Of myocardial infarctions (MIs) recorded in 2 large human immunodeficiency virus (HIV) observational studies from North America, approximately half were classified as type 2. In the REPRIEVE clinical trial of pitavastatin versus placebo in people with HIV (PWH) (<3% of participants were from Europe), 20.6% of MIs were type 2. The proportions of type 1 MI (T1MI) and type 2 MI (T2MI) in European PWH are unknown.

The study included a retrospective record review, ascertainment of prospectively recorded and medically validated MIs, differentiation of T1MI and T2MI, and MI time trend analysis in the Swiss HIV Cohort Study (1 January 2000 to 31 May 2021). Exploratory analysis was performed of the associations of T1MI and T2MI with blood leukocyte count and 2 validated genome-wide coronary artery disease-associated polygenic risk scores (metaGRS and GPS_mult).

Between 2000 and 2021, 16 027 Swiss HIV Cohort Study participants accumulated 181 598 years of follow-up, and 379 had a validated first MI. Of these participants, 359 (94.7%) had T1MI, and 20 (5.3%) had T2MI. Invasive coronary angiography was done in 95% and 60% of participants with T1MI and T2MI, respectively. We found no evidence for increasing or decreasing incidence trends over time for T1MI (P = .86) or T2MI (P = .85). Participants in the highest quintile for leukocyte count, metaGRS, and GPS_mult had significantly increased adjusted odds ratios for T1MI; power was limited for detecting associations with T2MI.

The proportion of T2MI in PWH in Switzerland is approximately 5%, consistent with data from the general population and lower than in previous North American reports among PWH.

The neutrophil-to-albumin ratio (NPAR), a novel marker of systemic inflammation, has been utilized to predict outcomes in patients with cancer and cardiovascular diseases. Since inflammation plays a critical role in the pathogenesis of constipation, understanding its connection to NPAR is essential. However, the association between NPAR and constipation remains unclear. This study aims to investigate the potential relationship between NPAR and constipation.

Data from the 2009-2010 National Health and Nutrition Examination Survey (NHANES) were utilized for this study. The neutrophil-to-albumin ratio (NPAR) was calculated as the ratio of the neutrophil percentage to serum albumin levels. To investigate the relationship between NPAR and chronic constipation, various statistical methods were applied, including interaction tests, subgroup analyses, and curve fitting techniques.

Among the 5,011 participants included in the analysis, 366 (7.30%) were identified as having chronic constipation. Higher NPAR levels were significantly associated with an increased likelihood of chronic constipation (OR = 1.05, 95% CI: 1.01-1.10, p < 0.05) based on a fully adjusted multiple logistic regression model. Further adjustments revealed that participants in the highest tertile of NPAR had an odds ratio of 1.31 (95% CI: 1.00-1.72, p < 0.05) for chronic constipation compared to those in the lowest tertile. Subgroup analyses indicated no significant association in most groups. However, a positive relationship between NPAR and chronic constipation was observed in specific subgroups, including individuals of Other Hispanic ethnicity, smokers, those with heart disease, alcohol consumers, diabetics, and those who were never married.

This study identified a significant positive association between NPAR and the prevalence of chronic constipation. These findings suggest that NPAR may serve as a potential inflammatory biomarker for chronic constipation. Further prospective research is necessary to clarify the long-term implications of elevated NPAR levels on chronic constipation.

Diabetic nephropathy is a common complication of diabetes. We investigated the risk factors for diabetic nephropathy in individuals newly diagnosed with type 2 diabetes.

Data from the Japanese Diagnosis Procedure Combination in-patient database (April 2008 to December 2018) were analyzed. The endpoint was subsequent diabetic nephropathy diagnosis or as the time when estimated glomerular filtration rate become <60 ml/min/1.73 m². Candidate risk factors included age, Hemoglobin A1c, log-transformed triglyceride, total cholesterol, and high-density lipoprotein cholesterol levels, body mass index, and estimated glomerular filtration rate. Eligible individuals with type 2 diabetes without complications who had pre- and post-diagnosis Hemoglobin A1c and serum creatinine measurements, and a history of hypertension or cardiovascular disease pre-diagnosis. Those with pre-existing kidney diseases, nephropathy onset pre-diagnosis, estimated glomerular filtration rate <60 ml/min/1.73 m² on or before diabetes diagnosis, or age <20 years at diabetes diagnosis were excluded. A multivariate Cox proportional hazards model (p = 0.2 backward selection) was employed.

Of 2,664 eligible individuals (1,775 men, 889 women), 325 men and 175 women developed diabetic nephropathy during follow-up. Cumulative incidence within 5 years was 29.0% in men and 32.5% in women. Age and estimated glomerular filtration rate in both sexes, and total cholesterol in men were significant.

Age, estimated glomerular filtration rate, and lipid pose potential risks for diabetic nephropathy onset within 5 years of diabetes diagnosis in individuals with hypertension. Collectively, our findings highlight the importance of early monitoring and intervention in this high-risk.

Idiopathic Intracranial Hypertension (IIH) presents an increasing health burden with changing demographic patterns. We studied nationwide trends in IIH epidemiology, treatment patterns, and associated outcomes using a large-scale database analysis within the United States (US).

We performed a retrospective analysis using the TriNetX US Collaborative Network database (1990-2024). We investigated demographic characteristics, time-based trends, geographic distribution, treatment pathway patterns, comorbidity profiles, and associated risks with IIH. We used multivariate regression, Cox proportional hazards modeling, and standardized morbidity ratios to assess various outcomes and associations.

Among 51,526 patients, we found a significant increase in adult IIH incidence from 16.0 per 100,000 in 1990-1999 to 127.0 per 100,000 in 2020-2024 (adjusted RR: 6.94, 95% CI: 6.71-7.17). Female predominance increased over time (female-to-male ratio: 3.29, 95% CI: 3.18-3.40). Southern regions showed the highest prevalence (43.0%, n=21,417). During the 2020-2024 period, initial medical management success rates varied between acetazolamide (42.3%) and topiramate (28.7%). Advanced interventional procedures showed 82.5% success rates in refractory cases during the same timeframe. Cox modeling for the entire study period (1990-2024) revealed significant associations between IIH and metabolic syndrome (HR: 2.14, 95% CI: 1.89-2.39) and cardiovascular complications (HR: 1.76, 95% CI: 1.58-1.94), independent of Body Mass Index.

Our findings highlight IIH as a systemic disorder with significant metabolic implications beyond its neurological manifestations. The marked regional disparities and rising incidence rates, especially among adults, suggest the need for targeted healthcare strategies. Early intervention success strongly predicts favorable outcomes, supporting prompt diagnosis and treatment initiation. These results advocate for an integrated approach combining traditional IIH management with broad metabolic screening care.

Controlling Nutritional Status (CONUT) score, a novel marker reflecting the malnutrition, has been demonstrated to predict all-cause mortality and major adverse cardiovascular events (MACE) in a wide range of diseases. The research intends to assess the clinical effects of malnutrition on patients who have percutaneous coronary intervention (PCI) after acute myocardial infarction (AMI).

In this retrospective observational study, we consecutively enrolled 3258 patients diagnosed with AMI from 2010 to 2016. Patients were categorized into three groups based on the CONUT score: normal, mild malnutrition, and moderate and severe malnutrition. The primary outcome was all-cause mortality. We develop cox proportional hazards models to investigate the relationship between the CONUT score and all-cause mortality among patients who underwent PCI after AMI.

According to the assessment via the CONUT score, a total of 43.7% patients experienced mild malnutrition, and 4.8% patients experienced moderate and severe malnutrition. During a median follow-up period of 8.6 years, there were 610 patients (18.7%) suffered from all-cause mortality. As malnutrition severity intensified, the occurrence of the primary endpoint saw a steady rise. After adjusting for multiple variables, the group classified with moderate and severe malnutrition exhibited an odds ratio of 1.56 (95% CI 1.13 to 2.15, p = 0.007) for the primary endpoint. Incorporating the CONUT score augments the prognostic accuracy of the GRACE risk score in predicting all-cause mortality (Absolute Integrated Discrimination Improvement = 0.008, p < 0.001; Category-free Net Reclassification Improvement = 0.144, p = 0.001).

Malnutrition is prevalent among patients with AMI and is significantly associated with an increased incidence of all-cause mortality. As a nutritional assessment tool, the CONUT score effectively aids in risk stratification and predicts poor prognosis in patients. Additional prospective clinical trials are required to evaluate the influence of nutritional interventions on outcomes in patients undergoing PCI after AMI.

Glioma is an aggressive brain tumor with a poor prognosis. Establishing an in vitro culture model that closely replicates the cellular composition and microenvironment of the original tumor has been challenging, limiting its clinical applications. Here, we present a novel approach to generate glioma organoids with a microenvironment (GlioME) from patient-derived glioma tissue. These organoids maintain the genetic and epigenetic characteristics of the primary tumor and preserve cell-to-cell interactions within the tumor microenvironment, including resident immune cells. Bulk RNA sequencing, whole exome sequencing, and DNA methylation analysis were used to confirm the molecular similarities between the organoids and primary glioma tissues. Immunofluorescence and flow cytometry were used to assess immune cell viability, comparing GlioME with floating glioma organoids. GlioME exhibited high responsiveness to chemotherapy and targeted therapy, demonstrating its potential for therapeutic screening applications. Notably, GlioME accurately predicted patient response to the recently approved MET inhibitor, vebreltinib. Thus, this organoid model provides a reliable in vitro platform for glioma microenvironment-related research and clinical drug screening.

Hemiplegia is characterized by muscle weakness on one side of the body, often resulting from damage to the brain, spinal cord, or associated nerves. This condition commonly occurs due to strokes, traumatic brain injuries (TBI), or spinal cord injuries (SCI), which can damage corticospinal neurons (CSNs) and the corticospinal tract (CST). However, there is still a notable lack of comprehensive studies that systematically characterize the anatomical and behavioral aspects of these hemiplegic animal models.

This study aimed to validate and compare existing models of TBI, stroke, and SCI in order to identify the most suitable preclinical hemiplegia models for future research.

Using viral-based retrograde tracing, we first mapped the cortical distribution of CSNs responsible for hindlimb movement. Anterograde and retrograde viral tracing techniques were then employed to label and evaluate the damage to CSNs and the CST in three models: photothrombotic stroke, Feeney's weight-drop TBI, and T10 hemi-section SCI. We also conducted behavioral tests to assess spontaneous motor function recovery, including open field and rotarod tests for gross motor function, as well as beam walking and irregular ladder walking tasks for assessing skilled motor function.

Our findings revealed that the CSNs controlling hindlimb movement are concentrated in the hindlimb region of the primary somatosensory cortex (S1HL). In the TBI and stroke models, there was complete destruction of ipsilateral CSNs in the S1HL and loss of CST fibers governing hindlimb movement. In the SCI model, ipsilateral CST fibers below T10 were also lost. After 8 weeks post-injury, all three groups of hemiplegic mice showed improvements in motor function, with gross motor function returning to normal levels; however, the recovery of skilled motor function was only modest. Notably, the degree of improvement in fine motor skills varied among the hemiplegia models, with mice subjected to brain injury (stroke and TBI) demonstrating significantly greater recovery in fine motor skills compared to those with SCI.

We confirmed and validated previous hemiplegia models by damaging CSNs or CST controlling hindlimb movement. Post-injury, gross motor function gradually returned to normal levels across all groups, whereas recovery of skilled motor function was limited. Furthermore, there were significant differences in the recovery of skilled motor function between brain injury models and the SCI model. These hemiplegic mouse models are valuable tools for studying post-injury skilled motor functions.

Not applicable.

This study aimed to identify, evaluate, and summarize the best available evidence on exercise rehabilitation for patients undergoing interventional treatment for heart valve disease, with the goal of informing clinical nursing practice and supporting evidence-based decision-making.

This scoping review was conducted in accordance with the PRISMA-ScR reporting guidelines and the Joanna Briggs Institute (JBI) framework for scoping reviews. A systematic search was performed across multiple databases and websites, including BMJ Best Practice, UpToDate, Cochrane Library, PubMed, EMBASE, CINAHL, China National Knowledge Infrastructure (CNKI), Wanfang Data Knowledge Service Platform, VIP Database, and China Medical Pulse Clinical Guidelines Network, to gather evidence on exercise rehabilitation for patients undergoing interventional treatment for heart valve disease. The search covered publications up to July 13, 2024. Researchers assessed the quality of the included literature using appropriate critical appraisal tools tailored to different types of evidence, extracted relevant content, and categorized the findings according to a pre-established evidence grading system.

Following a strict literature screening strategy, a total of 24 studies were included, consisting of 2 clinical decision articles, 1 guideline, 6 systematic reviews, 4 evidence summaries, 7 expert consensus reports, and 4 randomized controlled trials. A total of 27 evidence items were summarized and categorized into seven dimensions: team formation, exercise rehabilitation principles, assessment, preoperative prehabilitation, postoperative exercise rehabilitation, Outpatient and home-based rehabilitation, and health education.

This study consolidated 27 pieces of evidence on exercise rehabilitation for patients undergoing interventional therapy for heart valve disease based on the principles of evidence-based care. However, the evidence has not been implemented in clinical practice and its clinical effectiveness remains to be validated.

Cerebral infarction is a common cause of hypertrophic olive degeneration (HOD), while cerebral infarction is the most common type of stroke in China. When patients with a history of brainstem infarction present with new or progressively worsening symptoms, hypertrophic inferior olivary nucleus degeneration should be considered in the diagnosis, this report details a case of hypertrophic inferior olivary nucleus degeneration after cerebral infarction.

A 55-year-old male patient reported experiencing dizziness, unsteady walking, and persistent vertigo, along with blurred vision and reduced visual acuity two years ago, without any clear precipitating factors. With a medical history of hypertension, diabetes, and multiple strokes, the patient sought further diagnosis and treatment at various hospitals and was diagnosed with cerebral infarction. After being treated at our hospital, The examination indicates left finger-nose test (+), palatal myoclonus, nystagmus, and increased muscle tone in the left limb, Magnetic resonance imaging (MRI) scans and enhancements of the head conducted in the radiology department of our hospital revealed swelling of the inferior olivary nucleus of the medulla oblongata, with patchy T1WI isosignal and T2WI high-signal foci, FLAIR sequences showing high signal, without enhancement.Given symptomatic treatment, the patient improved and was discharged.

The diagnosis of HOD needs to fulfill the following three points: first, typical clinical manifestations; second, damage to the Guillain-Mollaret triangle; and third, enlarged T2WI high signal over the inferior olivary nucleus. The author reports the diagnosis and treatment of a patient with HOD, whose main manifestations were "dizziness and unsteady walking", with the aim of improving clinicians' understanding of the disease, especially raising the alertness of HOD after stroke, and reducing missed diagnosis and misdiagnosis.

The bone-specific protein osteocalcin (OCN) is an established marker of vascular calcification and vascular smooth muscle cell (VSMC) osteogenic trans-differentiation. Recent studies have revealed the regulatory function of externally administered OCN on atherosclerosis and vascular remodeling. However, the role of OCN in VSMCs involved in cell migration and neointima formation has not been clearly described.

Rat carotid-artery balloon-injury was performed to induce neointima formation. OCN expression was detected in injured carotid arteries by western blot and immunofluorescence staining. Rat primary cultured VSMCs were treated with tumor necrosis factor-α (TNF-α) and platelet-derived growth factor-BB (PDGF-BB). OCN overexpression was induced by virus infection. VSMC migration was detected by scratched wound-healing assay. The ratio of intima to media thickness and vascular cell adhesion molecule-1 (VCAM-1) expression were compared between wild type (WT) rat and OCN knockout (OCN-/-) rat after vascular injury. Blood pressure and vascular stiffness were detected between WT rat and OCN-/- rat by rat tail blood pressure test and small animal ultrasound.

OCN was significantly up-regulated in balloon-injured carotid arteries of rat and enhanced in VSMCs treated by the TNF-α and PDGF-BB. With OCN overexpression, VSMC proliferation and migration were simultaneously aggravated. OCN-/- rats maintained normal carotid artery architecture and function under physiological condition. After carotid artery injury, OCN-/- rats exhibited significantly reduced neointimal thickness and VCAM-1 expression of injured vessels compared to WT rats.

OCN participates in the pathological processes of vascular neointima formation and promotes inflammatory response of VSMC to vascular injury, but deletion of OCN does not affect vascular integrity under physiological condition, suggesting that OCN may provide new insights into the mechanism of intima hyperplasia.