Meta-Analysis on the Efficacy and Safety of Hyperbaric Oxygen as Adjunctive Therapy for Vascular Dementia

Background: Vascular dementia (VD) is a common type of disease in the elderly. Numerous clinical trials have suggested that hyperbaric oxygen is an effective and safe complementary therapy for aging-related disorders. However, there is no reliable systematic evidence regarding hyperbaric oxygen therapy (HBOT) for the treatment of VD. Therefore, we performed a meta-analysis to evaluate the clinical efficacy and safety of HBOT in treating VD.Methods: We methodically retrieved the clinical studies from eight databases (PubMed, Cochrane Library, Embase, Web of Science, Sino-Med, China National Knowledge Infrastructure (CNKI), China Science and Technology Journal Database (VIP), and WanFang) from their inception to November 2018. RevMan 5.3.5 was used for quality assessment and data analysis. Stata 15.1 was employed for publication bias detection and sensitivity analysis.Results: Twenty-five randomized clinical trials (RCTs) involving 1,954 patients met our inclusion criteria. These articles researched the HBOT + oxiracetam + conventional therapy (CT) vs. oxiracetam + CT (n = 13), HBOT + butylphthalide +CT vs. butylphthalide + CT (n = 5), HBOT + donepezil + CT vs. donepezil + CT (n = 4), HBOT + nicergoline + CT vs. nicergoline + CT (n = 2) and HBOT + CT vs. CT (n = 1). The results indicated that additional HBOT strikingly improved the Mini-Mental State Examination (MMSE) (MD = 4.00; 95% CI = 3.28–4.73; P < 0.00001), activities of daily living (ADL) (MD = −5.91; 95% CI = −6.45, −5.36; P < 0.00001) and ADL by Barthel index (BADL) (MD = 13.86; 95% CI = 5.63–22.10; P = 0.001) and increased the total efficacy rate (TEF) (OR = 4.84, 95% CI = 3.19–7.33, P < 0.00001). The adverse events rates were not statistically significant between the HBOT and CT groups (OR = 0.85, 95% CI = 0.26–2.78, P = 0.79).Conclusion: In view of the effectiveness and safety of HBOT, the present meta-analysis suggested that HBOT can be recommended as an effective and safe complementary therapy for the treatment of VD.Protocol Registration: PROSPERO (ID: CRD42019117178). Available online at: http://www.crd.york.ac.uk/PROSPERO/display_record.asp?ID=CRD42019117178

Oocyte stage-specific effects of MTOR determine granulosa cell fate and oocyte quality in mice.

MTOR (mechanistic target of rapamycin) is a widely recognized integrator of signals and pathways key for cellular metabolism, proliferation, and differentiation. Here we show that conditional knockout (cKO) of Mtor in either primordial or growing oocytes caused infertility but differentially affected oocyte quality, granulosa cell fate, and follicular development. cKO of Mtor in nongrowing primordial oocytes caused defective follicular development leading to progressive degeneration of oocytes and loss of granulosa cell identity coincident with the acquisition of immature Sertoli cell-like characteristics. Although Mtor was deleted at the primordial oocyte stage, DNA damage accumulated in oocytes during their later growth, and there was a marked alteration of the transcriptome in the few oocytes that achieved the fully grown stage. Although oocyte quality and fertility were also compromised when Mtor was deleted after oocytes had begun to grow, these occurred without overtly affecting folliculogenesis or the oocyte transcriptome. Nevertheless, there was a significant change in a cohort of proteins in mature oocytes. In particular, down-regulation of PRC1 (protein regulator of cytokinesis 1) impaired completion of the first meiotic division. Therefore, MTOR-dependent pathways in primordial or growing oocytes differentially affected downstream processes including follicular development, sex-specific identity of early granulosa cells, maintenance of oocyte genome integrity, oocyte gene expression, meiosis, and preimplantation developmental competence. Proc Natl Acad Sci U S A 2018 Jun 5; 115(23):E5326-E5333

ISMAC: An Intelligent System for Customized Clinical Case Management and Analysis

Clinical cases are primary and vital evidence for Traditional Chinese Medicine (TCM) clinical research. A great deal of medical knowledge is hidden in the clinical cases of the highly experienced TCM practitioner. With a deep Chinese culture background and years of clinical experience, an experienced TCM specialist usually has his or her unique clinical pattern and diagnosis idea. Preserving huge clinical cases of experienced TCM practitioners as well as exploring the inherent knowledge is then an important but arduous task. The novel system ISMAC (Intelligent System for Management and Analysis of Clinical Cases in TCM) is designed and implemented for customized management and intelligent analysis of TCM clinical data. Customized templates with standard and expert-standard symptoms, diseases, syndromes, and Chinese Medince Formula (CMF) are constructed in ISMAC, according to the clinical diagnosis and treatment characteristic of each TCM specialist. With these templates, clinical cases are archived in order to maintain their original characteristics. Varying data analysis and mining methods, grouped as Basic Analysis, Association Rule, Feature Reduction, Cluster, Pattern Classification, and Pattern Prediction, are implemented in the system. With a flexible dataset retrieval mechanism, ISMAC is a powerful and convenient system for clinical case analysis and clinical knowledge discovery

Prospects for detection rate of very-high-energy {\gamma}-ray emissions from short {\gamma}-ray bursts with the HADAR experiment

The observation of short gamma ray bursts (SGRBs) in the TeV energy range plays an important role in understanding the radiation mechanism and probing new areas of physics such as Lorentz invariance violation. However, no SGRB has been observed in this energy range due to the short duration of SGRBs and the weakness of current experiments. New experiments with new technology are required to detect sub-TeV SGRBs. In this work, we observe the very high energy (VHE) $\gamma$-ray emissions from SGRBs and calculate the annual detection rate with the High Altitude Detection of Astronomical Radiation HADAR (HADAR) experiment. First, a set of pseudo-SGRB samples is generated and checked using the observations of Fermi-GBM, Fermi-LAT, and SWIFT measurements. The annual detection rate is calculated from these SGRB samples based on the performance of the HADAR instrument. As a result, the HADAR experiment can detect 0.5 SGRB per year if the spectral break-off of $\gamma$-rays caused by the internal absorption is larger than 100 GeV. For a GRB09010-like GRB in HADAR's view, it should be possible to detect approximately 2000 photons considering the internal absorption. With a time delay assumption due to the Lorentz invariance violation effects, a simulated light curve of GRB090510 has evident energy dependence. We hope that the HADAR experiment can perform the SGRB observations and test our calculations in the future

Protective Effects of Li-Fei-Xiao-Yan Prescription on Lipopolysaccharide-Induced Acute Lung Injury via Inhibition of Oxidative Stress and the TLR4/NF- κ

Li-Fei-Xiao-Yan prescription (LFXY) has been clinically used in China to treat inflammatory and infectious diseases including inflammatory lung diseases. The present study was aimed at evaluating the potential therapeutic effects and potential mechanisms of LFXY in a murine model of lipopolysaccharide- (LPS-) induced acute lung injury (ALI). In this study, the mice were orally pretreated with LFXY or dexamethasone (positive drug) before the intratracheal instillation of LPS. Our data indicated that pretreatment with LFXY enhanced the survival rate of ALI mice, reversed pulmonary edema and permeability, improved LPS-induced lung histopathology impairment, suppressed the excessive inflammatory responses via decreasing the expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) and chemokine (MIP-2) and inhibiting inflammatory cells migration, and repressed oxidative stress through the inhibition of MPO and MDA contents and the upregulation of antioxidants (SOD and GSH) activities. Mechanistically, treatment with LFXY significantly prevented LPS-induced TLR4 expression and NF-κB (p65) phosphorylation. Overall, the present study suggests that LFXY protected mice from acute lung injury induced by LPS via inhibition of TLR4/NF-κB p65 activation and upregulation of antioxidative enzymes and it may be a potential preventive and therapeutic agent for ALI in the clinical setting