This paper analyzes the concept of hospital financial information management and the current situation.From the perspective of public hospital reform, we proposed the hospital should fulfill the information-based budget management and salary management, construct hospital information-based cost control flowsheet, build message conducting and transferring program, that budget should be achieved as soon as possible, information technology should be applied in hospital management, and build a complex financial information management team as soon as possible.

We retrospectively analyzed 23 cases of histiocytic necrotizing lymphadenitis (HNL) admitted to our hospital as fever of unknown origin (FUO).Fever,lymphadenopathy and skin rash were the most common clinical manifestation.The major laboratory features included cytopenia,abnormal liver enzyme and elevated inflammatory markers.Three of the 23 cases were finally diagnosed as infectious disease,5 as autoimmune disease,while the left 15 remained as HNL during the follow-up.Four of the 15 HNL patients resolved spontaneously,while the other 11 relieved by steroid use.Two patients relapsed during the follow-up.HNL was one of the rare causes of FUO.Since it would be accompanied with infectious,autoimmune or malignant diseases,long follow-up is necessary.

Objective To investigate the breeding densities and the seasonal distribution of Tyrophagus putrescentiae, Acarus siro, Lepidoglyphus destructor, and Dermatophagoides farinae in Bengbu City, 4 common storage acaroid mites during Feb.2006-Jan.2007. Methods The samples were collected and isolated by Waterflotation and Tullgren, then counted and identified the four acaroid mites from 20 different habitats. Results 4 species of acaroid mites had high breeding density in ham, wheat, seed and house dust. The number of the mite increased from Apr. or May, and to the peak during July and Aug. and declined from Sep. or Oct.. Seasonal distribution of the individual acaroid mites might be different. Conclusion 4 species of acaroid mites are widely distributed in Bengbu city with distinctive seasonal distribution.

Objective To review the clinical features,diagnostic work-up,classification,prognosis and treatment of systemic mastocytosis (SM).Methods The clinical data of 3 SM patients admitted to Peking Union Medical College Hospital (PUMCH) were retrospectively analyzed and the review of recent literatures was performed.Results All the 3 cases were pathologically diagnosed.According to WHO 2008 classification criteria,2 cases were diagnosed as aggressive SM (ASM) and the other one was diagnosed as indolent SM (ISM).Case 1 was a 60-year-old female patient who had overt mediator release syndrome manifesting as episodes of flushing,fever,vomiting,palpitation,hypotension and syncope.She was diagnosed as aggressive SM based on significantly increased number of abnormal mast cells (accounting for 6％ of all nucleated cells) in the bone marrow aspiration sample and biopsy specimen which accompanied with decreased other myeloid and erythroid elements.Her disease was refractory to the treatment of H2 antihistamines and led to a fatal outcome eventually.Case 2 was a 72-year-old male patient who underwent extended proximal gastrectomy with esophagogastric anastomosis due to endoscopically detected diffuse thickening of the gastric fundic mucosa.The diagnosis as indolent SM was established according to the dense infiltrate of abnormal mast cells in the surgically resected part of stomach and regional lymph nodes.He had been in complete remission for more than 6 years ever since then.Case 3 was a 41-year-old female patient who presented with fever,urticaria pigmentosa and diffuse bone lesions.A bone biopsy specimen demonstrated a dense infiltrate of mast cells while the assays for KIT-D816V mutation and FIP1L1-PDGFRα fusion gene yielded negative results.She was diagnosed as aggressive SM and a progression-free survival of more than 1 year had been achieved with the treatment of prednisone,interferon-α and pamidronate.Conclusions SM is a rare disease.Diagnosis is primarily dependent on histopathology.There is currently no curative therapy for systemic mastocytosis.Treatment is intended to reduce symptoms and improve quality of life.The prognosis of ISM is much better than that of ASM.

Objective To evaluate the feasibility of liver senescence model with senescence accelerated mouse prone 8 (SAMP8), and to explore the possible mechanism of oxidative stress in the process of liver aging in SAMP8. Methods Male SAMP8 mice at the age of 9 months were chosen as research objects, and senescence accelerated mouse resistance 1 (SAMR1) mice were used for normal control. Histopathological changes in the liver of SAMR1 and SAMP8 mice were observed by hematoxylin-eosin (HE), Sudan Ⅳ and Masson staining. Senescence associated β-galactosidase activity was measured by histoehemical staining method, and the activities of superoxide dismutase (SOD), eatalase (CAT), glutathione peroxidase (GSH-Px) and the level of malondialdehyde (MDA) in liver homogenate were examined by chemical colorimetry. Results Compared with SAMR1 group, the liver degenerative changes of SAMP8 mice were observed by microscopy, such as extensive fatty degeneration, focal necrosis of hepatocytes and inflammatory cells infiltration. Meanwhile, senescence associated β-galactosidase-positive cells were significantly increased in SAMP8 group [(78.1±11.0) vs.( 23.9±8.8),t=10.887, P<0.01]. In addition, the activities of SOD, CAT and GSH-Px in liver homogenate were decreased [SOD: (214.8 ± 34.8) vs. ( 295.3 ± 29.7), t = 4.975,P<0.01;CAT: (23.0±4.0) vs. ( 36.3±8.3),t=4.084,P<0.01;GSH-Px: (524.0±74.2) vs. (648. 4±102.8) ,t=2. 776, P<0. 05]and the level of MDA was markedly increased ((2.3±0.2) vs. (1.8±0. 1),t = 6. 329, P<0. 01]. Conclusions SAMP8 mice is a feasible animal model for the study of liver senescence, and oxidative stress may play an important role in the process of liver aging in SAMP8.

AIM: To observe the effect of mouse Sim2 (mSim2) eukaryotic expression vector transfection on the cell cycle in PC12 cells in vitro and to explore the role of Sim2 in the pathogenesis of Down syndrome. METHODS: The full open reading frame of mSim2 was amplified by reverse transcription-polymerase chain reaction (RT-PCR) and cloned into the vector pcDNA3. Then the constructed pcDNA3-Sim2 vectors were transiently transfected into PC12 with Lipofectamine~ TM . The expression of mSim2 was detected by RT-PCR. The effect of mSim2 on the cell cycle was observed by flow cytometry. RESULTS: The eukaryotic expression vector mSim2 was successfully constructed. There was notable expression of mSim2 in the cells transfected with pcDNA3-Sim2. There were more cells in G_0/G_1 phase in the pcDNA3-Sim2 transfected cells than that in the control (P

Objective To investigate clinical characteristics of smear- or culture-positive pulmonary tuberculosis (TB) in patients hospitalized at a general hospital to improve its diagnosis. Methods Clinical data of smear- or culture-positive pulmonary TB diagnosed in 50 patients hospitalized at Peking Union Medical College Hospital, Beijing during 2006 to 2009 were analyzed retrospectively. Results Seventeen (34%) of 50 cases of smear- or culture-positive pulmonary TB aged more than 60 years, with 30 males (32%), 16 retirees and nine farmers (18%). Their main symptoms included fever (80%), cough (94%) and sputum expectoration (92%), with elevated erythrocyte sedimentation rate (ESR) in 38 of 45 patients (84%). Chest X-ray examinations showed that lesions located mostly in the upper lobes or in both of the lungs diffusedly, with patchy infiltrations, nodular opacities and cavities. Acid-fast bacilli were demonstrated on sputum smear in 41 ( 82% ) and in specimens of six ( 12% ) cases obtained through bronchoscopy with brush or bronchoalveolar lavage fluid ( BALF), and M. Tuberculosis was cultured from sputum specimens in three (6%). Mean time interval between admission and diagnoses averaged 14 days.Conclusions Basic knowledge about prevention and control of pulmonary tuberculosis should be publicized comprehensively in general hospital keeping alert in its diagnosis with acid-fast staining for sputum smear as a routine test for patients with respiratory symptoms, and in some cases, bronchoscopy procedures ( brush or BALF) are reasonable options to improve its detection.

Objective To investigate the impact of hypoxia on the expression of early growth response-1 (Egr-1) and monocyte chemoattractant protein-1 (MCP-1) in mouse aorta,and to probe the underlying mechanism involving receptor for advanced glycation end-products (RAGE).Methods 3-month-old C57BL/6 mice were subjected to hypoxia [(6.0±0.5) ％ oxygen] to establish the global hypoxia model(n=6 rats for each).Aortas were dissected,Egr-1 mRNA and MCP-1 mRNA were detected by real time RT-PCR,Egr-1 and RAGE proteins were tested by Western blot,and Egr-1 DNA binding activity was assayed by electrophoretic mobility shift assay (EMSA).For blockade of RAGE,mice were pretreated with soluble RAGE (sRAGE) for 1 h by intra-peritoneal injection before they were exposed to hypoxia.Mice with normoxia were used as controls.Results After 30 minutes of hypoxic exposure,Egr-1 mRNA in aorta was increased to (28.3±0.9)folds compared with normoxic controls (F=617.17,P＜0.01),and the induction persisted for at least 3 hours.After 45 minutes of hypoxic exposure,Egr-1 proteins in aorta was increased to (5.7 ± 0.3) folds compared with normoxic controls (F =57.18,P＜ 0.01); the enhanced DNA binding activity of Egr-1 by hypoxia was attenuated by pretreatment with anti-Egr-1 lgG.After 4 hours of hypoxic exposure,MCP-1 mRNA expression in aorta was increased to(4.0±0.3)folds compared with normoxic controls (F=30.68,P＜0.01).RAGE antigen was increased significantly within 30 minutes of hypoxic exposure,with the peak at 15 minutes; hypoxia-induced Egr-1 mRNA expression was significantly attenuated by pretreatment with sRAGE (3.3 ± 0.2) folds compared with normoxic controls (F =30.20,P＜0.01).Conclusions Hypoxia significantly induces Egr-1 and MCP-1 upregulation expressions in mouse aorta,and blockade of RAGE significantly attenuates hypoxia-induced Egr-1 expression.Thcsc findings suggest RAGE signaling is involved in hypoxia-induced vascular inflammatory stress,and highlight this receptor as a potential therapeutic target to protect tissues injured by hypoxia.

The medical records of all 12 patients diagnosed as chronic active Epstein-Barr virus (CAEBV) infection at our hospital were analyzed retrospectively.There were 7 males and 5 females with a median onset age of 28 years.CAEBV was characterized by fever,splenomegaly,hepatomegaly and lymphadenopathy,etc.The abnormalities of laboratory examination included liver dysfunction,thrombocytopenia,anemia and leucopenia.EBV-DNA detected by real-time polymerase chain reaction was (1.7 × 103-3.5 × 107) copies/μg DNA in peripheral blood mononuclear cell.Among them,the outcomes were death (n =5),lost to follow-up (n =2) and T cell lymphoma (n =1).It is necessary to improve our awareness of CAEBV infection because of its poor prognosis and high mortality.

To investigate the effects of ischemia-reperfusion on the levels of nitric oxide and nitric oxide synthase isoforms (nNOS and iNOS), rat organotypic hippocampus slice were cultured in vitro and subjected to ischemia by oxygen-glucose deprivation (OGD) for 30 min and then placed in the normal culture condition. The ischemia-reperfusion produced a time-dependent increase in nitrite levels in the culture medium. Reverse transcriptional-polymerase chain reaction showed augmented levels of mRNA for both nNOS and iNOS when compared with control at 12 h and remained increase at 36 h after OGD (P < 0.05). The protein levels of both nitric oxide synthase isoforms increased significantly as determined by Western Blot. OGD also caused neurotoxicity in this model as revealed by the elevated lactate dehydrogenase (LDH) efflux into the incubation solution. The results suggest that organotypic hippocampus slice is a useful model in studying ischemia-reperfusion brain injury. NO and NOS may play a critical role in the ischemia-reperfusion brain damage in vitro.
Animals, Newborn ; Cell Hypoxia ; Hippocampus/cytology ; Hippocampus/*metabolism ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase Type I/*metabolism ; Nitric Oxide Synthase Type II/*metabolism ; RNA, Messenger/metabolism ; Rats, Sprague-Dawley ; Reperfusion Injury/*metabolism ; Tissue Culture Techniques