ABSTRACT
Blood purification is one of the commonly used techniques for the rescue of critically ill patients, which is used for acute and chronic kidney injury caused by various causes and renal replacement therapy (RRT) for a variety of critical diseases. Its main working principle is to drain the human blood into a variety of dialyzers through the artificial tube, exchange substances through a variety of ways, and remove harmful substances and some metabolites from patients' body. Then the purified blood is transfused back to the body, so as to maintain the patient's internal environment relatively stable. At present, there are different models of hemodialysis machines in clinical practice, but they are bulky and unable to move, and the method of heat dissipation is single, which cannot meet the needs of hemodialysis treatment in transport patients. Therefore, the medical staff of the Second Affiliated Hospital of Zunyi Medical University designed and developed a hemodialysis machine, which is suitable for patients who demand hemodialysis treatment during transport, and obtained the National Invention Patent of China (ZL 2020 1 0864737.3). The hemodialysis machine comprises a main body of the hemodialysis machine and a mobile vehicle. The main body of the hemodialysis machine is placed in the bottom of the mobile vehicle, and a protective cylinder with fixed airbags is designed around the main body of the hemodialysis machine. The fixed airbag is connected to the air storage tank through the pipeline, the air storage tank is connected to the Venturi tube through the control valve, and the throat of the Venturi tube is connected to the disinfection tank and cooling water tank. The outlet end of the Venturi tube is connected with the cooling pipe inside the main part of the hemodialysis machine and the sprinkler head placed on the top of the main body. By adding a mobile vehicle and designing an airbag and protective cylinder, the hemodialysis machine can be applied to the hemodialysis treatment during the transportation of patients. By designing the heat dissipation pipe, the main body of the hemodialysis machine can be cooled, the temperature of the hemodialysis machine can be reduced, and the hemodialysis machine can still work when the fan is damaged. By designing the sprinkler head, it is convenient to automatically disinfect the main screen and control keys of the hemodialysis machine, reduce the risk of cross infection of medical staff in the operation, and increase the safety and practicability of the hemodialysis machine. The hemodialysis machine is convenient, safe and efficient, which can be widely used in the hemodialysis treatment during transported patient, and is worthy of clinical promotion.
Subject(s)
Equipment Design , Renal Dialysis , Transportation of Patients , Renal Dialysis/instrumentation , Renal Dialysis/methods , Humans , Transportation of Patients/methodsABSTRACT
This corrects the article published in European Journal of Histochemistry 2023;67:3535. doi: 10.4081/ejh.2023.3535.
ABSTRACT
Patients who are bedridden are for a long-time prone to develop bedsores, especially in the hip and sacral areas and limbs, which causes eczema, ulcers, infection and other complications, resulting in pain and more medical costs. Therefore, the medical staff of the Second Affiliated Hospital of Zunyi Medical University designed and developed a kind of anti-bedsore turning pad, and has obtained the national utility model patent (ZL 2021 2 3004923.9), which is suitable for various long-term bedridden patients. The anti-bedsore turning pad includes the center axis of the turning pad, and ventilation pad 1 and ventilation pad 2 designed on the left and right of turning pad center axis. Under the ventilation pad 1 and the ventilation pad 2, the air pad 1 and the air pad 2 are respectively designed. There is a bedspread connected with ventilation pad 1 and ventilation pad 2 on the inflatable pad 1 and the inflatable pad 2. Through the design of inflatable pad 1 and inflatable pad 2, the left and right of the anti-bedsore turning pad can be lowered or raised independently, which is convenient for the patient's body to tilt and turn over, and can significantly reduce the number of nursing staff and the burden of nursing staff when turning over. In addition, it is convenient to replace the force site at any time and reduce the occurrence of pressure ulcers caused by long-term pressure on the force site. Through the design of ventilation cushion 1 and ventilation cushion 2, the internal gas flow of the turning pad can be made, and the ventilation between the patient and the turning pad can be kept dry, so as to reduce the occurrence of eczema, ulcers or infection and other complications, and ultimately reduce the occurrence of bedsores. In addition, through the design of the most superficial limb pad, the patient's limb can be appropriately elevated or massaged, which increases the comfort of the patient. The anti-bedsore turning pad is simple and effective, and can be widely used in long-term bedridden patients.
Subject(s)
Eczema , Pressure Ulcer , Humans , Pressure Ulcer/epidemiology , Ulcer , Respiration , Risk FactorsABSTRACT
The mortality and morbidity rates of ovarian cancer (OC) are high, but the underlying mechanisms of OC have not been characterized. In this study, we determined the role of Rho GTPase Activating Protein 30 (ARHGAP30) in OC progression. We measured ARHGAP30 abundance in OC tissue samples and cells using immunohistochemistry (IHC) and RT-qPCR. EdU, transwell, and annexin V/PI apoptosis assays were used to evaluate proliferation, invasiveness, and apoptosis of OC cells, respectively. The results showed that ARHGAP30 was overexpressed in OC tissue samples and cells. Inhibition of ARHGAP30 suppressed growth and metastasis of OC cells, and enhanced apoptosis. Knockdown of ARHGAP30 in OC cells significantly inhibited the PI3K/AKT/mTOR pathway. Treatment with the PI3K/AKT/mTOR pathway inhibitor buparlisib simulated the effects of ARHGAP30 knockdown on growth, invasiveness, and apoptosis of OC cells. Following buparlisib treatment, the expression levels of p-PI3K, p-AKT, and p-mTOR were significantly decreased. Furthermore, buparlisib inhibited the effects of ARHGAP30 upregulation on OC cell growth and invasiveness. In conclusion, ARHGAP30 regulated the PI3K/AKT/mTOR pathway to promote progression of OC.
Subject(s)
Acute Lung Injury , Hyperoxia , Ovarian Neoplasms , RNA, Long Noncoding , Humans , Female , Signal Transduction , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , RNA, Long Noncoding/metabolism , Membrane Potential, Mitochondrial , TOR Serine-Threonine Kinases/metabolism , Apoptosis , Cell Line, Tumor , Cell Proliferation , Alveolar Epithelial Cells/metabolism , Ovarian Neoplasms/metabolismABSTRACT
Resumo Fundamento A cardiopatia isquêmica atraiu muito atenção devido às altas taxas de mortalidade, custos do tratamento e a crescente morbidade na população jovem. Estratégias de reperfusão reduziram a mortalidade. Porém, a reperfusão pode levar à morte do cardiomiócito e subsequente dano irreversível ao miocárdio. No momento, não há um tratamento eficiente e direcionado para a lesão de isquemia-reperfusão (I/R). Objetivos Avaliar se a dexmedetomidina (DEX) tem efeito protetivo na I/R do miocárdio e explorar os possíveis mecanismos por trás dela. Métodos Corações de ratos foram perfundidos com o sistema de perfusão de Langendorff e aleatoriamente distribuídos em cinco grupos: grupo controle, perfundido com solução de Krebs-Henseleit (K-H) por 205 minutos sem isquemia; e quatro grupos de teste que foram submetidos a 40 minutos de isquemia global e 120 minutos de reperfusão. O Grupo DEX, o grupo ioimbina (IO) e o grupo DEX + IO foram perfundidos com DEX (10 nM), IO (1 μM) ou a combinação de DEX e IO antes da reperfusão, respectivamente. A hemodinâmica cardíaca, o tamanho do infarto do miocárdio e a histologia do miocárdio foram avaliados. A expressão da proteína-78 regulada pela glicose (GRP78), a proteína quinase do retículo endoplasmático (PERK), a PERK fosforilada, o fator de iniciação eucariótico 2α (eIF2α), eIF2α fosforilado, o fator de transcrição 4 (TCF-4) e a proteína homóloga à proteína ligadora do acentuador CCAAT (CHOP) foram avaliados. P< 0,05 foi considerado para indicar a diferença estatisticamente significativa. Resultados O pré-condicionamento com DEX melhorou a função cardíaca nos corações com I/R, reduziu o infarto do miocárdio, a apoptose do miocárdio e a expressão de GRP78, p-PERK, eIF2α, p-eIF2α, TCF-4 e CHOP. Conclusões O pré-tratamento com DEX reduziu a lesão de I/R no miocárdio ao suprimir a apoptose, o que foi induzido pela via PERK.
Abstract Background Ischemic heart disease has attracted much attention due to its high mortality rates, treatment costs and the increasing morbidity in the young population. Strategies for reperfusion have reduced mortality. However, reperfusion can lead to cardiomyocyte death and subsequent irreversible myocardial damage. At present, the timely and targeted treatment of ischemia-reperfusion (I/R) injury is often lacking. Objectives To evaluate if dexmedetomidine (DEX) has a protective effect in myocardiual I/R and explore the possible mechanism behind it. Methods Rat hearts were perfused with a Langendorff perfusion system, and randomly assigned to five groups: control group, perfused with Krebs-Henseleit (K-H) solution for 205 minutes without ischemia; and four test groups that underwent 40 minutes of global ischemia and 120 min of reperfusion. The DEX group, the yohimbine (YOH) group and the DEX + YOH group were perfused with DEX (10 nM), YOH (1 μM) or the combination of DEX and YOH prior to reperfusion, respectively. Cardiac hemodynamics, myocardial infarct size, and myocardial histology were evaluated. The expression of glucose-related protein 78 (GRP78), protein kinase R-like ER kinase (PERK), phosphorylated PERK, eukaryotic initiation factor 2α (eIF2α), phosphorylated eIF2α, activating transcription factor 4 (ATF4), and CCAAT/enhancer-binding protein homologous protein (CHOP) were assessed. P<0.05 was considered to indicate a statistically significant difference. Results DEX preconditioning improved the cardiac function of I/R hearts, reduced myocardial infarction, myocardial apoptosis, and the expression of GRP78, p-PERK, eIF2α, p-eIF2α, ATF4 and CHOP. Conclusions DEX pretreatment reduced myocardial I/R injury by suppressing apoptosis, which was induced by the PERK pathway.
Subject(s)
Animals , Rats , Myocardial Reperfusion Injury/prevention & control , Reperfusion Injury , Myocardial Ischemia , Dexmedetomidine/pharmacology , Myocardial Infarction/prevention & control , Myocardial Infarction/drug therapy , Signal TransductionABSTRACT
BACKGROUND: Ischemic heart disease has attracted much attention due to its high mortality rates, treatment costs and the increasing morbidity in the young population. Strategies for reperfusion have reduced mortality. However, reperfusion can lead to cardiomyocyte death and subsequent irreversible myocardial damage. At present, the timely and targeted treatment of ischemia-reperfusion (I/R) injury is often lacking. OBJECTIVES: To evaluate if dexmedetomidine (DEX) has a protective effect in myocardiual I/R and explore the possible mechanism behind it. METHODS: Rat hearts were perfused with a Langendorff perfusion system, and randomly assigned to five groups: control group, perfused with Krebs-Henseleit (K-H) solution for 205 minutes without ischemia; and four test groups that underwent 40 minutes of global ischemia and 120 min of reperfusion. The DEX group, the yohimbine (YOH) group and the DEX + YOH group were perfused with DEX (10 nM), YOH (1 µM) or the combination of DEX and YOH prior to reperfusion, respectively. Cardiac hemodynamics, myocardial infarct size, and myocardial histology were evaluated. The expression of glucose-related protein 78 (GRP78), protein kinase R-like ER kinase (PERK), phosphorylated PERK, eukaryotic initiation factor 2α (eIF2α), phosphorylated eIF2α, activating transcription factor 4 (ATF4), and CCAAT/enhancer-binding protein homologous protein (CHOP) were assessed. P<0.05 was considered to indicate a statistically significant difference. RESULTS: DEX preconditioning improved the cardiac function of I/R hearts, reduced myocardial infarction, myocardial apoptosis, and the expression of GRP78, p-PERK, eIF2α, p-eIF2α, ATF4 and CHOP. CONCLUSIONS: DEX pretreatment reduced myocardial I/R injury by suppressing apoptosis, which was induced by the PERK pathway.
FUNDAMENTO: A cardiopatia isquêmica atraiu muito atenção devido às altas taxas de mortalidade, custos do tratamento e a crescente morbidade na população jovem. Estratégias de reperfusão reduziram a mortalidade. Porém, a reperfusão pode levar à morte do cardiomiócito e subsequente dano irreversível ao miocárdio. No momento, não há um tratamento eficiente e direcionado para a lesão de isquemia-reperfusão (I/R). OBJETIVOS: Avaliar se a dexmedetomidina (DEX) tem efeito protetivo na I/R do miocárdio e explorar os possíveis mecanismos por trás dela. MÉTODOS: Corações de ratos foram perfundidos com o sistema de perfusão de Langendorff e aleatoriamente distribuídos em cinco grupos: grupo controle, perfundido com solução de Krebs-Henseleit (K-H) por 205 minutos sem isquemia; e quatro grupos de teste que foram submetidos a 40 minutos de isquemia global e 120 minutos de reperfusão. O Grupo DEX, o grupo ioimbina (IO) e o grupo DEX + IO foram perfundidos com DEX (10 nM), IO (1 µM) ou a combinação de DEX e IO antes da reperfusão, respectivamente. A hemodinâmica cardíaca, o tamanho do infarto do miocárdio e a histologia do miocárdio foram avaliados. A expressão da proteína-78 regulada pela glicose (GRP78), a proteína quinase do retículo endoplasmático (PERK), a PERK fosforilada, o fator de iniciação eucariótico 2α (eIF2α), eIF2α fosforilado, o fator de transcrição 4 (TCF-4) e a proteína homóloga à proteína ligadora do acentuador CCAAT (CHOP) foram avaliados. P< 0,05 foi considerado para indicar a diferença estatisticamente significativa. RESULTADOS: O pré-condicionamento com DEX melhorou a função cardíaca nos corações com I/R, reduziu o infarto do miocárdio, a apoptose do miocárdio e a expressão de GRP78, p-PERK, eIF2α, p-eIF2α, TCF-4 e CHOP. CONCLUSÕES: O pré-tratamento com DEX reduziu a lesão de I/R no miocárdio ao suprimir a apoptose, o que foi induzido pela via PERK.
Subject(s)
Dexmedetomidine , Myocardial Infarction , Myocardial Ischemia , Myocardial Reperfusion Injury , Reperfusion Injury , Animals , Dexmedetomidine/pharmacology , Myocardial Infarction/drug therapy , Myocardial Infarction/prevention & control , Myocardial Reperfusion Injury/prevention & control , Rats , Signal TransductionABSTRACT
BACKGROUND: Severe sepsis, a major health problem worldwide, has become one of the leading causes of death in ICU patients. Further study on the pathogenesis and treatment of acute kidney injury (AKI) is of great significance to reduce high mortality rate of sepsis. In this study, the mechanism by which ubiquitin specific peptidase 10 (USP10) reduces sepsis-induced AKI was investigated. Ligation and perforation of cecum (CLP) was employed to establish C57BL/6 mouse models of sepsis. Hematoxylin-eosin (H&E) staining was performed to detect renal injury. The concentrations of serum creatinine (Cr), urea nitrogen (BUN) and cystatin C (Cys C) were determined using a QuantiChrom™ Urea Assay kit. RT-qPCR and western blot were conducted to assess the USP10 expression level. DHE staining was used to detect reactive oxygen species (ROS) levels. H2O2, MDA and SOD levels were assessed using corresponding colorimetric kits. Western blot was used to examine the expression levels of Bcl-2, Bax, cleaved caspase-3, Sirt6, Nrf2 and HO-1. MTT assay was used to determine cell viability, whereas TUNEL staining and flow cytometry were used to assess cell apoptosis. RESULTS: In this study, we found that USP10 was decreased in CLP-induced mouse renal tissues. We identified that USP10 alleviated renal dysfunction induced by CLP. Moreover, USP10 was found to reduce oxidative stress, and abated LPS-induced renal tubular epithelial cell injury and apoptosis. Finally, we discovered that USP10 promoted activation of the NRF2/HO-1 pathway through SIRT6 and attenuated LPS-induced renal tubular epithelial cell injury. CONCLUSIONS: This study found that USP10 activates the NRF2/ARE signaling through SIRT6. USP10 alleviates sepsis-induced renal dysfunction and reduces renal tubular epithelial cell apoptosis and oxidative stress.