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Abstract: An efficient evaluation index system and evaluation method for enterprise informatization is critically important for guiding the implementation and development tasks of enterprise information systems. This paper, based on pre-research for a group of typical enterprises and item, factor and reliability analysis of acquired samples, presents a comprehensive evaluation index system which includes three key first-level indicator sets (consisting of the current status of enterprise informatization, the production management characteristics and the system functional requirements), 16 second-level indicators and 80 third-level indicators. According to the characteristics of the designed objectives in the evaluation index system, we propose to use the grey relative correlation analysis method to evaluate the influencing factors of the enterprise informatization, employ the grey comprehensive correlation analysis method to determine the production management characteristics of the enterprise and adopt the grey clustering assessment technology to assess the information system functional requirements based on Grey System Theory. Moreover, case studies for enterprise informatization that mainly focus on the process enterprises in southwest China were illustrated. The research results show that the proposed evaluation system and evaluation method is reliable, practical, and able to better reflect the level of enterprise information and demand characteristics. [Copyright &y& Elsevier]

A rat model of gastric ischemia–reperfusion injury (GI-RI) was established by clamping the celiac artery for 30 min and allowing reperfusion for 1 h, on which the regulatory effect of the paraventricular nucleus (PVN) and its neural mechanisms were investigated. The results were: 1. Electrical stimulation of the PVN obviously attenuated the GI-RI. Microinjection of L-glutamic acid into PVN produced an effect similar to that of PVN stimulation. 2. Electrolytic ablation of the PVN aggravated the GI-RI. 3. Nucleus tractus solitarius (NTS) ablation could eliminate the protective effect of electrical stimulation of PVN on GI-RI. 4. Hypophysectomy did not alter the effect of electrical stimulation of PVN. 5. Vagotomy or sympathectomy both could increase the effect of PVN stimulation on GI-RI. These results indicate that the PVN participates in the development of GI-RI as a specific area in the CNS, exerting protective effects on the GI-RI. The NTS and vagus and sympathetic nerve may be involved in the regulative mechanism of PVN on GI-RI, but the PVN mechanism here is independent of the PVN-hypophyseal pathway. [Copyright &y& Elsevier]

Abstract: We investigated the protective effects of chemical stimulation of cerebellar interpositus nucleus (IN) on gastric ischemia-reperfusion injury (GI-RI) and its possible regulatory mechanisms in rats. Gastric mucosal damage index (GMDI) indicated the severity of gastric mucosal injuries. Transferase dUTP nick end labeling (TUNEL) staining and proliferating cell nuclear antigen (PCNA) were performed to assess gastric mucosal cell apoptosis and proliferation. Microinjection of glutamate into IN markedly attenuated GI-RI. Either chemical lesion of IN or electrical ablation of the decussation of superior cerebellar peduncle (DSCP) obviously aggravated GI-RI. The protective effects of IN were reversed with the pretreatments of microinjection of 3-mercaptopropionic acid into IN or Bicuculline into lateral hypothalamic area (LHA), individually. The discharge frequency and intensity of greater splanchnic nerve (GSN) decreased and gastric mucosal blood flow increased after chemical stimulation of IN. The apoptosis of positive cells of gastric mucosa was decreased by chemical stimulation of IN, whereas proliferation increased. The gastric juice volume, acidity, and total acid output were all decreased after the chemical stimulation of IN. These results indicated that IN participates in regulation of GI-RI and is a specific area in central nervous system for exerting protective effects on GI-RI. DSCP, LHA and GSN may involve in this process. Apoptosis and proliferation may mediate this protective process in rats too. [Copyright &y& Elsevier]

Abstract: Cerebellum, primarily believed as a subcortical somatic motor center, is increasingly considered to be implicated in visceral activities. However, little is known about its regulation on gastrointestinal organs. In this research, we investigated the aggravated effect of microinjection of gamma-aminobutyric acid receptor subtype B (GABABR) agonist, Baclofen into cerebellar fastigial nucleus (FN) on stress gastric mucosal damage (SGMD) and its possible regulatory mechanism. The gastric mucosal damage index was chosen to indicate the severity of gastric mucosal injure. Immunohistochemistry and transferase-mediated dUTP-biotin nick-endlabeling (TUNEL) methods were used to detect the variations of lateral hypothalamic area (LHA) and gastric mucosa. It had been demonstrated that FN participates in regulation of SGMD via its GABABR and GABA neural pathway, which passes through the decussation of superior cerebellar peduncle and projects to the GABA receptors in LHA. Meanwhile, celiac sympathetic nerve involves in this process via mediating neural discharge, which results in the decrease of gastric mucosal blood flow. Additionally, apoptosis, proliferation and oxidation in gastric mucosa, and gastric acid contribute in the mechanism. It could be expected that these results might suggest insights to the cerebellar and hypothalamic function, and the treatment of gastrointestinal diseases. [Copyright &y& Elsevier]

In the study, we investigated the effect of histamine microinjected into cerebellar fastigial nucleus (FN) on stress gastric mucosal damage (SGMD), and its mechanisms in rats. The model of SGMD was established by restraining and water (21±1 °C)-immersion for 3 h. The gastric mucosal damage index (GMDI) indicated the severity of gastric mucosal damage. Histamine or receptor antagonist was microinjected into the FN. The decussation of superior cerebellar peduncle (DSCP) and the lateral hypothalamic area (LHA) were destroyed, respectively. The pathological changes of gastric mucosa were evaluated using biological signal acquisition system, Laser-Doppler flowmeter, and western blotting. We found that the microinjection of histamine (0.05, 0.5, and 5 μg) into FN significantly attenuated the SGMD, in a dose-dependent manner, whereas, the microinjection of histamine H 2 receptor antagonist, ranitidine, and glutamic acid decarboxylase antagonist, 3-mercaptopropionic acid (3-MPA) exacerbated the SGMD. The protective effect of histamine on SGMD was abolished by electrical lesion of DSCP or chemical ablation of LHA. The microinjection of histamine decreased the discharge frequency of the greater splanchnic nerve, and the gastric mucosal blood flow was increased. In addition, the cellular proliferation was enhanced, but the cellular apoptosis was reduced in the gastric mucosa. Also the pro-apoptosis protein, Bax, and caspase-3 were down-regulated, and the anti-apoptosis protein, Bcl-2 was up-regulated following microinjection of histamine. In conclusion, the FN participated in the regulation of SGMD after histamine microinjected into FN, and cerebellar–hypothalamic circuits (include: DSCP, LHA) contribute to the process, which may provide a new therapeutic strategy for SGMD. [ABSTRACT FROM AUTHOR]

Abstract: Objective: To explore the effect and mechanism of Phloretin on human γδ T cells killing colon cancer SW-1116 cells. Methods: γδ T cells were amplified in vitro from human peripheral blood mononuclear cells through isopentenyl pyrophosphate method (IPP). After cocultured different concentrations of Phloretin with γδ T cells or SW-1116 cells for 48h respectively, MTT assay was used to test the growth curve of these two cells; Flow cytometry to test the expression of Granzyme B (GraB), perforin (PFP), CD107a and IFN-γ of γδ T cells; Lactate dehydrogenase (LDH) release assay to test the cytotoxic activity of the γδ T cells on SW-1116 cells; and Western blot to test the Wnt3a expression of the γδ T cells. Results: After cultured with IPP for ten days, the percentage of γδ T cells increased from 3.31±3.00% to 78.40±10.30%. Compared to the control group, when the concentration of Phloretin increased from 2.35μg/ml to 18.75μg/ml, it could significantly proliferate the γδ T cell growth (P <0.05) and inhibit the growth of SW-1116 cells in dose–response, and the expression of GraB, PFP, CD107a and Wnt3a significantly increased (P <0.05). Significant positive relationships were observed among CD107a and PFP, GraB, cytotoxicity (P <0.05). The percentage of IFN-γ producing γδ T cells treated with Phloretin was significantly higher than control group. Conclusion: Phloretin can enhance the killing effect of γδ T cells on SW-1116 cells; the mechanism may be that Phloretin could proliferate the γδ T cell growth, increase the expression of PFP and GraB, activate the Wnt signaling pathway, and produce higher level of IFN-γ. Indeed CD107a expression probably correlates quite well with antitumor activity. [Copyright &y& Elsevier]

Abstract: Our previous study demonstrated that electrical stimulation of the hypothalamic paraventricular nucleus (PVN) protects against gastric ischemia-reperfusion (GI-R) injury, but it is still unknown whether angiotensin II (Ang II) in the PVN plays a role in the development of GI-R. The purpose of this study was to investigate the effect of Ang II in the PVN on GI-R injury. GI-R injury was induced in rats by clamping the celiac artery for 30 min, and then reperfusing for 30 min, 1 h, 3 h, 6 h or 24 h, respectively. A cannula was inserted into the unilateral PVN for microinjection of Ang II. The extent of gastric mucosal damage was determined by gross and histological methods. We found that microinjection of pharmacological doses of Ang II (3, 30, and 300 ng) into the PVN dose-dependently inhibited GI-R injury, and that Ang II (30 ng) markedly attenuated GI-R injury at 1 h and 3 h after reperfusion. The effect of Ang II was prevented by pretreatment with the Ang II AT1 receptor antagonist losartan (5 µg) into the lateral cerebral ventricle. Furthermore, the protective effect of Ang II on GI-R injury was abolished by propranolol (1 mg/kg, i.v.) or disconnection of the nerves innervating the adrenal glands, was augmented by sympathectomy or phentolamine (1 mg/kg, i.v.), and was not affected by subdiaphragmatic vagotomy or atropine (1 mg/kg, i.v.). These results indicate that the PVN is a responsive site for central Ang II-induced protection against GI-R injury. The central effects of Ang II are mediated by AT1 receptors in the PVN, and the peripheral effects by a sympathetic-adrenal gland/β-adrenoceptor pathway. [Copyright &y& Elsevier]

• We found that glutamate stimulation of PVN reduced visceral sensitivity in the CVH rats. • We clarified that chemical ablation of PVN or NTS reversed the effect of PVN on CVH. • The microinjection of AVP-V 1 receptor antagonist DPVDAV into NTS promoted CVH. • The vagal nerve is participated in the CVH process. • We first reported that PVN and NTS are involved in the regulation of CVH. Chronic visceral hypersensitivity (CVH) is a major pathophysiological feature of patients experiencing in irritable bowel syndrome (IBS) and other disorders with visceral pain. However, little is known about its regulation of the central nucleus. In this research, we investigated the protective effect of microinjection of glutamate into hypothalamus paraventricular nucleus (PVN) on CVH and its possible regulatory mechanism in rats. Visceral sensitivity was assessed by pain threshold, abdominal withdrawal reflex (AWR) score, and the abdominal external oblique muscle electromyography (EMG) amplitude. Pathological changes in colorectal mucosa were assessed using immunohistochemical, biochemical analysis and Western blot. Results showed that microinjection of different doses of glutamate into PVN reduced the visceral sensitivity in a dose-dependent manner. This effect can be reversed after chemical ablation of PVN or nucleus tractus solitarius (NTS) or pretreatment with the arginine vasopressin (AVP)-V 1 receptor antagonist ([Deamino-pen1,val4,D-Arg8]-vasopressin) DPVDAV into NTS. The vagus discharge frequency was significantly reduced after the glutamate microinjection into PVN. Additionally, oxidation, proliferation and apoptosis in colorectal mucosa were related to the CVH regulations. These findings suggested that PVN and NTS are involved in the regulatory process of CVH and exert the protective effect on CVH, providing new ideas and therapeutic targets for CVH research. [ABSTRACT FROM AUTHOR]