This report discusses a patient with chronic ankle pain for 2 years. No respiratory symptoms were present, but her father had tuberculosis (TB) when she was four. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were elevated. Empirical antibiotic therapy was initiated. The viral panel test was negative, while the purified protein derivative (PPD) test showed >20 mm induration. Chest radiograph and computed tomography (CT) scan were normal. Ankle radiograph revealed hypodense areas, osteolytic changes, and soft tissue swelling in the cuboid bone. Magnetic resonance imaging (MRI) confirmed soft tissue signal in the cuboid bone. Biopsy showed non-caseating necrotizing granulomatous reaction. The polymerase chain reaction (PCR) and culture confirmed M. tuberculosis infection. Anti-TB treatment was initiated. Skeletal TB in peripheral bones is very rare. Early-stage diagnosis can be challenging due to various potential causes, leading to irreversible complications. Thus, a high index of clinical suspicion should always be maintained. Imaging findings may be suggestive but not confirmative.

Real-time data collection, sharing, and analysis of health-related information are made feasible using the Internet of Things (IoT) in the healthcare field. IoT could transform patient care, enhance clinical results, and optimize healthcare operations by integrating remote monitoring, automation, and data-driven decision-making. Determining the blood type is essential for safe blood transfusions, organ transplant compatibility, and preventing immunological responses. Additionally, the ABO blood group system prediction supports research on associations between blood types and various medical conditions, such as susceptibility to infections, cardiovascular diseases, and clotting disorders. Antigens (A and B) and the Rhesus (Rh) factor (+ or -) are usually used to determine blood grouping. By combining known antibodies with blood samples, the blood group can be examined by the agglutination reactions through image processing techniques. In this work, we proposed an intelligent portable blood analyser for blood type prediction and determination using an IoT-based system. The blood group identification and detection in blood samples is performed with a fabricated simulation device using a 3D Printer and acrylic materials. This system determines a solution using the adaptive Hough transform algorithm and provides the highest level of efficiency and accuracy in blood group identification and counting. Thus, the proposed system lowers the possibility of transfusion-related allergic responses and stores precise outcomes that exclude human-made errors, enabling us to instantly determine a person's blood type.

Spinal ischemia is a rare condition and accounts for only 1-2% of all neurovascular diseases. In this case, spinal ischemia occurred in a 46-year-old patient after prolonged resuscitation after out-of-hospital cardiac arrest and following invasive coronary angiography and percutaneous coronary intervention under mechanical circulatory support with an Impella (Abiomed, Danvers, MA, USA). Magnetic resonance imaging showed an infarct demarcation from the 5^th thoracic vertebra to the conus medullaris. The supply areas of the anterior spinal artery (paraplegia, no response to pain stimulus) as well as the posterior spinal arteries (reduced sensation of touch) were affected. Magnetic resonance imaging of the brain showed both signs of hypoxic brain damage and embolic events. In terms of pathogenesis, the low-flow-phase of resuscitation with associated arterial thromboembolism as well as a thromboembolic event by the Impella need to be considered. To date, limited data on the prevalence and incidence of spinal ischemia after resuscitation and/or use of an Impella are available in the literature.

Impella (ventricular assist device) can be associated with thromboembolic events.The low flow phase of resuscitation can be associated with arterial thromboembolism.Spinal ischemia can occur after resuscitation.

Tryptophan (TRP) metabolism via the kynurenine (KYN) pathway links immune function, energy metabolism, and redox homeostasis. Dysregulation of this pathway has been implicated in inflammatory conditions and heart failure. Here, we investigated the acute effects of exercise on TRP-KYN metabolism and its relationship with natural killer (NK) cell function in controls and patients with heart failure with reduced ejection fraction (HFrEF).

Control (n=13) and HFrEF (n=16) groups had comparable composition regarding age and sex. Participants were investigated at baseline, immediately after a maximal symptom-limited cardiopulmonary exercise test (CPET), and after 2 hours of resting. Blood samples were obtained at all time points to assess NK cell counts and phenotypic parameters by flow cytometry, as well as tryptophan metabolites and protein secretome by mass spectrometry and targeted proteomics, respectively. NK cells and non-NK cells from blood of healthy donors were stimulated ex vivo prior to flow cytometry-based measurement, indoleamine 2,3-dioxygenase (IDO) mRNA expression analysis and mass spectrometry-based tryptophan metabolite analysis.

Plasma TRP levels decreased post-exercise in both study groups, with increased metabolism down the KYN route, albeit only in HFrEF patients, a significant accumulation of quinolinate (QUIN) was seen. Increases in plasma KYN-to-TRP ratios correlated with more circulating NK cell counts and IL-12p70 levels mainly in the HFrEF group. Ex vivo, IL-12 exposure of human total primary NK cells increased representation of the CD56-bright subset, IDO mRNA expression, and TRP-to-KYN conversion, resulting in net KYN accumulation and elevated QUIN production. In non-NK cells, IFN-γ exposure similarly promoted TRP-to-KYN flux and QUIN formation.

Collectively, our observations confirm earlier descriptive reports of exercise-induced upregulation of KYN production by NK cells and add mechanistic evidence that IL-12 induces a phenotype shift in NK cells, which is accompanied by accelerated TRP metabolism into KYN. Our data point to a concerted interaction between leukocyte subsets upon acute exercise, via the release of IL-12, with potential implications for differential energy metabolism and immune regulation in HFrEF.

Metabolic dysfunction-associated steatotic liver disease (MASLD), characterised by hepatic steatosis and metabolic dysfunction (i.e., obesity, type 2 diabetes, dyslipidaemia, and hypertension), is affecting over 30% of the adult population worldwide. It can progress to metabolic dysfunction-associated steatohepatitis (MASH) and fibrosis, cirrhosis and even hepatocellular carcinoma. However, most patients with non-cirrhotic MASLD die from extrahepatic causes, particularly cardiovascular disease and non-hepatic cancers, underscoring the need for a holistic approach to surveillance and treatment. Emerging research on MASLD has revealed a substantial heterogeneity in the MASLD population, driven by sex-specific factors, genetic susceptibility, cardiometabolic risk profile, lifestyle and socio-economic determinants, highlighting the necessity of individualised and holistic management of MASLD patients. Although lifestyle intervention remains the cornerstone of MASLD, the pharmacotherapeutic landscape is rapidly evolving, with resmetirom and semaglutide now approved for non-cirrhotic MASH with moderate-to-advanced fibrosis. In addition, metabolic/bariatric surgery has proven to be a highly effective option for patients with MASH. Given its close association with cardiometabolic and malignant comorbidities, MASLD requires individualised, holistic management integrating hepatic and extrahepatic risks. Multiprofessional care, involving among others behavioural therapists, dieticians and physiotherapists, may improve outcomes of lifestyle interventions, particularly in high-risk settings. A stepwise and integrated care model combining early case-finding, risk stratification, and tailored lifestyle and pharmacological interventions is essential to address both hepatic and extrahepatic complications. This review summarises the current understanding of MASLD heterogeneity, clinical assessment, and therapeutic advances, and outlines principles for individualised and coordinated care.

Atherosclerosis is a major contributor to cardiovascular disease globally, posing significant challenges for effective management. Conventional pharmacological therapies, particularly statins and lipid-lowering agents, remain pivotal due to their accessibility and long-term benefits, but are limited by suboptimal efficacy and side-effects. Nanomedicine presents promising targeted drug delivery systems that enhance treatment specificity while reducing toxicity, and has the potential for developing personalized therapy. In interventional cardiology, advances in stent technology from bare metal stents to drug-eluting stents and bioresorbable scaffolds have improved vascular healing, however complications such as delayed endothelialization, smooth muscle cell proliferation, and thrombosis persist. To further enhance stent performance and biocompatibility, innovative surface coatings have emerged, by precisely tailoring the chemistry, topography, and biofunctionalization to optimize healing, accelerate endothelialization, and minimize restenosis/thrombosis through diverse strategies. Despite progress, challenges pertaining to coating durability, manufacturing complexity, and limited long-term clinical evidence still continue. Future research should emphasize multifunctional coatings that synergistically enhance endothelial recovery and inhibit restenosis and thrombosis, with nanotechnology and biomimicry offering significant opportunities for next-generation stent development. This review explores a spectrum of anti-atherosclerotic approaches aimed at combating cardiovascular diseases, from pharmacological agents to stents, highlighting diverse material design principles and its biological performance, recent advances in nanoengineered stent coatings, and the overall clinical landscape.

Atherosclerosis, a chronic inflammatory disease, is pathologically associated with mitochondrial dysfunction. Mitochondria contribute to oxidative stress, vascular endothelial dysfunction, and chronic inflammatory cascades through pathways such as dynamic imbalance, abnormal epigenetic regulation, disruption of multi-organelle communication, and dysregulation of cell death signaling. Targeting mitochondria has therefore emerged as a promising therapeutic strategy beyond conventional treatments , which often fail to address this underlying pathology. Recent advances in nanomaterials enable precise mitochondrial intervention. Although conventional therapies such as statins and anti-inflammatory drugs can partially mitigate symptoms, they do not directly correct mitochondrial abnormalities and are often limited by systemic side effects. Recent progress in nanotechnology has enabled the development of mitochondria-targeted delivery systems, including liposomes, polymeric nanoparticles, and biomimetic carriers. These platforms enhance mitochondrial accumulation by incorporating targeting motifs or exploiting the negative mitochondrial membrane potential and specific interactions with outer membrane proteins. Among these, TPP⁺-modified liposomes can target the mitochondrial matrix via electrostatic interactions, effectively delivering drugs such as coenzyme Q10 to mitochondria, offering notable clinical potential. Moreover, Szeto-Schiller 31, which targets mitochondrial electron transport chain repair and reduces the secretion of inflammatory cytokines, has entered Phase II clinical trials. This review discusses the mechanistic role of mitochondrial dysfunction in atherosclerosis and evaluates the application of mitochondria-targeted delivery systems in atherosclerosis therapy. It also highlights the challenges these systems face, including issues related to delivery efficiency, biosafety, and targeting specificity. By linking molecular mechanisms with translational innovation, it highlights the significant potential of mitochondrial-targeted therapies.

Aging is an intricate process with physiological dysregulation across many systems; mechanisms like chronic inflammation and telomere attrition are key to the progressive deterioration of the organism. Although aging is universal, its rate varies widely among individuals, even among those of the same chronological age. Biological age reflects one's physiological status and is a measure for assessing aging rate and acceleration. There is also organ-specific aging with varying trajectories, with the molecular basis of this heterogeneity apparent across several organ systems, ascribed to complex genetic associations between blood-based epigenetic and organ-specific aging, demonstrating both homogeneity and heterogeneity. Chronic diseases may accelerate aging of the respective biological systems or subsystems and organs, with organ- and/or blood-specific epigenetic clocks determining aging heterogeneity. Aging is universal; its rate varies widely among individuals, even among those of the same chronological age. Biological age reflects an individual's physiological condition and is a useful measure for estimating aging rate and accelerated aging. Recently, the interest is growing regarding the link of accelerated aging with cardiovascular disease and mortality. Data indicate that persons with accelerated aging are at higher risk of progressing to multimorbidity and death. Elucidating these associations is crucial for informing strategies to prevent cardiovascular disease and premature death. Hopefully, a more specific quantitative assessment of individual aging may more precisely disclose one's aging and biological status. There is hope that pharmacologic intervention may tard the aging process, and also decrease or eliminate health disparities, which could foster better cardiovascular and general health for all populations.

Telemedicine usage surged during the COVID-19 pandemic, shaping how patients access healthcare services. Its sustained role in post-pandemic healthcare may uncover long-term trends and variations in utilization.

To characterize telemedicine utilization from 2019 to 2024 and identify patient characteristics associated with telemedicine use.

This retrospective cohort study analyzed outpatient visits across five hospitals within the University of Pennsylvania Health System (Penn Medicine) from January 1, 2019, to September 30, 2024.

The primary outcome was whether each outpatient encounter was conducted via telemedicine (vs in-person). We used multivariable logistic regression clustering on patients to assess associations between telemedicine use and patient- and encounter-level characteristics, including demographics, insurance, patient portal use, income, clinical comorbidity, distance from care, provider specialty, encounter type, hospital index, and visit year.

The study included 46,149,734 visits among 2,248,341 patients. Telemedicine surged from 1% of visits pre-pandemic to 17% in April 2020, stabilized at 8-13% through late 2020, and remained 4-6% from 2022 to 2024. Telemedicine use was lower among older adults (aOR 0.67 for ages 40-64; 0.47 for ≥ 65 vs. < 40 years), males (aOR 0.90), and new visits (aOR 0.46). Higher use was observed among unmarried (aOR 1.10), patient portal users (aOR 1.44), patients with fewer comorbidities, those living ≥ 15 miles from care (aOR 1.42 vs. < 5 miles), lower-income (< $50,000 aOR 1.06 vs. $50,000-$100,000), and primary care (aOR 1.23 vs. specialty care). Telemedicine use was lower among Non-Hispanic Black (aOR 0.88), Hispanic (aOR 0.94), and Asian (aOR 0.82) patients compared to Non-Hispanic White patients. Patterns differed by clinical condition, with disproportionately higher use among White patients with mental health disorders.

Telemedicine use persists post-pandemic but reflects differences in access by age, race/ethnicity, socioeconomic status, and prior engagement with the patient portal. Targeted policies are needed to ensure equitable telemedicine adoption and accessibility for all patients.

As US homelessness grows, so too does the forced removal of individuals and their belongings from where they are staying, also known as encampment sweeps, which have been associated with increased overdose and reduced healthcare access. We examined associations between past-year experiences of encampment sweeps and suboptimal health behaviors, outcomes, and healthcare access from 155 people who use drugs (PWUD) in Massachusetts. Thirty-eight percent of participants experienced a sweep in the past year, with 73% citing difficulty accessing health or social services following sweeps. Those who had been relocated were more likely to report worse mental health symptoms and feeling unwelcome in medical settings (both p < 0.05). Findings provide additional evidence that encampment sweeps disrupt access to essential services, likely further marginalizing PWUD and people who are homeless. Strategies that support, rather than punish, these populations are needed.