Identification of phase angle and Triglyceride-Glucose index as biomarkers for prediction and management of diabetic foot disease.

Introduction: Approximately 25 % of diabetic patients develop diabetic foot ulcers (DFUs), significantly increasing morbidity, mortality, and healthcare costs. Effective control and prevention are crucial. Objective: This study aims to identify easily measurable parameters for predicting DFU risk by assessing the correlation between Phase Angle (PA) and the Triglyceride-Glucose (TyG) index with DFU risk. Materials and methods: A comparative case-control study was conducted at the General Hospital of Elche from March to June 2023 with 70 participants (33 with diabetes, 37 without). Cases had diabetes for over five years and a diabetic foot risk grade of 0, 1, or 2 (IWGDF 2019). Exclusion criteria included inability to walk, prior use of orthoses, and severe complications like edema or wounds. Predictive variables were PA, TyG index, body composition, and biochemical markers. Statistical analyses included Pearson/Spearman tests for correlations, Student's t-test/Mann-Whitney test for group comparisons, and ANOVA/Kruskal-Wallis tests for normally and non-normally distributed variables. Results: PAand TyG index were strongly linked to diabetic foot risk, supporting their potential as biomarkers. Significant relationships with other relevant biomarkers were also confirmed. Conclusion: PA and TyG index are valuable, easily measurable biomarkers for assessing diabetic foot risk, and can be monitored in primary care settings. Implementing these biomarkers in routine practice could enhance the management of diabetic complications, particularly in resource-limited settings, by enabling early detection and intervention, thus improving patient outcomes and reducing the burden of advanced complications.

Characterization of latex particle arrays by gas adsorption.

Assemblies of colloidal particles are frequently used in novel applications, and this requires nondestructive methods allowing overall characterization of the sample and collection of information about the quality of the arrays. From suspensions of polystyrene, poly[styrene-co-(2-hydroxyethylmethacrylate)], poly[styrene-co-acrylic acid], and poly[styrene-co-methacrylic acid], assemblies of spherical particles were obtained by elimination of the solvent in different ways-evaporation, gravity deposition, and filtration. These latex particle packings were characterized by scanning and transmission electron microscopy and by gas adsorption to determine the efficiency of packing. The surface area, total pore volume, and pore size distributions obtained from the adsorption and desorption data were related to characteristic parameters calculated for cubic close-packed spherical particles.

BDNF induces glutamate release in cerebrocortical nerve terminals and in cortical astrocytes.

In this paper we report that BDNF is able to stimulate the release of glutamate not only in cerebrocortical nerve terminals, but also in cortical astrocytes. The process of glutamate release, in both nerve terminals and astrocytes, is dependent upon the extracellular and intracellular Ca2+ levels and involves exocytosis, since tetanus toxin treatment abolishes the release of glutamate from both preparations. Further, preincubation of nerve terminals or astrocytes with K252a (a tyrosine kinase inhibitor) inhibits BDNF-evoked glutamate release, suggesting the involvement of Trk B receptors in this process. In astrocytes, the level of BDNF-induced glutamate release is higher in immature than in more mature cells. The results suggest a new pathway of cross-talk between neurons and astrocytes, which may play a role in synaptic plasticity and neurotoxicity.

Astrocytes in culture express the full-length Trk-B receptor and respond to brain derived neurotrophic factor by changing intracellular calcium levels: effect of ethanol exposure in rats.

Although cultured astroglial cells were reported to express exclusively the truncated non-catalytic Trk B receptor for brain-derived neurotrophic factor (BDNF), we detect here, using a sensitive ribonuclease protection assay, mRNAs for both truncated (TrkB-T) and the full length catalytic (TrkB-fl) form of BDNF receptor in developing cortical astrocytes and neurons in culture. Cortical neurons and immature astroglia, such as radial glia and proliferating astrocytes, express both the protein and mRNAs for TrkB-fl and TrkB-T, whereas the differentiation of astrocytes leads to a decrease in the trkB-fl mRNA, being the truncated TrkB the predominant receptor in differentiating and confluent astrocytes. The levels of TrkB-fl expression in proliferating and differentiating astrocytes and neurons correlates with the cell response to BDNF, monitored by the rise in intracellular [Ca(2+)](i). Foetal exposure to ethanol alters astroglial development and delays the reduction in trkB-fl mRNA levels observed with differentiation of astrocytes. These results demonstrate that immature astrocytes are able to express the catalytic Trk B receptors and to respond to BDNF with the activation of conventional signal transduction pathways. The results suggest that this signalling pathway is more activated in ethanol-exposed cells.

[Nitroglycerin patches: properties and norms for correct use]. / Parches de nitroglicerina. Propiedades y normas de uso correcto.

The frequent application of Nitroglycerin Transdermal Systems in patients who need a prophylaxis of anginal episodes requires that medical section should know to use them and their pharmacological properties. These knowledges about their application should be explained to patients and their relatives clear and concisely for them to achieve an accurate use. Having checked the required bibliography, I want to show in this article both the characteristics of this pharmacological preparation and some important points about educational process that patients and relatives should follow: at the same time, this article tries to answer all the questions which might arise.

Ethanol exposure enhances cell death in the developing cerebral cortex: role of brain-derived neurotrophic factor and its signaling pathways.

Exposure to ethanol during fetal development induces brain damage, causing cell loss in several brain areas and affecting synaptic connections. Because neurotrophin signaling plays an important role in neuronal survival and differentiation, we have investigated the effect of ethanol exposure on cell death in the developing cerebral cortex and whether this effect correlates with alterations in brain-derived neurotrophic factor (BDNF) levels, expression of its receptors, TrkB, and its signaling. We report that chronic ethanol intake during gestation and lactation enhances natural cell death and induces cell necrosis, decreases BDNF levels, and increases the ratio of the truncated to full-length TrkB mRNA receptors during postnatal developing cerebral cortex. Furthermore, we provide evidence that during brain development BDNF activates the extracellular signal-regulated kinases (ERK1 and ERK2) and the phosphoinoside-3-kinase (PI-3-K/Akt) pathways. However, BDNF-induced cell signaling throughout the above-mentioned survival pathways is significantly reduced by ethanol exposure. These findings suggest that ethanol-induced alterations in BDNF availability and in its receptor function might impair intracellular signaling pathways involved in cell survival, growth, and differentiation, leading to enhanced natural cell death during cerebral cortex development.

Glial fibrillary acidic protein expression in rat brain and in radial glia culture is delayed by prenatal ethanol exposure.

The alterations in astrocyte proliferation and differentiation induced by prenatal exposure to alcohol (PEA) suggest that ethanol exposure affects the radial glial cells, the main astrocytic precursors. We have investigated the effects of ethanol on the early stages of astrogliogenesis by analyzing the developmental pattern of vimentin and glial fibrillary acidic protein (GFAP) immunoreactivity and their mRNA levels during embryonic/fetal brain development and in radial glia in primary culture. GFAP appeared late in gestation and at day 5 of culture of radial glia, whereas GFAP mRNA was first detected on fetal day 15 and increased in content on fetal day 21. In contrast, the levels of vimentin and its mRNA were high at fetal day 15 but decreased on day 21. Alcohol exposure delays the appearance of GFAP and its mRNA and significantly decreases the GFAP expression in fetal brain and in primary culture of radial glia. In addition, some morphological alterations were observed in PEA glial cells in culture. These results demonstrate that astroglial precursor cells are damaged by prenatal exposure to ethanol and suggest that abnormalities in the astrogliogenesis may underlie the disruption in neuronal migration and other CNS alterations observed after prenatal ethanol exposure.

Salivary caffeine clearance predicts survival in patients with liver cirrhosis.

OBJECTIVE: Quantification of liver function in patients with cirrhosis is difficult. Caffeine clearance (CCI) has been suggested as a more exact method than those commonly used. The aim of this work was to assess the usefulness of CCl in survival prediction for these patients. METHODS: Thirty-four patients with cirrhosis of the liver of various causes were included; 19 were class A or B in Child-Pugh's classification and 15 were class C. CCl was determined from saliva samples. The mean length of follow-up was 33.8 months. A bivariant survival analysis was carried out following the Kaplan-Meier method, together with a multivariant analysis using the Cox proportional hazards model. RESULTS: Twelve patients died during the follow-up period. CCl values < 0.24 ml/kg/min, age > 60 yr, and nonalcoholic cause of cirrhosis were factors predicting lower survival. CCl was the only independent predictive factor in the multivariant analysis. CONCLUSIONS: CCl enables us to predict survival in cirrhotic patients and, considering its harmlessness, simplicity, and cost, can be used as a routine procedure in the assessment of these patients.

Alcohol exposure alters the expression pattern of neural cell adhesion molecules during brain development.

Neural cell adhesion molecules (NCAMs) play critical roles during development of the nervous system. The aim of this study is to investigate the possible effect of ethanol exposure on the pattern of expression and sialylation of NCAM isoforms during postnatal rat brain development because alterations in NCAM content and distribution have been associated with defects in cell migration, synapse formation, and memory consolidation, and deficits in these processes have been observed after in utero alcohol exposure. The expression of NCAM isoforms in the developing cerebral cortex of pups from control and alcohol-fed mothers was assessed by western blotting, ribonuclease protection assay, and immunocytochemistry. The highly sialylated form of NCAM [polysialic acid (PSA)-NCAM] is mainly expressed during the neonatal period and then is down-regulated in parallel with the appearance of NCAM 180 and NCAM 140. Ethanol exposure increases PSA-NCAM levels during the neonatal period, delays the loss of PSA-NCAM, decreases the amount of NCAM 180 and NCAM 140 isoforms, and reduces sialyltransferase activity during postnatal brain development. Neuraminidase treatment of ethanol-exposed neonatal brains leads to more intense band degradation products, suggesting a higher content of NCAM polypeptides carrying PSA in these samples. However, NCAM mRNA levels are not changed by ethanol. Immunocytochemical analysis demonstrates that ethanol triggers an increase in PSA-NCAM immunolabeling in the cytoplasm of astroglial cells, accompanied by a decrease in immunogold particles over the plasma membrane. These findings indicate that ethanol exposure during brain development alters the pattern of NCAM expression and suggest that modification of NCAM could affect neuronal-glial interactions that might contribute to the brain defects observed after in utero alcohol exposure.

Intracellular location, temporal expression, and polysialylation of neural cell adhesion molecule in astrocytes in primary culture.

Neural cell adhesion molecules (NCAMs) constitute a group of cell surface glycoproteins that control cell-cell interactions and play important morphoregulatory roles in the developing and regenerating nervous system. NCAMs exist in a variety of isoforms differing in the cytoplasmic domain and/or their content in sialic acid. The highly sialylated form (PSA-NCAM) is expressed by neurons, whereas it is believed that the less sialylated NCAM forms are synthesised by astrocytes. Moreover, little is known about the molecular sequence of the events that contribute to its expression at the cell surface. Here we report that during the proliferation of cortical astrocytes, at 4 days in primary culture, these cells expressed PSA-NCAM as well as NCAM 180. Then, during cell differentiation these isoforms progressively disappeared and the NCAM 140 became predominant. By immunofluorescence and immunocytochemistry studies we also show that PSA-NCAM and NCAM are first observed in small cytoplasmic spots or vesicles, located in or near the Golgi apparatus, as demonstrated by their co-localization with labelled wheat germ agglutinin (WGA) in this cell organelle. Thereafter, immunostained cytoplasmic NCAM gradually disappeared and became detectable at the cell surface of differentiating astrocytes. We also describe for the first time sialyltransferase activity in these cells and report that the levels of this activity correlated with the decrease in PSA-NCAM expression during the differentiation of astrocytes. These results will contribute to our understanding of the PSA and NCAM intracellular transport pathways and their expression at the cell surface. Moreover, the presence of PSA-NCAM in astrocytes suggests their possible role in nerve branching, fasciculation, and synaptic plasticity.

Experiencia en el uso de tolvaptán en el servicio de urgencias en pacientes con insuficiencia cardiaca aguda e hiponatremia / Emergency department experience with tolvaptan in patients with acute heart failure and hyponatremia

La hiponatremia es una alteración electrolítica común en los pacientes con insuficiencia cardiaca aguda (ICA) en los servicios de urgencias (SU). Es de etiología multifactorial, y entre sus principales mecanismos de producción se encuentran la secreción inadecuada de vasopresina (AVP) y el tratamiento diurético. El tratamiento convencional de la hiponatremia en la ICA (restricción de consumo de líquidos orales, infusión de solución salina y diuréticos), aunque puede ser efectivo, es complejo y en ocasiones de resultados impredecibles. El tolvaptán es un antagonista de la AVP que induce una diuresis de agua libre sin electrolitos. Ensayos clínicos recientes han mostrado la efectividad del tolvaptán, tanto en pacientes con hiponatremia de diferente etiología como en la insuficiencia cardiaca. Presentamos una serie de 10 pacientes con ICA e hiponatremia que fueron tratados con tolvaptán asociado al tratamiento convencional desde su llegada al SU. Se objetivó una rápida mejoría de la hiponatremia sin afectación de la funcional renal ni de los electrolitos sanguíneos. En el presente artículo se describe nuestra experiencia y discutimos aspectos relacionados con dicha terapia diurética (AU)

Hyponatremia is a common electrolyte abnormality in emergency patients with acute heart failure. The condition is multifactorial in origin but one of the principal mechanisms is dysregulated vasopressin secretion. Treatment involves diuretics. Hyponatremia in acute heart failure is conventionally managed by restricting oral intake of fluids, infusing a saline solution, and administering diuretics. This approach may be effective, but it is complicated and results can be unpredictable. Tolvaptan is a vasopressin antagonist that induces diuresis of electrolyte-free water. Recent clinical trials have shown that tolvaptan is effective in patients with hyponatremia due to various conditions, including heart failure. We report10 cases of acute heart failure and hyponatremia treated with tolvaptan associated with conventional management in the emergency department. Sodium levels returned to normal rapidly without alteration of renal function or blood electrolytes. We describe our experience with this drug and discuss issues related to diuretic treatment (AU)