Cannabinoid type 1 receptor (CB1R) inhibition tends to be one of the promising strategies for the treatment of obesity and other related metabolic disorders. Although CB1R inhibition may cause adverse psychiatric effects including depression and anxiety, the investigation of the role of peripheral CB1R on weight loss and related metabolic parameters are urgently needed. We first explored the effect of rimonabant, a selective CB1R antagonist/inverse agonist, on some metabolic parameters in high fat-diet (HFD)-induced obesity in mice. Then, real-time PCR and electrophysiology were used to explore the contribution of high voltage-activated Ca2+ channels (HVACCs), especially Cav1.1, on rimonabant's effect in skeletal muscle (SM) in HFD-induced obesity. Five-week HFD feeding caused body weight gain, and decreased glucose/insulin tolerance in mice compared to those in the regular diet group (P<0.05), which was restored by rimonabant treatment compared to the HFD group (P<0.05). Interestingly, HVACCs and Cav1.1 were decreased in soleus muscle cells in the HFD group compared to the control group. Daily treatment with rimonabant for 5 weeks was shown to counter such decrease (P<0.05). Collectively, our findings provided a novel understanding for peripheral CB1R's role in the modulation of body weight and glucose homeostasis and highlight peripheral CB1R as well as Cav1.1 in the SM as potential targets for obesity treatment.

This study aims to explore the effect of microRNA-21 (miR-21) on the proliferation of human degenerated nucleus pulposus (NP) by targeting programmed cell death 4 (PDCD4) tumor suppressor. NP tissues were collected from 20 intervertebral disc degeneration (IDD) patients, and from 5 patients with traumatic spine fracture. MiR-21 expressions were tested. NP cells from IDD patients were collected and divided into blank control group, negative control group (transfected with miR-21 negative sequences), miR-21 inhibitor group (transfected with miR-21 inhibitors), miR-21 mimics group (transfected with miR-21 mimics) and PDCD4 siRNA group (transfected with PDCD4 siRNAs). Cell growth was estimated by Cell Counting Kit-8; PDCD4, MMP-2,MMP-9 mRNA expressions were evaluated by qRT-PCR; PDCD4, c-Jun and p-c-Jun expressions were tested using western blot. In IDD patients, the expressions of miR-21 and PDCD4 mRNA were respectively elevated and decreased (both P<0.05). The miR-21 expressions were positively correlated with Pfirrmann grades, but negatively correlated with PDCD4 mRNA (both P<0.001). In miR-21 inhibitor group, cell growth, MMP-2 and MMP-9 mRNA expressions, and p-c-Jun protein expressions were significantly lower, while PDCD4 mRNA and protein expressions were higher than the other groups (all P<0.05). These expressions in the PDCD4 siRNA and miR-21 mimics groups was inverted compared to that in the miR-21 inhibitor group (all P<0.05). MiR-21 could promote the proliferation of human degenerated NP cells by targeting PDCD4, increasing phosphorylation of c-Jun protein, and activating AP-1-dependent transcription of MMPs, indicating that miR-21 may be a crucial biomarker in the pathogenesis of IDD.

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.

This study proposes a methodology for evaluating the risk of coal bumps in multiple-seam longwall mining. Both the stress field and the total energy release (TER) during retreat were evaluated in the specified case involving multiple-seam mining using the LaModel program. The results of numerical simulations indicated that both the peak vertical stresses on the panel edges and the peak TERs in the outby longwalls increased significantly as the horizontal offsets were reduced from 60 m to zero. With the comprehensive consideration of the stress field and TERs, a conservative offset of 60 m was ultimately adopted when developing the gateroads of the lower panel in the field. The field measurements indicated that coal bumps were avoided completely by employing the proposed design, and the maximum roof-to-floor and rib-to-rib convergences of the tailgate during retreat were only 360 mm and 576 mm, respectively.

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.

Present studies show that nitrate accumulation is the major factor influencing the water uptake by vegetables, but there is lack of knowledge on how the relationship between nitrate and water concentrations in different vegetable tissues. We determined nitrate accumulation and water content in vegetables of rape, Chinese cabbage, and spinach under different nitrogen levels (experiment I), 29 spinach cultivars (experiment II), and 27 rape cultivars (experiment III). The results from experiments I-III showed a highly linear relationship between nitrate accumulation and water content, and the levels thereof in different organs of the vegetables revealed that the petiole exhibited the best correlation between them compared with the root and leaf blade. These suggest that (1) vegetables with high water content have high nitrate content, (2) water content in the petiole can be used to screen cultivars with low levels of nitrate accumulation, and (3) increasing soil water content in agronomic practice is essential to decreasing nitrate accumulation in vegetables.

To effectively control and treat river water pollution, it is very critical to establish a water quality prediction system. Combined Principal Component Analysis (PCA), Genetic Algorithm (GA) and Back Propagation Neural Network (BPNN), a hybrid intelligent algorithm is designed to predict river water quality. Firstly, PCA is used to reduce data dimensionality. 23 water quality index factors can be compressed into 15 aggregative indices. PCA improved effectively the training speed of follow-up algorithms. Then, GA optimizes the parameters of BPNN. The average prediction rates of non-polluted and polluted water quality are 88.9% and 93.1% respectively, the global prediction rate is approximately 91%. The water quality prediction system based on the combination of Neural Networks and Genetic Algorithms can accurately predict water quality and provide useful support for realtime early warning systems.

Gut-derived endotoxin and pathogenic bacteria have been proposed as important causative factors of morbidity and death during heat stroke. However, it is still unclear what kind of damage is induced by heat stress. In this study, the rat intestinal epithelial cell line (IEC-6) was treated with heat stress or a combination of heat stress and lipopolysaccharide (LPS). In addition, propofol, which plays an important role in anti-inflammation and organ protection, was applied to study its effects on cellular viability and apoptosis. Heat stress, LPS, or heat stress combined with LPS stimulation can all cause intestinal epithelial cell damage, including early apoptosis and subsequent necrosis. However, propofol can alleviate injuries caused by heat stress, LPS, or the combination of heat stress and LPS. Interestingly, propofol can only mitigate LPS-induced intestinal epithelial cell apoptosis, and has no protective role in heat-stress-induced apoptosis. This study developed a model that can mimic the intestinal heat stress environment. It demonstrates the effects on intestinal epithelial cell damage, and indicated that propofol could be used as a therapeutic drug for the treatment of heat-stress-induced intestinal injuries.