Physician well-being is vital to delivering high-quality emergency care. A supported and healthy emergency medicine workforce leads to better patient outcomes, fewer medical errors, and greater job satisfaction and staff retention.[1,2] Emergency physicians (EPs) face unique pressures, including shift work, high patient volumes and acuities, overcrowding, and systemic inefficiencies that escalate their risk of burnout. As a result, EPs have reported the highest rates of burnout among physician specialties.[1,3] Over the past decade, multiple attempts have been made to promote EP well-being. However, early initiatives were oriented around individual “wellness”, such as exercise, diet, sleep, yoga, and finding “work-life balance”. Recently, there has been evolving recognition of the effects of a number of aspects of burnout that are outside the control of individual EPs, including administrative duties superseding clinical duties, diminishing resources and support, overcrowding and boarding, adverse working conditions, and medico-legal challenges. These factors progressively constrain the ability and capacity of EPs to do the work that they are trained and entrusted to do - rapidly and effectively evaluate, treat, and dispose of acutely ill patients. This sense of “moral injury” has contributed to growing dissatisfaction and premature departure from emergency medicine through reduced hours, transitions to other fields, early retirement, and, tragically, suicide.[4,5]

Objective To investigate the role of the endothelin-1/nitric oxide （ET-1/NO） system in neurological function and cerebral hemodynamics after interventional surgery for cerebral infarction， as well as the association of the levels of ET-1 and NO with neurological recovery and cerebral blood flow after surgery. Methods A total of 108 patients with cerebral infarction who were treated in our hospital from January 2022 to June 2023 were enrolled， and serum samples were collected before surgery and on day 30 after surgery. ELISA was used to measure the levels of ET-1 and NO；National Institutes of Health Stroke Scale（NIHSS） was used to assess neurological function； transcranial Doppler was used to measure cerebral hemodynamic parameters， including mean blood flow velocity， peak systolic velocity， and pulsatility index. A Spearman correlation analysis was used to investigate the correlation of ET-1 and NO with neurological function and cerebral hemodynamics，and the receiver operating characteristic （ROC） curve was used to assess the value of ET-1 and NO in predicting poor neurological function. Results After interventional surgery， there was a significant reduction in the level of ET-1 and a significant increase in the level of NO（both P<0.001）. The patients were divided into good recovery group （NIHSS≤5） and poor recovery group.Compared with the poor recovery group， the good recovery group had a significant reduction in serum ET-1 and a significant increase in serum NO （both P<0.001）. The Spearman correlation analysis showed that the serum level of ET-1 was negatively correlated with neurological recovery and the improvement in cerebral hemodynamics， while the level of NO was positively correlated with these two indicators. The ROC curve analysis showed that ET-1 and NO could effectively predict poor neurological recovery after interventional surgery， with an area under the ROC curve of 0.881 and 0.981，respectively. Conclusion The ET-1/NO system plays an important role in neurological function and cerebral hemodynamics after interventional surgery for cerebral infarction. Reducing ET-1 and increasing NO can facilitate the recovery of neurological function and cerebral blood flow after surgery. The levels of ET-1 and NO can be used as biomarkers for predicting poor postoperative neurological function and provide a scientific basis for optimizing postoperative treatment strategies.
Endothelin-1

Neurocritical care involves complex pathophysiological mechanisms, and its incidence is higher, injuries are more severe, and treatment is more challenging in high-altitude environments. This consensus, based on the latest domestic and international evidence-based medical data, establishes a standardized, goal-oriented framework for neurocritical care management applicable in high-altitude regions and nationwide. The consensus was developed following international standards for evidence quality assessment and underwent two rounds of Delphi expert consultation, resulting in 32 recommendation statements covering three parts: management systems, monitoring and assessment, and core strategies. Key updates include: advocating for the establishment of independent neurocritical care units and implementing precise tiered diagnosis and treatment based on the "Five Differences in Critical Care" concept; constructing a "trinity" multimodal brain monitoring system centered on cerebral blood flow, cerebral oxygenation, and brain function, emphasizing routine bedside transcranial Doppler ultrasound, cerebral oximetry, and continuous electroencephalography monitoring; shifting management strategies from mild hypothermia therapy to targeted temperature management, and defining the "446" target management pathway for the supercritical stage; emphasizing the assessment of static and dynamic cerebrovascular autoregulation functions through multimodal methods to achieve individualized optimal mean arterial pressure management; elevating cerebrospinal fluid management goals to the level of "glymphatic system" function maintenance; implementing a multidisciplinary collaborative, whole-process management model focusing on patients' long-term neurological functional outcomes; de-escalation criteria include multidimensional indicators such as recovery of brain structure, restoration of cerebrovascular autoregulation, improvement in cerebrospinal fluid dynamics, and reduction in biomarker levels; and integrating cutting-edge technologies like artificial intelligence into post-critical care management and rehabilitation planning. This consensus systematically integrates the entire process of neurocritical care management, reflecting the modern connotation of goal-oriented, dynamic, and multimodal integration in neurocritical care medicine. It aims to adapt to new trends such as deepening understanding of pathophysiological mechanisms, the integration of medicine and engineering, and the empowerment of artificial intelligence, thereby further advancing the discipline of critical care medicine.

ObjectiveTo observe the effect of Xiao Qinglongtang on ferroptosis in allergic rhinitis rats and explore its specific mechanism of action. MethodsSixty SD rats were randomly divided into a blank group， a model group， a loratadine group （0.9 mg·kg^-1）， and low-， medium-， and high-dose Xiao Qinglongtang groups （2.14， 4.28， and 8.56 g·kg^-1）， 10 rats per group. After 2 weeks of drug treatment， behavioral scores were observed in 6 groups of rats. Hematoxylin-eosin （HE） staining was used to observe changes in nasal mucosal tissue morphology， and Prussian blue staining was used to observe iron deposition. Enzyme-linked immunosorbent assay （ELISA） was used to detect reactive oxygen species （ROS）， Fe²⁺ ions， malondialdehyde （MDA）， superoxide dismutase （SOD）， and glutathione peroxidase （GSH） in each group. Immunofluorescence assay was used to detect ROS content and sirtuin 1 （SIRT1） expression in nasal mucosal tissue. Western blot was used to detect the expression of SIRT1， solute carrier family 7 member 11 （SLC7A11）， p53 acyl-CoA synthetase long-chain family member 4 （ACSL4）， and glutathione peroxidase 4 （GPX4） proteins in nasal mucosal tissue. ResultsCompared with the blank group， the model group exhibited obviously increased behavioral scores， severe nasal mucosal damage， obvious increase in iron deposition， significant decreases in GSH and SOD levels， obvious increases in MDA， Fe²⁺， and ROS fluorescence area proportions （P<0.05）， decreased protein expression levels of GPX4， SLC7A11， and SIRT1， and obvious increases in p53 and ACSL4 expression （P<0.05）. Compared with the model group， Xiao Qinglongtang groups of all doses showed reduced rat behavioral scores， obviously improved nasal mucosal damage， obviously reduced iron deposition （P<0.05）， obviously increased GSH and SOD levels， obviously reduced MDA， Fe²⁺， ROS fluorescence area proportions （P<0.05）， increased GPX4， SLC7A11， and SIRT1 protein expression levels， and obviously reduced p53 and ACSL4 （P<0.05）. ConclusionXiao Qinglongtang may achieve the goal of treating allergic rhinitis by regulating the SIRT1/SLC7A11 signaling pathway and inhibiting lipid peroxidation and ferroptosis.

Objective: To analyze a case of hemolytic disease of the fetus and newborn (HDFN) caused by anti-Jk3 antibody, which was induced in a rare Jk (a-b-) blood type resulting from a gene mutation in the Kidd blood group system, so as to provide a reference for the diagnosis and treatment of HDFN associated with this antibody. Methods: HDFN-related blood group serological testing, antibody identification and specific blood group antigen identification were performed on blood samples from the infant and the mother. The mother's Kidd blood group was analyzed by molecular biology methods. Clinical data of the infant and the mother were collected, and changes in bilirubin, hemoglobin (Hb), and other results during the disease progression of the infant were analyzed. Results: The infant was blood type B, Rh (D) positive, and Kidd blood group Jk (a-b+). The mother was blood type O, Rh (D) positive. Due to an IVS5-1 G>A mutation, the mother exhibited a Jk (a-b-) phenotype. Anti-Jk3 antibodies were detected in the mother's plasma. The infant was diagnosed with HDFN due to anti-Jk3. During treatment, the total bilirubin (TBil) and indirect bilirubin (IBil) levels of the infant initially increased and then decreased, with peak monitored values of 228.2 μmol/L and 208.9 μmol/L, respectively. Hb decreased from 180 g/L at birth to 93 g/L. After phototherapy and symptomatic treatment, the infant's indicators stabilized, and the general condition improved. The infant was discharged after recovery. Conclusion: Clinically, HDFN caused by anti-Jk3 antibodies is relatively rare. For HDFN induced by this antibody, early detection, intervention, and treatment are essential to address the transfusion challenges posed by the extreme scarcity of Jk3-negative blood sources, thereby minimizing adverse outcomes in affected infants to the greatest extent possible.

The incidence and mortality rates of lung cancer have been continuously rising. Smoking is a crucial modifiable factor contributing to the high incidence of lung cancer, and quitting smoking is of great significance for the treatment and prognosis of lung cancer patients. This article systematically reviews the harms of smoking to lung cancer patients, such as carcinogenic substances triggering lung cancer, affecting the course of the disease, and the improvement of prognosis after quitting smoking. It also analyzes the current situation of smoking cessation among lung cancer patients, who face numerous difficulties and have a relatively small number of successful quitters. Meanwhile, this article provides a detailed introduction to the clinical diagnosis and treatment methods for smoking cessation interventions. This includes the explanation of the pathophysiology of smoking cessation, psychological supportive therapies [brief psychological intervention and 5A’s model (Ask, Advise, Assess, Assist, Arrange) psychological counseling], and pharmacotherapies (nicotine-based and non-nicotine-based smoking cessation medications). In addition, it covers the behavioral intervention therapies for smoking cessation, including the PRECEDE-PROCEED model, cognitive behavior theory model, capacity opportunity motivation-behavior (COM-B) theoretical model, information-motivation-behavioral skills (IMB) model, timing is right (TIR) theoretical model, and the economic incentive intervention model. Although some of the current intervention methods lack the support of clinical randomized controlled studies, existing research and practice have confirmed their positive effects on smoking cessation among lung cancer patients. It is hoped that relevant intervention methods can be further improved in the future to help lung cancer patients improve their quality of life.

OBJECTIVE To investigate the clinical efficacy of pramipexole combined with levodopa-benserazide in the treatment of Parkinson’s disease （PD）. METHODS A total of 108 PD patients treated at the Fifth People’s Hospital of Wuhu City from January 1， 2021， to February 28， 2023， were randomly divided into observation group and control group， with 54 cases in each group. Patients in the control group were administered levodopa-benserazide （initial dose of 62.5 mg per dose）， three times daily； after one month， the dose was increased to 250 mg per dose， four times daily. Patients in the observation group received the same treatment as the control group， with the addition of pramipexole （initial dose of 0.25 mg per dose） orally twice daily on an empty stomach； after 14 days， the dose was increased to 0.25 mg per dose， three times daily. Both groups were treated for 3 months. The short-term efficacy， safety and long-term prognosis of the two groups were compared. RESULTS After treatment， the observation group had significantly lower scores on the Unified Parkinson’s Disease Rating Scale part Ⅲ （UPDRS-Ⅲ）， the Hamilton Depression Scale （HAMD）， the Hamilton Anxiety Scale （HAMA）， and the Parkinson’s Disease Questionnaire-39（ PDQ- 39） compared to the control group； in contrast， the observation group had higher scores on the Montreal Cognitive Assessment （MoCA） scale， the Mini-mental State Examination （MMSE） scale， the Mattis Dementia Rating Scale （DRS）， and the Quality of Life （QOL） scale （P＜0.05）. Both groups showed a significant reduction in UPDRS-Ⅲ and PDQ-39 scores， and a significant increase in DRS scores compared to baseline （P＜0.05）. However， only the observation group showed a significant increase in MoCA scale， MMSE scale， and QOL scores， and a significant decrease in HAMD and HAMA scores compared to baseline （P＜ 0.05）. The total incidence of adverse drug reactions in both groups was not significantly different （P＞0.05）. The 12 months follow-up results showed that the incidence of dementia and mortality rates in the observation group were significantly lower than the control group （P＜0.05）. CONCLUSIONS Pramipexole combined with levodopa-benserazide significantly improves motor function， cognitive function， quality of life and symptoms of depression and anxiety in PD patients， and may reduce the long-term risk of dementia and mortality in these patients.

BACKGROUND:At present,osteoarthritis has become a major disease affecting the quality of life of the elderly,and the therapeutic effect is poor,often focusing on preventing the disease process,and the pathogenesis of osteoarthritis is still not fully understood.Bioinformatics analysis was carried out to explore the main pathogenesis of osteoarthritis and related mechanisms of gene coding regulation. OBJECTIVE:To screen core differential genes with a major role in osteoarthritis by gene expression profiling. METHODS:Datasets were downloaded from the Gene Expression Omnibus(GEO):GSE114007,GSE117999,and GSE129147.Differential genes in the GSE114007 and GSE117999 data collections were screened using R software,performing differential genes to weighted gene co-expression network analysis.The module genes most relevant to osteoarthritis were selected to perform protein interaction analysis.Candidate core genes were selected using the cytocape software.The candidate core genes were subsequently subjected to least absolute shrinkage and selection operator regression and COX analysis to identify the core genes with a key role in osteoarthritis.The accuracy of the core genes was validated using an external dataset,GSE129147. RESULTS AND CONCLUSION:(1)A total of 477 differential genes were identified,265 differential genes associated with osteoarthritis were obtained by weighted gene co-expression network analysis,and 8 candidate core genes were identified.The least absolute shrinkage and selection operator regression analysis finally yielded a differential gene ASPM with core value that was externally validated.(2)It is concluded that abnormal gene ASPM expression screened by bioinformatics plays a key central role in osteoarthritis.

ObjectiveTo investigate the effect and mechanism of Yijingtang （YJT） in treating diminished ovarian reserve （DOR） in rats by regulating the Toll-like receptor 4 （TLR4）/myeloid differentiation factor 88 （MyD88）/nuclear factor-κB （NF-κB） signaling pathway. MethodsFifty female SD rats with normal estrous cycles were randomly allocated into blank， model， low- and high-dose （12.579 and 25.158 g·kg^-1， respectively） YJT， and dehydroepiandrosterone （7.487 5 mg·kg^-1） groups， with 10 rats in each group. The rats in other groups except the blank group were administrated with the tripterygium glycosides tablet suspension （5 mg·kg^-1） by gavage for 14 days for the modeling of DOR. The rats in the drug treatment groups were administrated with corresponding drugs by gavage from day 15 for 30 consecutive days， and those in the blank and model groups received equal volumes of distilled water. The vaginal exfoliated cell smears were observed to assess the changes in the estrous cycle. The wet weight of bilateral ovaries was weighed for calculation of the ovarian index. Hematoxylin-eosin staining was performed to observe the histopathological changes in the ovaries and the proportions of follicles at various levels were calculated. The serum levels of sex hormones ［follicle-stimulating hormone （FSH）， luteinizing hormone （LH）， estradiol （E₂）， and anti-Müllerian hormone （AMH）］ and inflammatory factors ［tumor necrosis factor-alpha （TNF-α）， interleukin-1beta （IL-1β）， and interleukin-10 （IL-10）］ were determined by enzyme-linked immunosorbent assay. Real-time quantitative polymerase chain reaction（Real-time PCR） was conducted to determine the mRNA levels of TLR4， MyD88， NF-κB profilin α （IκBα）， NF-κB and inflammatory factors in the ovarian tissue. Western blot was employed to measure the protein levels of factors related to the TLR4/MyD88/NF-κB signaling pathway in the ovarian tissue. Immunofluorescence （IF） was used to detect the nuclear translocation of NF-κB p65 in the ovarian tissue. ResultsCompared with the blank group， the model group showed disturbed estrous cycles， increased inflammatory infiltration in the ovarian tissue， decreases in ovarian index and proportion of presinusoidal follicles， and an increase in the proportion of atretic follicles （P<0.05， P<0.01）. In addition， the model group showed elevated serum levels of FSH， LH， TNF-α， and IL-1β， up-regulated mRNA levels of TLR4， MyD88， IκBα， NF-κB， TNF-α， and IL-1β and protein levels of TLR4， MyD88， p-IκBα， and p-NF-κB p65 （P<0.01）， lowered serum levels of AMH， E₂， and IL-10， down-regulated mRNA level of IL-10 （P<0.01）， and massive nuclear translocation of NF-κB p65 in the ovarian tissue. Compared with the model group， dehydroepiandrosterone and low and high doses of YJT restored the disturbed estrous cycle， reduced inflammatory infiltration in the ovarian tissue， increased the ovarian index （P<0.01）， and changed the follicular composition ratio （P<0.01）. Furthermore， the drugs lowered the serum levels of FSH， LH， TNF-α， and IL-1β， down-regulated the mRNA levels of TLR4， MyD88， IκBα， NF-κB， TNF-α， and IL-1β and the protein levels of TLR4， MyD88， p-IκBα， and p-NF-κB p65 （P<0.05， P<0.01）， raised the serum levels of AMH， E₂， and IL-10， up-regulated the mRNA level of IL-10 （P<0.05， P<0.01）， and reduced the nuclear translocation of NF-κB p65 in the ovarian tissue. ConclusionYJT may inhibit the release and expression of inflammatory factors by regulating the TLR4/MyD88/NF-κB signaling pathway to attenuate the inflammatory responses in the ovarian tissue， thereby improving the ovarian function in DOR rats.

ObjectiveTo investigate the effect and mechanism of Yijingtang （YJT） in treating diminished ovarian reserve （DOR） in rats by regulating the Toll-like receptor 4 （TLR4）/myeloid differentiation factor 88 （MyD88）/nuclear factor-κB （NF-κB） signaling pathway. MethodsFifty female SD rats with normal estrous cycles were randomly allocated into blank， model， low- and high-dose （12.579 and 25.158 g·kg^-1， respectively） YJT， and dehydroepiandrosterone （7.487 5 mg·kg^-1） groups， with 10 rats in each group. The rats in other groups except the blank group were administrated with the tripterygium glycosides tablet suspension （5 mg·kg^-1） by gavage for 14 days for the modeling of DOR. The rats in the drug treatment groups were administrated with corresponding drugs by gavage from day 15 for 30 consecutive days， and those in the blank and model groups received equal volumes of distilled water. The vaginal exfoliated cell smears were observed to assess the changes in the estrous cycle. The wet weight of bilateral ovaries was weighed for calculation of the ovarian index. Hematoxylin-eosin staining was performed to observe the histopathological changes in the ovaries and the proportions of follicles at various levels were calculated. The serum levels of sex hormones ［follicle-stimulating hormone （FSH）， luteinizing hormone （LH）， estradiol （E₂）， and anti-Müllerian hormone （AMH）］ and inflammatory factors ［tumor necrosis factor-alpha （TNF-α）， interleukin-1beta （IL-1β）， and interleukin-10 （IL-10）］ were determined by enzyme-linked immunosorbent assay. Real-time quantitative polymerase chain reaction（Real-time PCR） was conducted to determine the mRNA levels of TLR4， MyD88， NF-κB profilin α （IκBα）， NF-κB and inflammatory factors in the ovarian tissue. Western blot was employed to measure the protein levels of factors related to the TLR4/MyD88/NF-κB signaling pathway in the ovarian tissue. Immunofluorescence （IF） was used to detect the nuclear translocation of NF-κB p65 in the ovarian tissue. ResultsCompared with the blank group， the model group showed disturbed estrous cycles， increased inflammatory infiltration in the ovarian tissue， decreases in ovarian index and proportion of presinusoidal follicles， and an increase in the proportion of atretic follicles （P<0.05， P<0.01）. In addition， the model group showed elevated serum levels of FSH， LH， TNF-α， and IL-1β， up-regulated mRNA levels of TLR4， MyD88， IκBα， NF-κB， TNF-α， and IL-1β and protein levels of TLR4， MyD88， p-IκBα， and p-NF-κB p65 （P<0.01）， lowered serum levels of AMH， E₂， and IL-10， down-regulated mRNA level of IL-10 （P<0.01）， and massive nuclear translocation of NF-κB p65 in the ovarian tissue. Compared with the model group， dehydroepiandrosterone and low and high doses of YJT restored the disturbed estrous cycle， reduced inflammatory infiltration in the ovarian tissue， increased the ovarian index （P<0.01）， and changed the follicular composition ratio （P<0.01）. Furthermore， the drugs lowered the serum levels of FSH， LH， TNF-α， and IL-1β， down-regulated the mRNA levels of TLR4， MyD88， IκBα， NF-κB， TNF-α， and IL-1β and the protein levels of TLR4， MyD88， p-IκBα， and p-NF-κB p65 （P<0.05， P<0.01）， raised the serum levels of AMH， E₂， and IL-10， up-regulated the mRNA level of IL-10 （P<0.05， P<0.01）， and reduced the nuclear translocation of NF-κB p65 in the ovarian tissue. ConclusionYJT may inhibit the release and expression of inflammatory factors by regulating the TLR4/MyD88/NF-κB signaling pathway to attenuate the inflammatory responses in the ovarian tissue， thereby improving the ovarian function in DOR rats.