Resumo Ligula intestinalis é um parasita cestódeo que acomete peixes de água doce em diversos países do mundo. O presente estudo visa revelar a diversidade filogenética, genética e de haplótipos das sequências do gene mt-CO1 enviadas ao banco de dados do NCBI de diferentes países, por meio de análise in-silico. As sequências gênicas de 105 mt-CO1 (371 pb) de L. intestinalis obtidas do NCBI foram utilizadas para análises bioinformáticas. As sequências foram submetidas a análise filogenética e de haplótipos. Como resultado da análise de haplótipos de L. intestinalis, 38 haplótipos foram obtidos de 13 países diferentes. Hap24 constituiu 44,76% da rede de haplótipos obtida. Mudanças nos nucleotídeos entre os haplótipos ocorreram em 1-84 pontos diferentes. A China e a Turquia apresentam os maiores valores do índice de fixação (Fst), 0,59761, enquanto o menor (-0,10526) foi encontrado entre a Rússia e a Turquia. Este estudo fornece uma linha de base para futuros estudos em larga escala sobre epidemiologia, aspectos ecológicos, padrão de distribuição, dinâmica de transmissão e dispersão populacional de L. intestinalis em todo o mundo.

Abstract Ligula intestinalis is a cestode parasite that affects freshwater fish in different countries of the world. The current study aims to reveal the phylogenetic, genetic and haplotype diversity of mt-CO1 gene sequences sent to the NCBI database from different countries by using in-silico analysis. The 105 mt-CO1 (371 bp) gene sequences of L. intestinalis obtained from NCBI were used for bioinformatics analyses. Sequences were subjected to phylogenetic and haplotype analysis. As a result of the haplotype analysis of L. intestinalis, 38 haplotypes were obtained from 13 different countries. Hap24 constituted 44.76% of the obtained haplotype network. Changes in nucleotides between haplotypes occurred at 1-84 different points. China and Turkey have highest fixation index (Fst) values of 0.59761, while the lowest (-0.10526) was found between Russia and Turkey. This study provides a baseline for future studies on extensive scale on the epidemiology, ecological aspects, distribution pattern, transmission dynamics and population dispersion of L. intestinalis worldwide.

The levels of serum inflammatory cytokines and the activation of nuclear factor kappa B (NF-κB) and hypoxia inducible factor-1α (HIF-1α) in heart tissues in response to different frequencies of intermittent hypoxia (IH) and the antioxidant tempol were evaluated. Wistar rats (64 males, 200-220 g) were randomly divided into 6 experimental groups and 2 control groups. Four groups were exposed to IH 10, 20, 30, or 40 times/h. The other 2 experimental groups were challenged with IH (30 times/h) plus tempol, either beginning on day 0 (IH30T0) or on day 29 (IH30T29). After 6 weeks of challenge, serum levels of tumor necrosis factor (TNF)-α, intracellular adhesion molecule (ICAM)-1, and interleukin-10 were measured, and western blot analysis was used to detect NF-κB p65 and HIF-1α in myocardial tissues. Serum levels of TNF-α and ICAM-1 and myocardial expression of NF-κB p65 and HIF-1α were all significantly higher in IH rats than in controls (P<0.001). Increased IH frequency resulted in more significant changes. Administration of tempol in IH rats significantly reduced levels of TNF-α, ICAM-1, NF-κB and HIF-1α compared with the non-tempol-treated group (F=16.936, P<0.001). IH induced an inflammatory response in a frequency-dependent manner. Additionally, HIF-1α and NF-κB were increased following IH administration. Importantly, tempol treatment attenuated this effect.

ABSTRACT Objective: To explain a definition of “interface respiratory failure” as arterial blood gas assay with arterial oxygen partial pressure in the range of 60–75 mmHg. Subjects and Methods: We compared arterial blood gases (ABGs), resting respiratory drive and its derivatives, mechanics of respiratory muscles, resistance and compliance of the respiratory tract and some important cytokines (interleukin-4 and interferon-γ) of stable chronic obstructive pulmonary diseases (COPD) subgroups (total 50 cases) and control group (25 cases). Results: The patients attaining the “interface respiratory failure” stage developed great changes in respiratory mechanics parameters and inflammatory mediator, which might cause the exacerbation of COPD and the inclination to generate “real respiratory failure” and COPD progression. Conclusions: The definition of interface respiratory failure is scientific, direct and its width is appropriate. We should intervene appropriately and positively to avoid progression from “interface respiratory failure” to the “real respiratory failure” stage, and this avoidance means a higher survival rate and a lower medical expense. Interventions should focus on oxygen therapy, bronchodilators, improving respiratory compliance, cytokines and anti-infective agents, respectively.

RESUMEN: Objetivo: Explicar una definición de “insuficiencia respiratoria de interfaz” como análisis de gasometría arterial con presión parcial de oxígeno arterial en el rango de 60–75 mmHg. Sujetos y métodos: Comparamos la gasometría arterial (ABG, por sus siglas en inglés), la dinámica respiratoria de descanso y sus derivados, la mecánica de los músculos respiratorios, la resistencia y com-pliancia (distensibilidad) de las vías respiratorias y algunas importantes citoquinas (Interleuquina-4 y el interferón-γ) de subgrupos estables de enfermedad pulmonar obstructiva crónica (EPOC) (total 50 casos) y grupo control (25 casos). Resultados: Los pacientes que alcanzaron la etapa de “insuficiencia respiratoria de interfaz” desarrollaron grandes cambios en los parámetros de mecánica respiratoria y mediador inflamatorio, que podrían causar la exacerbación de la EPOC y la inclinación a generar “insuficiencia respiratoria real” así como la progresión de la EPOC. Conclusiones: La definición de insuficiencia respiratoria de interfaz es científica, directa y su amplitud es apropiada. Debemos intervenir adecuadamente y positivamente para evitar la progresión de la “insuficiencia respiratoria de interfaz” a la etapa de “insuficiencia respiratoria real”. El hacerlo significa una mayor tasa de supervivencia y un menor gasto médico. Las intervenciones deben centrarse en la terapia de oxígeno, los broncodilatadores, el mejoramiento de la compliancia respiratoria, las citoquinas y los agentes antiinfecciosos, respectivamente.

To explore the effects of adipose tissue-derived stem cells (ADSCs) on the proliferation and invasion of pancreatic cancer cells in vitroand the possible mechanism involved, ADSCs were cocultured with pancreatic cancer cells, and a cell counting kit (CCK-8) was used to detect the proliferation of pancreatic cancer cells. ELISA was used to determine the concentration of stromal cell-derived factor-1 (SDF-1) in the supernatants. RT-PCR was performed to detect the expression of the chemokine receptor CXCR4 in pancreatic cancer cells and ADSCs. An in vitro invasion assay was used to measure invasion of pancreatic cancer cells. SDF-1 was detected in the supernatants of ADSCs, but not in pancreatic cancer cells. Higher CXCR4 mRNA levels were detected in the pancreatic cancer cell lines compared with ADSCs (109.3±10.7 and 97.6±7.6 vs 18.3±1.7, respectively; P<0.01). In addition, conditioned medium from ADSCs promoted the proliferation and invasion of pancreatic cancer cells, and AMD3100, a CXCR4 antagonist, significantly downregulated these growth-promoting effects. We conclude that ADSCs can promote the proliferation and invasion of pancreatic cancer cells, which may involve the SDF-1/CXCR4 axis.