During the outbreak of coronavirus disease 2019 (COVID-19), consistent and considerable differences in disease severity and mortality rate of patients treated in Hubei province compared to those in ...other parts of China have been observed. We sought to compare the clinical characteristics and outcomes of patients being treated inside and outside Hubei province, and explore the factors underlying these differences.
Collaborating with the National Health Commission, we established a retrospective cohort to study hospitalised COVID-19 cases in China. Clinical characteristics, the rate of severe events and deaths, and the time to critical illness (invasive ventilation or intensive care unit admission or death) were compared between patients within and outside Hubei. The impact of Wuhan-related exposure (a presumed key factor that drove the severe situation in Hubei, as Wuhan is the epicentre as well the administrative centre of Hubei province) and the duration between symptom onset and admission on prognosis were also determined.
At the data cut-off (31 January 2020), 1590 cases from 575 hospitals in 31 provincial administrative regions were collected (core cohort). The overall rate of severe cases and mortality was 16.0% and 3.2%, respectively. Patients in Hubei (predominantly with Wuhan-related exposure, 597 (92.3%) out of 647) were older (mean age 49.7
44.9 years), had more cases with comorbidity (32.9%
19.7%), higher symptomatic burden, abnormal radiologic manifestations and, especially, a longer waiting time between symptom onset and admission (5.7
4.5 days) compared with patients outside Hubei. Patients in Hubei (severe event rate 23.0%
11.1%, death rate 7.3%
0.3%, HR (95% CI) for critical illness 1.59 (1.05-2.41)) have a poorer prognosis compared with patients outside Hubei after adjusting for age and comorbidity. However, among patients outside Hubei, the duration from symptom onset to hospitalisation (mean 4.4
4.7 days) and prognosis (HR (95%) 0.84 (0.40-1.80)) were similar between patients with or without Wuhan-related exposure. In the overall population, the waiting time, but neither treated in Hubei nor Wuhan-related exposure, remained an independent prognostic factor (HR (95%) 1.05 (1.01-1.08)).
There were more severe cases and poorer outcomes for COVID-19 patients treated in Hubei, which might be attributed to the prolonged duration of symptom onset to hospitalisation in the epicentre. Future studies to determine the reason for delaying hospitalisation are warranted.
In this study, researchers describe the clinical characteristics of coronavirus disease 2019 in a selected cohort of 1099 patients with laboratory-confirmed disease throughout mainland China during ...the first 2 months of the current outbreak.
This study offers meta-analytic data on the potential association between epilepsy and depression especially for the prevalence of depression in epilepsy or vice versa.
The relevant studies were ...searched and identified from nine electronic databases. Studies that mentioned the prevalence and/or incidence of epilepsy and depression were included. Hand searches were also included. The search language was English and the search time was through May 2022. Where feasible, random-effects models were used to generate pooled estimates.
After screening electronic databases and other resources, 48 studies from 6,234 citations were included in this meta-analysis. The period prevalence of epilepsy ranged from 1% to 6% in patients with depression. In population-based settings, the pooled period prevalence of depression in patients with epilepsy was 27% (95% CI, 23-31) and 34% in clinical settings (95% CI, 30-39). Twenty studies reported that seizure frequency, low income, unemployment of the patients, perception of stigma, anxiety, being female, unmarried status, disease course, worse quality of life, higher disability scores, and focal-impaired awareness seizures were risk factors for depression.
Our study found that epilepsy was associated with an increased risk of depression. Depression was associated with the severity of epilepsy.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
This study aimed to explore the function of miR-24 in hypoxia/reoxygenation (H/R) -induced cardiomyocyte injury.We constructed a cardiomyocyte model of H/R using the primary cardiomyocytes isolated ...from Sprague-Dawley rats. To explore the role of miR-24, cells were transfected with a miR-24 mimic or miR-24 inhibitor. The RNA expression levels of miR-24 and Mapk14 were determined using qRT-PCR. The proliferation and apoptosis of cells were determined using a CCK8 assay and a flow cytometer. The TargetScan website was used to predict the targets of miR-24. A dual-luciferase reporter gene assay was conducted to verify whether Mapk14 is indeed a target of miR-24. A Western blot was applied for protein detection.H/R exposure decreased the expression of miR-24 in rat cardiomyocytes. Transfection of the miR-24 mimic into cardiomyocytes reduced H/R-induced injury as evidenced by an increase in proliferation and a decrease in the apoptotic rate. By contrast, transfection of the miR-24 inhibitor aggravated H/R-induced injury. The expression of Bcl-2 was increased while the levels of Bax and Active-caspase 3 were reduced in the H/R+miR-24 mimic group compared to those in the H/R group. H/R+miR-24 inhibitor group showed the opposite results. Mapk14 was identified as a target of miR-24. The mRNA level of Mapk14 and its protein (p38 MAPK) level were negatively affected by miR-24. Furthermore, we discovered that depletion of Mapk14 reduced the promoting effect of the miR-24 inhibitor on cell apoptosis.Overall, our results illustrated that miR-24 could attenuate H/R-induced injury partly by regulating Mapk14.
We examined gastric outlet obstruction (GOO) patients who received two weeks of strengthening pre-operative enteral nutrition therapy (pre-EN) through a nasal-jejenal feeding tube placed under a ...gastroscope to evaluate the feasibility and potential benefit of pre-EN compared to parenteral nutrition (PN). In this study, 68 patients confirmed to have GOO with upper-gastrointestinal contrast and who accepted the operation were randomized into an EN group and a PN group. The differences in nutritional status, immune function, post-operative complications, weight of patients, first bowel sound and first flatus time, pull tube time, length of hospital stay (LOH), and cost of hospitalization between pre-operation and post-operation were all recorded. Statistical analyses were performed using the chi square test and
-test; statistical significance was defined as
< 0.05. The success rate of the placement was 91.18% (three out of 31 cases). After pre-EN, the levels of weight, albumin (ALB), prealbumin (PA), and transferrin (TNF) in the EN group were significantly increased by pre-operation day compared to admission day, but were not significantly increased in the PN group; the weights in the EN group were significantly increased compared to the PN group by pre-operation day and day of discharge; total protein (TP), ALB, PA, and TNF of the EN group were significantly increased compared to the PN group on pre-operation and post-operative days one and three. The levels of CD3+, CD4+/CD8+, IgA, and IgM in the EN group were higher than those of the PN group at pre-operation and post-operation; the EN group had a significantly lower incidence of poor wound healing, peritoneal cavity infection, pneumonia, and a shorter first bowel sound time, first flatus time, and post-operation hospital stay than the PN group. Pre-EN through a nasal-jejunum feeding tube and placed under a gastroscope in GOO patients was safe, feasible, and beneficial to the nutrition status, immune function, and gastrointestinal function, and sped up recovery, while not increasing the cost of hospitalization.
Aims
The aim of this study was to determine FOXC1 expression in gastric tissues, and the clinical significance of FOXC1 in the development, progression and metastasis of gastric cancer (GC).
Methods ...and results
We screened GCs for the expression of FOXC1 using the Affymetrix U133 plus 2.0 Gene Chip Array, and found that expression was significantly higher in GC tissues than in controls. Furthermore, we validated the expression levels of FOXC1 using real‐time quantitative RT‐PCR (qRT‐PCR), and of FOXC1 using immunohistochemistry (IHC). Our study showed that expression levels of FOXC1 mRNA and FOXC1 in GC tissues were significantly higher than those in corresponding non‐tumour tissues. High FOXC1 expression correlated with the degree of histological differentiation (P < 0.01), TNM stage (P < 0.001), invasive depth (P < 0.05), lymph node metastasis (P < 0.05), and distant metastasis (P < 0.01). Survival analysis revealed that patients with high FOXC1 expression had shorter overall survival than those with low expression (P < 0.001). Multivariate analysis showed that high FOXC1 expression was an independent prognostic factor for GC patients (P < 0.01).
Conclusions
Overexpression of FOXC1 may play a key role in the progression of GC, and FOXC1 expression may serve as a useful marker for predicting the outcome of patients with GC.
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BFBNIB, DOBA, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, UILJ, UKNU, UL, UM, UPUK
To examine the expression of ALDOB in gastric cancer (GC) tissue and to reveal its potential clinicopathological and prognostic significance.
We screened for genes that were differentially expressed ...between GC and nontumor tissues using a microarray, specifically the Affymetrix U133 Plus 2.0 Array platform. We then verified the transcriptional and translational levels of ALDOB by performing quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC). In addition, a merged data set based on the Gene Expression Omnibus was generated and a survival analysis performed.
The microarray analysis revealed that
was downregulated (more than sevenfold) in GC compared with nontumor tissue. Both qRT-PCR and IHC validated the decrease of ALDOB in GC tissue. Moreover, we found that the expression of ALDOB was significantly related to tumor-invasion depth, lymph-node metastasis, distant metastasis, and TNM stage. The survival analysis, based on the IHC and merged data set, indicated that the overall survival was better in patients with high ALDOB expression. The Cox regression analysis showed that ALDOB expression was an independent prognostic factor for GC.
The expression of ALDOB in GC tissue was significantly related to the clinicopathological features and prognosis of the disease, thus suggesting that ALDOB could act as a novel molecular marker for GC.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Parkinson disease (PD) is an age-related neurodegenerative disease, which is associated with the loss of dopaminergic neurons (DA neurons) in the substantia nigra pars compacta (SNpc), and ...neuroinflammation may lead to the occurrence of PD. Wuzi Yanzong Pill (WYP) has demonstrated neuroprotective and anti-inflammatory properties, but its molecular mechanism of action is still unclear. In this study, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice and LPS-mediated BV2 microglia to explore WYP intervention, anti-inflammatory effect and molecular mechanism in vivo and in vitro. The results showed that oral administration of WYP in MPTP-induced PD mice for 2 weeks ameliorated abnormal motor dysfunction, attenuated the loss of TH + neurons in SNpc, protected dopaminergic neurons, and inhibited the activation of microglia in MPTP-induced PD mice and LPS-stimulated BV2 cell. Meanwhile, WYP intervention inhibited the expression of IL-6, TNF-α, Pro-IL-1β, IL-1β, Pro-IL-18, IL-18 and enhanced the expression of IL-10 in the SNpc of PD mice. Simultaneously, WYP intervention inhibited the expression of NLRP3 inflammasome, accompanied by the decrease of the TLR4/MyD88/NF-κB pathway. However, the exact target and interaction of WYP on NLRP3 inflammasome and TLR4/MyD88/NF-κB pathway still needs to be further investigated.
Highlights
WYP treatment increased the number of DA neurons in SNpc, improved the behavioral performance of MPTP-induced PD mice, and inhibited the activation of microglia and astrocytes.
WYP inhibits inflammatory factors in PD mice and BV2 cells.
WYP intervention inhibits NLRP3 inflammasome expression while decreasing TLR4/MyD88/NF-κB pathway.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Electroless Ni and Ni-P-B plating were conducted respectively on aromatic polysulfonamide (PSA) fibers following a new chlorine-aided silver activation system in the present work. Firstly, PSA fibers ...were treated in NaClO-HCl solution to impart chlorine to the surface area followed by immersion in AgNO3 solution to convert the chlorine to AgCl particles. After subsequent reduction of AgCl to metallic Ag seeds in NaBH4 solution, electroless Ni and Ni-P-B plating were performed respectively. These two kinds of adherent and continuous coatings activated and anchored by the silver seeds, which were both resistant against sonication, were deposited onto PSA fibers with different electrical, magnetic, electromagnetic shielding, and corrosion resistance properties. Both plated PSA fibers can act directly as electromagnetic interference shielding and static charge dissipation materials, or act as excellent base layers for other subsequent metallic coatings according to different requirements, and then show great potential applications in coaxial cables and wear protection for aerospace, aviation, microelectronics, military industry and telecommunications.
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•A chlorine-aided silver activation system is proposed to catalyze aromatic polysulfonamide fibers.•Electroless Ni and Ni-P-B alloy plating are designed and conducted, respectively.•The utilization of DMAB strongly promotes the activation capability of silver seeds and accelerates the plating process.•The obtained adherent Ni and Ni-P-B coatings have different morphologies, compositions, and structures.•The different performances of both coatings determine their different service conditions and application fields.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
It is well documented that statins protect atherosclerotic patients from inflammatory changes and plaque instability in coronary arteries. However, the underlying mechanisms are not fully understood. ...Using a previously established mouse model for vulnerable atherosclerotic plaque, we investigated the effect of atorvastatin (10 mg/kg/day) on plaque morphology. Atorvastatin did not lower plasma total cholesterol levels or affect plaque progression at this dosage; however, vulnerable plaque numbers were significantly reduced in the atorvastatin-treated group compared to control. Detailed examinations revealed that atorvastatin significantly decreased macrophage infiltration and subendothelial lipid deposition, reduced intimal collagen content, and elevated collagenase activity and expression of matrix metalloproteinases (MMPs). Because vascular inflammation is largely driven by changes in monocyte/macrophage numbers in the vessel wall, we speculated that the anti-inflammatory effect of atorvastatin may partially result from decreased monocyte recruitment to the endothelium. Further experiments showed that atorvastatin downregulated expression of the chemokines monocyte chemoattractant protein (MCP)-1, chemokine (C-X3-C motif) ligand 1 (CX3CL1) and their receptors CCR2 and, CX3CR1, which are mainly responsible for monocyte recruitment. In addition, levels of the plasma inflammatory markers C-reactive protein (CRP) and tumor necrosis factor (TNF)-α were also significantly decrease in atorvastatin-treated mice. Collectively, our results demonstrate that atorvastatin can improve plaque stability in mice independent of plasma cholesterol levels. Given the profound inhibition of macrophage infiltration into atherosclerotic plaques, we propose that statins may partly exert protective effects by modulating levels of chemokines and their receptors. These findings elucidate yet another atheroprotective mechanism of statins.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
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