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Obstet Gynecol Surv ; 76(8): 493-503, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34449852


Importance: Ten years have passed since the Institute of Medicine (IOM) released its recommendations for gestational weight gain (GWG), based on a woman's prepregnancy body mass index. Despite this, the majority of women do not gain the appropriate gestational weight; most women gain too much weight, and a small but substantial number gain too little. Objective: We review the literature concerning GWG, the opinions and practices of clinicians in managing their patients' weight, and how these practices are perceived by patients. We also review several randomized control trials that investigate the efficacy of clinical intervention in managing GWG. Evidence Acquisition: A literature review search was conducted with no limitations on the number of years searched. Results: The number of clinicians who are aware of and use the IOM recommendations has increased, but the prevalence of inappropriate GWG has not decreased. Clinicians report feeling less than confident in their ability to have an impact on their patients' weight gain, and there are discrepancies between what clinicians and patients report regarding counseling. Many randomized control trials demonstrate a beneficial impact of clinical intervention, highlighting the importance of collaboration and technology to provide educational information and support throughout a pregnancy. Conclusions: Pregnancy provides an opportunity for clinicians to have open and direct conversations with their patients about their weight. Providing clinicians with the tools, skillset, and confidence to assist in the management of GWG is essential to the health of women and their children, and warrants further investigation.

Gerenciamento Clínico , Ganho de Peso na Gestação , Papel do Médico , Guias de Prática Clínica como Assunto/normas , Terapia Comportamental , Aconselhamento , Grupos Étnicos , Feminino , Humanos , National Academies of Science, Engineering, and Medicine, U.S., Health and Medicine Division , Gravidez , Fatores Raciais , Tecnologia , Estados Unidos/epidemiologia
J Virol ; 90(7): 3400-10, 2016 Jan 13.
Artigo em Inglês | MEDLINE | ID: mdl-26764007


UNLABELLED: TRIM5α is an interferon-inducible retroviral restriction factor that prevents infection by inducing the abortive disassembly of capsid cores recognized by its C-terminal PRY/SPRY domain. The mechanism by which TRIM5α mediates the disassembly of viral cores is poorly understood. Previous studies demonstrated that proteasome inhibitors abrogate the ability of TRIM5α to induce premature core disassembly and prevent reverse transcription; however, viral infection is still inhibited, indicating that the proteasome is partially involved in the restriction process. Alternatively, we and others have observed that TRIM5α associates with proteins involved in autophagic degradation pathways, and one recent study found that autophagic degradation is required for the restriction of retroviruses by TRIM5α. Here, we show that TRIM5α is basally degraded via autophagy in the absence of restriction-sensitive virus. We observe that the autophagy markers LC3b and lysosome-associated membrane protein 2A (LAMP2A) localize to a subset of TRIM5α cytoplasmic bodies, and inhibition of lysosomal degradation with bafilomycin A1 increases this association. To test the requirement for macroautophagy in restriction, we examined the ability of TRIM5α to restrict retroviral infection in cells depleted of the autophagic mediators ATG5, Beclin1, and p62. In all cases, restriction of retroviruses by human TRIM5α, rhesus macaque TRIM5α, and owl monkey TRIM-Cyp remained potent in cells depleted of these autophagic effectors by small interfering RNA (siRNA) knockdown or clustered regularly interspaced short palindromic repeat (CRISPR)-Cas9 genome editing. Collectively, these results are consistent with observations that the turnover of TRIM5α proteins is sensitive to autophagy inhibition; however, the data presented here do not support observations that the inhibition of autophagy abrogates retroviral restriction by TRIM5 proteins. IMPORTANCE: Restriction factors are a class of proteins that inhibit viral replication. Following fusion of a retrovirus with a host cell membrane, the retroviral capsid is released into the cytoplasm of the target cell. TRIM5α inhibits retroviral infection by promoting the abortive disassembly of incoming retroviral capsid cores; as a result, the retroviral genome is unable to traffic to the nucleus, and the viral life cycle is extinguished. In the process of restriction, TRIM5α itself is degraded by the proteasome. However, in the present study, we have shown that in the absence of a restriction-sensitive virus, TRIM5α is degraded by both proteasomal and autophagic degradation pathways. Notably, we observed that restriction of retroviruses by TRIM5α does not require autophagic machinery. These data indicate that the effector functions of TRIM5α can be separated from its degradation and may have further implications for understanding the mechanisms of other TRIM family members.

Autofagia/genética , Proteínas de Transporte/metabolismo , Infecções por Retroviridae/virologia , Retroviridae/crescimento & desenvolvimento , Proteínas do Core Viral/metabolismo , Replicação Viral/genética , Animais , Aotidae , Proteínas Reguladoras de Apoptose/genética , Proteína 5 Relacionada à Autofagia , Proteína Beclina-1 , Proteínas de Transporte/genética , Linhagem Celular Tumoral , Repetições Palindrômicas Curtas Agrupadas e Regularmente Espaçadas/genética , Células HeLa , Humanos , Glicoproteínas de Membrana Associadas ao Lisossomo/metabolismo , Macaca mulatta , Macrolídeos/farmacologia , Proteínas de Membrana/genética , Camundongos , Proteínas Associadas aos Microtúbulos/genética , Proteínas Associadas aos Microtúbulos/metabolismo , Proteínas de Neoplasias/metabolismo , Proteólise , Interferência de RNA , RNA Interferente Pequeno/genética , Proteínas de Ligação a RNA/genética , Retroviridae/genética , Infecções por Retroviridae/imunologia , Proteínas com Motivo Tripartido , Ubiquitina-Proteína Ligases