Precision Clinical Medicine最新文献

{"title":"Aztreonam-avibactam: an option against carbapenem-resistant Enterobacterales with emerging resistance.","authors":"Shikai Wu, Zhiyong Zong","doi":"10.1093/pcmedi/pbac029","DOIUrl":"https://doi.org/10.1093/pcmedi/pbac029","url":null,"abstract":"The Enterobacterales are an order of Gram-negative bacteria comprising a few major human pathogens such as Escherichia coli and Klebsiella pneumoniae . However, carbapenem-resistant En-terobacterales (CRE) has risen as an urgent threat for human health, leading to high mortality with very limited antimicrobial options. The main mechanism mediating resistance to β - lactams including carbapenems in the Enterobacterales is production of β -lactamases, which are two categories of enzymes capable of hydrolyzing β -lactams: serine β -lactamases and metallo-β -lactamases (MBLs). Avibactam (AVI) is a non-β -lactam β - lactamase inhibitor able to inhibit almost all serine β -lactamases but not MBLs.AVI in combination with ceftazidime (CAZ) has been approved for treating infections caused by CRE but CAZ-AVI has no activities against those producing MBLs. Currently, no MBL inhibitors have been approved for clinical use. Aztreonam (ATM), a monobactam, is stable to the hydrolysis of MBLs,and AVI can protect ATM from the inactivation by serine β -lactamases. The ATM- AVIcombinationmaythereforebeaviablechoiceagainstCREpro-ducing","PeriodicalId":33608,"journal":{"name":"Precision Clinical Medicine","volume":"5 4","pages":"pbac029"},"PeriodicalIF":5.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9745765/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10731595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Blockade of integrin signaling reduces chemotherapy-induced premature senescence in collagen cultured bladder cancer cells.","authors":"","doi":"10.1093/pcmedi/pbac027","DOIUrl":"https://doi.org/10.1093/pcmedi/pbac027","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1093/pcmedi/pbac007.].</p>","PeriodicalId":33608,"journal":{"name":"Precision Clinical Medicine","volume":" ","pages":"pbac027"},"PeriodicalIF":5.3,"publicationDate":"2022-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9675475/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40506854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Precision prevention of monkeypox.","authors":"Kang An,&nbsp;Zhenmi Liu,&nbsp;Furong Qu,&nbsp;Zhenmei An","doi":"10.1093/pcmedi/pbac026","DOIUrl":"https://doi.org/10.1093/pcmedi/pbac026","url":null,"abstract":"1General Practice Ward/International Medical Center Ward, General Practice Medical Center, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, China 2West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu 610041, China 3Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu 610041, China 4Department of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu 610041, China ∗Correspondence: Zhenmei An, azmhxnfm@163.com","PeriodicalId":33608,"journal":{"name":"Precision Clinical Medicine","volume":" ","pages":"pbac026"},"PeriodicalIF":5.3,"publicationDate":"2022-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9639333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40468530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The latest breakthrough on NLRP6 inflammasome.","authors":"Runzhi Li,&nbsp;Yang Zan,&nbsp;Kaiwen Sui,&nbsp;Shu Zhu","doi":"10.1093/pcmedi/pbac022","DOIUrl":"https://doi.org/10.1093/pcmedi/pbac022","url":null,"abstract":"Abstract NLRP6, a Nod-like receptor family member, has been shown to affect intestinal homeostasis and microbial colonization through organizing a huge protein complex called inflammasome. NLRP6 inflammasome promotes the cleavage and secretion of inflammatory cytokines or the cleavage of pore-forming Gasdermin D to initiate the inflammatory cell death called pyroptosis, which plays important roles in responding to pathogen invasion. However, questions about the ligand(s) that trigger NLRP6 inflammasome activation, or the mechanisms that how a ligand triggers NLRP6 inflammasome assembly, are emerging. In this mini-review, we summarize the current understandings of ligand recognition of NLRP6, the role of liquid-liquid phase separation in NLRP6 inflammasome assembly, and potential links with human health and diseases.","PeriodicalId":33608,"journal":{"name":"Precision Clinical Medicine","volume":" ","pages":"pbac022"},"PeriodicalIF":5.3,"publicationDate":"2022-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/75/2e/pbac022.PMC9536861.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33496297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome-wide methylation profiling reveals differentially methylated genes in blood DNA of small-cell lung cancer patients.","authors":"Yanqi He,&nbsp;Calvin Wei,&nbsp;Zhifu Sun,&nbsp;Julie M Cunningham,&nbsp;Liang Wang,&nbsp;Zong Wei,&nbsp;Ping Yang","doi":"10.1093/pcmedi/pbac017","DOIUrl":"https://doi.org/10.1093/pcmedi/pbac017","url":null,"abstract":"the epige-netic biomarkers under investigation. We here report a study that identified aberrantly methylated genes between current and former smokers among SCLC patients, revealing a set of candidate biomarkers in peripheral blood DNA for better stratifying patients with high risk.","PeriodicalId":33608,"journal":{"name":"Precision Clinical Medicine","volume":"5 3","pages":"pbac017"},"PeriodicalIF":5.3,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9306013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10400146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory effect of lanosterol on cataractous lens of cynomolgus monkeys using a subconjunctival drug release system.","authors":"Keke Zhang,&nbsp;Wenwen He,&nbsp;Yu Du,&nbsp;Yugui Zhou,&nbsp;Xiaokang Wu,&nbsp;Jie Zhu,&nbsp;Xiangjia Zhu,&nbsp;Kang Zhang,&nbsp;Yi Lu","doi":"10.1093/pcmedi/pbac021","DOIUrl":"https://doi.org/10.1093/pcmedi/pbac021","url":null,"abstract":"<p><strong>Background: </strong>To evaluate the effect of lanosterol on cataractous lens of cynomolgus monkeys using a subconjunctival drug release system.</p><p><strong>Methods: </strong>Nine elder cynomolgus monkeys were used, consisting of three monkeys without cataract as controls, three monkeys with naturally occurring cortical cataract, and three monkeys with nuclear cataract as intervention groups. Nanoparticulated thermogel with lanosterol and fluorescein was administered by subconjunctival injection in the monkeys with cataract. Fluorescence changes of injected thermogel and cataract progression were observed. Lanosterol concentration in aqueous humor, solubility changes in lens proteins, and oxidative stress levels were analyzed in the lenses of the control and intervention groups.</p><p><strong>Results: </strong>Injected thermogel showed decreased fluorescence during follow up. Lanosterol concentration in aqueous humor increased in the first 2 weeks and then gradually decreased, which was in accordance with the changes in cortical lens clarity. However, lenses with nuclear opacification showed little change. In the cortical region of lenses with cortical cataract, solubility of α-crystallin was significantly increased after administration of lanosterol, as well as the reduction of oxidative stress.</p><p><strong>Conclusions: </strong>We demonstrated the effect of lanosterol on cataract progression based on <i>in vivo</i> models of primates. Lanosterol showed a short-term and reliable reversal effect on reducing cataract severity in cortical cataract in the early stages, possibly due to the increase in the solubility of lens proteins and changes in the oxidative stress status. Lanosterol administration using subconjunctival drug release system could be a promising nonsurgical approach for future clinical studies of cataract prevention and treatment.</p>","PeriodicalId":33608,"journal":{"name":"Precision Clinical Medicine","volume":" ","pages":"pbac021"},"PeriodicalIF":5.3,"publicationDate":"2022-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/cb/d7/pbac021.PMC9523460.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33488967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"JAM-A facilitates hair follicle regeneration in alopecia areata through functioning as ceRNA to protect VCAN expression in dermal papilla cells.","authors":"Minjuan Wu,&nbsp;Chen Xu,&nbsp;Junfeng Jiang,&nbsp;Sha Xu,&nbsp;Jun Xiong,&nbsp;Xiaoming Fan,&nbsp;Kaihong Ji,&nbsp;Yunpeng Zhao,&nbsp;Haitao Ni,&nbsp;Yue Wang,&nbsp;Houqi Liu,&nbsp;Zhaofan Xia","doi":"10.1093/pcmedi/pbac020","DOIUrl":"https://doi.org/10.1093/pcmedi/pbac020","url":null,"abstract":"<p><p>The dermal papilla cells in hair follicles function as critical regulators of hair growth. In particular, alopecia areata (AA) is closely related to the malfunctioning of the human dermal papilla cells (hDPCs). Thus, identifying the regulatory mechanism of hDPCs is important in inducing hair follicle (HF) regeneration in AA patients. Recently, growing evidence has indicated that 3' untranslated regions (3' UTR) of key genes may participate in the regulatory circuitry underlying cell differentiation and diseases through a so-called competing endogenous mechanism, but none have been reported in HF regeneration. Here, we demonstrate that the 3' UTR of junctional adhesion molecule A (JAM-A) could act as an essential competing endogenous RNA to maintain hDPCs function and promote HF regeneration in AA. We showed that the 3' UTR of JAM-A shares many microRNA (miRNA) response elements, especially miR-221-3p, with versican (VCAN) mRNA, and JAM-A 3' UTR could directly modulate the miRNA-mediated suppression of VCAN in self-renewing hDPCs. Furthermore, upregulated VCAN can in turn promote the expression level of JAM-A. Overall, we propose that JAM-A 3' UTR forms a feedback loop with VCAN and miR-221-3p to regulate hDPC maintenance, proliferation, and differentiation, which may lead to developing new therapies for hair loss.</p>","PeriodicalId":33608,"journal":{"name":"Precision Clinical Medicine","volume":" ","pages":"pbac020"},"PeriodicalIF":5.3,"publicationDate":"2022-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9486988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33474563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Precision management of brain oedema after acute ischaemic stroke.","authors":"Simiao Wu,&nbsp;Craig S Anderson","doi":"10.1093/pcmedi/pbac019","DOIUrl":"https://doi.org/10.1093/pcmedi/pbac019","url":null,"abstract":"Stroke is a leading cause of death and disability in the world, with acute ischaemic stroke accounting for ∼ 70% of all cases. 1 Some degree of brain oedema occurs in all cases of acute ischaemic stroke and, when severe, has major consequences on survival-free of disability. Pathophysiological studies indicate an evolu-tion of cytotoxic oedema, ionic oedema, and vasogenic oedema, 2 which implies brain oedema is a dynamic process and explains the various terminology used, such as large hemispheric infarc-tion,symptomatic infarct swelling,space-occupying infarction,or malignant middle cerebral artery (MCA) infarction . Heterogene-ity in manifestations and sequelae necessitates a new, precision medicine approach to individualizing prevention and treatment of brain oedema after stroke.","PeriodicalId":33608,"journal":{"name":"Precision Clinical Medicine","volume":" ","pages":"pbac019"},"PeriodicalIF":5.3,"publicationDate":"2022-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9384835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40645115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD4⁺ T cell metabolism, gut microbiota, and autoimmune diseases: implication in precision medicine of autoimmune diseases.","authors":"Wenjing Yang,&nbsp;Tianming Yu,&nbsp;Yingzi Cong","doi":"10.1093/pcmedi/pbac018","DOIUrl":"https://doi.org/10.1093/pcmedi/pbac018","url":null,"abstract":"<p><p>CD4⁺ T cells are critical to the development of autoimmune disorders. Glucose, fatty acids, and glutamine metabolisms are the primary metabolic pathways in immune cells, including CD4⁺ T cells. The distinct metabolic programs in CD4⁺ T cell subsets are recognized to reflect the bioenergetic requirements, which are compatible with their functional demands. Gut microbiota affects T cell responses by providing a series of antigens and metabolites. Accumulating data indicate that CD4⁺ T cell metabolic pathways underlie aberrant T cell functions, thereby regulating the pathogenesis of autoimmune disorders, including inflammatory bowel diseases, systemic lupus erythematosus, and rheumatoid arthritis. Here, we summarize the current progress of CD4⁺ T cell metabolic programs, gut microbiota regulation of T cell metabolism, and T cell metabolic adaptions to autoimmune disorders to shed light on potential metabolic therapeutics for autoimmune diseases.</p>","PeriodicalId":33608,"journal":{"name":"Precision Clinical Medicine","volume":" ","pages":"pbac018"},"PeriodicalIF":5.3,"publicationDate":"2022-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f4/7e/pbac018.PMC9384833.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40645116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of 2,2',4,4'-tetrabromodiphenyl ether (BDE47)-induced testicular toxicity via single-cell RNA-sequencing.","authors":"Wei Zhang,&nbsp;Siyu Xia,&nbsp;Xiaoru Zhong,&nbsp;Guoyong Gao,&nbsp;Jing Yang,&nbsp;Shuang Wang,&nbsp;Min Cao,&nbsp;Zhen Liang,&nbsp;Chuanbin Yang,&nbsp;Jigang Wang","doi":"10.1093/pcmedi/pbac016","DOIUrl":"https://doi.org/10.1093/pcmedi/pbac016","url":null,"abstract":"<p><strong>Background: </strong>The growing male reproductive diseases have been linked to higher exposure to certain environmental compounds such as 2,2',4,4'-tetrabromodiphenyl ether (BDE47) that are widely distributed in the food chain. However, the specific underlying molecular mechanisms for BDE47-induced male reproductive toxicity are not completely understood.</p><p><strong>Methods: </strong>Here, for the first time, advanced single-cell RNA sequencing (ScRNA-seq) was employed to dissect BDE47-induced prepubertal testicular toxicity in mice from a pool of 76 859 cells.</p><p><strong>Results: </strong>Our ScRNA-seq results revealed shared and heterogeneous information of differentially expressed genes, signaling pathways, transcription factors, and ligands-receptors in major testicular cell types in mice upon BDE47 treatment. Apart from disruption of hormone homeostasis, BDE47 was discovered to downregulate multiple previously unappreciated pathways such as double-strand break repair and cytokinesis pathways, indicative of their potential roles involved in BDE47-induced testicular injury. Interestingly, transcription factors analysis of ScRNA-seq results revealed that <i>Kdm5b</i> (lysine-specific demethylase 5B), a key transcription factor required for spermatogenesis, was downregulated in all germ cells as well as in Sertoli and telocyte cells in BDE47-treated testes of mice, suggesting its contribution to BDE47-induced impairment of spermatogenesis.</p><p><strong>Conclusions: </strong>Overall, for the first time, we established the molecular cell atlas of mice testes to define BDE47-induced prepubertal testicular toxicity using the ScRNA-seq approach, providing novel insight into our understanding of the underlying mechanisms and pathways involved in BDE47-associated testicular injury at a single-cell resolution. Our results can serve as an important resource to further dissect the potential roles of BDE47, and other relevant endocrine-disrupting chemicals, in inducing male reproductive toxicity.</p>","PeriodicalId":33608,"journal":{"name":"Precision Clinical Medicine","volume":" ","pages":"pbac016"},"PeriodicalIF":5.3,"publicationDate":"2022-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/dd/a4/pbac016.PMC9306015.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40535137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}