Vertigo is a kind of patients' subjective feelings. The severity of vertigo is closely related to many factors. But we are short of a well accepted quantitative evaluation method capable of accurately and comprehensively evaluating vertigo in clinics. Reducing the onset of vertigo, enhancing the re- covery of equilibrium function, and improving the quality of life of vertigo patients should be taken as the focus of evaluating therapeutic effects. As for establishing a Chinese medical effectiveness evaluation system for vertigo, we believe we should distinguish different "diseases". We could roughly identify it as systemic vertigo and non-systemic vertigo. For systemic vertigo, the efficacy of vertigo could be comprehensively evaluated by UCLA vertigo questionnaire or dizziness handicap inventory combined with equilibrium function testing indices. But for non-systemic vertigo, the efficacy of vertigo could be comprehensively evaluated by taking UCLA vertigo questionnaire or dizziness handicap inventory as main efficacy indices. Secondly, we should analyze different reasons for vertigo, choose symptoms and signs in line with vertigo features as well as with Chinese medical theories, and formulate corresponding syndrome effectiveness standards according to different diseases. We should not simply take syndrome diagnosis standards as efficacy evaluation standards.
China ; Dizziness ; diagnosis ; Humans ; Quality of Life ; Surveys and Questionnaires ; Vertigo ; diagnosis

Objective To assess the value of CT in diagnosis and clinical treatment of the traumatic rupture of spleen.Methods There were 35 cases with traumatic repture of spleen,32 cases were comfirmed by operation.Plain CT scans in all cases and contrast-enhanced scans in 4 cases were performed.Results 19 cases were subcapsular hematoma,8 cases were spleen hematoma,6 cases were rended in one place of spleen,2 cases were rended in many places of spleen.Conclusion The difinite diagnosis and classification of traumatic rupture of spleen can be made by CT.The rupture of the organs around the spleen also can be found by CT,that can provide reliable evidence for clinical treatment.

Objective To observe the tissular pathological and ultrastructural changes of gastric mucosa with experimental atrophic gastritis caused by salt-water in rats and to explore the relationship between atrophic gastritis and high-salt diet.Methods The atrophic gastritis rat model was made by salt-water perfusion(0.15g/ml,2.5ml/d).The tissue of sinus ventriculi was detected with histopathologic examination and the ultrastructure of gastric mucosa was observed by scanning electron microscope.Results Under light microscope,the gastric gland was shrunk obviously in high-salt water perfusion group after high-salt water was given for 24 weeks.The muscle in muscular layer was hyperplasia and cramped into the lamina propria.The glandular epithelium in the upper 1/3～2/3 edge of the gland was atrophic.The gastric micro-depression became broaden and the width of cervical part of gastric pit became narrow.Under the scanning electromicroscope,the gastric mucosa was comparted into many gastric areas in the control group.Round or elliptic epithelium cells lined on the wall of gastric pits were in the same size and had short and spare microvillus.The epithelium was lined regularly and covered by laminar mucus.In salt-water perfusion group after the salt-water was given for 24 weeks,the surface of the gastric mucosa became thin and flat,and the glandular cells became rough.The mucosa between lumens of gland was broadened and the limited exfoliation of mucosa also could be seen.When the salt-water was given for 32 weeks,the gastric epithelial cells were shrunk,and the diameter of lumen of gland was broadened.There was breakage in the cell surface.Erosions with various size and shape and fibrous exudation could be seen.Conclusion Salt-water perfusion may cause the damage of the epithelia of gastric mucosa in experimental rats and long-term high-salt stimulation can induce the injury and atrophy of gastric mucosa.

Objective To investigate the incidence and possible reasons of patients with rheumatoid arthritis (RA) who stopped taking slow-acting antirheumatic drugs (SAADs).Methods Two hundreds and twenty-four in-or out-patients with RA were prospectively followed up for 4-year,and their demographic and clinical information and reasons of SAADs cessation were recorded.The difference between patients who stuck to SAADs and those who stopped SAADs and the factors that resulting the cessation were analyzed.Results ① Fourty-eight percent of 224 patients with RA ceased taking SAADs during 4-year period.② The main reasons of ceasing SAADs,provided by patients themselves,were side effects of SAADs,ineffectiveness,lack of knowledge about drugs,short of SAADs,concurrent diseases,and intention to pregnancy.③ There was significant difference in low income,poor educational status,number of tender joints,and rheumatoid factor level between the patients who stuck to SAADs and those who did not.Conclusion The high incidence of SAADs cessation in RA patients should rise concern.Both medical and patient factors contribute to the cessation.

Objective To investigate the changes of blood pressure in rats with experimental brain infarction caused by use of mild hypothermia. Methods One hundred and twenty Sprague Dawley rats were used and divided randomly and equally into a control group and an experiment group. In all of the rats, the middle cerebral artery occlusion (MCAO) was made to cause the experimental brain infarction, and reperfused 2 hours later. Three hours after MCAO, the rats in the experiment group were placed in the 4℃ with the rectal temperature controlled at 34? 1.0℃ , while those in the control group in the room temperature. The heart rate, breath, blood pressure, oxygen saturation and rectal temperature were monitored. The rats were sacrificed 24 hours after MCAO and the infarction volume were observed. Results After MCAO, the blood pressure was significantly increased as compared with that prior to MCAO ( P 0.05) . Hypothermia significantly reduced the blood pressure after being used for more than 3 hours ( P

Objective To study the relationship between long-term high-salt water and the morbidity mechanism of chronic atrophic gastritis (CAG), The expression of HSP60 and ras protein were detected in the gastric mucosa of CAG rates induced by high-salt water.Methods The atrophic gastritis rat model was made by high-salt-hot water perfusion and the ultrastructure of gastric mucosa was observed by Laser Scanning ConfocaI Microscopy. Results There was no expression in gastric mucosa in normal group. The expression of HSP60 and ras was observed in the cell plasm of rats at 12 weeks. The higher expression was observed in the rats at 24, 32 and 65 weeks. Using laser scanning confocaI microscopy and immunofluorescence technique had observed coexistence of HSP60 and ras.Conclusion Long time high-salt-hot water can induce CAG and increasing the expression of HSP60 and ras. HSP60 and ras play an important role in the formation of atrophic gastritis.

Objective:To investigate the protective role of heme oxygenase-1 and its reaction product,carbon monoxide against acute liver injury induced by carbon tetrachloride in rats.Methods: Thirty male Sprague-Dawley rats were randomly divided into six groups with five in each.The control group received a single dose of corn oil injection.Carbon tetrachloride was injected intraperitoneally(i.p) to establish acute liver injury models in rats.Hemin(50 ?mol/kg) was administered i.p.12 hours before CCl_4 treatment,with an aim to induce HO-1 protein expression in the liver of rats.Carbon monoxide was injected i.p.12 hours prior to CCl_4 injection,resulting in about 8%-12% carboxyhemoglobin concentration in vivo.The expression of HO-1 in the liver of hemin-treated rats was determined by western blot method at different time points.At 24 h after carbon tetrachloride administration,all rats were sacrificed to collect blood samples for the examination of ALT,AST levels and to remove liver tissues for analysis of MDA concentration,SOD activity and caspase-3 activity as well as TNF-a contents.In addition,histopathological changes were investigated and hepatocyte apoptosis was detected by TUNEL method.Results: The administration of carbon tetrachloride to rats caused a marked hepatic damage,characterized by significant elevation of serum ALT,AST levels(2 136.3?163.4 U,1 422.7?221.7 U) and liver MDA con-tent(5.28?0.93 ?mol/g),caspase-3 activitiy(optical density value(4.69)?1.02) and TNF-? level(256.3?27.3 ng/L) combined with a remarkable reduction in liver SOD activity(45.9?14.8 U/mg) as compared with the control rats.Histopathological observations revealed severe damage in the liver and prominent hepatocyte apoptosis took place in CCl_4treated rats.However,pretreatment with hemin could induce high expression of HO-1 protein and exert potent protective effects against liver injury,as demonstrated by a significant decrease in ALT,AST levels(287.1?24.3 U,246.2?21.7 U) and MDA concentration(3.27?1.34 ?mol/g),reduction in caspase-3 activity(optical density value 2.49?1.47) and TNF-? level(132.6?19.5 ng/L),as compared with the CCl_4-treated rats.Moreover,hepatocyte apoptosis and liver injury were both attenuated remarkably in the liver of rats pretreated with hemin.In contrast to hemin administration,single injection of exogenous CO produced the same protective effects,as indicated by the remarkable reduction of ALT,AST levels and caspase-3 activity and TNF-a levels.Conclusion: The above results suggest that HO-1/CO system has a potent protective effect on acute liver injury induced by carbon tetrachloride in rats.Induction of HO-1 expression and low concentration of CO can inhibit the progress of hepatic damage,which might be due to the alleviation of lipid peroxidation and reduction of caspase-3 activity or inhibition of TNF-? level.

Adult ; Aged ; Breast Neoplasms ; diagnosis ; pathology ; Carcinoma, Papillary ; diagnosis ; pathology ; Female ; Humans ; Lymphatic System ; pathology ; Middle Aged ; Neoplasm Invasiveness

Objective To explore influencing factors for complete resection and operation time of endoscopic submucosal dissection( ESD) for colorectal tumors. Methods This retrospective study included 95 consecutive colorectal tumors in 88 patients whose pathological diagnosis was adenoma and carcinoma, treated with ESD at the Department of Endoscopy of the First Hospital of Jilin University from January 2013 to December 2014. Multiple logistic regression analysis was conducted on the factors related to complete resection and operation time. Results Average tumor size was 28. 7±14. 1 mm(range,8?80 mm), and the average procedure time was 80. 72±63. 90 min. The rate of complete resection was 92. 6%(88/95),and the rate of incomplete resection was 7. 4%(7/95). Multivariate logistic regression analysis revealed that fibrosis (P=0. 012,OR=52. 473, 95%CI:2. 571?1140. 438) contributed to incomplete resection. Fibrosis ( P=0. 001, OR=0. 045, 95%CI:0. 007?0. 289) ,tumor size ( P=0. 035,OR=0. 170, 95%CI:0. 033?0. 884) ,granular?type laterally spreading tumor ( P=0. 013, OR=34. 432, 95%CI:2. 138?554. 476 ) , non?granular?type laterally spreading tumor(P=0. 044,OR=31. 715, 95%CI:1. 093?919. 904) were independent factors for extending operation time of colorectal ESD. Conclusion The severer fibrosis can induce higher rate of incomplete resection. The more severe fibrosis is, the larger tumor size is, and the longer operation time is.

In the ApoE(-/-) mouse model of atherosclerosis (AS) stable plaque, the expression and location of intracellular tissue factor (TF) in the cellular components of AS stable plaque were investigated in order to explore the cellular mechanism of AS thrombosis. Pathological changes of the stable plaque were observed under a microscope. The expression of TF protein was examined in aortic stable plaque of mice by using immunohistochemistry. Color image planimetric system was used to analyze the histological components of the stable plaque and the TF distribution. Under the confocal microscope, the intracellular TF location in the stable plaque of mice was observed. The results showed the cellular area was the major part of stable plaque (67.36%+/-6.52%, P<0.01). The percentage of total area occupied by cellular area was significantly larger than atheromatous gruel and acellular area (P<0.01). Macrophages and smooth muscle cells (SMC) were major cells in the cellular area. The percentage of total area occupied by SMC was significantly larger than by macrophages (P<0.01). Multiple linear regression analysis showed there was a positive correlation between TF area and SMC area (r=0.616, P=0.008), and no correlation was found between TF area and macrophage area (r=0.437, P=0.08). Pictures of color image planimetric analysis of TF and SMC were merged to highlight areas with co-localization (yellow), it was concluded that the process could be a cell-mediated TF expression in the stable plaque. SMC may be the major source of TF in AS without plaque rupture.