Charcot Elbow Joint as the Initial Symptom in Chiari Malformation with Syringomyelia

Zhou, Yuan; Zhu, Lin; Lin, Yingbin; Cheng, Huilin

doi:10.4103/0366-6999.171466

Cited by 8 publications

(5 citation statements)

References 3 publications

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“…In terms of age of death, most deaths occurred at 60 years old and above for both men and women, which is basically consistent with the results of other studies [4] . This is because they are more prone to functional decline and diseases.…”

Section: Discussionsupporting

confidence: 92%

“…In this study, we analyzed the characteristics of inpatient death cases in a tertiary hospital in Hubei Province from 2018 to 2022 by exploring the development of causes of death among inpatients, the distribution characteristics of several factors, the trend of disease spectrum and in-hospital mortality. We discovered the main factors that threaten the lives of patients, discovered the weak points in the management of dead patients, formulated disease prevention and control strategies hospitals, optimized the allocation of medical resources, and provided a scientific basis for determining the focus of medical work, so as to further improve the hospital's medical service quality and social service capabilities [4] .…”

Section: Introductionmentioning

confidence: 99%

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Analysis of Characteristics of Inpatient Death Records in a Tertiary Hospital in Hubei Province

Lihan Huang,

Yu Luo,

Yurui Wu

et al. 2023

ssr

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Objective: To study the distribution characteristics of in-hospital death cases, explore the composition characteristics of death disease spectrum, and provide reference for hospital management. Methods: The first page information of inpatient death medical records from 2018 to 2022 in a tertiary hospital in Hubei Province was collected, and the main diagnoses were classified according to the International Classification of Diseases, Tenth Revision (ICD-10) standard for the cause of death. The t test and x² test were used to statistically analyze the distribution characteristics of the death cases in terms of gender, age group, season, cause of death, and other factors. Results: From 2018 to 2022, the total mortality rate in our hospital was 0.38%, the overall male-to-female death ratio was 2.04:1, and the overall average age at death was 65.89 years old; 65.87 years old for males and 65.91 years old for females. Most of the dead patients were over 60 years old, with the mortality rate in is the highest during the winters being the highest. The disease with the highest mortality rate of was circulatory system diseases. Conclusion: The professional, technical, and nursing skills of medical institutions, should be improved to reduce the in-hospital mortality rate.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Analysis of Characteristics of Inpatient Death Records in a Tertiary Hospital in Hubei Province

Lihan Huang,

Yu Luo,

Yurui Wu

et al. 2023

ssr

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“…Immunofluorescence Staining Zhou et al (2015) described the procedure of immunofluorescence staining, and this was performed to clearly visualize the images. Prior to this, the brain sections were incubated overnight at 4 • C with rabbit anti-S100A8 antibody (1:200; Abcam, Cambridge, MA, United States).…”

Section: Enzyme-linked Immunosorbent Assaymentioning

confidence: 99%

S100A8 Promotes Inflammation via Toll-Like Receptor 4 After Experimental Traumatic Brain Injury

Zhao

et al. 2021

Front. Neurosci.

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IntroductionS100 calcium-binding protein A8 (S100A8) is also known as macrophage-related protein 8, which is involved in various pathological processes in the central nervous system post-traumatic brain injury (TBI), and plays a critical role in inducing inflammatory cytokines. Accumulating evidences have indicated that toll-like receptor 4 (TLR4) is considered to be involved in inflammatory responses post TBI. The present study was designed to analyze the hypothesis that S100A8 is the key molecule that induces inflammation via TLR4 in TBI.MethodsThe weight-drop TBI model was used and randomly implemented on mice that were categorized into six groups: Sham, NS, S100A8, S100A8+TAK-242, TBI, and TBI+TAK-242 groups. In the S100A8+TAK-242 and TBI+TAK-242 groups, at half an hour prior to the intracerebroventricular administration of S100A8 or TBI, mice were intraperitoneally treated with TAK-242 that acts as a selective antagonist and inhibitor of TLR4. Furthermore, the protein recombinant of S100A8 was injected into the lateral ventricle of the brain of mice in the S100A8 and S100A8+TAK-242 groups. Sterile normal saline was injected into the lateral ventricle in the NS group. To evaluate the association between S100A8 and TLR4, Western blot, immunofluorescence, enzyme-linked immunosorbent assay (ELISA), and Nissl staining were employed. Simultaneously, the neurological score and brain water content were assessed. In the in vitro analysis, BV-2 microglial cells were stimulated with lipopolysaccharide LPS or S100A8 recombinant protein, with or without TAK-242. The expression of the related proteins was subsequently detected by Western blot or enzyme-linked immunosorbent assay.ResultsThe levels of S100A8 protein and pro-inflammatory cytokines were significantly elevated after TBI. There was a reduction in the neurological scores of non-TBI animals with remarkable severe brain edema after the intracerebroventricular administration of S100A8. Furthermore, the TLR4, p-p65, and myeloid differentiation factor 88 (MyD88) levels were elevated after the administration of S100A8 or TBI, which could be restored by TAK-242. Meanwhile, in the in vitro analysis, due to the stimulation of S100A8 or LPS, there was an upregulation of p-p65 and MyD88, which could also be suppressed by TAK-242.ConclusionThe present study demonstrated that the TLR4-MyD88 pathway was activated by S100A8, which is essential for the development of inflammation in the brain after TBI.

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“…BV-2 microglial cells were purchased from Cobioer BioScience Co., Ltd (Nanjing, China) and were cultured in Dulbecco's Modi ed Eagle Medium (DMEM) (Sigma-Aldrich, St. Louis, MO, USA) which contains 5% fetal bovine serum (FBS; Gibco, Grand Island, NY, USA) and 1% penicillin/streptomycin (pen/strep; Gibco, Grand Island, NY, USA); TAK-242 was added to the cells at the concentration of 10 nM just before the stimulation of S100A8 protein or LPS. Cells were treated with the S100A8 recombinant protein at nal concentrations of 0.5µ l/ml; LPS (Lipopolysaccharide, Sigma-Aldrich, St. Louis, MO, USA) was added to stimulate the BV-2 cell line at the nal concentration of 0.1 µg/mL according to the previous study [30].…”

Section: Bv-2 Microglial Cell Culturementioning

confidence: 99%

S100A8 Promotes Inflammation via Toll-Like Receptor 4 After Experimental Traumatic Brain Injury

Han

et al. 2020

Preprint

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Background: S100A8 is involved in the pathological processes of a variety of central nervous system(CNS) diseases related to inflammation including traumatic brain injury (TBI). However, the underlying mechanism for the induction of inflammation in the brain by S100A8 after TBI remains unclear, which was investigated in the present study.Methods: The weight-drop TBI model was used in this study. The mice were randomly assigned into 5 groups: the Sham, S100A8, S100A8 + TAK-242, TBI, and TBI + TAK-242 groups. In the S100A8 + TAK-242 and TBI + TAK-242 groups, mice were treated with TAK-242, an inhibitor of Toll-like receptor (TLR) 4, intraperitoneally at half an hour before TBI. In the S100A8 and S100A8 + TAK-242 groups, S100A8 recombinant protein was injected into the lateral ventricle of the brain. To explore the relationship between S100A8 and TLR4, Western Blot (WB), immunofluorescence, enzyme-linked immunosorbent assay (ELISA) and Nissl staining were employed. Neurological score and the brain water content were also assessed. Additionally, BV-2 microglial cells were stimulated with lipopolysaccharide (LPS) or S100A8 recombinant protein with/without TAK-242 in vitro. The expressions of the related proteins were subsequently detected with WB or ELISA.Results: The levels of S100A8 protein and pro-inflammatory cytokines were significantly increased after TBI. After intracerebroventricular administration of S100A8, the neurological scores of non-TBI animals were decreased remarkably with severe brain edema. Furthermore, the levels of TLR4, p-p65 and myeloid differentiation factor 88(MyD88) were all increased after S100A8 administration or TBI, which could be restored by TAK-242. Meanwhile, p-p65 and MyD88 were upregulated after S100A8 or LPS stimulation in vitro, which also could be suppressed by TAK-242.Conclusions: The present study demonstrated that TLR4-MyD88 pathway was activated by S100A8, which was essential to the development of inflammation in the brain after TBI.

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Charcot Elbow Joint as the Initial Symptom in Chiari Malformation with Syringomyelia

Cited by 8 publications

References 3 publications

Analysis of Characteristics of Inpatient Death Records in a Tertiary Hospital in Hubei Province

Analysis of Characteristics of Inpatient Death Records in a Tertiary Hospital in Hubei Province

S100A8 Promotes Inflammation via Toll-Like Receptor 4 After Experimental Traumatic Brain Injury

S100A8 Promotes Inflammation via Toll-Like Receptor 4 After Experimental Traumatic Brain Injury

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