When we study the effect of acupuncture-anaesthesia,we need to know the receptors in the muscle.The upper part of the musculus tibialis anterior was our object,which may contain the points of Zusanli and Shangjuxu.The musculi soleus and gastrocnemius were taken also for the purpose of comparation.We found there are four kinds of receptors in these muscles by Barkers method,the tradition gold method and so forth. The four kinds of receptors were the muscle spindles,the tendon organs,the Pacinian corpuscles and free nerve endings.We found no Pacinian corpuscles in the musculus tibialis anterior.So we suggests thar the muscle spindles may be the receptors for the acupuncture,but the free nerve endings may not be expelled.

The present investigation was performed in fifteen adult rats using four fluorescent tracers, including 4'-6-diamidino-2-phenylindol. 2 HC1 (DAPI), nuclear yellow (NY), propidium iodide (PI), and fast blue (FB), which were divided into four sets: PI-DAPI, PI-NY, DAPI-NY, and FB-NY. In each set two fluorescent tracers were used separately to label gastric corpus and pylorus antrum. In the medulla oblongata, the labelled cells in the dorsal motor nucleus of vagus (DmnX) were observed in every animal, but those in the nucleus ambiguus (nA) were only seen. in 11 cases and in the nucleus tractus solitarius (nTs) in 5 cases. In addition, labelled cells were also found in laminae V of the posterior grey columns of the thoracic (T6-9) spinal cords, spinal ganglia and sympathetic trunks. The results of counting and analysing the labelled cells of DmnX of both sides of 75 sections in four cases are as follows: 1233 cells on the left, including 1143 labelled cells of gastric corpus (92.7%), 63 labelled cells of pylorus antrum (5.1%), 27 double labelled cells (2.2%); 1007 cells on the right, including 930 labelled cells of gastric corpus (92.3%), 41 labelled cells of pylorus antrum (4.1%), and 36 double labelled cells (3.7%). The results indicate that PI is not fitted for 'long distance labelling in peripheral nervous system; the density of vagus innervation of gastric corpus is larger than that of pylorus antrum; a part of the nerve endings of vagus postganglionic neurons are distributed both in gastric corpus and in pylorus antrum; a part of postganglionic neurons of sympathetic fibres are located at the sympathetic trunk.

Objective To explore the role and correlation of peroxisome proliferator-activated receptor γ (PPAR-γ) and Toll-like receptor 4 (TLR4) on pulmonary vascular remodeling of chronic obstructive pulmonary disease(COPD).Methods Ninety male patients who underwent surgery for squamous cell carcinoma were enrolled as our subjects.All patients were divided into COPD group and uon-COPD group based on lung function,and 45 cases in each group.Peripheral lung tissues without tumor infiltrated after lobectomy were taken to assess the degree of arterial inflammation,percentage of wall thickness to vessel diamater (WT％) and percentage of wall area to total vascular area(WA％) were measured through Hematoxylin-Eosin(HE) staining under light microscope.The expression of PPARγand TLR4 were determined by immunohistochemistry.Results The distribution of WA％ and WT％ in COPD group were (43.98 ±6.43)％ and (27.37 ±3.34)％,higher than that of non-COPD group ((26.09 ± 2.82) ％,t =-13.949,P =0.000 ; (15.57 ± 1.75) ％,t =-7.140,P =0.000).The expression of PPAR-γand TLR4 in COPD group were (10.74 ± 8.81) ％,(3 1.41 ± 14.67) ％ respectively,and (28.22 ± 15.08)％,(4.67 ± 4.47)％ in non-COPD group.The differences were statistic significantly(t =5.483,P =0.000; t =-9.555,P =0.000).And there was negative correlation between the expression of PPARγand TLR4 (r =-0.404,P ＜ 0.01).Conclusion The pulmonary vascular of COPD patients showed the obviously inflammatory cell infiltration,fibrosis and proliferation,and PPAR-γ and TLR4 participate in the regulation of pulmonary vascular remodeling.

Objective To explore the correlation between the expressions of matrix metalloproteinase -9 (MMP-9), Toll-likeReceptor 4 ( TLR4) and lung revascularization in patients with chronic obstructive pulmonary disease .Methods Lung tissues frompatients with chronic obstructive pulmonary disease (COPD) (COPD group,n =25) and those without COPD (non-COPD group,n =25) were obtained from surgically resected specimens .The ratio of the area of the wall to that of the pulmonary arterioles (WA %) andthe ratio of the thickness of the wall to the external diameter of the pulmonary arterioles (WT %) were analyzed by computer-based imageanalysis system.Immunohistochemical technique was applied to investigate the expressions of TLR 4, proliferative cell nuclear antigen(PCNA) and MMP-9 in vascular smooth muscle cells.Results ⑴ The inflammatory infiltration degree, WA %, and WT %were significantly higher than that of non -COPD group ( P <0.01), respectively.⑵Compared with non-COPD group, the expressionsof PCNA, TLR4, and MMP-9 in vascular smooth muscle cells were increased significantly ( P <0.01).⑶The expressions of TLR4,MMP-9 had a positive correlation with WA%, WT%, degree of inflammatory infiltration, and the expression of PCNA ( r =0.67,0.74,0.47,0.44;0.59,0.71,0.61,0.33, P <0.01), up-regulated expression of TLR4 was closely related with the expression of MMP-9 ( r =0.55, P <0.01).Conclusions The pulmonary arterioles of COPD patients showed marked inflammatory and arteriolemuscularization, the TLR4 might aggravate inflammation,induced upregulation of MMP-9 expression, played an important role in the pulmonary vascular remodeling process.

Objective:To analyze the changes of serum metabolomics in rats with combined injuries caused by gas explosion and explore its possible mechanism.Methods:In April 2018, the large coal mine gas explosion test roadway and explosion test system were used to simulate the gas explosion experiment. All 32 SD rats were randomly divided into four groups, control group (not involved in the explosion) , close range (40 m) group, medium range (160 m) group and long range (240 m) group, 8 in each group. The respiratory function at 2 hours and the neural behavior at 48 hours were detected after the explosion. The rats were anesthetized and sacrificed after 48 hours, and the serum, lung, liver and other tissues of the rats were isolated and histopathological changes of lung and liver tissues were observed by HE staining. Serum samples were detected by liquid chromatography-high resolution mass spectrometry (UPLC-Orbitrap Elite/MS) , and metabolic spectrum differences between groups were evaluated by principal component analysis. Differential metabolites were screened and identified, and metabolic pathways were analyzed.Results:Compared with control group, respiratory function indexes (respiratory frequency, minute ventilation, peak inspiratory flow rate, peak expiratory flow rate and 1/2 tidal volume expiratory flow) of rats in different explosion groups were significantly decreased ( P<0.05) , but respiration pause, inspiratory time and 2/3 tidal volume required time were significantly increased ( P<0.05) in 2 hours after the explosion. However, the residence times of the neurobehavioral indicators of the 40 m group and 160 m group were significantly increased ( P<0.05) , and the movement distances were significantly decreased ( P<0.05) in 48 hours after the explosion. HE staining results showed that the lung and liver tissues of the rats in the gas explosion group structurally damaged, and the cells were disordered, with inflammatory cell infiltration, bleeding and edema. Metabonomics analysis showed that there were significant differences in metabolic profiles between groups. A total of 18 differential metabolites were identified in serum samples, including aconitum acid, citric acid, niacinamide and pyruvate, which involved in 12 major metabolic pathways, including the glutamic acid and glutamine metabolism, phenylalanine, tyrosine and tryptophan biosynthesis, glyoxylic acid and dicarboxylic acid metabolism, phenylalanine metabolism, nicotinic acid and nicotinamide metabolism, citric acid cycle (TCA cycle) . Conclusion:Gas explosion can cause multi-organ system damage in rats, the mechanism of which may be related to the biosynthesis of alanine, tyrosine and tryptophan, metabolism of niacin and niacinamide, metabolism of acetaldehyde and dicarboxylic acid, and TCA cycle, etc.

Objective:To analyze the changes of serum metabolomics in rats with combined injuries caused by gas explosion and explore its possible mechanism.Methods:In April 2018, the large coal mine gas explosion test roadway and explosion test system were used to simulate the gas explosion experiment. All 32 SD rats were randomly divided into four groups, control group (not involved in the explosion) , close range (40 m) group, medium range (160 m) group and long range (240 m) group, 8 in each group. The respiratory function at 2 hours and the neural behavior at 48 hours were detected after the explosion. The rats were anesthetized and sacrificed after 48 hours, and the serum, lung, liver and other tissues of the rats were isolated and histopathological changes of lung and liver tissues were observed by HE staining. Serum samples were detected by liquid chromatography-high resolution mass spectrometry (UPLC-Orbitrap Elite/MS) , and metabolic spectrum differences between groups were evaluated by principal component analysis. Differential metabolites were screened and identified, and metabolic pathways were analyzed.Results:Compared with control group, respiratory function indexes (respiratory frequency, minute ventilation, peak inspiratory flow rate, peak expiratory flow rate and 1/2 tidal volume expiratory flow) of rats in different explosion groups were significantly decreased ( P<0.05) , but respiration pause, inspiratory time and 2/3 tidal volume required time were significantly increased ( P<0.05) in 2 hours after the explosion. However, the residence times of the neurobehavioral indicators of the 40 m group and 160 m group were significantly increased ( P<0.05) , and the movement distances were significantly decreased ( P<0.05) in 48 hours after the explosion. HE staining results showed that the lung and liver tissues of the rats in the gas explosion group structurally damaged, and the cells were disordered, with inflammatory cell infiltration, bleeding and edema. Metabonomics analysis showed that there were significant differences in metabolic profiles between groups. A total of 18 differential metabolites were identified in serum samples, including aconitum acid, citric acid, niacinamide and pyruvate, which involved in 12 major metabolic pathways, including the glutamic acid and glutamine metabolism, phenylalanine, tyrosine and tryptophan biosynthesis, glyoxylic acid and dicarboxylic acid metabolism, phenylalanine metabolism, nicotinic acid and nicotinamide metabolism, citric acid cycle (TCA cycle) . Conclusion:Gas explosion can cause multi-organ system damage in rats, the mechanism of which may be related to the biosynthesis of alanine, tyrosine and tryptophan, metabolism of niacin and niacinamide, metabolism of acetaldehyde and dicarboxylic acid, and TCA cycle, etc.

Objective:The aims of this study were to investigate the effect of gas explosion on rats and to explore the pulmonary function alterations associated with gas explosion-induced acute blast lung injury (ABLI) in real roadway environment.Methods:In April 2018, the large coal mine gas explosion test roadway and explosion test system were used to simulate the real gas explosion roadway environment, fixed the cage and set the explosion parameters. 72 SD rats, male, SPF grade, were randomly divided into nine groups by completely random grouping method according to their body weight: control group, close range group (160 m) , and long range group (240 m) . In each group, there were wound groups (24 h group and 48h group, 8/group, total 48 in six groups) and no wound groups (8/group, total 24 in three groups) . Except for the control group, the other groups were placed in cages at different distances under anesthesia, the experiment of gas explosion was carried out by placing the rats in a position that could force the lungs. The changes of respiratory function of the rats in the non-invasive group were monitored with pulmonary function instrument at 2 h, 24 h, 48 h, 72 h and 168h after the explosion, and were killed under anesthesia 7 days later; the rats in invasive groups were anesthetized and killed at 24 h, 48 h and 168 h, respectively. Gross observation, lung wet-dry ratio and lung histopathology were performed.Results:Compared with the control group, f (respiratory frequency, f) , MV (minute ventilation, MV) , PEF (peak expiratory flow rate, PEF) , PIF (peak inspiratory flow rate, PIF) and EF50 (1/2 tidal volume expiratory flow, EF50) of rats in the close and long range groups decreased significantly after gas explosion 2 h. PAU (respiration pause, PAU) , Te (expiratory time, Te) , Ti (inspiratory time, Ti) and Tr (relaxation time, Tr) were significantly increased ( P<0.05) . After 48 h, TV (tidal volume, TV) , Penh (enhanced respiration pause, Penh) , PAU, and PIF of rats in the long range group were significantly increased ( P<0.05) . After 72 h, MV in the long range group was significantly decreased ( P<0.05) . Compared with the control group, Penh, PAU, Ti and Te were significantly decreased after 168 h in the close and long range groups, with statistical significance ( P<0.05) . At the same time, the body weight of rats in different range groups was significantly decreased ( P<0.05) . In addition, both HE staining and routine observation of lung tissues of rats in different range groups showed that gas explosion caused pulmonary edema, obviously congested pulmonary capillaries, a large number of inflammatory cells and infiltrated red blood cells. Conclusion:Gas explosion in real roadway environment can cause the change of respiratory function phase and lung tissue damage in rats, suggesting that the model of gas explosion-induced ABLI has been initially established successfully, which would provide a basis for further study on the pathogenesis of ABLI.

Objective:The aims of this study were to investigate the effect of gas explosion on rats and to explore the pulmonary function alterations associated with gas explosion-induced acute blast lung injury (ABLI) in real roadway environment.Methods:In April 2018, the large coal mine gas explosion test roadway and explosion test system were used to simulate the real gas explosion roadway environment, fixed the cage and set the explosion parameters. 72 SD rats, male, SPF grade, were randomly divided into nine groups by completely random grouping method according to their body weight: control group, close range group (160 m) , and long range group (240 m) . In each group, there were wound groups (24 h group and 48h group, 8/group, total 48 in six groups) and no wound groups (8/group, total 24 in three groups) . Except for the control group, the other groups were placed in cages at different distances under anesthesia, the experiment of gas explosion was carried out by placing the rats in a position that could force the lungs. The changes of respiratory function of the rats in the non-invasive group were monitored with pulmonary function instrument at 2 h, 24 h, 48 h, 72 h and 168h after the explosion, and were killed under anesthesia 7 days later; the rats in invasive groups were anesthetized and killed at 24 h, 48 h and 168 h, respectively. Gross observation, lung wet-dry ratio and lung histopathology were performed.Results:Compared with the control group, f (respiratory frequency, f) , MV (minute ventilation, MV) , PEF (peak expiratory flow rate, PEF) , PIF (peak inspiratory flow rate, PIF) and EF50 (1/2 tidal volume expiratory flow, EF50) of rats in the close and long range groups decreased significantly after gas explosion 2 h. PAU (respiration pause, PAU) , Te (expiratory time, Te) , Ti (inspiratory time, Ti) and Tr (relaxation time, Tr) were significantly increased ( P<0.05) . After 48 h, TV (tidal volume, TV) , Penh (enhanced respiration pause, Penh) , PAU, and PIF of rats in the long range group were significantly increased ( P<0.05) . After 72 h, MV in the long range group was significantly decreased ( P<0.05) . Compared with the control group, Penh, PAU, Ti and Te were significantly decreased after 168 h in the close and long range groups, with statistical significance ( P<0.05) . At the same time, the body weight of rats in different range groups was significantly decreased ( P<0.05) . In addition, both HE staining and routine observation of lung tissues of rats in different range groups showed that gas explosion caused pulmonary edema, obviously congested pulmonary capillaries, a large number of inflammatory cells and infiltrated red blood cells. Conclusion:Gas explosion in real roadway environment can cause the change of respiratory function phase and lung tissue damage in rats, suggesting that the model of gas explosion-induced ABLI has been initially established successfully, which would provide a basis for further study on the pathogenesis of ABLI.

Methotrexate (MTX) is a widely used immunosuppressive drug. Large-dose of MTX is used for the treatment of cancer while low-dose is used for the treatment of rheumatoid arthritis (RA). This study aimed to explore the effect of MTX on the urinary proteome of rats. MTX was given to rats orally to construct an MTX intragastric administration rat model. The urine of the rats were collected within 10 hours after giving MTX, and the urine proteins of the rats were analyzed by liquid chromatography tandem mass spectrometry (LC-MS/MS). A total of 31 differential proteins were identified, of which 7 proteins were related to the effect MTX and the symptom of RA. The biological processes of some rats reflected the effect of MTX on the body's glutathione metabolism and the JAK/STAT signaling pathway, which indicated that urine proteins have the ability to reflect the effects of MTX on the body of rats. The spectrum of the differential proteins of each single rat showed that different individuals respond to the drug quite differently.
Rats ; Animals ; Methotrexate/metabolism* ; Proteome ; Chromatography, Liquid/methods* ; Tandem Mass Spectrometry/methods* ; Arthritis, Rheumatoid/drug therapy*

Fatal Outcome ; Female ; Hepatic Encephalopathy/genetics* ; Humans ; Infant ; Male ; Metabolism, Inborn Errors/genetics* ; Mitochondrial Proteins/genetics* ; Mutation ; Peptide Elongation Factor G/genetics* ; Whole Exome Sequencing