Tobacco use remains a major public health concern worldwide. In residential treatment facilities for substance use disorders, little effort is made to help individuals quit smoking, even though the primary goal of treatment is to promote the overall health through abstinence from all drugs. The aim of this study was to analyze the perceptions of professionals and individuals in treatment regarding the management of tobacco use within residential therapeutic settings. We conducted a qualitative study in treatment centers in Spain, using thematic content analysis of focus groups with 29 professionals and 53 individuals. According to participants, tobacco use during substance use disorder treatment substitutes for the use of other drugs and serves as a tool for emotional regulation. Furthermore, many participants believed that quitting smoking may increase the risk of relapse for other substances, although scientific evidence shows otherwise. These insights suggest that prevailing attitudes toward tobacco use in treatment contexts are outdated, underscoring the need for a paradigm shift in how this issue is addressed. (PsycInfo Database Record (c) 2026 APA, all rights reserved).

Tactile contact during social interactions is believed to enhance the experience of pleasure. Dopaminergic neurons in the ventral tegmental area (VTA) are crucial for the regulation of pleasurable emotions. We aim to reveal the specific circuit mechanisms by which the VTA contributes to pleasure derived from tactile contact.

Paradigms of social interaction in the presence of physical contact (SIPPC) and social interaction in the absence of physical contact (SIAPC) were established. The expression of c-fos in different brain regions was detected by immunofluorescence. A combination of behavioural tests, fibre-optic calcium imaging, chemogenetics, patch-clamp techniques and molecular biological methods were used to investigate the circuit mechanism mediating pleasure of tactile contact.

Dopaminergic neurons in the VTA were implicated in triggering pleasurable emotions associated with SIPPC. Mechanistically, SIPPC promoted the disinhibition of presynaptic neurons and enhanced excitatory synaptic transmission. Furthermore, projections from the mPFC to VTA dopaminergic neurons were activated during SIPPC. Chemogenetic activation of the mPFC-VTA^DA circuit increased SIPPC-induced pleasure, whereas its inhibition decreased it. SIPPC triggered dopamine release in the nucleus accumbens (NAc), where the inhibition of dopamine receptors (D₁R) can reverse the pleasure-promoting effect of mPFC-VTA^DA circuit activation during SIPPC.

Collectively, these findings elucidate the key roles and mechanisms by which VTA^DA neurons receive projections from the mPFC and subsequently release dopamine in the NAc to regulate the pleasure induced by tactile contact, which provide new insights into the mechanisms underlying the association between tactile and social interaction.

Immunosuppressed patients with extensive skin barrier disruption face extraordinary risks for polymicrobial infections. The rapid, sequential emergence of multidrug-resistant (MDR) bacteremia and candidemia in such hosts constitutes a particularly lethal complication with limited therapeutic options.

We report a 74-year-old woman with refractory pemphigus vulgaris (PV), type 2 diabetes mellitus, and chronic obstructive pulmonary disease who developed a cascade of MDR infections over a 14-day hospitalization. Following initial methicillin-resistant Staphylococcus aureus (MRSA) skin colonization, she developed Serratia marcescens bacteremia, subsequently complicated by wound superinfection with carbapenem-resistant Acinetobacter baumannii (CRAB) and multiple Candida species, including the rare yeast Kodamaea ohmeri. Despite sequential antimicrobial escalation-from piperacillin-tazobactam/linezolid to meropenem/amikacin, and finally caspofungin-her condition deteriorated with diabetic ketoacidosis, culminating in the family's decision to pursue discharge with comfort care based on the patient's previously expressed wishes; she died three days later. K. ohmeri demonstrated reduced fluconazole susceptibility (MIC = 8 µg/mL), highlighting the diagnostic and therapeutic challenges posed by emerging fungal pathogens.

This case starkly illustrates the catastrophic potential of rapid, sequential MDR infections in profoundly immunocompromised hosts with skin barrier defects. It underscores the critical importance of early microbiological surveillance, the clinical urgency of dynamic antimicrobial stewardship, and the imperative for multidisciplinary management to navigate the irreconcilable conflict between necessary immunosuppression and life-threatening infection.

This study aimed to examine the level of adherence to self-care behaviors across socio-demographic and clinical characteristics in patients with type 2 diabetes mellitus (T2DM).

A total of 270 patients with diabetes who were referred to two medical centers in Gorgan, Iran, participated in this cross-sectional study. We assessed adherence using a reliable questionnaire, the Summary of Diabetes Self-Care Activities (SDSCA). The anthropometric measurements and blood pressure were assessed based on a standard protocol. The biochemical variables were gathered based on the medical documents of the centers. To compare adherence scores across clinical and demographic variables, independent t-test and ANOVA were used. A p-value less than 0.05 was considered statistically significant.

The mean age of participants was 57.16 ± 9.20 years, and nearly 66% of patients were female. The mean SDSCA score was 3.50 ± 0.87. Regarding self-care domains, the highest adherence scores were observed for medication use (6.07 ± 1.42) and foot care (6.05 ± 1.50), while blood glucose monitoring (2.16 ± 1.89) yielded the lowest score. A significant difference was observed between adherence scores and better glycemic control (P<0.001) and a more favorable lipid profile (P=0.001). No significant difference was observed between factors such as age, gender, duration of diabetes, BMI, and type of medication used with total score adherence.

Overall adherence to self-care practices among T2DM patients was suboptimal. Moreover, higher adherence to self-care behaviors is associated with a better metabolic situation. Targeted educational and awareness programs are recommended to enhance self-care behaviors and optimize metabolic outcomes in this population.

Subclinical myocardial dysfunction may precede overt heart failure in type 2 diabetes mellitus (T2DM), while conventional cardiac biomarkers largely reflect myocardial wall stress or cardiomyocyte injury. We systematically reviewed circulating fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15) across two distinct evidence domains: direct diagnostic or associative evidence for early myocardial dysfunction and longitudinal prognostic evidence for subsequent cardiovascular outcomes in T2DM. MEDLINE/PubMed, Embase, Scopus and Web of Science were searched from inception, and eligible studies related FGF21 and/or GDF15 to objective cardiac phenotypes or cardiovascular outcomes. Four GDF15 cohorts harmonised to a per-1-SD increase in log-transformed GDF15 showed higher cardiovascular risk (pooled HR 1.23, 95% CI 1.10-1.37; I² = 16.2%), with stable leave-one-out analyses. Three FGF21 cohorts yielded a pooled HR of 1.60 (95% CI 1.08-2.39; I² = 69.9%). In an exploratory leave-one-out analysis, omission of the Lenart-Lipińska 2013 cohort yielded HR 1.32 (95% CI 1.15-1.52; I² = 0%); this was interpreted as an influence analysis rather than an alternative primary estimate. Diagnostic evidence remained limited: FGF21 AUC ranged from 0.70 to 0.88, whereas one GDF15 study reported AUC 0.83 for asymptomatic diabetic cardiomyopathy. The current evidence therefore supports prognostic association rather than validated early diagnostic performance or demonstrated incremental predictive utility beyond established biomarkers; prospective head-to-head validation in subclinical disease is required.

Psoriasis is a systemic chronic inflammatory skin disease associated with musculoskeletal, cardiovascular, metabolic, psychiatric, and gastrointestinal comorbidities. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RAs have emerged as potential therapeutic adjuncts in psoriasis because, beyond their metabolic effects, these agents exhibit anti-inflammatory properties and may reduce expression of cytokines and inflammatory biomarkers. This review summarizes the current evidence from randomized trials and nonrandomized studies evaluating GLP-1 RAs and dual GIP/GLP-1 RAs in patients with psoriasis and discusses their potential role in disease management. Observational studies of liraglutide, semaglutide, exenatide, dulaglutide, and tirzepatide generally demonstrated improvements in psoriasis severity, body weight, metabolic parameters, inflammatory biomarkers, and quality of life, although most were limited by small sample sizes and uncontrolled designs. Randomized trials similarly suggest dermatologic benefit, particularly among patients with obesity and/or type 2 diabetes mellitus. Most notably, the phase 3b TOGETHER trial demonstrated greater skin clearance and weight reduction with ixekizumab plus tirzepatide compared with ixekizumab alone in patients with moderate-to-severe psoriasis and overweight or obesity. Complementary findings from the TOGETHER-PsA trial showed improvement in psoriatic arthritis disease activity as early as week 4, before clinically meaningful weight loss, supporting potential weight-independent anti-inflammatory effects of these agents. Future studies should include patients without obesity or diabetes to clarify the relative contributions of weight loss and direct anti-inflammatory effects to clinical response and determine whether the dermatologic benefits of GLP-1-based therapies extend to patients without underlying metabolic dysfunction.

Type 2 diabetes mellitus (T2DM) compromises bone quality and biomechanical integrity, driven by impaired microstructure, suppressed turnover, and collagen abnormalities. Crucially, this fragility occurs despite normal bone mineral density and may initiate early in the disease, underscoring the need for timely skeletal assessment.

Twelve male Sprague-Dawley rats were randomly assigned to either the control or the T2DM group. Within 2 weeks of model confirmation, all underwent dual-energy x-ray absorptiometry, in vivo magnetic resonance imaging of the liver and femur, and blood collection for comprehensive biochemical and lipid profiling. Subsequently, all right femurs were harvested for micro-computed tomography, biomechanical testing, and Masson's staining. The tibia and fibula were collected for the analysis of bone metabolism markers and advanced glycation end products (AGEs).

Compared with the control group, T2DM rats exhibited higher body weight from week 10 onward, along with increased fat mass and body fat percentage. Serum total cholesterol, alanine aminotransferase and aspartate aminotransferase levels were elevated. Hepatic proton density fat fraction (PDFF) was higher. No intergroup differences of serum calcium, magnesium and phosphorus, cancellous/cortical bone and biomechanical testing parameters. Femoral collagen fiber organization was impaired in T2DM rats. Procollagen type I N-terminal propeptide was upregulated, while osteocalcin relative mRNA expression was downregulated. Femoral collagen organization was strongly negatively correlated with hepatic PDFF.

In early-stage T2DM, bone damage follows a temporal sequence (organic before inorganic) and site-specific (pronounced in cancellous bone). These changes parallel systemic metabolic disturbances, and ameliorating adipose and hepatic dysfunction may help restore bone collagen matrix homeostasis.

Question How does the metabolic microenvironment shaped by adipose tissue redistribution affect bone microarchitecture in patients with early-stage T2DM? Findings In early-stage T2DM, bone damage may exhibit a temporal (organic-first) and spatial (cancellous-predominant) pattern, and coexists particularly with abnormal lipid metabolism and hepatic dysfunction. Relevance statement In early-stage T2DM, abnormal lipid metabolism and liver function may serve as a potential indicator of compromised bone quality. Therapeutic interventions aimed at ameliorating adipose and hepatic dysfunction in T2DM may help restore bone collagen matrix homeostasis.

Chronic kidney disease (CKD) represents a significant health burden worldwide, characterized by a gradual decline in kidney function and increased risk of cardiovascular events. Current therapeutic strategies like inhibition of the renin-angiotensin-aldosterone system or sodium-glucose cotransporter 2 inhibitors (SGLT2i), while beneficial, often fail to fully halt CKD progression, and a significant residual risk of disease progression persists. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), initially developed for the treatment of type 2 diabetes (T2D), have emerged as promising agents with pleiotropic effects extending beyond glycemic control and weight loss. Evidence from major cardiovascular outcome trials and dedicated CKD studies demonstrates that GLP-1 RAs can confer significant cardiovascular and nephroprotective benefits in patients with T2D and CKD. These benefits include reductions in major adverse cardiovascular events, slowing of kidney disease progression (as measured by estimated glomerular filtration rate (eGFR) decline), and decreased albuminuria. The mechanisms underlying these effects are complex and involve multiple pathways, including anti-inflammatory, anti-fibrotic, and antioxidative actions, as well as improvements in hemodynamic parameters. We provide a comprehensive overview of the current clinical and preclinical evidence supporting the use of GLP-1 RAs in CKD. We discuss the proposed mechanisms of action by which GLP-1 RAs exert their nephroprotective effects and explore the potential for these agents to improve kidney outcomes across a broad spectrum of patients with CKD and critically evaluate the potential risks and safety profile associated with GLP-1 RA use.

Vibrio vulnificus, a Gram-negative bacillus, is frequently present in warm estuarine and coastal waters and is a notable pathogen responsible for seafood-related fatalities globally. Infection typically arises from ingesting contaminated seafood or exposure of skin wounds to tainted seawater, resulting in primary or secondary sepsis, as well as severe skin and soft tissue infections.

Upon hospital admission, a 51-year-old man with chronic gastritis, long-term alcohol use, type 2 diabetes, thrombocytopenia, and active hepatitis B and C presented with acute right upper quadrant abdominal pain, high fever, and a history of consuming raw fish (sashimi) before symptom onset, suggesting a foodborne infection. Despite denial of recent seawater exposure or seafood handling, his condition rapidly deteriorated, resulting in septic shock, moderate acute respiratory distress syndrome, and necrotizing fasciitis of the left lower extremity within 72 hours. Laboratory findings revealed severe thrombocytopenia, hyperlactatemia, multiple organ dysfunction, and metabolic acidosis. Vibrio vulnificus was identified via peripheral blood metagenomic next-generation sequencing. Whole-exome sequencing incidentally detected a heterozygous missense variant in the DOCK2 gene (c.4511C>T, p. Thr1504Met), classified as a variant of uncertain significance. In silico analyses suggested a benign effect, leaving any potential link to disease severity undetermined without functional confirmation.

Severe V. vulnificus sepsis may develop through foodborne transmission, even in the absence of typical exposure to seawater or seafood handling. Disease severity in this patient was primarily influenced by chronic liver disease, alcohol abuse, and diabetes. Clinicians should watch for V. vulnificus infection in patients with these risk factors who present with septic shock or rapidly progressive soft tissue infections, regardless of exposure history.