Bronchial asthma is a kind of heterogeneous respiratory disease, and its emergency diagnosis and treatment face multiple challenges. This article, based on the evolution of domestic and international guidelines and consensus, explores the current confusions and shortcomings in the emergency treatment of asthma, considering the clinical specifics of emergency medicine. Due to the limited applicability of classifications such as "refractory asthma" and "severe asthma" in emergency settings, as well as the complex diagnostic process that makes clinical operations difficult, it is proposed to unify the diagnostic terminology as "acute exacerbation of bronchial asthma" (mild, moderate, severe, critical severe) in emergency work. Assessment indicators, such as arterial oxygen partial pressure (PaO₂), partial pressure of arterial carbon dioxide (PaCO₂), arterial oxygen saturation (SaO₂), peak expiratory flow (PEF). Simplified were simplified. The clinical diagnosis and emergency management should prioritize the approach outlined in the Chinese guidelines for the prevention and treatment of bronchial asthma (basic version). For mild-to-moderate and severe exacerbations, a tiered treatment strategy is recommended, focusing on rapid symptom relief, standardized glucocorticoid use, and dynamic efficacy assessment. Additionally, the urgent need for formulating a Chinese expert consensus on emergency diagnosis and treatment of bronchial asthma is highlighted, along with promoting multicenter prospective studies to optimize emergency protocols and improve patient prognosis.
Humans ; Asthma/therapy* ; Practice Guidelines as Topic

Objective:This study aimed to investigate the role of bone morphogenetic protein 2 (BMP2)/Smad8 signaling pathway in T-2 toxin-induced apoptosis of rat articular chondrocytes.Methods:Primary chondrocytes from SD rats were cultured in vitro and exposed to varying concentrations of T-2 toxin (0.00, 0.32, 1.60, 8.00 ng/ml). The changes in chondrocytes survival rate were determined by CCK8, and the apoptosis changes of chondrocytes were determined by TUNEL assay kit. Using a group design, chondrocytes were cultured in complete culture media and culture media containing T-2 toxin (1.60 ng/ml), BMP2 cytokine (500 ng/ml), or T-2 toxin (1.60 ng/ml) + BMP2 cytokine (500 ng/ml), referred to as the control group, T-2 toxin group, BMP2 group, and T-2 toxin + BMP2 group, respectively. The survival rate and apoptosis changes of chondrocytes in each group were determined. The expression levels of Caspase-3, BMP2, BMP receptor Ⅱ (BMP-R Ⅱ), and Smad1/4/5/8 were determined by quantitative real-time PCR. Results:Compared with the 0.00 ng/ml of T-2 toxin group [(100.00 ± 0.00)%, (4.33 ± 0.32)%], the chondrocyte survival rates [(85.77 ± 2.96)%, (72.79 ± 2.31)%, (48.87 ± 1.83)%] of the 0.32, 1.60, and 8.00 ng/ml of T-2 toxin groups were significantly lower ( P < 0.05), and the apoptosis rates [(5.43 ± 0.32)%, (6.17 ± 0.15)%, (5.07 ± 0.13)%] were significantly higher ( P < 0.05). Compared with the control group, the T-2 toxin group had a lower survival rate and a higher apoptosis rate of chondrocytes ( P < 0.05). Compared with the T-2 toxin group, the T-2 toxin + BMP2 group had a higher survival rate and lower apoptosis rate of chondrocytes ( P < 0.05). Compared with the control group, the T-2 toxin group showed higher expression level of Caspase-3 mRNA in chondrocytes, while the expression levels of BMP2, BMP-R Ⅱ, and Smad1/4/8 mRNA were lower ( P < 0.05). Compared with the T-2 toxin group, the expression level of Caspase-3 mRNA was lower in the T-2 toxin + BMP2 group, while the expression levels of BMP2 and Smad8 mRNA were higher ( P < 0.05). Conclusion:BMP2 may partially block the apoptosis of chondrocytes caused by T-2 toxin by regulating the BMP2/Smad8 signaling pathway.

In 2024, the European Society of Intensive Care Medicine published the end- of- life and palliative care in the Intensive Care Unit. This paper interpreted the key recommendations of the guideline, aiming to provide the latest evidence-based basis for medical and nursing staff, to inform the smooth development of hospice and palliative care practices in ICU in China, and to promote the progressive integration of intensive care and hospice and palliative care.

Objective:This study aimed to investigate the role of bone morphogenetic protein 2 (BMP2)/Smad8 signaling pathway in T-2 toxin-induced apoptosis of rat articular chondrocytes.Methods:Primary chondrocytes from SD rats were cultured in vitro and exposed to varying concentrations of T-2 toxin (0.00, 0.32, 1.60, 8.00 ng/ml). The changes in chondrocytes survival rate were determined by CCK8, and the apoptosis changes of chondrocytes were determined by TUNEL assay kit. Using a group design, chondrocytes were cultured in complete culture media and culture media containing T-2 toxin (1.60 ng/ml), BMP2 cytokine (500 ng/ml), or T-2 toxin (1.60 ng/ml) + BMP2 cytokine (500 ng/ml), referred to as the control group, T-2 toxin group, BMP2 group, and T-2 toxin + BMP2 group, respectively. The survival rate and apoptosis changes of chondrocytes in each group were determined. The expression levels of Caspase-3, BMP2, BMP receptor Ⅱ (BMP-R Ⅱ), and Smad1/4/5/8 were determined by quantitative real-time PCR. Results:Compared with the 0.00 ng/ml of T-2 toxin group [(100.00 ± 0.00)%, (4.33 ± 0.32)%], the chondrocyte survival rates [(85.77 ± 2.96)%, (72.79 ± 2.31)%, (48.87 ± 1.83)%] of the 0.32, 1.60, and 8.00 ng/ml of T-2 toxin groups were significantly lower ( P < 0.05), and the apoptosis rates [(5.43 ± 0.32)%, (6.17 ± 0.15)%, (5.07 ± 0.13)%] were significantly higher ( P < 0.05). Compared with the control group, the T-2 toxin group had a lower survival rate and a higher apoptosis rate of chondrocytes ( P < 0.05). Compared with the T-2 toxin group, the T-2 toxin + BMP2 group had a higher survival rate and lower apoptosis rate of chondrocytes ( P < 0.05). Compared with the control group, the T-2 toxin group showed higher expression level of Caspase-3 mRNA in chondrocytes, while the expression levels of BMP2, BMP-R Ⅱ, and Smad1/4/8 mRNA were lower ( P < 0.05). Compared with the T-2 toxin group, the expression level of Caspase-3 mRNA was lower in the T-2 toxin + BMP2 group, while the expression levels of BMP2 and Smad8 mRNA were higher ( P < 0.05). Conclusion:BMP2 may partially block the apoptosis of chondrocytes caused by T-2 toxin by regulating the BMP2/Smad8 signaling pathway.

In 2024, the European Society of Intensive Care Medicine published the end- of- life and palliative care in the Intensive Care Unit. This paper interpreted the key recommendations of the guideline, aiming to provide the latest evidence-based basis for medical and nursing staff, to inform the smooth development of hospice and palliative care practices in ICU in China, and to promote the progressive integration of intensive care and hospice and palliative care.

Objective To investigate the association of neutrophil gelatinase-associated lipocalin(NGAL)and severity of coronary stenosis in patients with stable coronary artery disease(SCAD).Methods Totally 144 patients who underwent coronary angiography firstly due to suspected coronary artery disease were enrolled.The patients were divided into SCAD group(n=101)and non-CAD group(n=43),and the clinical data were compared.The SCAD group was fuether divided into three subgroups accoding to Gensini score:mild stenosis group(Gensini<16,n=32),moderate stenosis(16≤Gensini<30,n=33)and severe stenosis group(Gensini≥36,n=35).The clinical data of each group were compared.Odinal Logistic regression was used to analysis the influencing factors of severe stenosis.The receiver operating characteristic(ROC)curve was performed to evaluated the ability of NGAL in discriminating severe stenosis.Results Serum NGAL,high sensitive C-reactive protein(hs-CRP)level in SCAD group were higher than those in non-CAD group(P<0.01).Comparing with mild and moderate stenosis groups,NGAL and hs-CRP level were more higher in severe stenosis group(P<0.01).Multivariable Logistic regression analysis showed that NGAL and hs-CRP were independent risk factors for severe coronary stenosis(both P<0.05).Receiver operating characteristic(ROC)curve analysis showed that the areas under the curve of NGAL and hs-CRP were 0.771,0.702 respectively(both P<0.01).The difference between two AUCs was 0.069 which was insignificant(P>0.05).Conclusion Serum NGAL increased is closely associated with severe coronary stenosis in patients with SCAD,which has a certain ability of discriminating severity of coronary stenosis.

Ascites is the most common complication in patients with decompensated cirrhosis. This condition results in a severely impaired quality of life, excessive healthcare use, recurrent hospitalizations and significant morbidity and mortality. While loop diuretics and mineralocorticoid receptor antagonists are commonly employed for symptom relief, our understanding of their impact on survival remains limited. A comprehensive understanding of the underlying pathophysiological mechanism of ascites is crucial for its optimal management. The renin-angiotensin-aldosterone system (RAAS) is increasingly believed to play a pivotal role in the formation of cirrhotic ascites, as RAAS overactivation leads to a reduction in urine sodium excretion then a decrease in the ability of the kidneys to excrete water. In this review, the authors provide an overview of the pathogenesis of cirrhotic ascites, the challenges associated with current pharmacologic treatments, and the previous attempts to modulate the RAAS, followed by a description of some emerging targeted RAAS agents with the potential to be used to treat ascites.

Objective To investigate the cause of a suspected outbreak of carbapenem-resistant Klebsiella pneumoniae infection(CRKP)in the neurological ICU,to find out the reason for infection and the way of transmission to provide evidence for the prevention and control of nosocomial infection.Methods Four patients with CRKP infection in the department of neurological ICU of a hospital from Au-gust 4 to August 20,2020 were investigated epidemiologically and environmental hygiene monitoring of the ward was carried out.Compre-hensive measures were taken to control the outbreak.Results All four CRKP infection cases were hospital-acquired,and the isolated strains showed consistent drug susceptibility test results,indicating they were the same clone.Environmental hygiene monitoring revealed the presence of the same clone in samples from patient bedside items,suction devices,oxygen therapy equipment,and personal belongings of healthcare workers.After implementing comprehensive corrective measures,no new cases of CRKP infection occurred,and subsequent surface sampling did not isolate any CRKP strains.Conclusion Environmental surface contamination in the neurointensive care unit and inadequate disinfection procedures were likely the main causes of the suspected outbreak of CRKP infection.Prompt identification of the outbreak,activation of emergency response plans,and implementation of corrective measures are crucial for controlling the outbreak of multidrug-resistant bacterial infections in hospitals.After adopting comprehensive measures,there were no new CRKP infection cases.

Objective:To explore the effect of chronic intermittent hypoxia(CIH)on learning and memory dysfunc-tion in rats,as well as the expression of high mobility group box-1(HMGB1)and nuclear transcription factor-KB(NF-κB)in the hippocampus region.Methods:The CIH rat model was established,and forty SD rats were randomly divid-ed into four groups:normoxia group,hypoxia for 4 weeks group(CIH4 group),hypoxia for 8 weeks group(CIH8 group),and hypoxia for 12 weeks group(CIH12 group).Morris water maze was used to assess the learning memory ability of rats,and immunohistochemistry and ELISA were used to detect the expression of HMGB1 and NF-κB in the hippocampus of rats.Results:Compared with the normoxia group,the CIH12 and CIH8 groups had longer escape la-tency,the number of crossing the platform and the residence time in the quadrant of the platform were significantly shortened,but there was no significant difference in the CIH4 group.Additionally,there was no significant expression of HMGB1 and NF-κB in the hippocampal region of the normoxia group,but little expression was observed in CIH4 group,and significantly expressed in CIH8 group and CIH12 group,and the expression of CIH12 group was significantly higher than that of CIH8 group.Conclusion:CIH can lead to a decline in learning and memory function in rats,and the longer time of intermittent hypoxia led to the more significant effect on their learning and memory function.In addi-tion,CIH also leads to increased expression levels of HMGB1 and NF-κB in the hippocampus region,and the expres-sion increased more significantly after hypoxia for 12 weeks,comparing to hypoxia for 8 weeks.

Objective:To investigate the role of m.4435A>G and YARS2 c.572G>T(p.G191V)mutations in the development of essential hypertension.Methods:A hypertensive patient with m.4435A>G and YARS2 p.G191V mutations was identified from previously collected mitochondrial genome and exon sequencing data.Clinical data were collected,and a molecular genetic study was conducted in the proband and his family members.Peripheral venous blood was collected,and immortalized lymphocyte lines constructed.The mitochondrial transfer RNA(tRNA),mitochondrial protein,adenosine triphosphate(ATP),mitochondrial membrane potential(MMP),and reactive oxygen species(ROS)in the constructed lymphocyte cell lines were measured.Results:Mitochondrial genome sequencing showed that all maternal members carried a highly conserved m.4435A>G mutation.The m.4435A>G mutation might affect the secondary structure and folding free energy of mitochondrial tRNA and change its stability,which may influence the anticodon ring structure.Compared with the control group,the cell lines carrying m.4435A>G and YARS2 p.G191V mutations had decreased mitochondrial tRNA homeostasis,mitochondrial protein expression,ATP production and MMP levels,as well as increased ROS levels(all P<0.05).Conclusion:The YARS2 p.G191V mutation aggravates the changes in mitochondrial translation and mitochondrial function caused by m.4435A>G through affecting the steady-state level of mitochondrial tRNA and further leads to cell dysfunction,indicating that YARS2 p.G191V and m.4435A>G mutations have a synergistic effect in this family and jointly participate in the occurrence and development of essential hypertension.