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Fulltext Stigma of mental illness and cultural factors in Pacific Rim region: a systematic review

Ran MS, Hall BJ, Su TT, Prawira B, Breth-Petersen M, Li XH, et al.

BMC Psychiatry, 2021 01 07;21(1):8.
PMID: 33413195 DOI: 10.1186/s12888-020-02991-5

BACKGROUND: Although cultural factors play a crucial role in experience of stigma, there is scant review on the impact and importance of culture on stigma of mental illness across Pacific Rim Region. This study aims to investigate: 1) the cultural factors related to stigmatizing beliefs about mental illness in Pacific Rim region, and 2) culture-specific measures and interventions on stigma of mental illness.
METHODS: A systematic search of papers was conducted in the MEDLINE, Embase, CINAHL, Web of Science, PsycINFO, Scopus, Cochrane Library and Google scholar through January 2003 to April 2019.
RESULTS: Forty-one studies in Pacific Rim region which met the inclusion criteria were included in the study. The rate of stigma of mental illness (e.g., public stigma: from 25.4 to 85.2%) was relatively high in Pacific Rim region. Culture factors (e.g., Collectivism, Confucianism, face concern and familism, religion and supernatural beliefs) contributed to people's stigmatizing behaviors and attitudes toward persons with mental illness, their relatives and mental health professionals. Certain measurements were developed and employed to assess different type of cultural factors related to stigma of mental illness.
CONCLUSIONS: Cultural factors play an important role in influencing the rate and performance of stigma of mental illness. Further research on stigma of mental illness and culture-specific interventions to reduce the stigma should be conducted in the Pacific Rim region.
Fulltext Mass spectrometry-based proteomic platforms for better understanding of SARS-CoV-2 induced pathogenesis and potential diagnostic approaches

Ahsan N, Rao RSP, Wilson RS, Punyamurtula U, Salvato F, Petersen M, et al.

Proteomics, 2021 05;21(10):e2000279.
PMID: 33860983 DOI: 10.1002/pmic.202000279

While protein-protein interaction is the first step of the SARS-CoV-2 infection, recent comparative proteomic profiling enabled the identification of over 11,000 protein dynamics, thus providing a comprehensive reflection of the molecular mechanisms underlying the cellular system in response to viral infection. Here we summarize and rationalize the results obtained by various mass spectrometry (MS)-based proteomic approaches applied to the functional characterization of proteins and pathways associated with SARS-CoV-2-mediated infections in humans. Comparative analysis of cell-lines versus tissue samples indicates that our knowledge in proteome profile alternation in response to SARS-CoV-2 infection is still incomplete and the tissue-specific response to SARS-CoV-2 infection can probably not be recapitulated efficiently by in vitro experiments. However, regardless of the viral infection period, sample types, and experimental strategies, a thorough cross-comparison of the recently published proteome, phosphoproteome, and interactome datasets led to the identification of a common set of proteins and kinases associated with PI3K-Akt, EGFR, MAPK, Rap1, and AMPK signaling pathways. Ephrin receptor A2 (EPHA2) was identified by 11 studies including all proteomic platforms, suggesting it as a potential future target for SARS-CoV-2 infection mechanisms and the development of new therapeutic strategies. We further discuss the potentials of future proteomics strategies for identifying prognostic SARS-CoV-2 responsive age-, gender-dependent, tissue-specific protein targets.
Fulltext Establishing an online resource to facilitate global collaboration and inclusion of underrepresented populations: Experience from the MJFF Global Genetic Parkinson's Disease Project

Vollstedt EJ, Madoev H, Aasly A, Ahmad-Annuar A, Al-Mubarak B, Alcalay RN, et al.

PLoS One, 2023;18(10):e0292180.
PMID: 37788254 DOI: 10.1371/journal.pone.0292180

Parkinson's disease (PD) is the fastest-growing neurodegenerative disorder, currently affecting ~7 million people worldwide. PD is clinically and genetically heterogeneous, with at least 10% of all cases explained by a monogenic cause or strong genetic risk factor. However, the vast majority of our present data on monogenic PD is based on the investigation of patients of European White ancestry, leaving a large knowledge gap on monogenic PD in underrepresented populations. Gene-targeted therapies are being developed at a fast pace and have started entering clinical trials. In light of these developments, building a global network of centers working on monogenic PD, fostering collaborative research, and establishing a clinical trial-ready cohort is imperative. Based on a systematic review of the English literature on monogenic PD and a successful team science approach, we have built up a network of 59 sites worldwide and have collected information on the availability of data, biomaterials, and facilities. To enable access to this resource and to foster collaboration across centers, as well as between academia and industry, we have developed an interactive map and online tool allowing for a quick overview of available resources, along with an option to filter for specific items of interest. This initiative is currently being merged with the Global Parkinson's Genetics Program (GP2), which will attract additional centers with a focus on underrepresented sites. This growing resource and tool will facilitate collaborative research and impact the development and testing of new therapies for monogenic and potentially for idiopathic PD patients.
Fulltext Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Klionsky DJ, Abdelmohsen K, Abe A, Abedin MJ, Abeliovich H, Acevedo Arozena A, et al.

Autophagy, 2016;12(1):1-222.
PMID: 26799652 DOI: 10.1080/15548627.2015.1100356
Fulltext Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1

Klionsky DJ, Abdel-Aziz AK, Abdelfatah S, Abdellatif M, Abdoli A, Abel S, et al.

Autophagy, 2021 Jan;17(1):1-382.
PMID: 33634751 DOI: 10.1080/15548627.2020.1797280

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.