[Objective] To evaluate the efficacy and safety of sacral neuromodulation (SNM) in the treatment of patients with benign prostatic hyperplasia (BPH) complicated with underactive bladder (UAB) who respond poorly to transurethral resection of the prostate (TURP). [Methods] A retrospective analysis was performed on 10 patients with BPH and UAB treated with TURP by the same surgeon in Zhongda Hospital Southeast University during Jan.2018 and Jan.2023.The residual urine volume was not significantly relieved after operation, and the maximum urine flow rate and urine volume per discharge were not significantly improved.All patients underwent phase I SNM, and urinary diaries were recorded before and after surgery to observe the average daily frequency of urination, volume per urination, maximum urine flow rate, and residual urine volume. [Results] The operation time was (97.6±11.2) min.During the postoperative test of 2-4 weeks, if the residual urine volume reduction by more than 50% was deemed as effective, SNM was effective in 6 patients (60.0%). Compared with preoperative results, the daily frequency of urination [(20.2±3.8) times vs. (13.2±3.2) times], volume per urination [(119.2±56.7) mL vs. (246.5±59.2) mL], maximum urine flow rate [(8.7±1.5) mL/s vs. (16.5±2.6) mL/s], and residual urine volume [(222.5±55.0) mL vs. (80.8±16.0) mL] were significantly improved, with statistical significance (P<0.05). There were no complications such as bleeding, infection, fever or pain.The 6 patients who had effective outcomes successfully completed phase II surgery, and the fistula was removed.During the follow-up of 1 year, the curative effect was stable, and there were no complications such as electrode displacement, incision infection, or pain in the irritation sites.The residual urine volume of the other 4 unsuccessful patients did not improve significantly, and the electrodes were removed and the vesicostomy tube was retained. [Conclusion] SNM is safe and effective in the treatment of BPH with UAB patients with poor curative effects after TURP.

OBJECTIVE To explore the effects and potential mechanism of plumbagin on the inflammatory response and oxidative stress in rats with acute exacerbation of chronic obstructive pulmonary disease （AECOPD） based on Notch1/GATA3 signaling pathway. METHODS Ten rats were randomly selected as the control group； another 65 rats were used to establish the AECOPD model by inhaling cigarette smoke， intratracheal administration of endotoxin， and nasal inoculation of bacteria. The 50 successfully modeled rats were randomly divided into the AECOPD group， plumbagin low-dose group （10 mg/kg）， plumbagin high-dose group （50 mg/kg）， positive control group （dexamethasone 0.09 mg/kg）， and high-dose plumbagin+Jagged1 （Notch1 activator） group （50 mg/kg+25 mg/kg）， with 10 rats in each group. Each group was administrated intragastrically or intraperitoneally with the corresponding drug solution or normal saline， once a day for 28 consecutive days. After the last administration， the lung function indicators （peak expiratory flow， the ratio of forced expiratory volume in 0.3 seconds to forced vital capacity）， the number of inflammatory cells （white blood cells， lymphocytes， neutrophils， macrophages） in bronchoalveolar lavage fluid， the levels of inflammatory factors [interleukin-6 （IL-6）， IL-10， tumor necrosis factor-α （TNF-α）] in lung tissue， and the contents of oxidative stress indicators [superoxide dismutase （SOD）， malondialdehyde （MDA）] in lung tissue were all determined in each group； the pathological changes of lung tissue and the pathological scores， as well as protein expressions of mucin 5ac （Muc5ac）， Notch1 and GATA3 in lung tissue were also detected. RESULTS Compared with the control group， the lung tissue of the AECOPD group rats showed severe damage to the alveolar wall structure， with a large number of inflammatory cells infiltration and accompanied by pathological changes such as thickening of the airway wall； their lung function indicators， IL-10 level， and SOD content were significantly decreased； while the number of various inflammatory cells， IL-6 and TNF-α levels， MDA content， pathological score， as well as protein expressions of Muc5ac， Notch1 and GATA3 were significantly increased or upregulated （P＜0.05）. Compared with the AECOPD group， the pathological changes in the lung tissue of the rats in each plumbagin dose group were significantly alleviated， and the above quantitative indicators were significantly improved， and the improvement was more obvious in the plumbagin high- dose group （P＜0.05）. Jagged1 significantly reversed the protective effect of high-dose plumbagin on lung injury and related indicators in AECOPD rats （P＜0.05）. CONCLUSIONS Plumbagin can inhibit the inflammatory response and oxidative stress in the lungs of AECOPD rats， alleviate lung damage， and improve lung function. The above effects may be related to the inhibition of the Notch1/GATA3 signaling pathway.

Objective To develop a scale suitable for assessing work stressors among intensive care unit (ICU) nurses and to examine its reliability and validity. Methods The initial questionnaire of the ICU Nurses' Work Stressors Scale was constructed through literature review, ICU nurse interviews, and Delphi expert consultation. A total of 434 ICU nurses were selected as the validation subjects using the convenient sampling method. Item analysis, exploratory factor analysis, and confirmatory factor analysis were conducted to finalize the version of the ICU Nurses' Work Stressors Scale and evaluate its reliability and validity. Results The ICU Nurses' Work Stressors Scale included six dimensions and 34 items. Exploratory factor analysis extracted six common factors with a cumulative variance contribution rate of 77.8%. The results of confirmatory factor analysis demonstrated good model fit. The scale-level content validity index of the scale was 0.965, with item-level content validity index ranging from 0.850 to 1.000. The overall Cronbach's α coefficient of the questionnaire was 0.958, and the test-retest reliability was 0.986. In a survey of 434 ICU nurses testing with the scale, the total score ranged from 22.0-160.0 (82.6±20.6) points. The scores of each dimension including nursing profession, workload, working environment, patient care, family factors and interpersonal relationship were (14.5±4.2), (21.9±5.8), (7.0±2.1), (14.1±4.2), (6.3±2.5) and (18.8±5.7) points, respectively. Conclusion ICU Nurses' Work Stressors Scale demonstrates good reliability and validity and can serve as an effective tool for evaluating work stress among ICU nurses.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Sensorineural hearing loss (SNHL), the most commonly-occurring form of hearing loss, is caused mainly by injury to or the loss of hair cells and spiral ganglion neurons in the cochlea. Numerous environmental and physiological factors have been shown to cause acquired SNHL, such as ototoxic drugs, noise exposure, aging, infections, and diseases. Several programmed cell death (PCD) pathways have been reported to be involved in SNHL, especially some novel PCD pathways that have only recently been reported, such as ferroptosis, necroptosis, and pyroptosis. Here we summarize these PCD pathways and their roles and mechanisms in SNHL, aiming to provide new insights and potential therapeutic strategies for SNHL by targeting these PCD pathways.
Humans ; Hearing Loss, Sensorineural/metabolism* ; Necroptosis/drug effects* ; Pyroptosis/drug effects* ; Ferroptosis/drug effects* ; Animals

Ventriculostomy drainage is one of the commonly used surgical techniques in neurocritical care, which can relieve intracranial hypertension and facilitate postoperative cerebrospinal fluid and intracranial pressure monitoring. By placing a drainage tube in the ventricle, blood and fluid accumulation within the ventricle are drained out of the brain, reducing intracranial pressure and preventing brain tissue damage. Clinically, the speed of ventriculostomy drainage is often controlled by measuring the height difference between the drainage opening and the plane of the ventricle, ensuring the safe and effective reduction of intracranial pressure, facilitating the implementation of clinical management plans, and preventing complications. However, how to easily, safely, and effectively measure the height difference between the drainage opening and the ventricular plane remains a challenge in nursing management. Currently, clinical practice often uses a tape measure to measure the height of the ventriculostomy drainage, a process that is cumbersome and time-consuming and susceptible to human error, leading to inaccurate measurements. However, the challenge of easily, safely, and effectively detecting the height difference between the drainage opening and the ventricular plane remains a difficult problem in nursing management. To address this issue, the medical and nursing staff of the intensive care unit (ICU) at Zhongda Hospital, Southeast University, jointly designed a novel ventriculostomy drainage height measurement device, which has been granted a national utility model patent (patent number: ZL 2022 2 1400920.9). This device can be easily and securely fixed to an infusion stand. Using a level within the horizontal measuring part and a rotational structure, the vertical measuring part of the device is adjusted to be perpendicular to the ground. After opening the limit clip, the horizontal part is manually guided down to the appropriate height. The front end of the horizontal measuring part is then extended towards the patient's head, and after confirming the position, the limit clip is closed. At this point, the horizontal height difference between the drainage opening and the ventricular plane can be accurately measured. When temporarily finishing the height measurement of the drainage tube, the device can be folded and stored by retracting the horizontal measuring part and rotating components. This measuring device has a simple operation process, which can improve the accuracy and reliability of the drainage height measurement, enhance treatment outcomes and patient safety, reduce the workload of nursing staff, and has certain clinical promotion and practical value.
Humans ; Ventriculostomy/methods* ; Drainage/instrumentation* ; Equipment Design ; Cerebral Ventricles

With the continuous advancement and innovation in medical equipment technology, the transition between high-flow oxygen therapy, non-invasive ventilation, and invasive ventilation can be easily achieved by adjusting the ventilation mode of ventilators. During the weaning phase for tracheotomized patients, it is necessary to disconnect the ventilator circuit, change the ventilator mode, and gradually extend the weaning time to achieve complete ventilator liberation. During the weaning process, due to patients' excessive dependence on the ventilator, there may be situations where respiratory endpoints and Y-connectors of the ventilator are reconnected for invasive ventilation. However, during the weaning process, the Y-connector and expiratory end connectors are exposed to the air, which cannot ensure the tightness of the ventilator circuit, easily increasing the probability of ventilator circuit contamination and subsequently the risk of ventilator-associated pneumonia (VAP). To overcome these issues, the research team of department of critical care medicine of Zhongda Hospital Southeast University has designed a ventilator circuit interface protective device for weaning and has obtained a National Utility Model Patent of China (ZL 2023 2 1453385.8). The main body of the protective device is a Y-connector plug, consisting of multiple components, including a sealing piece, a protective cover, a sealing plug, an interface 1 (connects with the patient's tracheal tube), an interface 2 (connects with the respiratory branch of the ventilator), and an interface 3 (connects with the expiratory branch of the ventilator), featuring a unique design and easy operation. During the patient's weaning training process, the interface 1 and interface 2 is disconnected from the patient's tracheal tube and respiratory branch, respectively. The interface 1 is plugged with a stopper, and the interface 2 is covered with a protective cover to ensure the tightness of the expiratory branch and Y-connector of the ventilator. During the period when the patient is using the ventilator, the protective cover and plug are removed, and connecting them together ensures the tightness of the device itself, reducing the incidence of VAP caused by ventilator circuit contamination, avoiding nosocomial infections, and shortening the prolonged use of invasive ventilation, increased complication rate, extended hospital stay, and increased medical cost associated with weaning.
Humans ; Ventilator Weaning/methods* ; Equipment Design ; Ventilators, Mechanical ; Respiration, Artificial/instrumentation* ; Pneumonia, Ventilator-Associated/prevention & control*

Extracorporeal membrane oxygenation (ECMO) is a key continuous extracorporeal life support technology that can partially or completely replace a patient's cardiopulmonary function, thereby winning valuable time for the diagnosis and treatment of the primary disease. With the widespread application of ECMO, the need for transport has increased. However, during transfers, the standard heater unit is often large and inconvenient to carry, while alternative warming measures tend to be ineffective. This frequently leads to complications such as hypothermia or the inability to maintain body temperature, which can seriously affect the patient's prognosis. In response to this challenge, the medical and nursing staff of the critical care medicine department at Zhongda Hospital Affiliated to Southeast University jointly designed an insulation device for ECMO transport pipelines. The device was successfully granted a National Utility Model Patent of China (patent number: ZL 2021 2 0653569.3). It primarily consists of key components such as a heating pad, velcro straps, a cover layer, a backing layer, an electric heating layer, and a wiring plug. Its advantages include portability, the ability to effectively wrap around and warm the ECMO circuit during transit, and a reduction in the incidence of hypothermia-related complications. Furthermore, its transparent material design allows for real-time monitoring of the ECMO system's status, making it both economical and practical.
Extracorporeal Membrane Oxygenation/instrumentation* ; Humans ; Equipment Design

Patients requiring extracorporeal membrane oxygenation (ECMO) often need concurrent continuous renal replacement therapy (CRRT). At present, there are various connection methods between ECMO and CRRT circuits, among which in-series integration is the most common. However, ECMO blood flow and catheter type, pressure changes at the pre-pump, post-pump pre-oxygenator, and post-oxygenator segments frequently result in circuit pressures that exceed the alarm threshold of the device. Excessive negative or positive pressures may compromise blood withdrawal and return within the CRRT circuit, leading to frequent system alarms, interruptions in therapy, filter occlusion, and an increased risk of thrombus formation. To address this issue, the critical care nursing team of Zhongda Hospital Affiliated to Southeast University, developed a novel pressure-regulating clamp for CRRT vascular access in ECMO patient, which has been granted a National Utility Model Patent of China (patent number: ZL 2021 2 1496610.7). The device comprises opposing left and right clamp arms joined at the top by a flexible plastic bridge, with dual internal compression surfaces designed to fit CRRT tubing of various calibers. A locking mechanism and serrated strip at the base enable precise adjustment of the compression distance, thereby modulating the tubing's cross-sectional area. This configuration allows real-time regulation of blood flow and stabilization of pressures at blood withdrawal and return sites within the CRRT circuit. By reducing pressure-related alarms and extending filter life, the device may enhance the safety and efficiency of CRRT delivery during ECMO. It is user-friendly, cost-effective, and well-suited for broad clinical implementation, with the potential to alleviate the overall treatment burden on patients and their families.
Extracorporeal Membrane Oxygenation/instrumentation* ; Humans ; Continuous Renal Replacement Therapy/instrumentation* ; Equipment Design ; Pressure