Men who have sex with men (MSM) is one of the key populations affected by HIV epidemic with infection rates exceeding five percentages. Due to a strict and prohibitive socio-cultural and legal environment, male-to-male sexual practices are often misunderstood and highly stigmatised, thus creating barriers for MSM to access HIV prevention, treatment, care and support services.
The reduced capacity for social and interpersonal interactions, social anhedonia, is an important aspect of various psychiatric disorders, especially schizophrenia-spectrum disorders. The goal of the present study was to validate a Malay translation of the adult version of the Anticipatory and Consummatory Interpersonal Pleasure Scale (ACIPS; Gooding and Pflum, 2014), a relatively short and easy to administer indirect measure of social anhedonia. This cross-sectional study included 95 (47 male, 48 female) schizophrenia patients and 300 (77 male, 223 female) healthy subjects. Participants were given Malay versions of the ACIPS, Snaith Hamilton Pleasure Scale (SHAPS-M), and Beck Depression Inventory (BDI-M). The ACIPS exhibited good internal consistency (Ordinal alpha = 0.966). Total ACIPS scores were inversely correlated with the BDI-M scores, and positively correlated with total SHAPS-M scores. Factor analysis yielded a three-factor solution which accounted for 52.06% of the variance. As expected, the schizophrenia patients scored significantly lower than the healthy community participants on the ACIPS, t(130) = 4.26, p
Type I interferon (IFN-α/β) is a fundamental antiviral defense mechanism. Mouse models have been pivotal to understanding the role of IFN-α/β in immunity, although validation of these findings in humans has been limited. We investigated a previously healthy child with fatal encephalitis after inoculation of the live attenuated measles, mumps, and rubella (MMR) vaccine. By targeted resequencing, we identified a homozygous mutation in the high-affinity IFN-α/β receptor (IFNAR2) in the proband, as well as a newborn sibling, that rendered cells unresponsive to IFN-α/β. Reconstitution of the proband's cells with wild-type IFNAR2 restored IFN-α/β responsiveness and control of IFN-attenuated viruses. Despite the severe outcome of systemic live vaccine challenge, the proband had previously shown no evidence of heightened susceptibility to respiratory viral pathogens. The phenotype of IFNAR2 deficiency, together with similar findings in STAT2-deficient patients, supports an essential but narrow role for IFN-α/β in human antiviral immunity.
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.