Gradient boosting DD-MLP Net: An ensemble learning model using near-infrared spectroscopy to classify after-stroke dyskinesia degree during exercise.

This study aims to develop an automatic assessment of after-stroke dyskinesias degree by combining machine learning and near-infrared spectroscopy (NIRS). Thirty-five subjects were divided into five stages (healthy, patient: Brunnstrom stages 3, 4, 5, 6). NIRS was used to record the muscular hemodynamic responses from bilateral femoris (biceps brachii) muscles during passive and active upper (lower) limbs circular exercise. We used the D-S evidence theory to conduct feature information fusion and established a Gradient Boosting DD-MLP Net model, combining the dendrite network and multilayer perceptron, to realize automatic dyskinesias degree evaluation. Our model classified the upper limb dyskinesias with high accuracy: 98.91% under the passive mode and 98.69% under the active mode, and classified the lower limb dyskinesias with high accuracy: 99.45% and 99.63% under the passive and active modes, respectively. Our model combined with NIRS has great potential in monitoring the after-stroke dyskinesias degree and guiding rehabilitation training.

Age-related difference in muscle metabolism patterns during upper limb's encircling exercise: a near-infrared spectroscopy study.

Aging is usually accompanied by decrease in limb motor function and change in muscle metabolism patterns. However, few studies have investigated the aging effect on muscle hemodynamics of the upper extremity. This study aims to explore the aging effect on muscle metabolism patterns during upper limb's exercise. Twelve middle-aged and elderly subjects and 12 young subjects were recruited, and muscle oxygenation signals from these subjects' biceps brachii muscles were collected during active and passive upper limb's encircling exercise with near-infrared spectroscopy (NIRS). The old group showed stronger muscle hemodynamic metabolism than the young group. The multiscale fuzzy approximate entropy and multiscale transfer entropy analyses indicated higher complexity and stronger interlimb coupling of the muscle oxygenation signals for the old group. Based on the selected muscle metabolism features, the constructed support vector machine model showed a high accuracy rate for classifying the two groups of subjects: 91.6% for the passive mode and 87.5% for the active mode. Our results proved the specific muscle metabolism patterns in the upper limb's exercise for old subjects, promoting the understanding of the aging effect on muscle hemodynamics.

Selenium deficiency induces duodenal villi cell apoptosis via an oxidative stress-induced mitochondrial apoptosis pathway and an inflammatory signaling-induced death receptor pathway.

Selenium (Se) is an important nutritional trace element possessing antioxidant properties. Our goal was to elucidate the effect and mechanism of Se deficiency on the intestinal cell fate. One-day-old three-yellow chickens were fed a low Se diet for 1, 3, and 5 weeks. Histologic characteristics, protein expression profiles, antioxidant activities, inflammatory signaling, and the apoptosis status in duodenum mucosa were investigated. Histological results showed that Se deficiency could increase inflammatory cell infiltration, karyopyknosis of the epithelial cells, cytoplasm vacuolization and dissolution of goblet cells. The proteomics results indicated that Se deficiency could induce apoptosis of cells in duodenal villi via inhibition of antioxidant redox signaling and activation of NF-κB signaling. Further analysis results showed that Se deficiency decreased the total antioxidant capacity of duodenum mucosa via down-regulating the transcription level and activities of glutathione peroxidase (GPX), reduced glutathione (GSH), and thioredoxin reductase (TrxR). The NF-κB signaling pathway was activated by Se deficiency-induced reactive oxygen species (ROS). TUNEL, DNA ladder, immunohistochemical assay, and western blotting proved that selenium deficiency could induce duodenal villi cell apoptosis. The results also indicated that Se deficiency can cause duodenal villi cell apoptosis via an oxidative stress-induced mitochondrial apoptosis pathway (intrinsic pathway) and an inflammatory signaling-induced death receptor pathway (extrinsic pathway). Our data may provide new insight into the prevention and treatment of chronic diarrhea caused by Se deficiency.

Selenium deficiency induces splenic growth retardation by deactivating the IGF-1R/PI3K/Akt/mTOR pathway.

Selenium (Se) deficiency impairs the development and function of immune system in human beings and animals. We investigated the effect and molecular mechanism of Se deficiency on spleen development in chicken. The concentration of Se in blood and spleen, the spleen weight and splenocyte number, the histological characteristics of spleen, the concentration of growth factors in serum, the transcription level of growth factor receptor gene and the activity of growth and proliferation pathway in spleen were investigated. We found that the growth of the spleen and the splenocyte number were significantly lower in the chicken fed with Se-deficient diet for 21 and 35 days. The ELISA and qRT-PCR results showed that the serum IGF-I concentration and the transcription level of IGF1R gene in spleen were significantly lower in the SD group. The Western blotting and immunohistochemistry results showed that Se deficiency could deactivate the PI3K/Akt/mTOR pathway in spleen. In summary, the results indicated that Se deficiency decreases the growth rate of spleen and the number of splenic lymphocytes by deactivating the IGF-1R/PI3K/Akt/mTOR pathway.

Low-level laser therapy attenuates LPS-induced rats mastitis by inhibiting polymorphonuclear neutrophil adhesion.

The aim of this study was to investigate the effects of low-level laser therapy (LLLT) on a rat model of lipopolysaccharide (LPS)-induced mastitis and its underlying molecular mechanisms. The rat model of mastitis was induced by inoculation of LPS through the canals of the mammary gland. The results showed that LPS-induced secretion of IL-1ß and IL-8 significantly decreased after LLLT (650 nm, 2.5 mW, 30 mW/cm(2)). LLLT also inhibited intercellular adhesion molecule-1 (ICAM-1) expression and attenuated the LPS-induced decrease of the expression of CD62L and increase of the expression of CD11b. Moreover, LLLT also suppressed LPS-induced polymorphonuclear neutrophils (PMNs) entering the alveoli of the mammary gland. The number of PMNs in the mammary alveolus and the myeloperoxidase (MPO) activity were decreased after LLLT. These results suggested that LLLT therapy is beneficial in decreasing the somatic cell count and improving milk nutritional quality in cows with an intramammary infection.