Antimicrobial peptide HI-3 from Hermetia illucens alleviates inflammation in lipopolysaccharide-stimulated RAW264.7 cells via suppression of the nuclear factor kappa-B signaling pathway.

Hermetia illucens-3 (HI-3), an active insect antimicrobial peptide extracted from H. illucens larvae, exerts antibacterial and anticancer activity. However, the inflammatory effects and their relative molecular mechanisms remain unclear. To explore the inflammatory effects of HI-3, an inflammatory model was induced using 1 ng/mL LPS in RAW264.7 cells. The cell viability and phagocytosis of LPS-stimulated RAW264.7 cells were then detected after HI-3 treatment. Furthermore, the antioxidant activity, the levels of proinflammatory cytokines, and the expression levels of both p65 and inhibitor of nuclear factor kappa B (IκB) were measured. Results showed that HI-3 could inhibit the differentiation, proliferation, phagocytosis, and antioxidant ability, as well as the secretion and messenger RNA expression levels of IL-6, TNF-α, and IL-1ß of LPS-induced RAW264.7 cells in a dose-dependent manner. At the same time, the level of the anti-inflammatory cytokine IL-10 was increased after HI-3 treatment. Western blotting results showed that HI-3 suppressed LPS-induced p65 and IκB activation in a dose-dependent manner. Therefore, HI-3 exerts its anti-inflammatory effect by inhibiting the expression of proinflammatory cytokines and the activation of p65 and IκB, which indicated that HI-3 could be a promising therapeutic medicine for inflammation.

Marginal parental donors for pediatric living donor liver transplantation.

PURPOSE OF REVIEW: Living donor liver transplantation (LT) has been increasingly recognized as an effective treatment modality with excellent patient survival. Indications for LT have evolved not only for cholestatic liver disease, but also metabolic liver diseases. Living donor selection, particularly for pediatric inherited disease, is essential to prevent morbidity, both in the donor and recipient. RECENT FINDINGS: Based on 30 years of experience in pediatric living donor LT in Japan, we could identify marginal parental living donors who have potential risks following LT, including heterozygous mothers with ornithine transcarbamylase deficiency, heterozygous protein C deficiency, heterozygous hypercholesterolemia, heterozygous protoporphyria, asymptomatic parental donors with paucity of intrahepatic bile duct, and human leukocyte antigen-homozygous parental donors. SUMMARY: Although these situations seem rare due to infrequency of the condition, careful living donor evaluation is required to optimize the outcomes for pediatric recipients. In the setting of an appropriate selection of a living donor, we should avoid any additional hazards, given that the procedure itself has risks for a healthy individual.

High expression of TNFSF13 in tumor cells and fibroblasts is associated with poor prognosis in non-small cell lung cancer.

OBJECTIVES: To examine high expression of tumor necrosis factor ligand superfamily member 13 (TNFSF13), which is correlated with several malignancies. METHODS: TNFSF13 messenger RNA expression in tumor cells and fibroblasts in a cohort of patients with non-small cell lung cancer (NSCLC) was analyzed by quantitative real-time polymerase chain reaction and immunohistochemistry using a tissue microarray. RESULTS: TNFSF13 expression was significantly higher in lung adenocarcinomas compared with squamous cell carcinomas (P = .022). High TNFSF13 expression in NSCLC stroma was related with low differentiation (P = .045) and sex (male > female, P = .005). Cox proportional hazards regression univariate and multivariable analysis revealed TNFSF13 expression in NSCLC tumor cells (P = .007) or fibroblasts (P = .027) as an independent prognostic factor in the 5-year overall survival rate. CONCLUSIONS: Our findings indicate TNFSF13 is a prognostic factor in NSCLC and suggest TNFSF13 may be a novel therapeutic target for NSCLC.

Evidence for schema theory from surface electromyography: an artificial neural network approach.

In order to study voluntary movement control, we applied artificial neural networks (ANNs) to define the temporal patterns of surface electromyography (SEMG) activity used by normal subjects in performing three tasks, namely, wrist extension, continuous extension-flexion movements and extension-flexion movements for which the pause time between extension and flexion were 250 ms. SEMGs of 8 muscles were simultaneously recorded together with wrist movement. The results provided some evidence for the schema theory.

The use of artificial neural networks in the motor program.

Though it is commonly assumed that the brain creates "motor programs" which store the information essential to perform a motor skill, little direct evidence exists for such motor programs. Electromyography (EMG) provides a look into the motoneurons--level of a movement by measuring the electrical activity in relation to the muscle's involvement in the movement In this paper, artificial neural networks (ANNs) were applied to define the temporal patterns of EMG activity used by normal subjects in performing step-tracking tasks, and how such patterns change with practice. Our results demonstrate that ANNs could be trained to detect the input-output relationship between muscles' onset times and reaction times, and provided evidence to support the existence of a motor program.

[Role of nitric oxide in iron-induced toxicity in rat hearts].

The aim of the present study was to explore the effect of nitric oxide (NO) on iron-induced toxicity in rat hearts. Langendorff perfused rat heart and enzymatically isolated cardiomyocytes were used. It was shown that lipophilic Fe-HQ reduced the contractile amplitude, velocity and end-diastolic cell length in the cardiomyocyte, while the left ventricular developed pressure (LVDP), +/-dp/dt(max), heart rate and coronary flow showed biphasic alterations, which increased in the first 2 min and then was followed by a decline in isolated perfused rat heart; the contents of lactate dehydrogenase (LDH) and creatine kinase (CK) in the coronary effluent and the malondialdehyde (MDA) in the myocardium were increased. L-arginine (L-Arg), an NO precursor, reduced the contractile amplitude and end-diastolic cell length in the cardiomyocyte; but reversibly increased LVDP, +/-dp/dt(max), and coronary flow in isolated perfused rat heart. Pretreatment with L-Arg aggravated the Fe-HQ-induced decrease in contractile amplitude, velocity and end-diastolic cell length in the cardiomyocyte; LVDP, +/-dp/dt(max), heart rate and coronary flow were significantly reduced in the perfused heart, and the levels of LDH and CK increased in the coronary effluent. In contrast, the NOS inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) blocked the Fe-HQ induced change in contractile amplitude, velocity and end-diastolic cell length in the cardio- myocyte; it inhibited the decrease in LVDP, LVEDP and +/-dp/dt(max), and reduced the LDH and CK. Removing endothelial cells in coronary vessels attenuated the increase in LVDP and +/-dp/dt(max) at the beginning of Fe-HQ perfusion. It is suggested that L-Arg aggravates the iron-induced cardiac dysfunction, NO can mediate the iron-induced toxicity in heart, and endothelial cells in coronary vessels play an important role in the early stage of the effect of iron.