Objective To clarify the role of hypothalamic IL-6 in gastric mucosal blood flow, gastric juice pH value and gastric mucosal injury. Method Model of gastric stress ulcer was established by fluid percussion to make craniocerebral trauma. Twenty male SD rats fed for one week in the experiment room were randomly(random number) divided into control group, one hour group, six hours group and 12 hours group after injury. The levels and distribution of IL-6 in hypothalamus were detected by using immunohistochemistry and Western blot. Simultaneously, gastric pH value, gastric mucosal blood flow and gastric mucosal injury index of rats in each group were measured, and the histology of gastric mucosa was observed. Results IL-6 immunoreactive cells were widely distributed in neuronal cells of hypothalamus of the stressed rats especially in the para-ventricular nucleus (PVN).One hour after injury, the pH value rapidly declined, and the lowest point appeared 6 hours later. One hour after injury, the injury of gastric mucosa was found, and the injury became worse and worse as time got longer and longer. The ulcer index (UI) was increased. One hour after injury, there was a brief increase in blood flow to the peak in gastric mucosa, and then the blood flow declined until 6 hours elapsed and got stable. The experiment prompted the gastric stress ulcer appeared. Conclusions In the SD rats with gastric stress ulcer induced by craniocerebral injury incurred by hydraulic percussion, the hypothalamic IL-6 may activate neuronendocrine metabolism mediated through the activation of PVN, inducing gastric mucosal injury.

Objective To investigate the effect of acute high intracranial pressure on the static pressure-volume curve of dogs' total respiratory system in order to evaluate the relationship between brain injury and respiratory insufficiency.Methods Fourteen dogs were divided into two groups.Animals were anesthetized,paralyzed and mechanical ventilated.The intracranial hypertension in experimental group(n=8)was induced by injecting blood-clots into the right frontal lobe.The other six dogs served as control.The intracranial pressure was monitored by an optical fiber transmitter inserted into the left cerebral hemisphere.The pressure-volume curves of the respiratory system were measured before and after induction of high intracranial pressure by a self-made apparatus consisting of two sealed bottles and a U shaped glass tube.The curves were also measured correspondingly in control group.The static compliance was calculated by equation C=?V/?P.The volume of intracerebral hematoma was calculated.The histopathology of lung was studied under microscope.Results The intracerebral hematoma was located in the right frontal lobe with volume from 4.8-11.5ml(average 8.48ml).The intracranial pressure was elevated from 18.13?5.96mmHg to 46.88?16.42mmHg,which induced a shift of pressure-volume curve to the right in experimental group,while no obvious change was found in control group.Compared to pre-injection,the static compliance of total respiratory system decreased significantly(P

Objective To investigate standard diagnosis and treatment of cerebrospinal fluid (CSF) leakage to improve the prognosis of the patients. Methods A retrospective study was done on 75 patients with CSF leakage from January 2004 to March 2007 in our hospital. There were 51 patients with rhinorrhea, nine with otorrhea and 15 with wound/incision leakage. Of all, 39 patients had traumatic leakage, 32 postoperative leakage and four spontaneous leakage. In the study, 23 patients were cured by position testing and drug therapy and 16 by cerebrospinal fluid drainage and/or wound debridement but 36 were treated with surgeries including craniotomy repair in 17, extracranial repair in 17 and CSF shunt in five (three received CSF shunt after repair). Results Of all, 64 patients were cured, 10 gained im-provement but one died. Conclusion Standard diagnosis and treatment of CSF leakage helps improve cure rate and reduce complications.

Objective To evaluate the neuroprotective benefits of histone deacetylases (HDAC)inhibitor MS-275 in rats with moderate traumatic brain injury (TBI).Methods Sixty-eight adult male SD rats were assigned to sham injury + placebo treatment (control group),TBI + placebo treatment (injury group),TBI + MS-275 (15 mg/kg) treatment (treatment group Ⅰ) and TBI + MS-275 (45 mg/kg)treatment (treatment group Ⅱ) according to the random number table.An experimental model of moderate TBI in the rat was induced using a lateral fluid percussion device.MS-275 was dissolved in DMSO and administered (15 and 45 mg/kg) intraperitoneally in seven consecutive days(once a day).The first administration was done in 30 minutes postinjury.Alteration in body weight of rats in each group was recorded after injury.Spatial learning and memory retention in rats was assessed using the Morris Water Maze in days 10-14 after TBI.Brain tissues were sectioned to measure acetyl-histone H3 and neuronal survivals in the hippocampus CA2-3 region using immunohistochemistry and cresyl-violet staining techniques.Results TBI rats showed significant body weight loss in 3 days postinjury as compared with the controls (P ＜0.05) and then gradually gained the body weight in 4-5 days postinjury.No significant difference in actual body weight loss after injury was found among injury group and treatment groups (F =0.149,P ＞0.05).Behavioral result revealed that the animals in treatment groups had significant improvement in cognitive performance as compared with injury group (P ＜ 0.01).Immunohistochemical results presented a markedly increased level of acetyl-histone H3 in both treatment groups,with no significant difference as compared with control group and a trend of increase in the survived neurons in the CA2-3 hippocampus in 14 days postinjury (P ＞ 0.05).Conclusions MS-275 achieves visible improvement of acetyl-histone H3 level and cognitive performance in the acute phase of TBI.Simultaneously,this treatment has an ameliorative effect on pathological changes associated with TBI as well and provides a neuroprotective effect against TBI.

Objective To evaluate the influence of positive end-expiratory pressure (PEEP) on intracranial pressure and cerebral perfusion pressure in dogs with or without intracranial hypertension caused by frontal intracerebral hematoma. Methods Eighteen dogs were randomly divided into three groups. In Group B and Group C, the intracranial hypertension was respectively higher than 25 mmHg but less than 40 mmHg and higher than 40 mmHg induced by autoblood clotting injection into the right frontal lobe, while Group A as control was of normal intracranial pressure. PEEP was applied in increment of 3 cmH2O from 0 to 18 cmH2O, each level lasting 20 min. The intracranial pressure (ICP) was monitored by an optical fiber transducer implanted into left frontal lobe. Mean arterial pressure (MAP), heart rate (HR), and central venous pressure (CVP) were recorded simultaneously. Cerebral perfusion pressure (CPP) was calculated by the equation (CPP=MAP-ICP). Results With increasing PEEP level, ICP increased and CPP fell in Group A; ICP fell, MAP and CPP increased in Group B; ICP fell, MAP and CPP increased in Group C. CVP increased in all groups, and the increment was significantly higher in Group C than the other two groups (P

Objective:To investigate the effect of astragaloside IV (AS-IV) on the secretion of stromal cell-derived factor-1α (SDF-1α) and CXC chemokine receptor 4 (CXCR4) by high glucose injured human umbilical vein endothelial cells (HUVECs), so as to lay a foundation for further study on AS-IV improving angiogenesis by regulating SDF-1 α/CXCR4 axis of endothelial cells.Methods:HUVECs were isolated and cultured from the umbilical vein of full-term healthy newborns and identified by von Willebrand factor (vWF) combined with 4-diamino-2-phenylindole (DAPI) nuclear staining. The obtained HUVECs was cultured in EGM-2 medium with 30 mmol/L glucose for 120 h to obtain high glucose damaged HUVECs. After intervention with different concentration gradients (25 mg/L, 50 mg/L, 100 mg/L, 200 mg/L, 400 mg/L) AS-IV for 72 hours, the contents of SDF-1α and CXCR4 were detected by enzyme linked immunosorbent assay (ELISA) method to determine the best concentration of AS-IV. The supernatant of damaged HUVECs were collected at 6, 12, 24, 48 and 72 hours after intervention with the best concentration of AS-IV, and the contents of SDF-1α and CXCR4 were detected by ELISA method to determine the best action time of AS-IV. The damaged HUVECs was randomly divided into experimental group and control group, and the blank group was set up at the same time. The experimental group was treated with the best concentration of AS-IV and the best time, the control group and the blank group were treated with the same volume of phosphate buffered saline (PBS) solution, and the contents of SDF-1α and CXCR4 in each group were detected by ELISA method.Results:The vWF factor on the cell membrane was green fluorescence, and the nucleus was blue after DAPI staining. When the fusion image showed green fluorescence, HUVECs were identified by blue fluorescence. The expression of SDF-1α in damaged HUVECs was the best when treated with AS-IV of 100 mg/L for 24 hours (1 642.87 pg/ml), and the expression of CXCR4 in damaged HUVECs was the best when treated with AS-IV of 50 mg/L for 48 hours (8.44 ng/ml). Compared with the control group, the contents of SDF-1α and CXCR4 in the experimental group were significantly increased, and the difference was statistically significant ( P<0.05). While the contents of SDF-1α and CXCR4 in the experiment group were slightly less than those in the blank group and there was no statistically significant difference ( P>0.05). Conclusions:AS-IV can promote the expression of SDF-1α and CXCR4 in HUVECs damaged by high glucose to return to normal physiological level, so as to play the role of vascular repair and neovascularization.

OBJECTIVE: To investigate the protective effects of mild hypothermia (33-35 degrees C) on the outcome of patients with severe traumatic brain injury (TBI) (GCS<8). METHODS: Patients in the mild hypothermia group were cooled to 33-35 degrees C by cooling blanket with muscular relaxant, and patients in the normothermia group were maintained at 37-38 degrees C. RESULTS: The result showed that the mortality was 26.1% (6/23) in the mild hypothermia group and 58.3% (14/24) in the normothermia group respectively (P<0.05). The mild hypothermia also markedly reduced intracranial pressure (P<0.01 and inhibited hyperglycermia (P<0.05). No significant side-effects were found during hypothermic treatment. CONCLUSIONS: Our clinical data have demonstrated that mild hypothermia is a useful method for management of patients with severe traumatic brain injury.

Objective To investigate the effect of intracranial pressure fluctuation on the prognosis of patients with traumatic brain injury (TBI).Methods A retrospective case series study was conducted on the clinical data of 30 patients with TBI hospitalized between June 2012 and June 2014.There were 21 males and 9 females,aged (43.0 ± 19.8) years.After the intracranial pressure probe was implanted,the intracranial pressure of TBI patients was monitored continuously and the data were recorded per minute.A single cosine method was used in analyzing the circadian rhythm of intracranial pressure data.Furthermore,the ratio of the amplitude of the circadian parameter (A) to the median (M) value (A/M) was selected to evaluate the biologic rhythm of patients.The correlations of circadian rhythm parameter A/M with Glasgow Outcome Scale (GCS) and with extended Glasgow Outcome Scale (GOS-E) were analyzed using linear regression.Results The circadian rhythm was observed in all patients regardless of injury severity (P ＜ 0.01).The circadian rhythm parameter A/M of intracranial pressure was positively correlated with the GCS of patients at discharge (R2 =0.346,F =14.797,P ＜0.01) and with the GOS-E (R2 =0.356,F =15.502,P ＜ 0.01).Conclusion The intracranial pressure fluctuation of TBI patients follows circadian rhythm,which might be correlated with the prognosis of TBI patients.

Objective To investigate independent risk factors for unintended initial dissection of the posterior plane(UIDPP)during small incision lenticule extraction(SMILE)by surgeons with different qualifications.Methods A total of 1 600 patients(3 003 eyes)who underwent SMILE performed by three surgeons with different qualifications from April to September 2021 were selected as the research subjects,including 911 males and 689 females,with an average age of(21.82±3.55)years.The incidence of UIDPP in patients was recorded,along with a comprehensive summary of the age,gender,eyes,surgeons,surgical proficiency,subjective refraction,central corneal thickness,lenticule thickness,side cut angle,and peripheral lenticule thickness of the patients.Independent risk factors of UIDPP were analyzed using the binary logistic regression.Test level:α=0.05.Results In this study,the incidence of UIDPP was 6.56％(197/3 003),and the lenticule was successfully removed in all eyes.Multivariate logistic regression analysis demonstrated that surgeon(P=0.035),surgical proficiency(P=0.026),eyes(P=0.007),lenticule thickness(P＜0.001),and peripheral lenticule thick-ness(P＜0.001)were independent risk factors associated with the UIDPP during SMILE surgery.No significant differences were observed in other parameters(all P＞0.05).Conclusion Surgeons,surgical proficiency,eyes,lenticule thick-ness,and peripheral lenticule thickness are independent risk factors of UIDPP.

Objective The objective is to probe into the effects of astragaloside Ⅳ (AS-Ⅳ) on activity and proliferative function of endothelial progenitor cells (EPCs),which lays a foundation for further study on the effects of AS-Ⅳ on vascular neovascularization mediated by endothelial progenitor cells.Methods The mononuclear cells were isolated by the density gradient centrifugation in umbilical cord blood of full-term healthy infants,and EPCs were obtained by subculture and cell identification when the cells presented spindle shapes.The obtained EPCs were randomly divided into the experimental group and the control group.In the experimental group,EPCs were cultured by AS-Ⅳ with different concentration gradients (25 mg/L,50 mg/L,100 mg/L,200 mg/L and 400 mg/L),while in the control group,they were treated with the same amount of phosphate buffer saline (PBS) solutions.The effects of AS-Ⅳ on the proliferation of endothelial progenitor cells was studied by cell counting kit-8 (CCK-8) cell proliferation experiment,and the activity rate of EPCs cells was measured at the optimum concentration of EPCs proliferation.Results EPCs were successfully obtained after confirming nuclear staining test of CD31 antibody and 4',6-diamidi-no-2-phenylindole (DAPI).Further study showed that AS-Ⅳ can promote the proliferation of EPCs,and its optimal concentration of EPCs proliferation is 100 mg/L.Compared with the normal control group,the activity rate of endothelial progenitor cells after intervention of AS-Ⅳ was 98.7％,higher than 98.12％ in the control group,with significant difference (x2 =49.59,P ＜0.01).Conclusions AS-Ⅳ can enhance the activity of human EPCs and promote their proliferation in vitro.