Turmeric is a spice widely used in China, Southeast Asia, and in traditional Ayurvedic medicine. Its safety profile and efficacy as an antioxidant, anti-inflammatory, antimicrobial, antitumor, antidiabetic, and anti-obesity agent have led to extensive research into its potential role in preventing and treating metabolic diseases. The active compound in turmeric is curcumin, which exhibits low systemic bioavailability after oral administration. However, it is detectable in the gut, where it bidirectionally interacts with the gut microbiota (GM), which plays a crucial role in maintaining host health. The favorable effects of curcumin, particularly its hypoglycemic properties, are linked to alteration in intestinal dysbiosis observed in type 2 diabetes mellitus and metabolic syndrome patients. Restoration of the eubiotic GM may contribute to glycemic homeostasis. Preclinical and clinical studies have demonstrated the involvement of the GM in the regulation of glucose and lipid metabolism. Although the underlying mechanism remains incompletely understood, intestinal dysbiosis is associated with insulin resistance, hyperglycemia, and low-grade inflammation. In the present overview, we summarize the biological properties of curcumin, focusing on its link with GM and, therefore, on its potential role in metabolic diseases.

Background: Evaluation of donor lung function relies on the arterial oxygen partial pressure to inspired oxygen fraction ratio (PaO ₂ /FiO ₂ ) measurement. Hemodynamic, metabolic derangements, and therapeutic intervention occurring during brain dead observation may influence the evaluation of gas exchange. Methods: We performed a mathematical analysis to explore the influence of the extrapulmonary determinants on the interpretation of PaO ₂ /FiO ₂ in the brain‐dead donor and during Ex‐Vivo Lung Perfusion (EVLP). Results: High FiO ₂ and increased mixed venous oxygen saturation, caused by increased delivery and reduced consumption of oxygen, raise the PaO ₂ /FiO ₂ despite substantial intrapulmonary shunt. Anemia does not modify the PaO ₂ /FiO ₂ —intrapulmonary shunt relationship. During EVLP, the reduced artero‐venous difference in oxygen content increases the PaO ₂ /FiO ₂ without this corresponding to an optimal graft function, while the reduced perfusate oxygen‐carrying capacity linearizes the PaO ₂ /FiO ₂ —intrapulmonary shunt relationship. Conclusions: Adopting PaO ₂ /FiO ₂ to evaluate graft suitability for transplantation should account for extrapulmonary factors affecting its interpretation.

A study was carried out to investigate the presence of Echinococcus multilocularis in red foxes (Vulpes vulpes) in two regions of Turkey—central Anatolia (in Asia Minor) and Thrace (in the European part of Turkey). A total of 405 putative fox feces were collected from central Anatolia (186 specimens in 59 locations) and from Thrace (219 specimens in 114 locations). All samples were examined by the flotation and sieving method for taeniid eggs, and positive and putative samples were further analyzed by multiplex PCR. In seven samples from three locations in central Anatolia (5.1%) and in one (0.9%) from Thrace, E. multilocularis DNA was amplified, and this result was confirmed with another PCR specific for E. multilocularis. In addition, Echinococcus granulosus s.l. was found in two (0.5%) of the samples. Although alveolar echinococcosis (AE) is known as a serious zoonosis in Turkey, this is the first field study detecting E. multilocularis in collected fecal samples documenting the environmental contamination with eggs of this zoonotic parasite.

The acceptable duration of donor warm ischemia time (DWIT) after cardiocirculatory death (DCD) is still debated. We analyzed the biomolecular profile and function during ex vivo lung perfusion (EVLP) of DCD lungs and their correlation with lung transplantation (LuTx) outcomes. Donor data, procurement times, recipient outcomes, and graft function up to 1 year after LuTx were collected. During EVLP, the parameters of graft function and metabolism, perfusate samples to quantify inflammation, glycocalyx breakdown products, coagulation, and endothelial activation markers were obtained. Data were compared to a cohort of extended-criteria donors after brain death (EC-DBD). Eight DBD and seven DCD grafts transplanted after EVLP were analyzed. DCD’s DWIT was 201 [188;247] minutes. Donors differed only regarding the duration of mechanical ventilation that was longer in the EC-DBD group. No difference was observed in lung graft function during EVLP. At reperfusion, “wash-out” of inflammatory cells and microthrombi was predominant in DCD grafts. Perfusate biomolecular profile demonstrated marked endothelial activation, characterized by the presence of inflammatory mediators and glycocalyx breakdown products both in DCD and EC-DBD grafts. Early graft function after LuTx was similar between DCD and EC-DBD. DCD lungs exposed to prolonged DWIT represent a potential resource for donation if properly preserved and evaluated.

Serum vitamin D (VitD) levels have been inversely related with metabolic syndrome (MetS), although the direct impact of VitD is still debated. This study examined 879 subjects of working age from an obesity and occupational clinic in Milan, Italy. Among these participants, 316 had MetS, while 563 did not. A multiple logistic regression analysis was conducted to determine the odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) for MetS in relation to serum VitD levels. After controlling for age, sex, leisure time physical activity, and body mass index (BMI), individuals with VitD levels between 20 and 29.9 ng/dL, or at least 30 ng/dL, had approximately half the risk of developing MetS (OR: 0.52, 95% CI: 0.32–0.86 and OR: 0.50, 95% CI: 0.25–0.99, respectively) compared to those with VitD levels below 10 ng/dL. This study presents further evidence of the beneficial effect of adequate VitD levels on the risk of MetS in a population of overweight/obese workers, even after adjusting for BMI. This study supports the importance of testing for and—if required—supplementing VitD in individuals with metabolic risk factors.