Diabetic foot ulcers (DFUs) are the fastest growing chronic complication of diabetes mellitus, with more than 400 million people diagnosed globally, and the condition is responsible for lower extremity amputation in 85% of people affected, leading to high-cost hospital care and increased mortality risk. Neuropathy and peripheral arterial disease trigger deformities or trauma, and aggravating factors such as infection and edema are the etiological factors for the development of DFUs. DFUs require identifying the etiology and assessing the co-morbidities to provide the correct therapeutic approach, essential to reducing lower-extremity amputation risk. This review focuses on the current treatment strategies for DFUs with a special emphasis on tissue engineering techniques and regenerative medicine that collectively target all components of chronic wound pathology.

The two primary pathophysiological characteristics of patients with type 2 diabetes mellitus (T2DM) are insulin resistance (IR) and beta cell dysfunction. It has been proposed that the development of IR is secondary to the accumulation of triacylglycerols and fatty acids in the muscle and liver, which is in turn thought to be secondary to an enzymatic defect in mitochondrial beta-oxidation. The purpose of the present study was to analyze the molecules of intermediary metabolism to determine if an alteration in mitochondrial function exists in T2DM patients and, if so, to determine whether this alteration is caused by excess nutrients or an enzymatic defect. Seventy-seven subjects were recruited and divided into four groups (21 T2DM patients, 17 non-diabetic overweight/obese subjects, 20 offspring of T2DM patients, and 19 healthy subjects). Anthropometric parameters were determined by air plethysmography, and biochemical and metabolic parameters were measured, including 31 acylcarnitines (ACs) and 13 amino acids quantified by MS/MS and 67 organic acids measured by GC/MS. Patients with T2DM showed elevation of short-chain ACs (C2, C4), a glycogenic amino acid (valine), a glycogenic and ketogenic amino acid (tyrosine), and a ketogenic amino acid (leucine) as well as altered excretion of dicarboxylic acids. T2DM offspring with abnormal glucose tolerance test GTT showed increased levels of C16. Subjects in the obese group who were dysglycemic also showed altered urinary excretion of dicarboxylic acids and lower levels of a long-chain AC (C14:2). These results suggest that mitochondrial beta-oxidation is altered in T2DM patients and that the alteration is most likely caused by nutrient overload through a different pathway from that observed in obese subjects.

The primary strategy to avoid adverse impacts from insect-mediated pathogen transmission is the chemical control of vector populations through insecticides; its continued use has led to insecticide resistance and unknown consequences on vector competence. This review aims to systematically analyze and synthesize the research on the influence of insecticide resistance (IR) on vector competence (VC). Thirty studies met the inclusion criteria. Twenty studies, conducted either in laboratory or field settings, described the influence of phenotypic insecticide resistance and mechanisms on VC in vectors of human pathogens. Seven studies showed the effect of exposure to insecticides on VC in vectors of human pathogens. Three studies reported the influence of phenotypic resistance and mechanisms on VC in crop pests. The evidence shows that IR could enhance, impair, or have no direct effect on VC in either field or laboratory-designed studies. Similar positive and negative trends are found in pest vectors in crops and studies of insecticide exposure and VC. Even though there is evidence that exposure to insecticides and IR can enhance VC, thus increasing the risk of pathogen transmission, more investigations are needed to confirm the observed patterns and what implications these factors could have in vector control programs.

Background: Risk factors for developing long COVID are not clearly established. The present study was designed to determine if any sign, symptom, or treatment of the acute phase, or personal characteristics of the patient, is associated with the development of long COVID. Methods: A cohort study was carried out, randomly selecting symptomatic COVID-19 patients and not vaccinated. The severity of the acute illness was assessed through the number of compatible COVID-19 symptoms, hospitalizations, and the symptom severity score using a 10-point visual analog scale. Results: After multivariate analysis, a severity score ≥8 (RR 2.0, 95%CI 1.1–3.5, p = 0.022), hospitalization (RR 2.1, 95%CI 1.0–4.4, p = 0.039), myalgia (RR 1.9, 95%CI 1.08–3.6, p = 0.027), tachycardia (RR 10.4, 95%CI 2.2–47.7, p = 0.003), and use of antibiotics (RR 2.0, 95%CI 1.1–3.5, p = 0.022), was positively associated with the risk of having long COVID. Higher levels of education (RR 0.6, 95%CI 0.4–0.9, p = 0.029) and type positive B blood group (B + AB, RR 0.44, 95%CI 0.2–0.9, p = 0.044) were protective factors. The most important population attributable fractions (PAFs) for long COVID were myalgia (37%), severity score ≥8 (31%), and use of antibiotics (27%). Conclusions: Further studies in diverse populations over time are needed to expand the knowledge that could lead us to prevent and/or treat long COVID.

Iron and copper chelation restricts Plasmodium growth in vitro and in mammalian hosts. The parasite alters metal homeostasis in red blood cells to its favor, for example metabolizing hemoglobin to hemozoin. Metal interactions with the mosquito have not, however, been studied. Here, we describe the metallomes of Anopheles albimanus and Aedes aegypti throughout their life cycle and following a blood meal. Consistent with previous reports, we found evidence of maternal iron deposition in embryos of Ae. aegypti, but less so in An. albimanus. Sodium, potassium, iron, and copper are present at higher concentrations during larval developmental stages. Two An. albimanus phenotypes that differ in their susceptibility to Plasmodium berghei infection were studied. The susceptible white stripe (ws) phenotype was named after a dorsal white stripe apparent during larval stages 3, 4, and pupae. During larval stage 3, ws larvae accumulate more iron and copper than the resistant brown stripe (bs) phenotype counterparts. A similar increase in copper and iron accumulation was also observed in the susceptible ws, but not in the resistant bs phenotype following P. berghei infection. Feeding ws mosquitoes with extracellular iron and copper chelators before and after receiving Plasmodium-infected blood protected from infection and simultaneously affected follicular development in the case of iron chelation. Unexpectedly, the application of the iron chelator to the bs strain reverted resistance to infection. Besides a drop in iron, iron-chelated bs mosquitoes experienced a concomitant loss of copper. Thus, the effect of metal chelation on P. berghei infectivity was strain-specific.

Bruxism is a jaw muscle activity that involves physio-pathological, psycho‑social, hereditary and genetic factors. The purpose of this study was to determine the associations between self‑reported bruxism, anxiety, and neuroticism personality trait with the rs6313 polymorphism in the gene HTR2A. A sample of 171 subjects of both sexes (14‑53 years of age) was included. The control group (group 1, n=60) exhibited no signs or symptoms of bruxism. The case group had signs and symptoms of bruxism (n=112) and was subdivided into group 2, bruxism during sleep (n=22); group 3, awake bruxism (n=44); and group 4 combined bruxism (n=46). As diagnostic tools, the Self‑Reported Bruxism Questionnaire (SBQ), the Beck Anxiety Inventory (BAI) and the Eysenck Personality Questionnaire Revised‑Abbreviated (EPQR‑A) were used. HTR2A (rs6313) SNPs were determined by qPCR for all the participants. The packages SPSS, maxLik and EPI‑INFO were used for data analysis. The combined bruxism group reported higher scores in bruxism symptoms, mean = 32.21; anxiety symptoms, mean = 14.80; and neuroticism, mean = 3.26. Combined bruxism was associated with a higher degree of neuroticism (OR=15.0; CI 1.52‑148.32) and anxiety in grade 3‑moderate (OR=3.56; CI 1.27‑10.03), and grade 4‑severe (OR=8.40; CI 1.45‑48.61), as determined using EPISODE computer software. Genotypic homogeneity analysis revealed no significant differences in allele frequency (P=0.612) among the four groups. The population was in Hardy‑Weinberg equilibrium (maxLik package). In conclusion, the three instruments confirm traits of bruxism, anxiety and neuroticism in individuals with bruxism. These data were ratified when the sample was divided by genotypic homo­geneity. On the other hand, there was no significant difference between the groups in the SNPs rs6313 from the HTR2A gene.