat. 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“In the field of proteomics AZD5153 manufacturer extensive efforts have been focused on the knowledge of proteins expressed by different cell types. In particular, enormous progress has been done in the characterization of blood cellular components. In this work, we have established a public 2-DE database for human peripheral blood mononuclear cells (PBMCs) proteins. Two hundred and forty-six spots corresponding

to 174 different proteins have been identified on 2-DE gels from PBMCs isolated from six healthy individuals. All the identified proteins have been classified in thirteen categories on the basis of their differential functions or cellular localization and annotated at the http://physiology.unile.it/proteomics. The role of several proteins has been discussed in relation to their biological function. We intend Pifithrin-�� purchase to show the potentiality of PBMCs to investigate the proteomics changes possibly associated with a large number of pathologies such as autoimmune, neurodegenerative and cancer diseases.”
“After uptake into target cells, many nonenveloped viruses undergo conformational changes in the low-pH environment of the endocytic compartment. This results in exposure of amphipathic viral peptides and/or hydrophobic protein domains that are inserted into and either disrupt or perforate the vesicular membranes. The viral nucleic acids thereby gain access to the cytosol and initiate replication. We here demonstrate the in vitro transfer of the single-stranded positive-sense RNA genome of human rhinovirus 2 into liposomes decorated with recombinant very-low-density lipoprotein receptor fragments.

Our findings suggest that the frequency of use might have a particular critical impact R428 research buy on intact parahippocampal functioning in cannabis users. Increased activity within the encoding-related network might reflect functional compensation to maintain cognitive functioning.”
“Background We did a meta-analysis

to assess factors associated with disparities in HIV infection in black men who have sex with men (MSM) in Canada, the UK, and the USA.

Methods We searched Embase, Medline, Google Scholar, and online conference proceedings from Jan 1, 1981, to Dec 31, 2011, for racial comparative studies with quantitative outcomes associated with HIV risk or HIV infection. Key words and Medical Subject Headings (US National Library of Medicine) see more relevant to race were cross-referenced with citations pertinent to homosexuality in Canada, the UK, and the USA. Data were aggregated

across studies for every outcome of interest to estimate overall effect sizes, which were converted into summary ORs for 106 148 black MSM relative to 581 577 other MSM.

Findings We analysed seven studies from Canada, 13 from the UK, and 174 from the USA. In every country, black MSM were as likely to engage similarly in serodiscordant unprotected sex as other MSM. Black MSM in Canada and the USA were less likely than other MSM to have a history of substance use (odds ratio, OR, 0.53, 95% CI 0.38-0.75, for Canada and 0.67, 0.50-0.92, for C646 research buy the USA). Black MSM in the UK (1.86, 1.58-2.18) and the USA (3.00, 2.06-4.40) were more likely to be HIV positive than were other MSM, but HIV-positive black MSM in each country were less likely (22% in the UK and 60% in the USA) to initiate combination antiretroviral therapy (cART) than other HIV-positive MSM. US HIV-positive black MSM were also less likely to have health insurance, have a high CD4 count, adhere to cART, or be virally suppressed than were other US HIV-positive MSM. Notably, despite a two-fold greater odds of having any structural barrier that increases HIV risk (eg, unemployment, low income, previous

incarceration, or less education) compared with other US MSM, US black MSM were more likely to report any preventive behaviour against HIV infection (1.39, 1.23-1.57). For outcomes associated with HIV infection, disparities were greatest for US black MSM versus other MSM for structural barriers, sex partner demographics (eg, age, race), and HIV care outcomes, whereas disparities were least for sexual risk outcomes.

Interpretation Similar racial disparities in HIV and sexually transmitted infections and cART initiation are seen in MSM in the UK and the USA. Elimination of disparities in HIV infection in black MSM cannot be accomplished without addressing structural barriers or differences in HIV clinical care access and outcomes.