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  • Oxford University Press (OUP)  (15)
  • Wang, Hui  (15)
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  • Oxford University Press (OUP)  (15)
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  • 1
    In: European Heart Journal, Oxford University Press (OUP), Vol. 41, No. 22 ( 2020-06-07), p. 2058-2066
    Abstract: It remains unknown whether the treatment of hypertension influences the mortality of patients diagnosed with coronavirus disease 2019 (COVID-19). Methods and results This is a retrospective observational study of all patients admitted with COVID-19 to Huo Shen Shan Hospital. The hospital was dedicated solely to the treatment of COVID-19 in Wuhan, China. Hypertension and the treatments were stratified according to the medical history or medications administrated prior to the infection. Among 2877 hospitalized patients, 29.5% (850/2877) had a history of hypertension. After adjustment for confounders, patients with hypertension had a two-fold increase in the relative risk of mortality as compared with patients without hypertension [4.0% vs. 1.1%, adjusted hazard ratio (HR) 2.12, 95% confidence interval (CI) 1.17–3.82, P = 0.013]. Patients with a history of hypertension but without antihypertensive treatment (n = 140) were associated with a significantly higher risk of mortality compared with those with antihypertensive treatments (n = 730) (7.9% vs. 3.2%, adjusted HR 2.17, 95% CI 1.03–4.57, P = 0.041). The mortality rates were similar between the renin–angiotensin–aldosterone system (RAAS) inhibitor (4/183) and non-RAAS inhibitor (19/527) cohorts (2.2% vs. 3.6%, adjusted HR 0.85, 95% CI 0.28–2.58, P = 0.774). However, in a study-level meta-analysis of four studies, the result showed that patients with RAAS inhibitor use tend to have a lower risk of mortality (relative risk 0.65, 95% CI 0.45–0.94, P = 0.20). Conclusion While hypertension and the discontinuation of antihypertensive treatment are suspected to be related to increased risk of mortality, in this retrospective observational analysis, we did not detect any harm of RAAS inhibitors in patients infected with COVID-19. However, the results should be considered as exploratory and interpreted cautiously.
    Type of Medium: Online Resource
    ISSN: 0195-668X , 1522-9645
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 2001908-7
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  • 2
    In: International Journal of Epidemiology, Oxford University Press (OUP), Vol. 52, No. 3 ( 2023-06-06), p. 690-702
    Abstract: Limited studies have examined the effect of prenatal exposure to particulate matter with diameter of & lt;2.5 µm (PM2.5) and & lt;1 μm (PM1) on fetal growth using ultrasound measurements with inconsistent results. No study has evaluated the joint effect of the indoor air pollution index and ambient particulate matter on fetal growth. Methods We conducted a prospective birth cohort study in Beijing, China in 2018, including 4319 pregnant women. We estimated prenatal PM2.5 and PM1 exposure using a machine-learning method and calculated the indoor air pollution index based on individual interviews. Gender- and gestational age-adjusted Z-score of the abdominal circumference (AC), head circumference (HC), femur length (FL) and estimated fetal weight (EFW) was calculated and then undergrowth was defined. A generalized estimating equation was used to evaluate the individual and joint effect of indoor air pollution index, PM2.5 and PM1 on fetal Z-score and undergrowth parameters. Results One unit increase in the indoor air pollution index was associated with −0.044 (95% CI: −0.087, −0.001) and −0.050 (95% CI: −0.094, −0.006) decrease in the AC and HC Z-scores, respectively. PM1 and PM2.5 were associated with decreased AC, HC, FL and EFW Z-scores, and higher risk of undergrowth. Compared with exposure to lower PM1 (≤ median) and no indoor air pollution, those exposed to higher PM1 ( & gt; median) and indoor air pollution had decreased EFW Z-scores (β = −0.152, 95% CI: −0.230, −0.073) and higher risk of EFW undergrowth (RR = 1.651, 95% CI: 1.106, 2.464). Indoor air pollution and ambient PM2.5 exposure had a similar joint effect on the Z-scores and undergrowth parameters of fetal growth. Conclusions This study suggested that indoor air pollution and ambient PM exposure had individual and joint negative effects on fetal growth.
    Type of Medium: Online Resource
    ISSN: 0300-5771 , 1464-3685
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 1494592-7
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  • 3
    In: International Journal of Neuropsychopharmacology, Oxford University Press (OUP), Vol. 23, No. 10 ( 2020-12-10), p. 673-686
    Abstract: We recently identified neuronal expression of farnesoid X receptor (FXR), a bile acid receptor known to impair autophagy by inhibiting cyclic adenosine monophosphate response element-binding protein (CREB), a protein whose underfunctioning is linked to neuroplasticity and depression. In this study, we hypothesize that FXR may mediate depression via a CREB-dependent mechanism. Methods Depression was induced in male C57BL6/J mice via chronic unpredictable stress (CUS). Subjects underwent behavioral testing to identify depression-like behaviors. A variety of molecular biology techniques, including viral-mediated gene transfer, Western blot, co-immunoprecipitation, and immunofluorescence, were used to correlate depression-like behaviors with underlying molecular and physiological events. Results Overexpression of FXR, whose levels were upregulated by CUS in hippocampal CA1, induced or aggravated depression-like behaviors in stress-naïve and CUS-exposed mice, while FXR short hairpin RNA (shRNA) ameliorated such symptoms in CUS-exposed mice. The behavioral effects of FXR were found to be associated with changes in CREB-brain-derived neurotrophic factor (BDNF) signaling, as FXR overexpression aggravated CUS-induced reduction in BDNF levels while the use of FXR shRNA or disruption of FXR-CREB signaling reversed the CUS-induced reduction in the phosphorylated CREB and BDNF levels. Molecular analysis revealed that FXR shRNA prevented CUS-induced cytoplasmic translocation of CREB-regulated transcription coactivator 2 (CRTC2); CRTC2 overexpression and CRTC2 shRNA abrogated the regulatory effect of FXR overexpression or FXR shRNA on CUS-induced depression-like behaviors. Conclusions In stress conditions, increased FXR in the CA1 inhibits CREB by targeting CREB and driving the cytoplasmic translocation of CRTC2. Uncoupling of the FXR-CREB complex may be a novel strategy for depression treatment.
    Type of Medium: Online Resource
    ISSN: 1461-1457 , 1469-5111
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 1501053-3
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  • 4
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2021
    In:  The Journals of Gerontology: Series A Vol. 76, No. 10 ( 2021-09-13), p. 1707-1713
    In: The Journals of Gerontology: Series A, Oxford University Press (OUP), Vol. 76, No. 10 ( 2021-09-13), p. 1707-1713
    Abstract: Alzheimer’s disease (AD) is a chronic neurodegenerative disease, which is characterized by cognitive and synaptic plasticity damage. Rapamycin is an activator of autophagy/mitophagy, which plays an important role in identifying and degrading damaged mitochondria. The aim of this study was to investigate the effect of rapamycin on cognitive and synaptic plasticity defects induced by AD, and further explore if the underlying mechanism was associated with mitophagy. The results show that rapamycin increases Parkin-mediated mitophagy and promotes fusion of mitophagosome and lysosome in the APP/PS1 mouse hippocampus. Rapamycin enhances learning and memory viability, synaptic plasticity, and the expression of synapse-related proteins, impedes cytochrome C-mediated apoptosis, decreases oxidative status, and recovers mitochondrial function in APP/PS1 mice. The data suggest that rapamycin effectively alleviates AD-like behaviors and synaptic plasticity deficits in APP/PS1 mice, which is associated with enhanced mitophagy. Our findings possibly uncover an important function of mitophagy in eliminating damaged mitochondria to attenuate AD-associated pathology.
    Type of Medium: Online Resource
    ISSN: 1079-5006 , 1758-535X
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2043927-1
    SSG: 12
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  • 5
    In: Cerebral Cortex, Oxford University Press (OUP), ( 2021-10-13)
    Abstract: Sex differences in human emotion and related decision-making behaviors are recognized, which can be traced back early in development. However, our understanding of their underlying neurodevelopmental mechanisms remains elusive. Using developmental functional magnetic resonance imaging and computational approach, we investigated developmental sex differences in latent decision-making dynamics during negative emotion processing and related neurocognitive pathways in 243 school-aged children and 78 young adults. Behaviorally, girls exhibit higher response caution and more effective evidence accumulation, whereas boys show more impulsive response to negative facial expression stimuli. These effects parallel sex differences in emotion-related brain maturity linking to evidence accumulation, along with age-related decrease in emotional response in the basolateral amygdala and medial prefrontal cortex (MPFC) in girls and an increase in the centromedial amygdala (CMA) in boys. Moreover, girls exhibit age-related decreases in BLA–MPFC coupling linked to evidence accumulation, but boys exhibit increases in CMA–insula coupling associated with response caution. Our findings highlight the neurocomputational accounts for developmental sex differences in emotion and emotion-related behaviors and provide important implications into the neurodevelopmental mechanisms of sex differences in latent emotional decision-making dynamics. This informs the emergence of sex differences in typical and atypical neurodevelopment of children’s emotion and related functions.
    Type of Medium: Online Resource
    ISSN: 1047-3211 , 1460-2199
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 1483485-6
    SSG: 12
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  • 6
    In: American Journal of Epidemiology, Oxford University Press (OUP), Vol. 188, No. 4 ( 2019-04-01), p. 776-784
    Type of Medium: Online Resource
    ISSN: 0002-9262 , 1476-6256
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2030043-8
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  • 7
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2017
    In:  The Journal of Infectious Diseases Vol. 216, No. 9 ( 2017-11-27), p. 1150-1158
    In: The Journal of Infectious Diseases, Oxford University Press (OUP), Vol. 216, No. 9 ( 2017-11-27), p. 1150-1158
    Type of Medium: Online Resource
    ISSN: 0022-1899 , 1537-6613
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2017
    detail.hit.zdb_id: 1473843-0
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  • 8
    In: PNAS Nexus, Oxford University Press (OUP), Vol. 2, No. 4 ( 2023-04-03)
    Abstract: Acinetobacter baumannii has been listed as one of the most critical pathogens in nosocomial infections; however, the key genes and mechanisms to adapt to the host microenvironment lack in-depth understanding. In this study, a total of 76 isolates (from 8 to 12 isolates per patient, spanning 128 to 188 days) were longitudinally collected from eight patients to investigate the within-host evolution of A. baumannii. A total of 70 within-host mutations were identified, 80% of which were nonsynonymous, indicating the important role of positive selection. Several evolutionary strategies of A. baumannii to increase its potential to adapt to the host microenvironment were identified, including hypermutation and recombination. Six genes were mutated in isolates from two or more patients, including two TonB-dependent receptor genes (bauA and BJAB07104_RS00665). In particular, the siderophore receptor gene bauA was mutated in multiple isolates from four patients with three MLST types, and all mutations were at amino acid 391 in ligand-binding sites. With 391T or 391A, BauA was more strongly bound to siderophores, which promoted the iron-absorption activity of A. baumannii at acidic or neutral pH, respectively. Through the A/T mutation at site 391 of BauA, A. baumannii displayed two reversible phases to adapt to distinct pH microenvironments. In conclusion, we demonstrated the comprehensive within-host evolutionary dynamics of A. baumannii, and discovered a key mutation of BauA site 391 as a genetic switch to adapt to different pH values, which may represent a model in the pathogen evolutionary adaption of the host microenvironment.
    Type of Medium: Online Resource
    ISSN: 2752-6542
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 3120703-0
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  • 9
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 108, No. 1 ( 2020-07-01), p. 189-198
    Abstract: Acupuncture is a centuried and unfading treatment of traditional Chinese medicine, which has been proved to exert curative effects on various disorders. Numerous works have been put in to uncover the effective mechanisms of acupuncture. And the interdependent interaction between acupuncture and acupoint microenvironment is a crucial topic. As a benign minimally invasive stimulation, the insertion and manipulation of needle at acupoint could cause deformation of local connective tissue and secretion of various molecules, such as high mobility group box 1 and ATP. The molecules are secreted into extracellular space and bind to the corresponding receptors thus active NF-κB, MAPK, ERK pathways on mast cells, fibroblasts, keratinocytes, and monocytes/macrophages, among others. This is supposed to trigger following transcription and translation of immune factors and neural active substance, as well as promote the free ion movement (such as Ca2+ influx) and the expansion of blood vessels to recruit more immune cells to acupoint. Finally, acupuncture could enhance network connectivity of local microenvironment at acupoints. The earlier mentioned substances further act on a variety of receptors in local nerve endings, transmitting electrical and biochemical signals to the CNS, and giving full play to the acupuncture action. In conclusion, we portrayed a neuro-immune microenvironment network of acupoints that medicates the acupuncture action, and would lay a foundation for the systematic study of the complex network relationship of acupoints in the future.
    Type of Medium: Online Resource
    ISSN: 0741-5400 , 1938-3673
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 2026833-6
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2022
    In:  Rheumatology Vol. 61, No. 9 ( 2022-08-30), p. 3830-3840
    In: Rheumatology, Oxford University Press (OUP), Vol. 61, No. 9 ( 2022-08-30), p. 3830-3840
    Abstract: This study was initiated to evaluate mammalian target of rapamycin (mTOR) activation in renal tissue of LN patients. Methods This retrospective study included 187 LN patients, 20 diabetic nephropathy (DN) patients, 10 minimal change disease (MCD) patients and 10 normal controls (NCs). Seven of 187 LN patients had repeated renal biopsies. mTORC1/2 activation was evaluated by immunohistochemistry and multiplexed immunofluorescence. The association of mTORC1/2 activation with the clinicopathologic indices and prognostic outcomes was analysed among 187 LN patients. Proteomics was performed in renal biopsies of 20 LN patients. Proteomics was employed to comprehensively evaluate the impact of mTOR activation on intrarenal gene expression. Results mTORC1/2 was significantly activated in podocytes, mesangial cells, endothelial cells and tubular epithelial cells of LN patients as compared with those with MCD or NC. The glomerular mTORC1 activation was higher in LN patients compared with DN patients. mTORC1, but not mTORC2, activation strongly correlated with serum albumin, complement C3, proteinuria and the following pathological biomarkers of LN: crescent formation, interstitial inflammation and fibrosis. Moreover, mTORC1 activation was identified as a prognostic marker in LN patients. Bioinformatic analyses of proteomics and immunohistochemical data unveiled increased complement activation, antigen presentation and phagocytosis in LN patients with mTORC1 activation. Conclusion Renal mTORC1 activation could be a biomarker to reveal disease activity and predict clinical prognosis in LN patients.
    Type of Medium: Online Resource
    ISSN: 1462-0324 , 1462-0332
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 1474143-X
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