This study aimed to elucidate the effects of different soil water contents on the yield and quality of R.glutinosa.Different soil water contents were adjusted in different periods of growth of R.glutinosa.The yield,content of water extract,catalpol,verbascoside and polysaccharide were determined and analysed by the grey pattern recognition after harvests.The impacts of soil water content from the most important to the least important were medium moisture content (M2),high moisture content (M3),low moisture content (M1) and blank (M4).In the cultivation of R.glutinosa,the soil water content should be remained in the range of 40％-50％ at seedling stage,while 50％-60％ at the stage of root formation and tuber enlargement,and 20％-30％ during harvesting,which can significantly improve the yield and quality of R.glutinosa.

OBJECTIVETo evaluate the effects of different oxygen therapy technique (different concentrations of normobaric oxygen and the hyperbaric oxygen) on the ultrastructure of cardiac muscle, lung and liver in rats with acute hydrogen sulfide intoxication.

METHODSOne hundred healthy male Wistar rats were randomly divided into five groups: normal control group (A), poisoned group (B), oxygen therapy group (C), oxygen therapy group (D) and oxygen therapy group (E). After the exposure to 300 ppm H2S for 60 min in a static exposure tank (1 m3), the rats were treated with oxygen therapy, C, D and E groups were given 33% oxygen, 50% oxygen of atmospheric oxygen and hyperbaric oxygen therapy for 100 min, respectively. The rats in normal control group inhaled air under the same environment. After exposure and therapy, the tissues of lung, heart and liver were observed under light microscope and electron microscope.

RESULTSThe results of light microscope examination showed that the broken and not well aligned cardiac myofilaments, cytoplasmic edema and pyknosis could be seen in group B. The well aligned and clear cardiac myofilaments appeared in group C, D and E. The alveolar hemorrhage, edema and inflammatory cells exudation could not be seen in group A. Alveolar epithelial cell edema, unsmooth alveolar edge and alveolar inflammatory cells exudation could be found in group B. The unsmooth alveolar septal borders and pulmonary edema could be seen occasionally in group C and D, the alveolar inflammatory cells exudation could not be seen in group E. The regular hepatic boards and the uniform hepatic cellular nuclei were found in group A. The disordered hepatic boards, widened cellular gaps and cytoplasmic edema could be seen occasionally in group B. The irregular hepatic boards and ballooning degeneration could be seen in group C and D. The regular hepatic boards and uniform cytoplasm could be found in group E. The results of electron microscope examination indicated that the mitochondrial swelling, autolyzing, fuzzy and breakage of myocardial cells were observed in group B; the clear mitochondrial structure appeared in group E. The apoptosis and organelle vacuole of alveolar epithelial cells could be observed in group B. The relatively normal nuclei of alveolar epithelial cells could be seen in group E. The lax cytoplast structure of hepatocytes, unclear nuclear membrane, lumped chromatin, slightly swelled mitochondria and phagosomes were observed in group B. However, no improved change was observed in group C, D and E.

CONCLUSIONHydrogen sulfide could induce the extensive and severe damage of myocardial mitochondria, alveolar epithelial cells and hepatocytes, the oxygen therapy in good time could reduce significantly the myocardial injury, and improve the lung injury to some extent. High-pressure oxygen therapy is better than the normobaric oxygen therapy.

Animals ; Hydrogen Sulfide ; poisoning ; Hyperbaric Oxygenation ; Liver ; pathology ; Lung ; pathology ; Male ; Myocardium ; pathology ; Oxygen Inhalation Therapy ; Pulmonary Alveoli ; pathology ; Rats ; Rats, Wistar

AIM To investigate the effects of imperatorin and isoimperatorin on the expression of mouse liver cytochrome P450s and hepatic toxicity in mice.METHODS C57BL/6 mice were randomly divided into control and administration groups,which were treated with imperatorin or isoimperatorin by intragastric administration for two weeks.The effects of two compounds on mRNA expressions of major P450s isoforms were analyzed by RT-PCR.The P450 expression was determined by Western blot.The serum levels of glutamicpyruvic transaminase (GPT),glutamic-oxalacetic transaminase (GOT) and blood total bilirubin (TBIL) were detected by kits.The change of liver tissue was observed with HE staining.RESULTS The Cyp1a2 mRNA expression was significantly induced by 40 mg/kg imperatorin as compared with the control group.For isoimperatorin,the Cyp2c37 mRNA expression was significantly induced.Western blot results showed that CYP1 A2 expression was significantly induced by imperatorin.For isoimperatorin,the CYP2C and CYP2E1 expressions were significantly induced.Blood biochemical indices showed that 40 mg/kg isoimperatorin led to increased serum GOT and TBIL levels.Pathological analysis showed that both compounds (at the doses of 20 mg/kg and 40 mg/kg) could cause liver edema to a certain degree.CONCLUSION Imperatorin is the inducer of CYP1A2,while isoimperatorin is the inducer of CYP2C and CYP2E1.These two compounds (at the doses of 20 mg/kg and 40 mg/kg) can lead to damage for mouse liver.The toxicity of isoimperatorin is stronger than that of imperatorin.

Objectives:To explore the relationship between insomnia symptoms and neuroticism in patients with COVID-19,and to explore the role of anxiety and psychological capital in the relationship.Methods:Totally 687 patients with COVID-19 were recruited from Shanghai Fangcang Hospital.The Athens Insomnia Scale(AIS),Eysenck Personality Questionnaire-Revised Short Scale for Chinese Neuroticism Subscale(EPQ-RSC-N),Self-Rat-ing Anxiety Scale(SAS)and Psychological Capital Questionnaire(PCQ)were used to measure insomnia symp-toms,neuroticism personality trait,anxiety symptoms and psychological capital levels.The deviation-corrected per-centile Bootstrap method was used to test the mediating effect,and the PROCESS program was used to test the moderated effect.Results:The detection rate of insomnia symptoms was 49.93％.The AIS scores were lower in male patients than in female patients(P＜0.01).The SAS scores partly mediated the relationship between neuroti-cism scores and AIS scores,with an effect size of 0.03,accounting for 18.29％of the total effect.With the im-provement of PCQ scores,the predictive effect of SAS scores on AIS scores gradually decreased(β=-0.01,t=-4.41,P＜0.001).Conclusions:Anxiety symptoms in patients with COVID-19 play a partial mediating role in the positive relationship between insomnia symptoms and neuroticism.The psychological capital moderates the relation-ship between insomnia and anxiety symptoms.

Exercise fatigue is a complex physiological and psychological phenomenon that includes peripheral fatigue in the muscles and central fatigue in the brain. Peripheral fatigue refers to the loss of force caused at the distal end of the neuromuscular junction, whereas central fatigue involves decreased motor output from the primary motor cortex, which is associated with modulations at anatomical sites proximal to nerves that innervate skeletal muscle. The central regulatory failure reflects a progressive decline in the central nervous system’s capacity to recruit motor units during sustained physical activity. Emerging evidence highlights the critical involvement of central neurochemical regulation in fatigue development, particularly through neurotransmitter-mediated modulation. Alterations in neurotransmitter release and receptor activity could influence excitatory and inhibitory signal pathways, thus modulating the perception of fatigue and exercise performance. Increased serotonin (5-HT) could increase perception of effort and lethargy, reduce motor drive to continue exercising, and contribute to exercise fatigue. Decreased dopamine (DA) and noradrenaline (NE) neurotransmission can negatively impact arousal, mood, motivation, and reward mechanisms and impair exercise performance. Furthermore, the serotonergic and dopaminergic systems interact with each other; a low 5-HT/DA ratio enhances motor motivation and improves performance, and a high 5-HT/DA ratio heightens fatigue perception and leads to decreased performance. The expression and activity of neurotransmitter receptors would be changed during prolonged exercise to fatigue, affecting the transmission of nerve signals. Prolonged high-intensity exercise causes excess 5-HT to overflow from the synaptic cleft to the axonal initial segment and activates the 5-HT1A receptor, thereby inhibiting the action potential of motor neurons and affecting the recruitment of motor units. During exercise to fatigue, the DA secretion is decreased, which blocks the binding of DA to D1 receptor in the caudate putamen and inhibits the activation of the direct pathway of the basal ganglia to suppress movement, meanwhile the binding of DA to D2 receptor is restrained in the caudate putamen, which activates the indirect pathway of the basal ganglia to influence motivation. Furthermore, other neurotransmitters and their receptors, such as adenosine (ADO), glutamic acid (Glu), and γ‑aminobutyric acid (GABA) also play important roles in regulating neurotransmitter balance and fatigue. The occurrence of central fatigue is not the result of the action of a single neurotransmitter system, but a comprehensive manifestation of the interaction between multiple neurotransmitters. This review explores the important role of neurotransmitters and their receptors in central motor fatigue, reveals the dynamic changes of different neurotransmitters such as 5-HT, DA, NE, and ADO during exercise, and summarizes the mechanisms by which these neurotransmitters and their receptors regulate fatigue perception and exercise performance through complex interactions. Besides, this study presents pharmacological evidence that drugs such as agonists, antagonists, and reuptake inhibitors could affect exercise performance by regulating the metabolic changes of neurotransmitters. Recently, emerging interventions such as dietary bioactive components intake and transcranial electrical stimulation may provide new ideas and strategies for the prevention and alleviation of exercise fatigue by regulating neurotransmitter levels and receptor activity. Overall, this work offers new theoretical insights into the understanding of exercise central fatigue, and future research should further investigate the relationship between neurotransmitters and their receptors and exercise fatigue.

BACKGROUND: Anterior thalamic nuclei (ATN) deep brain stimulation (DBS) is an effective method of controlling epilepsy, especially temporal lobe epilepsy. Mossy fiber sprouting (MFS) plays an indispensable role in the pathogenesis and progression of epilepsy, but the effect of ATN-DBS on MFS in the chronic stage of epilepsy and the potential underlying mechanisms are unknown. This study aimed to investigate the effect of ATN-DBS on MFS, as well as potential signaling pathways by a kainic acid (KA)-induced epileptic model. METHODS: Twenty-four rhesus monkeys were randomly assigned to control, epilepsy (EP), EP-sham-DBS, and EP-DBS groups. KA was injected to establish the chronic epileptic model. The left ATN was implanted with a DBS lead and stimulated for 8 weeks. Enzyme-linked immunosorbent assay, Western blotting, and immunofluorescence staining were used to evaluate MFS and levels of potential molecular mediators in the hippocampus. One-way analysis of variance, followed by the Tukey post hoc correction, was used to analyze the statistical significance of differences among multiple groups. RESULTS: ATN-DBS is found to significantly reduce seizure frequency in the chronic stage of epilepsy. The number of ectopic granule cells was reduced in monkeys that received ATN stimulation (P < 0.0001). Levels of 3',5'-cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) in the hippocampus, together with Akt phosphorylation, were noticeably reduced in monkeys that received ATN stimulation (P = 0.0030 and P = 0.0001, respectively). ATN-DBS also significantly reduced MFS scores in the hippocampal dentate gyrus and CA3 sub-regions (all P < 0.0001). CONCLUSION ATN-DBS is shown to down-regulate the cAMP/PKA signaling pathway and Akt phosphorylation and to reduce the number of ectopic granule cells, which may be associated with the reduced MFS in chronic epilepsy. The study provides further insights into the mechanism by which ATN-DBS reduces epileptic seizures.
Adenosine Monophosphate ; Anterior Thalamic Nuclei ; Cyclic AMP-Dependent Protein Kinases ; Deep Brain Stimulation ; Epilepsy/therapy* ; Epilepsy, Temporal Lobe/therapy* ; Hippocampus ; Humans ; Mossy Fibers, Hippocampal ; Signal Transduction