Myocardial infarction (MI) and atrial fibrillation (AF), a common complication during hospitalisation of critically ill MI patients, have a complex and close bidirectional relationship, and the two frequently occur together.

To develop a nomogram to predict the risk of in-hospital mortality in critically ill patients with MI and AF.

For this retrospective cohort research, we selected 1240 critically ill patients with AF and MI from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) (version 3.1) database. A 7:3 random division of the dataset was made into training and test sets. LASSO regression plus 10-fold cross-validation was used to screen predictors, and multivariate logistic regression was used to build prediction models using the screened predictors. We assessed our outcome model using the calibration curve and the area under the receiver operating characteristic curve (AUROC). We assessed the clinical usefulness of the predictive models using decision curve analysis (DCA).

This study included 1240 patients with both MI and AF, of whom 212 died during hospitalisation, yielding a mortality rate of 17.1%. The final seven predictors were chronic obstructive pulmonary disease, continuous renal replacement therapy, metoprolol, vasopressor use, red blood cell distribution width, anion gap and blood urea nitrogen. The model achieved an Area under the receiver operating characteristic curve (AUC) of 0.802 in the training set and 0.814 in the test set. Both calibration and decision curves demonstrated good model performance.

For patients with MI and AF, this nomogram offers an early evaluation of the risk of inpatient death.

By utilising risk prediction algorithms, nurses may precisely evaluate the risk of early mortality in patients with MI and AF promptly and execute targeted preventative interventions. This method enhances nursing decision-making and resource distribution, demonstrating clinical significance in critical care practice.

Rural-urban disparities in access to acute stroke care exist and have widened over time. We sought to quantify the rural-urban disparities that may exist in access to endovascular thrombectomy (EVT) for patients experiencing strokes with large vessel occlusions in Colorado.

This was a retrospective cohort study looking at all Colorado residents aged ≥18 years with large vessel occlusions undergoing EVT, between January 1, 2015, and November 30, 2022. Eleven sites performed EVTs in Colorado during the study period, and each site submitted data independently to the coordinating center. Rural designation at the patient level was defined as either (1) the patient first presented to a rural hospital or (2) the patient lived in a rural area based on their 5-digit residential zip code. Primary outcomes include time from last known normal to groin puncture and unfavorable outcome, defined as a modified Rankin Scale score >2 at discharge. Secondary outcomes include the length of stay and whether the patient was discharged home.

A total of 3100 patients were included in the study: 346 (11%) rural and 2754 (89%) urban patients. The adjusted geometric mean time from last known normal to EVT in rural patients was 6.0 (95% CI, 4.6-7.9) hours compared with 4.5 (95% CI, 3.5-5.8) hours for urban patients. Rural patients took 33.3% (P=0.001) longer than urban patients to undergo EVT. Rural patients had a 10% higher risk of unfavorable outcomes (P=0.016). The lengths of stay for rural patients were 14% longer than urban patients (P<0.01). Rural patients were 11% more likely not to be discharged home after a stroke than urban patients (P=0.007).

Rural patients experienced longer time to intervention and had worse outcomes after a stroke with large vessel occlusions. Each rural patient with large vessel occlusions lost ≈1.7 years of disability-free life compared with an urban patient with the same severity stroke. More work needs to be done to identify and quantify the sources of delay for rural patients.

Based on latent structure model and association rule analysis, this study investigates the prescription patterns used by professor YANG Zhong-qi in treating hypertension with traditional Chinese medicine(TCM) and infers the associated TCM syndromes, providing a reference for clinical syndrome differentiation and treatment. The observation window spanned from January 8, 2013, to June 26, 2024, during which qualified herbal decoction prescriptions meeting efficacy criteria were extracted from the outpatient medical record system of the First Affiliated Hospital of Guangzhou University of Chinese Medicine and compiled into a standardized database. Statistical analysis of high-frequency herbs included frequency counts and herbal property-channel tropism analysis. Latent structure modeling and association rule analysis were performed using R 4.3.2 and Lantern 5.0 software to identify core herbal combinations and infer TCM syndrome patterns. A total of 2 436 TCM prescriptions were included in the study, involving 263 drugs with a cumulative frequency of 29 783. High-frequency herbs comprised Uncariae Ramulus cum Uncis, Poria, Glycyrrhizae Radix et Rhizoma, Puerariae Lobatae Radix, and Alismatis Rhizoma, predominantly categorized as deficiency-tonifying, heat-clearing, and blood-activating and stasis-resolving herbs. Latent structure analysis identified 18 latent variables, 74 latent classes, 5 comprehensive clustering models, and 15 core herbal combinations, suggesting that the core syndrome clusters include liver Yang hyperactivity pattern, Yin deficiency with Yang hyperactivity pattern, phlegm-stasis intermingling pattern, and liver-kidney insufficiency pattern. Association rule analysis revealed 22 robust association rules. RESULTS:: indicate that hypertension manifests as a deficiency-rooted excess manifestation, significantly associated with functional dysregulation of the liver, lung, spleen-stomach, heart, and kidney. Key pathogenic mechanisms involve liver Yang hyperactivity, phlegm-stasis interaction, and liver-kidney insufficiency. Therapeutic strategies should prioritize liver-calming, spleen-fortifying, and deficiency-tonifying principles, supplemented by dynamic regulation of Qi-blood and Yin-Yang balance according to syndrome evolution, alongside pathogen-eliminating methods such as phlegm-resolving and stasis-dispelling. Synergistic interventions like mind-tranquilizing therapies should be tailored to individual conditions.

Workplace bullying, a widespread phenomenon, significantly impacts interpersonal relationships, mental health, professional performance, and organizational efficiency in healthcare. Defined as repeated behaviors intended to intimidate or degrade, bullying thrives in hierarchical, high-stress environments like hospitals, where nurses face disproportionate risk. Such behaviors harm morale, increase turnover, and jeopardize patient safety through errors and negligence. Understanding its prevalence and contributors is essential for fostering healthier work environments and improving healthcare outcomes.

This cross-sectional descriptive study followed the STROBE guidelines. A Slovak adaptation of the Negative Act Questionnaire-Revised, developed as part of this study, was administered to nurses, resulting in a final sample of 244 participants. Spearman's correlation and Welch's ANOVA tests analyzed variable relationships using jamovi software.

Nearly one-third of nurses were victims of bullying (32.2%, >45 points), with another third experiencing occasional bullying (32.2%, 33-44 points). The median score per responder was 38 (IQR: 23), with person-related bullying scoring highest (median 19, IQR: 13). Younger nurses with less experience reported higher mobbing levels (p < 0.001). Nurses in frontline roles (operating rooms, intensive care units, and surgical units) experienced significantly more bullying than those in outpatient clinics (p = 0.01). Doctoral degree holders had the lowest mobbing scores (p < 0.001), while nurses in frontline roles reported higher mobbing levels than Ward/Charge Nurses (p < 0.001).

The study highlights a significant correlation between nurses' experiences of mobbing and factors such as age, experience, education, position, and workplace type. The high incidence of bullying among Slovak nurses requires immediate attention from healthcare leaders.

To address workplace bullying, healthcare institutions should implement zero-tolerance policies, provide ongoing education in professional conduct, emotional intelligence, and conflict resolution and integrate these topics into nursing curricula. Leadership should model respectful behavior, while mentorship frameworks and resilience training support novice nurses. Finally, accessible reporting systems must ensure accountability.

Heart failure (HF) is characterized by a significant imbalance of the autonomic nervous system (ANS), with chronic sympathetic nervous system (SNS) overactivity leading to maladaptive cardiac remodeling, arrhythmia, and hemodynamic instability. In this review, we aim to discuss current and emerging therapies and the potential path forward for developing future novel neuromodulatory therapies in HF.

Neuromodulatory therapies including splanchnic nerve modulation (SNM), vagal nerve stimulation (VNS), baroreflex activation therapy (BAT), and renal denervation (RDN) reduce sympathetic output in individuals with HF, leading to improved cardiac function, neurohormonal regulation, and vascular resistance. However, implementation of these strategies in clinical practice is limited owing to variability in response, patient selection criteria, and insufficient long-term efficacy data. Gene therapy targeting Gαi2 proteins, and adenylyl cyclase isoforms have demonstrated potential in reducing sympathetic overactivation. Endovascular BAT such as the Mobius HD has shown early indications of improvements in symptoms, left ventricular function, and biomarkers in patients with HF. These emerging therapies warrant further investigation. Neuromodulation is a characteristic method for reducing disease progression and improving outcomes in individuals with autonomic dysfunction-driven HF. Although initial studies demonstrate benefits, long-term impact of neuromodulation on HF development, symptom load, and survival has not yet been thoroughly demonstrated. Future studies should prioritize deep phenotyping using genetic and biomarker profiles to improve patient selection. Comparative trials are required to assess the efficacy and safety of neuromodulatory therapies relative to conventional approaches. Large-scale trials are needed to optimize procedural procedures, and assess the long-term efficacy of treatment interventions.

Atherosclerosis (AS) is a vascular disorder characterized by lipid accumulation, fibrous tissue proliferation, and calcium deposition in the intima, contributing significantly to the mortality associated with cardiovascular disease, and the pathogenesis of AS is multifaceted. Recent studies have identified copper (Cu) overlap induced cuproptosis as a key mechanism underlying cellular dysfunction in AS. Cuproptosis impacts the function and survival of multiple cell types within AS lesions by several downstream pathways, and regulating cellular cuproptosis may be a very promising clinical treatment strategy. In this review, we explored the influence of key regulatory proteins and signaling pathways associated with copper homeostasis and cuproptosis in AS, and the potential regulators of cuproptosis in AS therapy, especially the endogenous metabolites, copper ionophore, Cu oxide nanoparticles and natural products, we also discuss emerging therapeutic strategies and offering insights into future developments and translational medicine or challenge by targeting cuproptosis in AS pathogenesis.

One-year mortality following acute myocardial infarction (AMI) has declined over time, yet the reasons for this improvement remain unclear. Understanding the drivers of these changes is essential for informing clinical strategies and health policy.

We analysed 852 914 adult patients admitted with AMI across England and Wales between 2005 and 2019 using national registry data. We examined changes in 1-year all-cause mortality and quantified the contribution of clinical, treatment and demographic factors to this trend using decomposition analysis.

Between 2005 and 2019, 1-year all-cause mortality declined from 22.8% (95% CI 22.4% to 23.2%) to 14.2% (95% CI 13.7% to 14.7%), an absolute reduction of 8.6 percentage points. Approximately 68.2% of this decline was explained by measured factors. The greatest contributor was increased use of evidence-based pharmacological therapies-including statins, beta blockers and ACE inhibitors-accounting for 27.7% of the reduction (95% CI 26.0% to 29.5%). Increased use of percutaneous coronary intervention (PCI) contributed 17.6% (95% CI 16.3% to 19.0%). Mortality improvements were observed in both ST-elevation myocardial infarction (STEMI) and non-STEMI populations. However, older adults and women continued to experience higher mortality rates throughout the study period.

One-year survival after AMI improved substantially over 15 years in England and Wales largely due to advances in pharmacotherapy and PCI. Nevertheless, about one-third of the mortality decline remains unexplained, underscoring the need to investigate other contributors such as postdischarge care and health system factors.

To observe the effect of "Xingnao Kaiqiao" (regaining consciousness and opening orifice) acupuncture on cerebral ischemia/reperfusion injury(CI/RI), autophagy and adenosine 5'-monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/UNC-51-like autophagy-activated kinase 1 (ULK1) signaling pathway, so as to explore its underlying mechanisms in improving CI/RI.

Male Sprague Dowley (SD) rats were randomly divided into sham-operation group, CI/RI model group, and acupuncture group, with 10 rats in each group. The CI/RI model was replicated by occlusion of the middle cerebral artery with intraluminal filament embolization. Two hours after successful modeling, the rats in the acupuncture group received manual acupuncture stimulation of "Shuigou" (GV26), "Neiguan"(PC6), and "Sanyinjiao" (SP6) with "Xingnao Kaiqiao" needling method, and electroacupuncture (EA) stimulation (2 Hz/15 Hz, 1 mA, 20 min) of PC6 and SP6 on the affected side during needle retention. The intervention was conducted twice a day (10:00 and 16:00) for 7 times altogether. The severity of neurological deficits was assessed using Zausinger's six-point method. TTC staining was used to detect the volume of cerebral infarction. H.E. staining was used to observe the histopathological and morphological changes of the infarct brain tissues. A transmission electron microscopy (TEM) was used to observe the neuronal ultrastructure and autophagosome formation in the hippocampal tissue. Western blot was used to detect the protein expression levels of microtubule-associated protein light chain 3-II (LC3-II), AMPK, p-AMPK, mTOR, p-mTOR, ULK1 and p-ULK1 in the hippocampal tissues on the ischemic side.

Compared with the sham-operation group, the model group had a significantly reduced neurological deficit score (P<0.001), significantly decreased expression levels of LC3-II, ratios of p-AMPK/AMPK and p-ULK1/ULK1 (P<0.001), and significantly increased percentage of cerebral infarct volume and p-mTOR/mTOR ratio (P<0.001). In comparison with the model group, the acupuncture group had a significant increase in the neurological deficit score and expression of LC3-II, ratios of p-AMPK/AMPK and p-ULK1/ULK1 (P<0.001, P<0.05), and a significant decrease in the percentage of cerebral infarct volume and p-mTOR/mTOR ratio (P<0.001). Results of H.E. staining showed loose arrangement and reduction in the number of neurons, with pyknotic nucleus, obvious cavities, and appearance of degenerated and necrotic neurons in the ischemic brain tissue, which was relatively milder in the severity of CI/RI of the acupuncture group. Results of TEM showed injured and fractured membrane of neurons, moderate cell edema, mitochondrial swelling and reduction in number, dilation of the endoplasmic reticulum, and appearance of autophagosomes in the hippocampus of the model group, while in the acupuncture group, the nuclear membrane of nerve cells was relatively intact, the numbers of normal mitochondria and endoplasmic reticulum were increased, with appearance of typical autophagosomes.

"Xingnao Kaiqiao" acupuncture can improve neurological behavior and reduce infarction volume in rats with CI/RI, which may be related to its functions in regulating AMPK/mTOR/ULK1 signaling, and promoting cellular autophagy.

To observe the effect of electroacupuncture (EA) on cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING)/NOD-like receptor family pyrin domain containing 3 (NLRP3) pathway of the cerebral cortex in rats with cerebral ischemia reperfusion injury and investigate the underlying mechanisms of EA in improving cerebral ischemia reperfusion injury.

A total of 45 SD rats were randomly assigned into sham-operation group, model group and EA group, with 15 rats in each group. The modified thread embolism method was used to establish the model of cerebral ischemia reperfusion injury. Rats in the EA group received EA at "Baihui" (GV20), "Fengfu" (GV16), and "Dazhui" (GV14) for 20 min, once daily for 7 consecutive days. The modified neurological severity score (mNSS) was used to assess the neurological deficit condition. TTC staining was used to detect the percentage of cerebral infarction. HE staining was used to detect the pathological morphology in the cerebral cortex of infarcted side of rats. TUNEL staining was used to detect the apoptosis rate of cerebral cortical nerve cells. ELISA was used to detect the contents of interleukin (IL)-1β and IL-18 in the cerebral cortex of infarcted side. Western blot and qPCR were respectively used to detect the protein and mRNA expressions of cGAS, STING, TANK binding kinase-1(TBK1), Interferon regulatory factor 3(IRF3) and NLRP3 in the cerebral cortex of infarcted side.

In comparison with the sham-operation group, the mNSS and the percentage of cerebral infarction were increased (P<0.01);there were structural disorders and neuronal damage in the cerebral cortex of infarcted side;the apoptosis rate of nerve cells was increased (P<0.01), the contents of IL-1β and IL-18 were increased (P<0.01), and the protein and mRNA expressions of cGAS, STING, TBK1, IRF3 and NLRP3 were elevated (P<0.01) in the model group. In comparison with the model group, the mNSS and the percentage of cerebral infarction were decreased (P<0.01);the pathological damage was alleviated;the apoptosis rate of nerve cells was decreased (P<0.01), the contents of IL-1β and IL-18 were decreased (P<0.01), and the protein and mRNA expressions of cGAS, STING, TBK1, IRF3 and NLRP3 were reduced (P<0.01) in the EA group.

EA can improve cerebral ischemia reperfusion injury, which is related to the inhibition of the cGAS/STING/NLRP3 pathway and inflammatory response in the cerebral cortex.

To observe the effect of acupuncture on the expression of brain-derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB), extracellular signal-regulated kinase (ERK), cyclic adenosine monophosphate (cAMP)-response element binding protein (CREB), as well as synapsin1 (Syn1) and synaptophysin (Syp) in the striatum of neonatal rats with hypoxic-ischemic brain damage ( HIBD), so as to explore its mechanisms underlying improvement of motor control.

Seven-day-old neonatal SD rats were randomly and equally assigned to 4 groups:blank control, sham-operation, model, and acupuncture groups (n=12 per group) according to the randomized numerical table method. The HIBD model was established by using modified Rice's method. For rats in the acupuncture group, manual acupuncture stimulation of "Dazhui"(GV14), "Baihui"(GV20), "Shuigou"(GV26) and "Mingmen"(GV4) was given 24 h after modeling. In the sham operation group, only the left common carotid artery was isolated without clamping, and no intervention was given. The neonatal rats in each group were subjected to the balance beam test 28 d after modeling. After the acupuncture intervention, the striatum tissue of neonatal rats in each group was taken for observing histopathological and morphological changes after H.E. staining. The ultrastructural changes of the neurons of striatum were observed by transmission electron microscopy, and the immunoactivity of Syp was detected by immunohistochemistry, and the expression levels of BDNF, TrkB, p-ERK, p-CREB, Syn1, and Syp proteins were detected by using Western blot.

There were no significant differences between the blank control and sham operation groups in the Longa score, balance beam test score, Syp immunoactivity, and expression levels of BDNF, TrkB, p-ERK, p-CREB, Syn1 and Syp proteins. Compared with the sham operation group, the balance beam test score at 28^th day after modeling was significantly increased (P<0.01), and the Syp immunoactivity and the expression levels of BDNF, TrkB, p-ERK, p-CREB, Syn1 and Syp proteins were considerably down-regulated (P<0.01, P<0.05, P<0.001) in the model group. In contrast to the model group, the balance beam test score at 28 d after modeling was obviously decreased (P<0.05), the immunoactivity of Syp, and the expression levels of BDNF, TrkB, p-ERK, p-CREB, Syn1 and Syp proteins were strikingly up-regulated (P<0.05, P<0.01) in the acupuncture group. H.E. staining showed disordered arrangement of the striatal neurons, unclear layers, reduced cell density, with vacuolization and nuclear pyknosis in some cells in the model group, which was milder in the injury severity of the striatal neurons in the acupuncture group. Ultrastructure results displayed that in the model group, the distribution density of striatum synaptosome was lower, the thickness of postsynaptic dense area and the length of active area were reduced, and the boundary became blurred. Whereas in the acupuncture group, the synaptic structure of the striatum was more regular, the distribution density of synaptosomes, the thickness of the postsynaptic dense area and the length of the active area were increased.

Manual acupuncture stimulation can improve the motor control ability in neonatal rats with HIBD, which may be achieved by up-regulating the endogenous BDNF and its receptor TrkB, activating the MAPK/ERK signaling pathway, promoting the phosphorylation of CREB, and up-regulating the expression of Syn1 and Syp proteins, thereby promoting synaptic regeneration and remodeling.