Even though trade liberalisation seems to have positive effects on economic growth, it is not sufficient to boost growth. in several countries, trade reforms have not translated into enhanced economic expansion

because complementary policies are needed. Trade liberalisation and openness are associated with greater wage inequality and raised economic insecurity. Trade liberalisation has facilitated availability of highly processed, calorie-rich, nutrient-poor food in developing countries, but further research CX-5461 clinical trial is needed to better understand the effects of trade on unhealthy diets. Policyrnakers and health professionals need to be aware that the global economy affects the health of populations and understand how risks associated with trade liberalisation can be mitigated.”
“Magnetic resonance spectroscopy (MRS) studies in human MRT67307 alcoholics report decreases in N-acetylaspartate (NAA) and choline-containing (Cho) compounds. Whether alterations in brain metabolite levels are attributable to alcohol per se or to physiological effects of protracted withdrawal or impaired

nutritional or liver status remains unclear. Longitudinal effects of alcohol on brain metabolites measured in basal ganglia with single-voxel MRS were investigated in sibling pairs of wild-type Wistar rats, with one rat per pair exposed to escalating doses of vaporized alcohol, the other to vapor chamber air. MRS was conducted before alcohol exposure and twice during exposure. After 16 weeks of alcohol exposure, rats achieved average blood alcohol levels (BALs) of similar to 293 mg per 100 ml and had higher Cho and a trend for higher glutamine + glutamate (Glx) than controls. After 24 weeks of alcohol exposure, BALs rose to similar to 445 mg per 100 ml, and alcohol-exposed rats had higher Cho, Glx, and glutamate than controls. Thiamine and thiamine monophosphate levels were significantly lower in the alcohol than the control group but did not reach levels low enough to be considered clinically relevant. Histologically, livers of alcohol-exposed rats exhibited

greater steatosis and lower glycogenosis than controls, but were not cirrhotic. This study demonstrates a specific pattern of neurobiochemical changes Rebamipide suggesting excessive membrane turnover or inflammation, indicated by high Cho, and alterations to glutamate homeostasis in the rat brain in response to extended vaporized alcohol exposure. Thus, we provide novel in vivo evidence for alcohol exposure as causing changes in brain chemistry in the absence of protracted withdrawal, pronounced thiamine deficiency, or severe liver damage.”
“The 2008 G8 summit in Toyako, Japan, produced a strong commitment for collective action to strengthen health systems in developing countries, indicating Japan’s leadership on, and the G8′s increasing engagement with, global health policy.

003). The NUP98-HOXA9 fusion was strongly associated with KRAS and WT1 mutations (P = 0.015 and P = 0.0018, respectively). We characterized four varieties of this fusion, among which NUP98 exon 12/HOXA9 exon 1b was present in all 11 patients. We developed a highly sensitive and specific assay to quantify the abundance of leukemic cells, and found that the fusion Tucidinostat remained detectable in morphological complete remission, even after allogeneic stem cell transplantation, suggesting that this disease was highly refractory to very intensive treatment. AML with NUP98-HOXA9 fusion therefore appears to have a distinct clinical and biological profile, and should be regarded as a poor prognostic

group. Leukemia (2009) 23, 1303-1310; doi: 10.1038/leu.2009.25; published online 19 February 2009″
“Symptomatic ischemia following aneurysmal subarachnoid hemorrhage (SAH) is common but poorly understood and inadequately treated. Severe constriction of the major arteries at the base of the brain, termed vasospasm, traditionally has been thought to be a proximal event underlying these ischemias, although microvascular changes also have been described. The vast majority of studies aimed at understanding the pathogenesis of ischemic deficits, and vasospasm have focused on the interaction of the “”spasmogen”" of the extravasated blood Lapatinib mw with the smooth muscle and endothelium of the arteries. This has led to a comparative neglect of the contribution of the CNS to

the maintenance of cerebral perfusion. In the present study, we focused on the role of the rostral ventromedial medulla (RVM) in modulating cerebral perfusion at rest and following an experimental

SAH in the rat. Changes in cerebral blood Fossariinae flow (CBF) were measured using laser-Doppler flowmetry and three-dimensional optical microangiography. Focal application of a GABA(A) receptor agonist and antagonist was used to respectively inactivate and activate the RVM. We show here that the RVM modulates cerebral blood flow under resting conditions, and further, contributes to restoration of cerebral perfusion following a high-grade SAH. Failure of this brainstem compensatory mechanism could be significant for acute perfusion deficits seen in patients following subarachnoid hemorrhage. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Erythroleukemia induced by Friend Murine Leukemia Virus (F-MuLV) serves as a powerful tool for the study of multistage carcinogenesis and hematological malignancies in mice. Fli-1, a proto-oncogene and member of the Ets family, is activated through viral integration in F-MuLV-induced erythroleukemia, and is the most critical event in the induction of this disease. Fli-1 aberrant regulation is also observed in human malignancies, including Ewing’s sarcoma, which is often linked to expression of the EWS/Fli-1 fusion oncoprotein. Here we examined the effects of Fli-1 inhibition to further elucidate its role in these pathological occurrences.

The complete genome of one of the isolates was sequenced, and phylogenetic analysis was conducted. The

analysis showed that this isolate belonged to genotype VII, specifically, to subgenotype VIIa, and clustered closely with isolates characterized from Indonesia in the 1990s. Interestingly, the isolate showed significant differences from previously characterized APMV-1 isolates from commercial and rural chickens in Pakistan. The work presented here is the first complete genome sequence of any APMV-1 isolate from wild birds in the region and therefore highlights the need for this website increased awareness and surveillance in such bird species.”
“We describe an improved Phos-tag SDS-PAGE (Zn(2+)-Phos-tag SDS-PAGE) using a dizinc(II) complex of Phos-tag acrylamide in conjunction with a Bis-tris-buffered neutral-pH gel system to detect shifts in the mobility of phosphoproteins. An existing technique (Mn(2+)-Phos-tag SDS-PAGE) using a polyacrylamide-bound Mn(2+)-Phos-tag and a conventional Laemmli’s buffer system under alkaline pH conditions has limitations for separating certain phosphoproteins. The major improvements were demonstrated

by visualizing novel up-shifted bands of commercially available pepsin, recombinant Tau treated in vitro with tyrosine kinases, and endogeneous beta-catenin in whole-cell lysates. Additionally, the Zn(2+)-Phos-tag SDS-PAGE gels showed better long-term selleck chemical stability than the Mn(2+)-Phos-tag SDS-PAGE gels. We can

therefore provide a simple, convenient, and more reliable homemade gel system for phosphate-affinity SDS-PAGE.”
“Adolescence is a time of continued brain maturation, particularly in limbic and cortical regions, which undoubtedly plays a role in the physiological and emotional changes coincident with adolescence. An emerging line of research has indicated that stressors experienced Cobimetinib mouse during this crucial developmental stage may affect the trajectory of this neural maturation and contribute to the increase in psychological morbidities, such as anxiety and depression, often observed during adolescence. In this review, we discuss the short- and long-term effects of periadolescent stress exposure on the structure and function of the brain. More specifically, we examine how stress at prepubertal and early adolescent stages of development affects the morphological plasticity of limbic and cortical brain regions, as well as the enduring effects of adolescent stress exposure on these brain regions in adulthood. We suggest that, due to a number of converging factors during this period of maturation, the adolescent brain may be particularly sensitive to stress-induced neurobehavioral dysfunctions with important consequences on an individual’s immediate and long-term health and well-being. (C) 2012 IBRO. Published by Elsevier Ltd.

The aim of the current study was to determine whether infusion of small interfering RNAs (siRNA) targeting MOP-r into the midbrain could knock down MOP-r mRNA and affect heroin-induced

locomotor activity or heroin-induced conditioned place preference. Ten-week-old male C57BL/6J mice were surgically implanted bilaterally with guide cannulae directed between the substantia nigra and ventral SHP099 research buy tegmental area. After 4 days’ recovery, mice were infused bilaterally with siRNAs that target the MOP-r (2 mM x 0.75 mu l/side/day for 3 days) or control siRNA. Seven days after the last infusion, a procedure for conditioned place preference was begun with four heroin (3 mg/kg i.p.) administration sessions alternating with four saline sessions. While heroin induced an increase in locomotor activity in all groups, siRNAs targeting specific regions of MOP-r significantly attenuated this effect. Of particular interest, mice infused with specific siRNAs MK-8931 cell line targeting the MOP-r failed to develop and express conditioned place preference to heroin, or showed a significantly attenuated preference. These alterations in reward-related behaviors are likely due to the reduction in MOP-r mRNA and protein, shown in separate studies by in situ hybridization and

autoradiography using the same MOP-r- siRNA infusions. Taken together, these studies demonstrate the utility of siRNA in the neurobiological study of specific components of Low-density-lipoprotein receptor kinase the reward system and should contribute to the study of other complex behaviors. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Lack of sexual interest is the most common sexual complaint among women. However, factors affecting sexual desire in women have rarely been studied. While the role of the brain in integrating the sensory, attentional, motivational, and motor aspects of sexual response is commonly acknowledged as important, little is known about specific patterns of brain activation and sexual

interest or response, particularly among women. We compared 20 females with no history of sexual dysfunction (NHSD) to 16 women with hypoactive sexual desire disorder (HSDD) in a functional magnetic resonance imaging (fMRI) study that included assessment of subjective sexual arousal, peripheral sexual response using a vaginal photoplethysmograph (VPP), as well as brain activation across three time points. Video stimuli included erotic, sports, and relaxing segments. Subjective arousal to erotic stimuli was significantly greater in NHSD participants compared with HSDD. In the erotic-sports contrast, NHSD women showed significantly greater activation in the bilateral entorhinal cortex than HSDD women. In the same contrast, HSDD females demonstrated higher activation than NHSD females in the medial frontal gyrus (Brodmann area (BA) 10), right inferior frontal gyrus (BA 47) and bilateral putamen.

The methodology followed that of the WHO/Euro Multicenter Study on Parasuicide. A stratified analysis was performed using the Mantel-Haenszel procedure in order to control for the effects of gender and diagnosis. Adolescents used significantly more over-the-counter medicines. Adults were significantly more certain of the possible fatal outcome of their attempt and had a significantly more severe intention when harming themselves. Individuals appear to use the methods that are available to them to attempt suicide. Adolescents may display more impulsive

and less lethal directed behavior than adults or, alternatively, they are more frequently admitted for less severe attempts. (c) 2007 Elsevier Ireland Ltd. All rights reserved.”
“Affinity column chromatography check details is a promising method for the purification of flavivirus particles that can supplement or potentially replace diafiltration and sucrose density centrifugation. In this study, the purification of West Nile Virus (WNV) antigens via Cellufine Sulfate column chromatography Repotrectinib was examined. Virus-like particles (VLPs) produced by the expression of the prM and E genes were separated

from most of the contaminant proteins with 0.2-0.4 M NaCl, but still retained their spherical forms and immunogenicity in mice. The column, with a 1 mL bed-volume, concentrated WN-VLPs a minimum of 15 fold from TCL culture supernatants. A heparin analogue, suramin, competitively eluted WN-VLPs, but sulphated polysaccharides, such as heparin, heparin sulfate and dextran sulfate, did not. Furthermore, 2.4 x 10(9) plaque forming units of WNV and 196 mu g of the viral antigens were recovered from 60 mL of infected culture medium at high yields (93% and 96%, respectively). These results indicate that, in addition to conventional methods, Cellufine Sulfate column chromatography is an effective preparation technique for

WNV particulate antigens that does not impair the antigen virological characteristics. (C) 2011 Elsevier B.V. All rights reserved.”
“Patients with insulin resistance and early type 2 diabetes exhibit an increased propensity to develop a diffuse and extensive pattern of arteriosclerosis. Various risk factors such as hypertension, dyslipidemia, and a proinflammatory and prothrombotic state contribute to atherogenesis in this high-risk population, but the pathophysiologic mechanisms leading to this characteristic pattern remain largely unexplored. Recent data suggest that the proinsulin cleavage product C-peptide could play a causal role in atherogenesis by promoting monocyte and CD4-positive lymphocyte recruitment in early arteriosclerotic lesions and by inducing the proliferation of vascular smooth muscle cells.

9% vs. 41.5%, P=0.001). None of the serious adverse events reported were attributed to the trial

interventions.

Conclusions: When given at birth, monovalent type 1 oral poliovirus vaccine is superior to trivalent oral poliovirus vaccine in inducing humoral antibodies against type 1 poliovirus, overcoming high preexisting BMS-777607 levels of maternally derived antibodies, and increasing the resistance to excretion of type 1 poliovirus after administration of a challenge dose. (Current Controlled Trials number, ISRCTN76316509.).”
“Background: The number of cases of paralytic poliomyelitis has declined in Nigeria since the introduction of newly licensed monovalent oral poliovirus vaccines and new techniques of vaccine delivery. Understanding the relative contribution

of these vaccines and the improved coverage to the decline in incident cases is essential for future planning.

Methods: We estimated the field efficacies of monovalent type 1 oral poliovirus vaccine and trivalent oral poliovirus vaccine, using the reported number of doses received by Paclitaxel concentration people with poliomyelitis and by matched controls as identified in Nigeria’s national surveillance database, in which 27,379 cases of acute flaccid paralysis were recorded between 2001 and 2007. Our estimates of vaccine coverage and vaccine-induced immunity were based on the number of doses received by children listed in the database who had paralysis that was not

caused by poliovirus.

Results: The estimated efficacies per dose of monovalent type 1 oral poliovirus vaccine and trivalent oral poliovirus vaccine against type 1 paralytic poliomyelitis were 67% (95% confidence interval [CI], 39 to 82) and 16% (95% CI, 10 to 21), respectively, and the estimated efficacy per dose of trivalent oral poliovirus vaccine against type 3 paralytic poliomyelitis was 18% (95% CI, 9 to 26). In the northwestern region of Nigeria, Ketanserin which reported the majority of cases during the study period, coverage with at least one dose of vaccine increased from 59 to 78%. Between 2005 and 2007, vaccine-induced immunity levels among children under the age of 5 years more than doubled, to 56%.

Conclusions: The higher efficacy of monovalent type 1 oral poliovirus vaccine (four times as effective as trivalent oral poliovirus vaccine) and the moderate gains in coverage dramatically increased vaccine-induced immunity against serotype 1 in northern Nigeria. Further increases in coverage in Nigerian states with infected populations are required to achieve the levels of vaccine-induced immunity associated with the sustained elimination achieved in other parts of the country.”
“Purpose: DNA methylation is, a key regulator of gene transcription and genomic stability, and alterations in DNA methylation patterns are frequently detected in human tumors.

Consequently, the mechanism of intussusceptive angiogenesis is often overlooked in angiogenesis research. Here, the mechanism of intussusceptive angiogenesis is reviewed and the current techniques and

models for investigating intussusceptive angiogenesis are summarized. In addition, other mechanisms of vascular growth are briefly reviewed. Copyright (C) 2012 S. Karger AG, Basel”
“Herpesviruses are ubiquitous human pathogens that establish lifelong persistent infections. Clinical manifestations range from mild self-limiting outbreaks such as childhood rashes and cold sores to the more severe and life-threatening outcomes of disseminated infection, encephalitis, and cancer. NU7026 supplier Nucleoside analog drugs that target viral DNA replication provide the primary means of treatment. However, extended use of these LEE011 solubility dmso drugs can result in selection for drug-resistant strains, particularly in immunocompromised patients. In this review we will present recent observations about the participation of cellular protein kinases in herpesvirus biology and discuss the potential for targeting these protein kinases as well as the herpesvirus-encoded protein

kinases as an anti-herpesvirus therapeutic strategy.”
“Purpose: To study the power of CRF stimulation test to predict relapse in a sample of melancholic depressive patients in depressed phase, followed-up over a two-year period from the moment they achieved complete remission of depressive symptoms.

Methods: Fifty-one outpatients diagnosed with unipolar depressive disorder with melancholic features according to DSM-IV were assessed with the CRF test. The Structured Clinical

Interview for DSM-IV (SCID-IV) was used for diagnosis. Monthly follow-up visits were held over a two-year period after remission; relapse was established using HDRS according to Frank’s criteria [Frank E, Prien RF, Jarret RB, Keller MB, Kupfer DJ, Lavori PW, et al. Conceptualization and rationale for next consensus definitions of terms in major depressive disorder: remission, recovery, relapse, and recurrence. Arch Gen Psychiatry 1991;48:851-5]. Forty-three patients completed the study. Non-controlled antidepressant treatment protocols were used. Predictive statistical analysis was performed through logistic regression.

Findings: The final predictive model included three variables: net area under cortisol curve (NAUCC), previous suicide attempt, and stress during follow-up. Sensitivity was of 89%, and specificity was of 92%. NAUCC has shown a predictive power of 80%, with an optimal cut-off point of 251.24 mu g/ml/min.

Conclusions: Cortisol is the hormone of the HPA axis which shows the highest power to predict relapse. NAUCC is the most relevant variable. The complete predictive model is a complex combination of biological, clinical and psychoenvironmental variables (NAUCC, previous suicide attempts, and stress during follow-up).

In turn, viral antagonists have adapted to changes in PKR. As a result of this “”arms race,”" modern TRS1 alleles in CMVs may function differently in cells derived from alternative species. We have previously shown that human CMV TRS1 (HuTRS1)

blocks the PKR pathway Selleckchem Tubastatin A and rescues replication of a vaccinia virus mutant lacking its major PKR antagonist in human cells. We now demonstrate that HuTRS1 does not have these activities in Old World monkey cells. Conversely, the rhesus cytomegalovirus homologue of HuTRS1 (RhTRS1) fulfills these functions in African green monkey cells, but not rhesus or human cells. Both TRS1 proteins bind to double-stranded RNA and, in the cell types in which they can rescue VV Delta E3L replication, they also bind to PKR and prevent phosphorylation of the alpha-subunit of eukaryotic initiation factor 2. However, while HuTRS1 binds to inactive human PKR and prevents its autophosphorylation, RhTRS1 binds to phosphorylated African green monkey PKR. These studies reveal that evolutionary adaptations click here in this critical host defense protein have altered its binding interface in a way that has resulted in a qualitatively altered mechanism of PKR antagonism by viral TRS1 alleles from different

CMVs. These results suggest that PKR antagonism is likely one of the factors that contributes to species specificity of cytomegalovirus replication.”
“This study examined cocaine self-administration after pretreatments with three structurally related compounds that bind selectively to dopamine D3 receptors (D3Rs) relative to the D2 receptor subtype (D2Rs) and exhibit varying intrinsic activities in the forskolin-stimulated adenylyl cyclase assay. The compounds are: a) WC10, a D3R weak partial agonist/antagonist with 42-fold D3R:D2R selectivity,

b) WC26, a 51-fold selective D3R partial agonist, c) WC44, a 23-fold selective D3R agonist. Rats were stabilized on a multiple variable-interval 60-s (VI60) schedule with alternating components of sucrose (45 mg pellets) or cocaine reinforcement (0.375 mg/kg, IV) and then tested for effects of the WC compounds (0.0, 1.0, 3.0, 5.6, or 10.0 mg/kg, IP). Another cohort was trained to self-administer cocaine FAD (0.75 mg/kg, IV) on a VI60 schedule then tested with various doses of cocaine available (0.0-1.5 mg/kg, IV) following pretreatment with WOO (5.6 or 10.0 mg/kg) or WC44 (10.0 mg/kg). WC10 and WC26 decreased both cocaine and sucrose reinforcement rates at the 10.0 mg/kg dose, whereas WC44 decreased only cocaine reinforcement rate at this dose. Furthermore, WC26 and WC44 increased response latency for cocaine but not sucrose. In the cocaine dose response experiment, WC10 and WC44 flattened the dose-effect function of cocaine reinforcement rate. All compounds decreased spontaneous locomotion. WC10 and WC26 also reduced cocaine-induced locomotion.

HepG2 cells develop polarity over time, resulting in the formation and remodeling of bile canalicular (BC) structures. HepG2 cells expressing CD81 provide a model system to study the effects of hepatic polarity on HCV infection. We found an inverse association between HepG2-CD81 polarization and HCV pseudoparticle entry. As HepG2 cells polarize, discrete pools of claudin-1 (CLDN1) at the TJ and basal/lateral membranes develop, consistent

with the pattern of receptor staining observed in liver tissue. The TJ and nonjunctional pools of CLDN1 show an altered association with CD81 and localization in response to the PKA antagonist Rp-8-Br-cyclic AMPs (cAMPs). Rp-8-Br-cAMPs reduced CLDN1 expression at the basal membrane and inhibited HCV infection, supporting a model where the nonjunctional Citarinostat cell line pools of CLDN1 DMXAA mouse have a role in HCV entry. Treatment of HepG2 cells with proinflammatory cytokines, tumor necrosis factor alpha and gamma interferon,

perturbed TJ integrity but had minimal effect(s) on cellular polarity and HCV infection, suggesting that TJ integrity does not limit HCV entry into polarized HepG2 cells. In contrast, activation of PKC with phorbol ester reduced TJ integrity, ablated HepG2 polarity, and stimulated HCV entry. Overall, these data show that complex hepatocyte-like polarity alters CLDN1 localization and limits HCV entry, suggesting that agents which disrupt hepatocyte polarity may promote HCV infection and transmission within the liver.”
“Active compounds in cannabis such as tetrahydrocannabinol

(THC) interact with the inhibitory neurotransmitter delta-aminobutyric acid (GABA) but little is known about the functional effects of cannabis on human cortical brain processes. Therefore, the aim of the study was to investigate whether patients with chronic cannabis use Quisqualic acid demonstrate abnormalities in cortical inhibition or excitability. In all, 42 chronic cannabis using subjects (divided into heavy and light using subjects) and 19 controls were included in the study. Single and paired pulse transcranial magnetic stimulation were used to assess a number of parameters of cortical inhibition and cortical excitability. In addition, psychomotor function and THC plasma levels were measured. Both cannabis using groups (heavy and light use) demonstrated a reduction in short interval cortical inhibition compared with healthy controls, but there was no difference in other measures of cortical inhibition or cortical excitability. There was also no difference between the two groups on measures of psychomotor performance. Chronic cannabis use is associated with a reduction in cortical inhibition potentially related to activity at the GABA(A) receptors.

Biochemical fractionation of BV and ODV into the nucleocapsid and envelope components followed by Western blotting showed that 38K was associated with the nucleocapsids. Immunoelectron microscopic analysis revealed that 38K was specifically localized to the nucleocapsids

in infected cells and appeared to be distributed over the cylindrical capsid sheath of nucleocapsid. Yeast two-hybrid assays were performed to examine potential interactions between 38K and nine known nucleocapsid shell-associated proteins (PP78/83, PCNA, VP1054, FP25, VLF-1, VP39, BV/ODV-C42, VP80, and P24), three non-nucleocapsid shell-associated proteins (P6.9, PP31, and BV/ODV-E26), and itself. The results revealed that 38K interacted with the nucleocapsid selleck proteins VP1054, VP39, VP80, and 38K itself. These interactions were confirmed by coimmunoprecipitation assays in vivo. These data demonstrate that 38K is a novel nucleocapsid protein and provide a rationale for why 38K is essential for nucleocapsid assembly.”
“The central role of plasmacytoid dendritic cells (pDC) in activating host immune responses stems from their high capacity to express alpha interferon (IFN-alpha) after

stimulation of Toll-like receptors 7 and 9 (TLR7 and -9). This involves the adapter MyD88 and the kinases interleukin-1 receptor-associated kinase 1 (IRAK1), IRAK4, and I kappa B kinase alpha (IKK alpha), which activates IFN regulatory factor 7 (IRF7) and is independent of the canonical kinases TBK1 and IKK epsilon. We have https://www.selleckchem.com/products/8-bromo-camp.html recently shown that the immunosuppressive measles virus (MV) abolishes TLR7/9/MyD88-dependent IFN induction in human pDC (Schlender et al., J. Virol. 79: 5507-5515, 2005), but the molecular mechanisms remained elusive. Here, we have reconstituted the pathway in cell lines and identified IKK alpha and IRF7 as specific targets Tryptophan synthase of the MV

V protein (MV-V). Binding of MV-V to IKK alpha resulted in phosphorylation of V on the expense of IRF7 phosphorylation by IKK alpha in vitro and in living cells. This corroborates the role of IKK alpha as the kinase phosphorylating IRF7. MV-V in addition bound to IRF7 and to phosphomimetic IRF7 and inhibited IRF7 transcriptional activity. Binding to both IKK alpha and IRF7 required the 68-amino-acid unique C-terminal domain of V. Inhibition of TLR/MyD88-dependent IFN induction by MV-V is unique among paramyxovirus V proteins and should contribute to the unique immunosuppressive phenotype of measles. The mechanisms employed by MV-V inspire strategies to interfere with immunopathological TLR/MyD88 signaling.”
“Alphaviruses are mosquito-transmitted viruses that cause significant human disease, and understanding how these pathogens successfully transition from the mosquito vector to the vertebrate host is an important area of research.