The paper conducts a case study of Yangzhou No.1 People′s Hospital, introduces the practice of outpatient process opti-mization based on informatization support platform, analyzes the operation status of self-service outpatient service platform and existing problems.Based on the M/M/s model in queuing theory, the queuing model of payment for outpatient service in the hospital is construc-ted, the characteristics of queuing payment problems for outpatient service are revealed, the relationship between the sharing rate of self-service terminals and the average length of the queue in service windows, the average waiting time of patients.

Treatment with traditional Chinese medicinal composite is one of the most important characteristics of traditional Chinese medicine (TCM). Studying material base of TCM composite and its mechanism is a key to modernizing the industry of Chinese medicinal herbs. The research for TCM composite can be carried out from many different angles, including multiple components, multiple actions, multiple levels and multiple targets. Such a way to study TCM composite will be beneficial to improving the theory of TCM composite, guiding clinical administration and developing new products.

Liver cancer has always been a threat to national health since liver disease has a high incidence rate in China. At present, methods for the prevention and treatment of liver cancer have unsatisfactory effects in clinical practice, and with in-depth studies, scholars have changed their focus to cancer-associated fibroblasts (CAFs) in tumor microenvironment. More and more evidence has shown that CAFs may provide a new target for the prevention and treatment of liver cancer. This article summarizes the role of CAFs in the development and progression of liver cancer and the potential of CAFs in the treatment of liver cancer.

OBJECTIVETo discuss the mechanism of cerebral vessel spasm caused by concussion and the effect of Nimodipine on concussion.

METHODSA total of 224 patients who were treated from March 1995 to October 1999 were divided into two groups randomly, ie, Nimodipine group (113 cases) and control group (111 cases). Middle cerebral artery (MCA), basilar artery (BA) and the average peak forward velocity of cerebral blood flow were observed by color three-dimensional transcranial Doppler (3D-TCD) within 24 hours after admission and at the end of 3-6 days of treatment. Cerebral blood flow changes, characteristics and treatment effect were analyzed and determined by clinical main symptom disappearance rate.

RESULTSIn concussion, cerebral blood flow was divided into 3 phases: cerebral blood flow low infusion dilation phase, cerebral blood vessel spasm phase and cerebral blood flow recovery phase. In the Nimodipine group, clinical main symptom disappearance rate was higher than that in the control group in the cerebral spasm and recovery phases with a significant difference (P < 0.01).

CONCLUSIONSCerebral vessel spasm, hypoxia and ischemia lesion are the main pathological changes. Whether cerebral dysfunction is reversible or not is mainly determined by spasm time of cerebral blood vessel. Nimodipine has a good effect on releasing spasm and diminishing the cerebral blood flow velocity. It not only improves curative effect on concussion, but also reduces and prevents concussion sequelae. Hence, concussion patients who have cerebral spasm confirmed by 3D-TCD should be given Nimodipine routinely and early.

Adolescent ; Adult ; Aged ; Blood Flow Velocity ; Brain Concussion ; complications ; diagnostic imaging ; Cerebral Arteries ; diagnostic imaging ; drug effects ; Cerebrovascular Circulation ; drug effects ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Drug Therapy, Combination ; Female ; Follow-Up Studies ; Humans ; Infusions, Intravenous ; Injury Severity Score ; Male ; Mannitol ; administration & dosage ; Middle Aged ; Nimodipine ; administration & dosage ; Reference Values ; Treatment Outcome ; Ultrasonography, Doppler, Transcranial ; Vasospasm, Intracranial ; drug therapy ; etiology ; physiopathology

Objective To study changes and significance of endothelin(ET) in rat cerebral concussion.Methods 80 Wistar male rats were used for animal model of cerebral concussion,which were sacrificed on 1,3,7,14 and 30 days after injury and the brain tissue were taken off. The expression of ET was studied in the course of cerebral concussion by means of immunohistochemistry.Results Typical clinical manifestation was observed in the 100 g group in which the pathological changes included cerebral vascular constriction and dilatation,congestion and edema of cerebral tissue,neuronal degeneration,necrosis,and obviously decreased even disappeared Nissl bodies.Increased expression of ET was observed on the first day,the positive area was seen in the plasma of endothelial cells in cerebral cortex,hippocampus,cerebellum and thalamus.ET expression peak occurred on the 7th day,the positive area was also found in the plasma of Purkinje cells in the cerebellum.Decreased ET expression was found on 14th day and returned to normal level on the 30th day.Conclusion The main pathological changes of cerebral concussion contained blood circulation disorder,and degeneration and necrosis of substantial cells.ET was involved in the brain tissue injury during the pathological process of cerebral concussion and might be related to regulation of cerebral vascular reaction,and neuron degeneration and necrosis.

At present, hepatic encephalopathy has a relatively high mortality and thus greatly affects patients’ quality of life. This article describes the changes of intestinal flora in patients with hepatic encephalopathy and analyzes the mechanism of action of intestinal flora in hepatic encephalopathy and related treatment methods. It is pointed out that the development of hepatic encephalopathy is closely associated with intestinal flora, and clinical treatment by regulating intestinal flora has achieved a marked effect in patients with hepatic encephalopathy. In the future, the research on intestinal flora in patients with hepatic encephalopathy can be deepened to provide better regimens for the treatment of hepatic encephalopathy.

As a novel form of programmed cell death different from cell necrosis, apoptosis, and autophagy discovered in recent years, pyroptosis is characterized by cell membrane rupture and release of cell contents and proinflammatory factors mediated by gasdermin, thus leading to cell death. Pyroptosis signaling pathways can be classified into classical pathways dependent on caspase-1 and non-classical pathways dependent on caspase-4/5/11; the activation of caspase-1 in classical pathways depends on the function of inflammasome, while the direct activation of caspase-4/5/11 is observed in non-classical pathways, which leads to the lysis of gasdermin D and induce the formation of membrane pores, the maturation and release of interleukin-1β and interleukin-18, and the rupture of cell membrane to cause pyroptosis. Latest research has shown that pyroptosis plays an important role in the development and progression of chronic liver diseases. This article introduces the mechanism of pyroptosis and summarizes the role of pyroptosis in the development and progression of nonalcoholic fatty liver disease, alcoholic liver disease, viral hepatitis, liver cirrhosis, and hepatocellular carcinoma, in order to provide new ideas and methods for the prevention and treatment of liver diseases in clinical practice.

Objective The aim of this experiment was to explore the effect and mechanism of intestinal microbiota on shaping the growth performance by fecal microbiota transplantation from pigs to pseudo-germ-free mice. Methods Thirty-six barrows with a similar initial body weight of 30 kg were raised for 42 days(ad libitum)within individual metabolic cages. Feed intake and body weight of each pig were recorded every week to calculate the feed conversion rate and average daily gain. At the end of the experiment,feed conversion ratio and average daily gain were integrated to divide the pigs into 3 groups, namely, high growth performance(HP), moderate growth performance(MP)and low growth performance(LP)groups. Feces were collected to calculate the total intestinal nutrient digestibility and prepare for fecal microbiota transplantation to pseudo-germ-free mice, which were induced with several antibiotics for four weeks. Fecal microbiome structure was assayed by profiling V3-V4 region of the 16S rRNA gene. Results Fecal microbiota transplantation from pigs to pseudo-germ-free mice resulted in reappearance of the original phenotype. Compared with the LP pigs, the microbial species richness and microbial diversity in feces were higher in the HP pigs. The HP pigs had improved digestibility of gross energy(P =0.01)and higher abundance of Methanobrevibacter. Enterococcus and Akkermansia were also more abundant in the recipient pseudo-germ-free mice from the HP pigs which may be correlated with a high energy utilization. Conclusions Fecal microbiota transplantation from pigs to mice results in reappearance of the original phenotype and microbial species richness,microbial diversity,and their growth ability. Different nutritional metabolism is shown among pigs with different feed efficiency and the HP pigs have improved energy utilization(P=0.01). At the same time, the bacteria correlated with high energy utilization are more abundant in feces of HP pigs than in LP pigs.

The development and progression of nonalcoholic fatty liver disease (NAFLD) have complex potential mechanisms. The traditional “two-hit” pathophysiological theory has been challenged, and in recent years, an increasing number of studies have been performed to investigate the interaction between insulin resistance, adipokines, and other unknown pathogenic factors in various organs. This article summarizes the factors of the liver, intestinal tract, hypothalamus, and extracellular cysts, as well as genetic factors, with an emphasis on the synergistic mechanism of action of the liver and extrahepatic organs in the pathogenesis of NAFLD, in order to provide a reference for obtaining new insights into NAFLD regulatory network and determining new targets for the prevention and treatment of NAFLD.

Background Chronic excessive exposure to fluoride can cause damage to the central nervous system and a certain degree of learning and memory impairment. However, the associated mechanism is not yet clear and further exploration is needed. Objective Using 4D unlabelled quantitative proteomics techniques to explore differentially expressed proteins and their potential mechanisms of action in chronic excessive fluoride exposure induced brain injury. Methods Twenty-four SPF-grade adult SD rats, half male and half male, were selected and divided into a control group and a fluoride group by random number table method, with 12 rats in each group. Among them, the control group drank tap water (fluorine content<1 mg·L⁻¹), the fluoride group drank sodium fluoride solution (fluorine content 10 mg·L⁻¹), and both groups were fed with ordinary mouse feed (fluoride content<0.6 mg·kg⁻¹). After 180 d of feeding, the SD rats were weighed, and then part of the brain tissue was sampled for pathological examination by hematoxylin-eosin (HE) staining and Nissl staining. The rest of the brain tissue was frozen and stored at −80 ℃. Three brain tissue samples from each group were randomly selected for proteomics detection. Differentially expressed proteins were screened and subcellular localization analysis was performed, followed by Gene Ontology (GO) function analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, cluster analysis, and protein-protein interaction analysis. Finally, Western blotting was used to detect the expression levels of key proteins extracted from the brain tissue samples. Results After 180 d of feeding, the average weight of the rats in the fluoride group was significantly lower than that in the control group (P<0.05). The brain tissue stained with HE showed no significant morphological changes in the cerebral cortex of the fluoride treated rats, and neuron loss, irregular arrangement of neurons, eosinophilic changes, and cell body pyknosis were observed in the hippocampus. The Nissl staining results showed that the staining of neurons in the cerebral cortex and hippocampus of rats exposed to fluoride decreased (Nissl bodies decreased). The proteomics results showed that a total of 6927 proteins were identified. After screening, 206 differentially expressed proteins were obtained between the control group and the fluoride group, including 96 up-regulated proteins and 110 down-regulated proteins. The differential proteins were mainly located in cytoplasm (30.6%), nucleus (27.2%), mitochondria (13.6%), plasma membrane (13.6%), and extracellular domain (11.7%). The GO analysis results showed that differentially expressed proteins mainly participated in biological processes such as iron ion transport, regulation of dopamine neuron differentiation, and negative regulation of respiratory burst in inflammatory response, exercised molecular functions such as ferrous binding, iron oxidase activity, and cytokine activity, and were located in the smooth endoplasmic reticulum membrane, fixed components of the membrane, chloride channel complexes, and other cellular components. The KEGG significantly enriched pathways included biosynthesis of secondary metabolites, carbon metabolism, and microbial metabolism in diverse environments. The results of differential protein-protein interaction analysis showed that the highest connectivity was found in glucose-6-phosphate isomerase (Gpi). The expression level of Gpi in the brain tissue of the rats in the fluoride group was lower than that in the control group by Western blotting (P<0.05). Conclusion Multiple differentially expressed proteins are present in the brain tissue of rats with chronic fluorosis, and their functions are related to biosynthesis of secondary metabolites, carbon metabolism, and microbial metabolism in diverse environments; Gpi may be involved in cerebral neurological damage caused by chronic overdose fluoride exposure.