Prevalence of chronic venous disease in health staff and its impact on quality of life at 6 months.

OBJECTIVE: To determine the frequency and stages of chronic venous disease (CVD) in health staff and its impact on the quality of life. METHOD: Cross-sectional study on health workers, between the ages of 20 and 60, indistinct gender, to remain standing position ≥6.5 hours per day for at least 5 days a week. Socio demographic variables were recorded. The Clinical-Etiology-Anatomy-Pathophysiology (CEAP) scale was used to stage the CVD; to measure the quality of life, the CIVIQ-20 (Chronic Venous Insufficiency Questionnaire) survey was applied at baseline, at 3 and 6 months. All patients underwent detailed clinical examination followed by color Doppler ultrasound and angiology review. RESULTS: Included 37 patients, 62.1% woman. Average age was 36.6 ± 8.8 years. By CEAP the 78.3% of the patients presented CVD and the highest prevalence was C1; corroborating by Doppler ultrasound only in 29.7% of the patients. The predominant symptoms were night cramps (54.5%). CONCLUSION: The frequency of CVD is like the literature. Patients with chronic venous disease have poor quality of life which improves with treatment.

OBJETIVO: Determinar la frecuencia y estadios de la enfermedad venosa crónica (EVC) en personal de salud y su impacto en calidad de vida. MATERIAL Y MÉTODOS: Estudio transversal en trabajadores de la salud, edad de 20 a 60 años, sexo indistinto, con bipedestación ≥ 6.5 horas/día por al menos 5 días a la semana. Se registraron variables sociodemográficas. La EVC se estadifico con la escala CEAP (Clinical-Etiology-Anatomy-Pathophysiology); la calidad de vida se midió basal, a 3 y 6 meses con la encuesta CIVIQ-20 (Chronic Venous Insufficiency Questionnaire 20). Además, se realizó examen clínico, ultrasonido Doppler y valoración por angiología. RESULTADOS: Incluyó 37 participantes, el 62.1% mujeres, edad promedio 36.6 ± 8.8 años. Acorde a la CEAP el 78.3% de los pacientes presentaron EVC (prevalencia mayor de C1). Se corroboró por ultrasonido Doppler en el 29.7%. El 54.5% presentaba calambres nocturnos. CONCLUSIONES: La frecuencia de EVC en personal de salud es similar a la reportada en la literatura; los individuos con EVC tienen mala calidad de vida.

An Antimicrobial Peptide Induces FIG1-Dependent Cell Death During Cell Cycle Arrest in Yeast.

Although most antibiotics act on cells that are actively dividing and non-dividing cells such as in microbe sporulation or cancer stem cells represent a new paradigm for the control of disease. In addition to their relevance to health, such antibiotics may promote our understanding of the relationship between the cell cycle and cell death. No antibiotic specifically acting on microbial cells arrested in their cell cycle has been identified until the present time. In this study we used an antimicrobial peptide derived from α-pheromone, IP-1, targeted against MATa Saccharomyces cerevisiae cells in order to assess its dependence on cell cycle arrest to kill cells. Analysis by flow cytometry and fluorescence microscopy of various null mutations of genes involved in biological processes activated by the pheromone pathway (the mitogen-activated protein kinase pathway, cell cycle arrest, cell proliferation, autophagy, calcium influx) showed that IP-1 requires arrest in G0/G1 in order to kill yeast cells. Isolating cells in different cell cycle phases by elutriation provided further evidence that entry into cell cycle arrest, and not into G1 phase, is necessary if our peptide is to kill yeast cells. We also describe a variant of IP-1 that does not activate the pheromone pathway and consequently does not kill yeast cells that express the pheromone's receptor; the use of this variant peptide in combination with different cell cycle inhibitors that induce cell cycle arrest independently of the pheromone pathway confirmed that it is cell cycle arrest that is required for the cell death induced by this peptide in yeast. We show that the cell death induced by IP-1 differs from that induced by α-pheromone and depends on FIG1 in a way independent of the cell cycle arrest induced by the pheromone. Thus, IP-1 is the first molecule described that specifically kills microbial cells during cell cycle arrest, a subject of interest beyond the process of mating in yeast cells. The experimental system described in this study should be useful in the study of the mechanisms at play in the communication between cell cycle arrest and cell death on other organisms, hence promoting the development of new antibiotics.

Expression pattern of transcription factors and intracellular cytokines reveals that clinically cured tuberculosis is accompanied by an increase in Mycobacterium-specific Th1, Th2, and Th17 cells.

Tuberculosis (TB) remains a major global health problem and is the second biggest cause of death by infectious disease worldwide. Here, we investigate in vitro the Th1, Th2, Th17, and Treg cytokines and transcriptional factors produced after Mycobacterium-specific antigen stimulation in patients with active pulmonary tuberculosis, clinically cured pulmonary tuberculosis, and healthy donors with a positive tuberculin skin test (TST+). Together, our data indicate that clinical cure after treatment increases the percentages of Mycobacterium-specific Th1, Th2, and Th17 cells compared with those found in active-TB and TST+ healthy donors. These results show that the host-parasite equilibrium in latent TB breaks in favor of the microorganism and that the subsequent clinical recovery posttreatment does not return the percentage levels of such cells to those observed in latent tuberculosis. Additionally, our results indicate that rather than showing an increase in the percentage of Mycobacterium-specific Tregs, active-TB patients display lower Th1 : Treg and Th17 : Treg ratios. These data, together with lower Th1 : Th2 and Th17 : Th2 ratios, may indicate a mechanism by which the breakdown of the host-parasite equilibrium leads to active-TB and changes in the repertoire of Mycobacterium-specific Th cells that are associated with clinical cure after treatment of pulmonary tuberculosis.

Monolayer formation of human osteoblastic cells on vertically aligned multiwalled carbon nanotube scaffolds.

Monolayer formation of SaOS-2 (human osteoblast-like cells) was observed on VACNT (vertically aligned multiwalled carbon nanotubes) scaffolds without purification or functionalization. The VACNT were produced by a microwave plasma chemical vapour deposition on titanium surfaces with nickel or iron as catalyst. Cell viability and morphology studies were evaluated by LDH (lactate dehydrogenase) release assay and SEM (scanning electron microscopy), respectively. The non-toxicity and the flat spreading with monolayer formation of the SaOs-2 on VACNT scaffolds surface indicate that they can be used for biomedical applications.