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We investigated the effect of lipopolysaccharide (LPS)-induced maternal immune activation used as a model for producing neurodevelopmental disorders on hippocampal neurogenesis and behaviors in rat offspring by exploring the antioxidant effects of alpha-glycosyl isoquercitrin (AGIQ). Pregnant Sprague-Dawley rats were intraperitoneally injected with LPS (50 μg/kg body weight) at gestational days 15 and 16. AGIQ was administered in the diet to dams at 0.5% (w/w) from gestational day 10 until weaning at postnatal day 21 and then to offspring until adulthood at postnatal day 77. During postnatal life, offspring of LPS-injected animals did not show neuroinflammation or oxidative stress in the brain. At weaning, LPS decreased the numbers of type-2b neural progenitor cells (NPCs) and PCNA

Lead (Pb) causes developmental neurotoxicity. Developmental exposure to Pb acetate (PbAc) induces aberrant hippocampal neurogenesis by increasing or decreasing neural progenitor cell (NPC) subpopulations in the dentate gyrus (DG) of rats. To investigate whether hippocampal neurogenesis is similarly affected by PbAc exposure in a general toxicity study, 5-week-old Sprague-Dawley rats were orally administered PbAc at 0, 4000, and 8000 ppm (w/v) in drinking water for 28 days. After exposure to 4000 or 8000 ppm PbAc, Pb had accumulated in the brains. Neurogenesis was suppressed by 8000 ppm PbAc, which was related to decreased number of type-2b NPCs, although number of mature granule cells were increased by both PbAc doses. Gene expression in the 8000 ppm PbAc group suggested suppressed NPC proliferation and increased apoptosis resulting in suppressed neurogenesis. PbAc exposure increased numbers of metallothionein-I/II

This study examined the ameliorating effect of alpha-glycosyl isoquercitrin (AGIQ), an antioxidant, on disrupted hippocampal neurogenesis in the dentate gyrus (DG) in a rat model of autism spectrum disorder induced by prenatal valproic acid (VPA) exposure. Dams were intraperitoneally injected with 500 mg/kg VPA on gestational day 12. AGIQ was administered in the diet at 0.25 or 0.5% to dams from gestational day 13 until weaning at postnatal day (PND) 21 and then to pups until PND 63. At PND 21, VPA-exposed offspring showed decreased numbers of type-2a and type-3 neural progenitor cells (NPCs) among granule cell lineage subpopulations. AGIQ treatment at both doses rescued the reduction in type-3 NPCs. AGIQ upregulated Reln and Vldlr transcript levels in the DG at 0.5% and ≥ 0.25%, respectively, and increased the number of reelin

Drinking alcohol during pregnancy may cause fetal alcohol spectrum disorder. In rats, developmental exposure to ethanol (EtOH) at high doses has shown to induce aberrant neurogenesis in neural progenitor cells (NPCs) during weaning and suppress synaptic plasticity of newborn granule cells after maturation; neuroinflammation was even sustained until the adult stage in the hippocampal dentate gyrus (DG). To investigate whether hippocampal neurogenesis is affected by EtOH exposure in a general toxicity study, EtOH was administered orally to 5-week-old Sprague-Dawley rats at 0%, 10%, and 16% (w/v) in drinking water for 28 days. Exposure to 16% EtOH decreased type-1 neural stem cells (NSCs) and type-2a NPCs in the DG subgranular zone. A reduction in reelin-positive (reelin

As no reported randomized control trials (RCTs) directly compare the three administration doses of anticoagulants (prophylactic dose, treatment dose, and no treatment), the most recommended dose to be administered to patients with coronavirus disease 2019 (COVID-19) remains unclear. The purpose of this study was to examine the effects of anticoagulant doses administered to patients with COVID-19, using a network meta-analysis (NMA) including high-quality studies.All eligible trials from the Cochrane Central Register of Controlled Trials, MEDLINE, and Clinicaltrials.gov were included. We included RCTs and observational studies adjusted for covariates for patients aged ≥ 18 years and hospitalized due to objectively confirmed COVID-19. The main study outcome was mortality.In patients with moderate COVID-19, the prophylactic (relative risk (RR) 0.64 [95% confidence interval (CI) 0.52-0.80]) and treatment dose (RR 0.57 [95% CI 0.45-0.72] were associated with a lower risk of short-term mortality than that with no anticoagulant treatment. However, the prophylactic and treatment dose groups were not significantly different. The hierarchy for efficacy in reducing short-term mortality was treatment dose (P score 92.4) prophylactic dose (57.6) no treatment (0.0). In patients with severe COVID-19, due to the absence of trials with the no-treatment group, NMA could not be conducted. However, pairwise comparison did not show a significant difference between the prophylactic and treatment dose groups.Treatment and prophylactic doses of anticoagulants showed similar effects on mortality; however, the treatment dose is preferred over the prophylactic dose for patients with both moderate and severe COVID-19.PROSPERO (registration number: CRD42021245308, 05/21/2021).

Aluminum (Al), a common light metal, affects the developing nervous system. Developmental exposure to Al chloride (AlClsub3/sub) induces aberrant neurogenesis by targeting neural stem cells (NSCs) and/or neural progenitor cells (NPCs) in the dentate gyrus (DG) of rats and mice. To investigate whether hippocampal neurogenesis is similarly affected by AlClsub3/subexposure in a general toxicity study, AlClsub3/subwas orally administered to 5-week-old Sprague Dawley rats at dosages of 0, 4000, or 8000 ppm in drinking water for 28 days. AlClsub3/subdownregulated Sox2 transcript level in the DG at the highest dosage and produced a dose-dependent decrease of SOX2sup+/supcells without altering numbers of GFAPsup+/supor TBR2sup+/supcells in the subgranular zone, suggesting that AlClsub3/subdecreases Type 2a NPCs. High-dose exposure downregulated Pcna, upregulated Pvalb, and altered expression of genes suggestive of oxidative stress induction (upregulation of Nos2 and downregulation of antioxidant enzyme genes), indicating suppressed proliferation and differentiation of Type 1 NSCs. AlClsub3/subdoses also increased mature granule cells in the DG. Upregulation of Reln may have contributed to an increase of granule cells to compensate for the decrease of Type 2a NPCs. Moreover, upregulation of Calb2, Gria2, Mapk3, and Tgfb3, as well as increased numbers of activated astrocytes in the DG hilus, may represent ameliorating responses against suppressed neurogenesis. These results suggest that 28-day exposure of young-adult rats to AlClsub3/subdifferentially targeted NPCs and mature granule cells in hippocampal neurogenesis, yielding a different pattern of disrupted neurogenesis from developmental exposure.

We have previously reported that the valproic acid (VPA)-induced disruption pattern of hippocampal adult neurogenesis differs between developmental and 28-day postpubertal exposure. In the present study, we performed brain region-specific global gene expression profiling to compare the profiles of VPA-induced neurotoxicity between developmental and postpubertal exposure. Offspring exposed to VPA at 0, 667, and 2000 parts per million (ppm) via maternal drinking water from gestational day 6 until weaning (postnatal day 21) were examined, along with male rats orally administered VPA at 0, 200, and 900 mg/kg body weight for 28 days starting at 5 weeks old. Four brain regions-the hippocampal dentate gyrus, corpus callosum, cerebral cortex, and cerebellar vermis-were subjected to expression microarray analysis. Profiled data suggested a region-specific pattern of effects after developmental VPA exposure, and a common pattern of effects among brain regions after postpubertal VPA exposure. Developmental VPA exposure typically led to the altered expression of genes related to nervous system development (Msx1, Xcl1, Foxj1, Prdm16, C3, and Kif11) in the hippocampus, and those related to nervous system development (Neurod1) and gliogenesis (Notch1 and Sox9) in the corpus callosum. Postpubertal VPA exposure led to the altered expression of genes related to neuronal differentiation and projection (Cd47, Cyr61, Dbi, Adamts1, and Btg2) in multiple brain regions. These findings suggested that neurotoxic patterns of VPA might be different between developmental and postpubertal exposure, which was consistent with our previous study. Of note, the hippocampal dentate gyrus might be a sensitive target of developmental neurotoxicants after puberty.

Background Although Chlamydophila pneumoniae (CP) is known to play a role in atherosclerosis and endothelial injury, its effect on the clinical course of coronavirus disease 2019 (COVID-19), which was also reported to be a vascular disease, remains unknown. Methods In this retrospective cohort study, we examined 76 COVID-19 patients and 44 bacterial pneumonia patients who visited a tertiary emergency center in Japan between April 1, 2021, and March 31, 2022. CP antibody levels, including IgM, IgG, and IgA, were measured. Results Among all patients, the CP IgA-positive rate was significantly associated with age (P = 0.002). Between the COVID-19 and non-COVID-19 groups, no difference in the positive rate for both CP IgG and IgA was observed (P = 1.00, and 0.51, respectively). However, in univariate analysis, age, proportion of males, and mortality were significantly higher in the IgA-positive group than in the IgA-negative group (60.35 vs. 76.33, P = 0.001; 59.6 vs. 95.2, P = 0.002; 11.5 vs. 33.3, P = 0.042, respectively). Age-adjusted and sex-adjusted logistic regression analyses revealed that IgA positivity was not significantly associated with higher mortality (odds ratio [OR], 0.36; 95% confidence interval [CI], 0.10–1.29; P = 0.12, and OR, 0.38; 95% CI, 0.11–1.30; P = 0.12, respectively). Conclusion Persistent infection with CP may be a contributing factor to the higher mortality of elderly male patients with COVID-19.

Neurofibromatosis type 1 (NF1) is not known to cause serious vascular complications. This report describes a 49-year-old man with NF1 who presented to our hospital in hemorrhagic shock due to vascular leakage within a neurofibroma tumor. Physicians should be aware that NF1 can cause a wide variety of vascular lesions.

We previously reported that exposure to α-glycosyl isoquercitrin (AGIQ) from the fetal stage to adulthood facilitated fear extinction learning in rats. The present study investigated the specific AGIQ exposure period sufficient for inducing this behavioral effect. Rats were dietarily exposed to 0.5% AGIQ from the postweaning stage to adulthood (PW-AGIQ), the fetal stage to postweaning stage (DEV-AGIQ), or the fetal stage to adulthood (WP-AGIQ). Fear memory, anxiety-like behavior, and object recognition memory were assessed during adulthood. Fear extinction learning was exclusively facilitated in the WP-AGIQ rats. Synaptic plasticity-related genes showed a similar pattern of constitutive expression changes in the hippocampal dentate gyrus and prelimbic medial prefrontal cortex (mPFC) between the DEV-AGIQ and WP-AGIQ rats. However, WP-AGIQ rats revealed more genes constitutively upregulated in the infralimbic mPFC and amygdala than DEV-AGIQ rats, as well as FOS-immunoreactive(+) neurons constitutively increased in the infralimbic cortex. Ninety minutes after the last fear extinction trial, many synaptic plasticity-related genes (encoding Ephs/Ephrins, glutamate receptors/transporters, and immediate-early gene proteins and their regulator, extracellular signal-regulated kinase 2 [ERK2]) were upregulated in the dentate gyrus and amygdala in WP-AGIQ rats. Additionally, WP-AGIQ rats exhibited increased phosphorylated ERK1/2+ neurons in both the prelimbic and infralimbic cortices. These results suggest that AGIQ exposure from the fetal stage to adulthood is necessary for facilitating fear extinction learning. Furthermore, constitutive and learning-dependent upregulation of synaptic plasticity-related genes/molecules may be differentially involved in brain regions that regulate fear memory. Thus, new learning-related neural circuits for facilitating fear extinction can be established in the mPFC.

We previously found downregulation of low-density lipoprotein receptor class A domain-containing protein 4 (LDLRAD4), a negative regulator of transforming growth factor (TGF)-β signaling, in glutathione S-transferase placental form (GST-P) expressing (+ ) pre-neoplastic lesions produced by treatment with nongenotoxic hepatocarcinogens for up to 90 days in rats. Here, we investigated the relationship between LDLRAD4 downregulation and TGFβ signaling in nongenotoxic hepatocarcinogenesis. The transcripts of Tgfb and Hb-egf increased after ≥28 days of treatment. After 84 or 90 days, Snai1 increased transcripts and the subpopulation of GST-P+ foci downregulating LDLRAD4 co-expressed TGFβ1, phosphorylated EGFR, or phosphorylated AKT2, and downregulated PTEN, showing higher incidences than those in GST-P+ foci expressing LDLRAD4. The subpopulation of GST-P+ foci downregulating LDLRAD4 also co-expressed caveolin-1 or TACE/ADAM17, suggesting that disruptive activation of TGFβ signaling through a loss of LDLRAD4 enhances EGFR and PTEN/AKT-dependent pathways via caveolin-1-dependent activation of TACE/ADAM17 during nongenotoxic hepatocarcinogenesis. The numbers of c-MYC+ cells and PCNA+ cells were higher in LDLRAD4-downregulated GST-P+ foci than in LDLRAD4-expressing GST-P+ foci, suggesting a preferential proliferation of pre-neoplastic cells by LDLRAD4 downregulation. Nongenotoxic hepatocarcinogens markedly downregulated Nox4 after 28 days and later decreased cleaved caspase 3+ cells in LDLRAD4-downregulated GST-P+ foci, suggesting an attenuation of apoptosis by LDLRAD4 downregulation through activation of the EGFR pathway. At the late hepatocarcinogenesis stage in a two-stage model, LDLRAD4 downregulation was higher in adenoma and carcinoma than in pre-neoplastic cell foci, suggesting a role of LDLRAD4 downregulation in tumor development. Our results suggest that nongenotoxic hepatocarcinogens cause disruptive activation of TGFβ signaling through downregulating LDLRAD4 toward carcinogenesis in the rat liver.

Review question What is the most preferable insertion cite ofcentral venous catheter for reducing infectious, thrombotic and mechanical complications in critically ill adult patients? Searches We will search for the eligible trials in the following databases: 1. MEDLINE via PubMed; 2. The Cochrane Central Register of Controlled Trials (CENTRAL); 3. Web of science; 4. Ichushi, a database of papers in the Japanese language; 5.Clinicaltrials.gov; 6. WHO ICTRP. Types of study to be included We will accept randomized controlled trials of publication status published. The language and the country in which the studies were conducted are not restricted. Randomized crossover trials, cluster randomized trials and quasi-experiment trials will be excluded. Condition or domain being studied Secure and reliable venous access is a cornerstone in the care of hospitalized adult patients, as well as for a variety of outpatient situations. Central venous catheter, which is inserted into deep vein, a key component of this practice. However, there are different complications among insertion sites, including jugular, subclavian, femoral, and peripheral vein. It is unclear which site is the most acceptable for central venous catheter considering various complications in hospitalized patients. It is important for clinicians to estimate the risk of complication, and for manager decreasing complication may be associated with a reduction in health care cost. Participants/population Inclusion We will include hospitalized patients aged 18 years or older who are inserted central venous access using maximal sterile barrier precautions Exclusion 1)Coated catheter（e.g., antimicrobial- impregnated, chlorhexidine/silver sulfadiazine, heparin） 2)Tunneled catheter Venous access port Catheter exchange over guidewire Intervention(s), exposure(s) Internal jugular: Any insertion techniques, any antiseptics and any number of lumenswill beacceptable. Subclavian: Any insertion techniques, any antiseptics and any number of lumens will be acceptable. Femoral: Any insertion techniques, any antiseptics and any number of lumens will be acceptable. Peripherally: The catheter is inserted peripherally, and the tip is placed in central venous. Any insertion techniques, any antiseptics and any number of lumens will be acceptable. If comparingcentral venous catheterwith peripherally insertedcentral venous catheter, we will adopt the most indwelling site, as an insertion site. Comparator(s)/control All above mentioned intervention can be controls. Main outcomes Clinically important infectious complication, which is related with catheter insertion and with systemic symptoms (e.g., sepsis, blood stream infection) Clinically important thrombotic complication with clinical symptoms or which requires treatment Clinically important mechanical complication, which requires procedures or careful observation (e.g., pneumothorax, hemothorax, hematoma, and bleeding) * Measures of effect The number of each outcome and total participant in group to calculate Relative Risk Additional outcome(s) None Data extraction (selection and coding) We will use machine learning algorithms for systematic reviews (high‐sensitivity strategies) to identify RCTs (https://robotsearch.vortext.systems/#).Two of four physicians (HO, SY, SN, KK) will screen the title and abstract at the first screening and the full text at the second screening for relevant studies and will independently extract data from included studies into standardized data recording forms. Disagreements will be resolved by discussion with one of three physicians who did not screen the study. We will ask the original author as necessary. If the study has only abstract and we do not evaluate whether they will meet our review criteria, we will attempt to contact the authors. If there is a discrepancy between the two reviewers, they will be discussed and solved by themselves. Discrepancy will be resolved by discussing with the third reviewer as necessary. We will extract the following study characteristics. We extracted the following study characteristics: Methods: study design, total study duration, number and locations of study centres, study setting, withdrawals, date of study initiation, and funding sources. Participants: number, age, sex, body mass index (BMI), setting, and inclusion/exclusion criteria. Interventions: insertion site, catheter type, duration of catheter placement, operator experience, antiseptic, dressing, and insertion technique. Outcomes: outcomes that were specified and collected and the timepoints reported. One review author (HO) will copy the data from the data collection form into the Review Manager 5 file. Risk of bias (quality) assessment We will assess the risk of bias of primary outcomes in included studies independently by two of four review authors (HO, SY, SN, KK) using Cochrane Risk of Bias tool 2.0 with respect to the following eight domains: (a) random sequence generation, (b) allocation concealment, (c) blinding of participants and personnel, (d) blinding of outcome assessors, (e) incomplete outcome data, (f) selective outcome reporting and (g) other sources of bias. Each bias will be graded as either ‘low-risk’, ‘unclear-risk’ or ‘high-risk’. The risk of bias of secondary outcomes in included studies will be assessed using Cochrane Risk of Bias tool 2.0 with respect to the following six domains: (a) Bias arising from the randomization process, (b) Bias due to deviations from intended interventions, (c) Bias due to missing outcome data, (d) Bias in measurement of the outcome, (e) Bias in selection of the reported result, (f) Overall risk of bias. If there is a discrepancy between the two reviewers, they will be discussed and solved by themselves. Discrepancy will be resolved by discussing with the third reviewer as necessary. Each domain will be evaluated in one of three categories: High risk, Low risk, Some concerns. Strategy for data synthesis Give the planned general approach to be used. Where appropriate a brief outline of analytic approach should be given. Data synthesis: Forest plots will be used for the meta-analysis, and effect size will be expressed as relative risk with 95% confidence interval for categorical data and as weighted mean differences with 95% CI for continuous data. Outcome measures will be pooled using a random effect model to take into account study-specific effects in measures. For all analyses, a two-sided p-value < 0.05 is considered significant. We will synthesize the data using Revman 5.3 (RevMan 2014) for pairwise meta-analysis. Assessment of heterogeneity: Study heterogeneity between trials for each outcome will be assessed by visual inspection of the forest plots and with an I² statistic for quantifying inconsistency (RevMan) (I squared values of 0% to 40%: might not be important; 30% to 60%: may represent moderate heterogeneity; 50% to 90%: may represent substantial heterogeneity; 75% to 100%: considerable heterogeneity). When heterogeneity is identified (I² statistic> 50%), we will investigate the reason. We will quantify it by the χ² test. Network meta-analysis will be performed by a frequentist-based approach with multivariate random effects meta-analysis. Inconsistency of the network model was estimated by using inconsistency factors and their uncertainty. In addition, ranking plots (rankograms) were constructed using the probability that a given treatment had the highest event rate for each outcome. The surface under the cumulative ranking curve (SUCRA), which is a simple transformation of the mean rank, was used to set the hierarchy of the treatments. We will assess the certainty of evidence by using the GRADE Working Group Approach for a network meta-analysis. Analysis of subgroups or subsets If data from the studies are sufficient, we will conduct the following subgroup analyses in order to investigate the impact of bias risk and assess the participants' heterogeneity in each study. Excluding studies comparing central venous catheters inserted in multiple sites withperipherally insertedcentral venous catheter Only for critically ill patients In addition, we will perform post-hoc sensitivity analyses to explore the sources of significant incoherence that were present for the primary outcomes, if necessary. Contact details for further information Masaaki Sakuraya masaaki.sakuraya@gmail.com Organizational affiliation of the review JA Hiroshima General Hospital, Jigozen 1-3-3, Hatsukaichi-city, Hiroshima, 738-8503, Japan Review team members and their organizational affiliations Dr. Masaaki Sakuraya Dr. Hiromu Okano Dr. Shodai Yoshihiro Dr. Niida Shoko Dr. Keina Kimura Funding sources/sponsors Not applicable. Conflicts of interest None known. Language No restriction. Country Japan

Polyinosinic-polycytidylic acid (PIC) provides a model of developmental neuropathy by inducing maternal immune activation. We investigated the effects of an antioxidant, alpha-glycosyl isoquercitrin (AGIQ), on PIC-induced developmental neuropathy in rats, focusing on postnatal hippocampal neurogenesis. On gestational day 15, PIC at 4 mg/kg body weight was administered to dams intravenously. AGIQ either at 0.25% or 0.5% was administered through the diet to dams from gestational day 10 until weaning on day 21 post-delivery and, thereafter, to offspring until postnatal day 77 (adult stage). At weaning, the numbers of TBR2

We encountered a case of cutaneous squamous cell carcinoma (SCC) in a 17-year-old female koala at a zoo. A fragile, papillary, elevated mass was found on the third digit of the right hind limb. SCC was identified histopathologically: squamous cell-like polygonal tumor cells showed a nest-like growth pattern with epidermal down growth, central keratinization and necrotic foci, and invaded dermal connective tissues. Metastatic lesions were observed in various organs, including the lung and axillary lymph node: in the lung, multiple metastatic foci similar to the primary lesion, and in the axillary lymph node, individual polygonal tumor cells infiltrated the sinusoids. Immunohistochemistry revealed that the tumor cells were positive for proliferating cell nuclear antigen, which exhibited 32-33% of labeling indices in the tumor cells. To our knowledge, this is the first report of a case of SCC in a digit of a koala.

Increasing evidence indicates that glyphosate (GlyP)-based herbicides (GBHs) induce developmental neurotoxicity. The present study investigated the developmental exposure effect of GlyP and GBH on hippocampal neurogenesis in rats. Dams were treated from gestational day 6 to day 21 post-delivery on weaning with a diet containing 1.5% or 3.0% GlyP or drinking water with 1.0% GBH (containing 0.36% GlyP). Dams in the 1.5%-GlyP, 3.0%-GlyP, and GBH groups received 1.04, 2.16, and 0.25 g GlyP/kg body weight (BW)/day during gestation, and 2.27, 4.65, and 0.58 g GlyP/kg BW/day during lactation, respectively. On weaning, 3.0% GlyP- and GBH-exposed offspring decreased the BW, and the latter also decreased the brain weight. Both compounds suppressed neural progenitor cell proliferation in the neurogenic niche, and GlyP-exposed offspring showed a decreased number of TUBB3

Background: Although non-invasive respiratory managements are preformed to avoid intubation, patients with de novo acute hypoxaemic respiratory failure (AHRF) are high risk for treatment failure. Choosing the most effective primary respiratory management for adults with de novo AHRF is a complex problem. In the previous meta-analyses, the effect of non-invasive ventilation was not sufficiently evaluated according to ventilation modes in patients with AHRF. Furthermore, no meta-analyses comparing non-invasive respiratory managements with invasive mechanical ventilation (IMV) have been reported. We performed a network meta-analysis to compare the efficacy of non-invasive ventilation according to ventilation modes with high-flow nasal oxygen (HFNO), standard oxygen therapy (SOT), and IMV in adult patients with AHRF.Methods: The Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, and Ichushi databases were searched. Studies including adults with AHRF and randomised controlled trials comparing two different respiratory managements (continuous positive airway pressure [CPAP], pressure support ventilation [PSV], HFNO, SOT, or IMV) were reviewed. A network meta-analysis was performed via a frequentist approach with a multivariate random-effects meta-analysis. The certainty of evidence was assessed based on the Grades of Recommendation, Assessment, Development and Evaluation Working Group approach. The primary outcome was short-term mortality.Results: Using SOT as the reference, CPAP (risk ratio [RR], 0.55; 95% confidence interval [CI], 0.31–0.95; very low certainty) was significantly associated with a lower risk of mortality. Compared with SOT, PSV (RR, 0.81; 95% CI, 0.62–1.06; low certainty) and HFNO (RR, 0.90; 95% CI, 0.65–1.25; very low certainty) were not associated with a significantly lower risk of mortality. Compared with IMV, no non-invasive respiratory management was associated with a significantly lower risk of mortality, although all certainties of evidence were very low. The probability of being best in reducing short-term mortality among all possible interventions was higher for CPAP, followed by PSV and HFNO; IMV and SOT were tied for the worst.Conclusions: Our findings imply that CPAP may be the most effective strategy as the primary non-invasive respiratory management for AHRF to avoid unnecessary pressure support. Trial registration: protocols.io (Protocol integer ID 49375, April 23, 2021). dx.doi.org/10.17504/protocols.io.buf7ntrn.

Background Although non-invasive respiratory management strategies have been implemented to avoid intubation, patients with de novo acute hypoxaemic respiratory failure (AHRF) are high risk of treatment failure. In the previous meta-analyses, the effect of non-invasive ventilation was not evaluated according to ventilation modes in those patients. Furthermore, no meta-analyses comparing non-invasive respiratory management strategies with invasive mechanical ventilation (IMV) have been reported. We performed a network meta-analysis to compare the efficacy of non-invasive ventilation according to ventilation modes with high-flow nasal oxygen (HFNO), standard oxygen therapy (SOT), and IMV in adult patients with AHRF. Methods The Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, and Ichushi databases were searched. Studies including adults with AHRF and randomized controlled trials (RCTs) comparing two different respiratory management strategies (continuous positive airway pressure (CPAP), pressure support ventilation (PSV), HFNO, SOT, or IMV) were reviewed. Results We included 25 RCTs (3,302 participants: 27 comparisons). Using SOT as the reference, CPAP (risk ratio [RR] 0.55; 95% confidence interval [CI] 0.31–0.95; very low certainty) was associated significantly with a lower risk of mortality. Compared with SOT, PSV (RR 0.81; 95% CI 0.62–1.06; low certainty) and HFNO (RR 0.90; 95% CI 0.65–1.25; very low certainty) were not associated with a significantly lower risk of mortality. Compared with IMV, no non-invasive respiratory management was associated with a significantly lower risk of mortality, although all certainties of evidence were very low. The probability of being best in reducing short-term mortality among all possible interventions was higher for CPAP, followed by PSV and HFNO; IMV and SOT were tied for the worst (surface under the cumulative ranking curve value: 93.2, 65.0, 44.1, 23.9, and 23.9, respectively). Conclusions When performing non-invasive ventilation among patients with de novo AHRF, it is important to avoid excessive tidal volume and lung injury. Although pressure support is needed for some of these patients, it should be applied with caution because this may lead to excessive tidal volume and lung injury. Trial registration protocols.io (Protocol integer ID 49375, April 23, 2021). https://doi.org/10.17504/protocols.io.buf7ntrn.

The present study investigated the role of neuroinflammation and brain oxidative stress induced by neonatal treatment with lipopolysaccharides (LPS) on the development of autism spectrum disorder (ASD)-like behaviors and disruptive hippocampal neurogenesis in rats by exploring the chemopreventive effects of alpha-glycosyl isoquercitrin (AGIQ) as an antioxidant. AGIQ was dietary administered to dams at 0.25% or 0.5% (w/w) from gestational day 18 until postnatal day (PND) 21 on weaning and then to pups until the adult stage on PND 77. The pups were intraperitoneally injected with LPS (1 mg/kg body weight) on PND 3. At PND 6, LPS alone increased Iba1

Background COVID‐19 pneumonia has lesions with a decreased blood flow. Dual‐energy computed tomography is suitable to elucidate the pathogenesis of COVID‐19 pneumonia because it highlights the blood flow changes in organs. We report the dual‐energy computed tomography findings of a successfully treated case of COVID‐19 pneumonia. Case Presentation An obese 49‐year‐old man with COVID‐19 pneumonia was transferred from another hospital on day 11 after onset of illness. Although he was hypoxemic (PaO2/FiO2 = 100), tracheal intubation was not performed after anticipating difficulty in weaning from mechanical ventilation. Prone position therapy and nasal high flow therapy were administered, and the patient was discharged after his condition improved. Dual‐energy computed tomography was performed three times during hospitalization, and it revealed improvement in the blood flow defect, unlike plain computed tomography that did not show much improvement. Conclusion Dual‐energy computed tomography can assess perfusion in COVID‐19 pneumonia in real time and may be able to predict its severity., Dual‐energy computed tomography (DECT) is suitable to elucidate the pathogenesis of COVID‐19 pneumonia because it highlights the blood flow changes in organs. DECT can assess perfusion in COVID‐19 pneumonia in real time and may be able to predict its severity.