To investigate causes and clinical picture of fever of unknown origin (FUO), and to sum up the experiences in diagnosis of FUO, the medical records of 107 patients with FUO were reviewed retrospectively. Specific causes were identified in 99. 1% of these patients, including infections in 50 patients(46. 7%) , rheumatic problems in 22(20. 6%) and malignancies in 17(15. 9%). The main pathogens responsible for the infections were pyogenic bacteria(72. 0% , 36/50) and M tuberculosis (18. 0% , 9/50), mostly extrapulmonary. Lymphatic and he-mopoietic tissue neoplasms were the main forms of malignancy (88. 2%, 15/17), including histiocytosis, malignant lymphoma and leukemia. Drug fever was another common cause of FUO, accounting for 8. 4% in our series.

Objective:To investigate the risk factors for refeeding syndrome (RFS) in patients with severe stroke.Methods:Patients with stroke admitted to the Neuro Intensive Care Unit, Nanfang Hospital, Southern Medical University and received enteral nutrition support >72 h from January 2013 to July 2019 were enrolled retrospectively. RFS was defined as a new onset of hypophosphatemia within 72 h after the start of nutritional support, that is, blood phosphorus <0.65 mmol/L and a decrease of >0.16 mmol/L from the baseline value. The independent risk factors for RFS were identified by multivariate logistic regression model. Results:A total of 209 patients with severe stroke were included, with a median age of 65 years (interquartile range [ IQR] 53 to 72 years), and 154 were males (73.7%); 136 patients had cerebral infarction (65.1%), 73 had intracerebral hemorrhage (34.9%). The baseline median National Institutes of Health Stroke Scale (NIHSS) score was 15 ( IQR, 11-20), the median Glasgow Coma Scale score was 9 ( IQR, 6-12), the median Acute Physiology and Chronic Health Score was 16 ( IQR, 11-20), the median Nutrition Risk in Critically Ill (NUTRIC) score was 3 ( IQR 2-5), and the median Sequential Organ Failure Assessment (SOFA) score was 4 ( IQR, 3-6); the baseline median serum phosphorus was 1.05 mmol/L ( IQR, 0.90-1.19 mmol/L). A total of 34 patients (16.3%) developed RFS. Multivariate logistic regression analysis showed that male (odds ratio 3.565, 95% confidence interval 1.150-11.053; P=0.028) and patients with higher SOFA score (odds ratio 1.246, 95% confidence interval 1.077-1.442; P=0.032) were more likely to develop RFS. Conclusions:RFS is not rare in patients with severe stroke. Males and patients with severe disease are more likely to develop RFS.

Objective To investigate the role of acid-sensing ion channels (ASICs) in global cerebral ischemia-reperfusion (I/R) injury in rats. Methods Forty-eight adult male Sprague-Dawley rats weighing 250-310 g were randomly divided into 4 groups ( n = 12 each): sham operation group (group S); global cerebral I/R group (group I/R); normal saline group (group NS) and specific ASIC blocker amiloride group (group A). Global cerebral I/R was produced by occlusion of 3 vessels ( 10 min occlusion of the bilateral common carotid arteries and basilar artery) followed by reperfusion. In group NS and A, NS 6 ml/kg and amiloride 0.6 mg/kg were injected through femoral vein immediately before reperfusion respectively. Six rats in each group were selected, the dialysate in CA1 area was collected before ischemia (baseline), immediately after ischemia and during 20 min reperfusion (once every 10 min) for determination of lactate concentrations. The left 6 rats in each group were elected at 8 h of reperfusion and the open field test and inclined plane test were peeformed to assess neurological behavior.The rats were then sacrificed and brain tissues taken for microscopic examination and brain water content was calculated. Results Compared with group S, the concentration of lactate in the dialysate and brain water content were significantly increased and neurological deficits developed in group I/R and NS (P ＜ 0.05). Compared with group I/R, the concentration of lactate in the dialysate and brain water content were significantly decreased and neurological deficits were improved in group A ( P ＜ 0.05 ), but no significant change in the parameters mentioned above was found in group NS ( P ＞ 0.05). Microscopic examination showed that the damage to the brain tissues was attenuated in group A compared with group I/R. Conclusion ASICs are involved in the development of global cerebral I/R injury in rats.

Objective To study the resistances of CDl33 + subset purified from gastric cancer cell line to chemotherapy drugs and the mechanism of this resistance regarding to the mRNA expressions of both Bcl-2 and BAX in relation to the relative apoptotic genes.Methods CD133 + subset and CD133-subset were purified from KATOⅢ cell linc by magnetic activated cell sorting.The proliferating ability of these two subsets resistantnt to 5-FU,Cisplatin(DDP,PDD) and Etoposide was checked and compared by CCK-8 test.The apoptotic changes of these two subsets regarding to the expression of mRNA of both Bcl-2 and BAX were also analized by RT-PCR.Results In CD133 + subset,the contant percentage of CD133 + expression rate was 90％ via analysis of flow cytometye.Twelve hours after treatment of5-FU,DDP and VP-16,the cells in both CD133 + subgroup and CD133-subgroup would gradually start to change in apoptotic morphology.The growth inhibiting rate by CCK-8 measurement for 5-FU,DDP and VP-16 groups in CD133 + subgroup was significantly lower than that in CD133-subgroup.The data under different treatment respectively was,5-FU:(30.56 ± 1.99) ％-(88.60 ± 1.95) ％ vs (32.81 ± 2.67) ％-(95.73±2.12)％,P=0.045,cisplatin:(45.89 ±3.64)％-(81.20 ± 1.18)％ vs (50.21 ±3.22)％-(90.46±1.89)％,P=0.043,VP-16:(37.21 ±3.80)％-(78.49 ±3.22)％ vs (35.55 ±3.23)％-(89.32 ±-3.54) ％,P =0.048).After treatment of these three kind of anti-tumour drugs,the expression level of Bcl-2 mR-NA decreased significantly and the expression level of BAX mRNA increased significantly in both CD133 + subgroup and CD133-subgroup.However,these changing ranges of Bcl-2 mRNA and BAX mRNA were more obvious in CD133 + subgroup in comparison with those in CD133-subgroup.Conclusions In some degree,resistent potentiality of CD133 + cells to 5-FU,DDP and VP-16 has been identified,which may probably be due to the up-regulation of the expression of BAX and down-regulation of the expression of Bcl-2.

In the course of emerging infectious disease learning,comprehensive methods including comparing the similarity of emerging infectious disease and classical infectious disease,uniting the general introduction and the typical examples explanation,strengthening the multimedia teaching and the case based teaching were adopted to strengthen the effect of teaching.

Objective:To investigate the relationship between serum vascular endothelial growth factor (VEGF), peripheral blood microRNA-126 (miR-126) and the number and distribution of cerebral microbleeds (CMBs).Methods:Consecutive patients with non-acute ischemic cerebrovascular disease admitted to the Department of Neurology, the First Affiliated Hospital of Baotou Medical College from June 2019 to June 2020 were enrolled. The clinical data were collected, 3.0 T MRI examination was performed, and susceptibility-weighted imaging was used to detect CMBs. The serum VEGF concentration was detected by enzyme-linked immunosorbent assay, and miR-126 was detected by fluorescence quantitative polymerase chain reaction. Multivariate logistic regression analysis was used to determine the independent influencing factors of CMBs. Multiple linear regression analysis was used to determine the correlation between serum VEGF concentration, miR-126 in peripheral blood and the number of CBMs. Receiver operating characteristic (ROC) curve was used to evaluate the predictive value of serum VEGF concentration and relative expression of miR-126 in peripheral blood for CMBs. Results:A total of 193 patients with non-acute ischemic cerebrovascular disease were enrolled, including 110 patients (57.0%) in the non-CMBs group, 20 (10.4%) in the strictly lobar CMBs group and 63 patients (32.6%) in non-strictly lobar CMBs group. The comparison among the three groups showed that age might be a risk factor for strictly lobar CMBs, while higher VEGF, higher cystatin C level, lower relative expression of miR-126 in peripheral blood, hypertension and previous stroke or transient ischemic attack might be the risk factors for non-strictly lobar CMBs. Multivariate logistic regression analysis showed that higher serum VEGF concentration was an independent risk factor for non-strictly lobar CMBs (odds ratio 1.186, 95% confidence interval 1.035-1.358; P=0.014), while the higher relative expression of miR-126 was an independent protective factor for non-strictly lobar CMBs (odds ratio 0.154, 95% confidence interval 0-0.269; P=0.026). Multiple linear regression analysis showed that higher serum VEGF concentration ( r=0.848, P<0.001) and the lower relative expression of miR-126 ( r=-0.043, P=0.035) significantly increased the number of CMBs. ROC curve analysis showed that the area under the curve of serum VEGF for predicting non-strictly lobar CMBs was 0.803 (95% confidence interval 0.741-0.865), the optimal cut-off value was 120.55 ng/L, the sensitivity was 70.7%, and the specificity was 75.5%. Conclusions:In patients with non-acute ischemic cerebrovascular disease, there is a significant correlation between serum VEGF concentration and the relative expression of miR-126 in peripheral blood and the number and distribution of CMBs. Serum VEGF can be used as a biomarker for predicting the presence of non-strictly lobar CMBs.

Objective:To analyze the clinicopathological characteristics of patients with unknown etiology of portal hypertension and investigate the efficacy of endoscopic management of gastroesophageal varices in these patients.Methods:Patients with unknown etiology of portal hypertension and gastroesophageal varices who received liver biopsy between January, 2017 and January, 2020 in Zhongshan Hospital were included. The characteristics of pathology, portal computed tomography (CT) angiography, and endoscopy were recorded and follow-up for the occurrence of bleeding after treatment.Results:A total of 31 patients were included and divided into cirrhosis with unknown etiology group ( n=10) and non-cirrhotic portal hypertension group ( n=21). Patients in the non-cirrhotic group were younger [28.0(29.5-49.5) vs 58.5(43.5-65.8), P=0.004] and mostly male (71.4%), and fewer comorbidities including diabetes (4.8% vs 40.0%, P=0.027). The features of pathology finding including vasculopathy, cholestasis, and hepatic sinusoidal dilatation as well as the Sarin classification and bleeding rate of gastroesophageal varices, proportion of patients receiving endoscopic treatment were shown similar between the two groups ( P>0.05). The hepatic venous pressure gradient (HVPG) was significantly lower in the non-cirrhotic group [4.5(2.8-12.8)mmHg vs 12(8-18)mmHg, P=0.018]. Among them, 21 patients received endoscopic treatment, and the bleeding rate had no difference between these two groups after endoscopic treatment ( P=0.751). Conclusions:Non-cirrhotic portal hypertension in a predominantly young male population has similar clinicalpathological characteristics when compared to cirrhotic portal hypertension with unknown etiology. HVPG can not reflect the actual portal pressure in these patients. Endoscopic treatment is the effective treatment option for the prevention of variceal bleeding.

Objective: To investigate the influence of CD133+expression on patients' survival and resistance of CD133+cells to anti-tumor agents in gastric cancer (GC).
Methods: Influence of CD133 expression on prognosis was analyzed employing sam-ples from patients with GC. GC cell lines were utilized to separate CD133+and CD133?subpopulations by immunomagnetic separation and to analyze the biological features of two subpopulations in vitro and in vivo, especially in resistant to anti-tumor reagents and its apoptotic mechanism.
Results: The lower CD133+group showed a significantly better survival compared with the higher CD133+group. The highest content of CD133+subpopulations for KATO-III cells had stronger proliferative ability than CD133?subpopulations. A single CD133+cell was capable of generating new cell colony and the tumorigenicity rate in nude mice was 100% for CD133+ clonal spheres or for CD133+ cells, but 0% for CD133? cells. Furthermore, the higher expression levels of Oct-4, Sox-2, Musashi-1 and ABCG2 in CD133+ clonal spheres were identified compared with CD133+ cells or CD133? cells. Under the treatment of anti-tumor reagents, CD133+ cells had lower suppression rates compared with CD133? cells while lower level of Bcl-2 and higher level of Bax were found in CD133+cells compared with CD133?cells.
Conclusions: The patients with lower CD133+expression had a better survival. Enriched CD133+ cells in clonal sphere shared the ability to be self-renewable, proliferative, tumorigenic and resistant to anti-tumor agents as probably regulated by Bcl-2 and Bax.

Objective To evaluate the effect of chronic low potassium on K+uptake rate in the my?ocardium and skeletal muscle of rabbits. Methods Thirty?two adult male rabbits, aged 12-14 weeks, weighing 2?0-2?7 kg, were randomly divided into 4 groups ( n=8 each) using a random number table:normal feeding group ( group N) , low potassium feeding group ( group L) , potassium supplementation con?trol group ( group SC ) and potassium supplementation experimental group ( group SE ) . N and SC groups were given a normal diet only, and L and SE groups were fed with a low potassium diet for 15 days. Potassi?um chloride ( KCl) 0?5 mol∕L was then infused intravenously at the initial rate of 60 μmol·kg-1 ·min-1 in SE and SC groups. Blood samples were obtained from the central artery of the left ear every 5 min for meas?urement of plasma K+ concentrations. The infusion rat of KCl was then adjusted until the plasma K+concen?tration reached 5?5 mmol∕L and maintained at this level for 1 h, and then infusion was stopped. The total volume of KCl infused was recorded. The hearts and soleus muscle of animals were excised for determination of K+content. K+uptake and uptake rate were calculated. Results Compared with N group, the plasma K+concentration, and K+content in the myocardium and soleus muscle were significantly decreased in group L ( P<0?05) . Compared with SC group, the total volume of KCl infused, and K+uptake and uptake rate in the myocardium and soleus muscle were significantly increased in group SE ( P<0?05) . Conclusion Chro?nic hypokalaemia can increase K+ uptake rate in the myocardium and skeletal muscle of rabbits.

ObjectiveTo investigate the expression of CXCR4 and CD133mRNA in primary lesion of primary gastric adenocarcinoma and the relation with clinicopathological features,and to explore the correlation of CXCR4 and CD133.MethodsThe primary lesion of primary gastric adenocarcinoma and normal tissues adjacent to gastric cancer were obtained from 50 patients.The diction of CXCR4 and CD133 protein expression was detected by the immunohistochemical staining,and the relative gray scale values of CXCR4 and CD133mRNA by semi-quantitative RT-PCR (Fisher' s exact probability method).Their relationship with clinicopathological features was also investigated ( Spearman relation analysis).ResultsThe positive rates of CXCR4 and CD133 protein in gastric cancers were 76.0％ and 66.0％ respectively,which were significantly higher than that in normal tissues adjacent to gastric cancer ( 16.0％ and 10％ ; P =0.000,P =0.000).The increment of relative gray scale values of CXCR4mRNA was associated with the larger tumor diameter,the later TNM stage and the occurrence of lymphatic metastasis( P ＜ 0.05 ).And the larger diameter of tumor,the later TNM stage were associated with the higher relative gray scale values of CD133mRNA (P ＜0.05).The levels of the relative gray scale values of CXCR4 mRNA and CD133mRNA were positively related(r =0.453,P ＜ 0.01 ).ConclusionsThe higher expression of CXCR4 and CD133mRNA correlateswith tumour diameter,TNM stage and lymphatic vessel invasion. The relative gray scale values of CD133mRNA increase with the increment of the relative gray scale values of CXCR4.