Problem-based learning ( PBL ) has become the major teaching method to cultivate medical student's autonomous learning and their ability to solve problems.It's basic elements are the scene authenticity and problem construction.Thoratic surgery clinical probation is the most important part of clinical teaching.The author summerized and analysized the PBL teaching experience in thoratic surgery and had some new understanding and experience on the problem construction,and therefore made some exploration and improvement to it and got some good teaching effect.

Objective To explore the relationship between oncology and military medicine in order to remove theoretical barriers to the development of oncology in military hospitals .Methods The documentary evidence was obtained from cita-tion networks .Results Military hospitals and institutes in China and abroad have conducted studies on oncology , including the long-term survival of Hodgkin′s disease patients in a study of 388 military cases during World War Ⅱ, a study of leuke-mia within the former West Germany Armed Forces , and a study on melanoma in the Armed Forces .Also,some foreign doc-umentation paid special attention to special weapons and equipment , special military operations and special military envi-ronment-related issues of cancer epidemiology , such as cancer following nuclear weapon tests , the association of selected cancers with service in the U .S.military in Vietnam or after the Gulf War .The Military Cancer Institute of the United States published a total of 206 articles between 2001 and 2013 .Conclusion To make closer the relationship between oncol-ogy and military medicine , we should find out more about the relationship between general medicine and military medicine , learn foreign from experience on development of oncology , and explore the military medical value of oncology .

The endocrine system with the normal aging is characterized by a progressive loss of reserve capacity,resulting in a decreased ability to adapt to environmental demands.This loss of homeostatic regulation reflects important alterations in hormonal synthesis,metabolism,and action.However,these changes may have no significant clinical manifestations,especially under non-stress conditions.This review discusses the endocrine system in the elderly in general.

Infection can complicate different stages of acute pancreatitis.The probability of infection is related to the existence and extent ofpancreatic necrosis: up to 30% of patients with pancreatic necrosis develop infection.The timing of infection is variable and usually peaks in the second to fourth week after the onset of pancreatitis.IPN(infected pancreatic necrosis)is the most common type of secondary pancreatic infection.Infectious complications in severe acute pancreatitis are associated with considerable morbidity and mortality.Antimicrobial therapy is one of the fundamental elements of therapy.Diagnosis of secondary pancreatic infection is challenging and radiologic characteristic (air bubble sign) and CT guided fine-needle aspiration (FNA) are reliable diagnostic strategies.Antibioticuse should be rational in terms of a rational indication, a rational spectrum, and a rationalduration.Prophylactic antibiotics are not beneficial in improving prognosis.The only rational indication for antibiotics is documented infection.The empirical antibiotics should cover common microbials of hospital-acquired intra-abdominal infection and with good pancreatic penetration.Also, fungal infections are often present in thesepatients, and early diagnosis and antifungal coverage should be considered.Duration is in fact largely determined by the presence and efficacy of source control.When there is no or minimal residual infection left after a source control procedure, a duration of 7 to 10 days is probably sufficient.On the other hand, if the source of infection has not been removed completely, prolonged courses until the residual necrosis has been sterilized are necessary.

As an important organ of the human body,vascular endothelial cells (VECs) play a vital role in heat stressinduced tissue damage.Its integrity not only serves as a barrier for maintaining vascular permeability but also has major impact on cellular structure and function during acute phase response to heat stress.In heat stroke,a series of acute and complicated pathophysiological changes,including microcirculation change,damage VECs and thereby induce or aggravate multiple organ dysfunction syndrome (MODS).Meanwhile,studies have shown that,during heat stroke,VECs are the major responding cells and one of the most common cells that experience morphological and functional changes.Therefore,VECs damage might be an important mechanism involved in heat stroke.This article reviews the mechanism of heat-induced damage of VECs and its effect on vital organs.

There exist a series of problems in heat stroke treatment,such as,pathogenesis is still unclear,clinical classification is too simple and has no intrinsic relation with pathophysiological process and prognosis,missing of indexes for hierarchical diagnosis and prognosis prediction,and lack of targeted therapeutic norms.All of these factors could lead to high mortality and disability by heat stroke.Our research team started an epidemiological investigation of heat stroke since 2002.On the basis of discovering organ injury rule,system info and treatment technology on critical medicine were applied to heat stroke treatment.Research on organ injury mechanism for heatstroke was carried out based on translational medicine idea,and periodic research results were also achieved.A series of key technologies for heat stroke treatment were obtained.These technologies were popularized in 30 hospitals across the country,thus improving ability of heat stroke treatment.

Objective To explore the relationship of the levels of adhesion molecules and cytokines with vascular disease in patients with type 2 diabetes (T2DM).Methods Ninety-six T2DM patients were selected as case group and divided into non-vascular group (28 cases),micro-vascular group (33 cases) and major vascular group(35 cases) according to vascular disease.Meanwhile,30 healthy persons were selected as control group.Serum levels of serum soluble intercellular adhesion molecule-1 (ICAM-1),vascular cell adhesion molecule-1 (VCAM-1),interleukin-6 (IL-6),tumor necrosis factor-α (TNF-α) and yon willebrand factor (vWF) were determined by Enzyme-Linked Immuno Sorbent Assay (ELISA),and the expression of adhesion molecule and cytokines of patients with T2MD at 2 weeks after treatment.Results Compared with control group,the levels of ICAM-1,VCAM-1,TNF-α and IL-6 in all subgroup of T2DM patients were significantly elevated(P ＜ 0.05),and the levels showed an increasing trend with function deterioration (P ＜ 0.05).The levels of ICAM-1,VCAM-1,IL-6 and TNF-α in case group before treatment were (505.34 ± 56.42) μg/L,(570.85 ±59.54) μg/L,(94.51 ± 18.04) ng/L,(70.57 ± 18.34) ng/L respectively,significant different from those of after treatment ((390.53 ±45.23) μg/L,(482.93 ± 69.85) μg/L,(77.31 ± 15.49) ng/L,(50.45 ± 12.66) ng/L; t =16.281,8.712,7.697,8.445; P ＜ 0.05).There were significant positive correlation between ICAM-1,VCAM-1,IL-6,TNF-α and vWF in the case group(r =0.482,0.453,0.576,0.534 respectively,P ＜ 0.05).Conclusion Adhesion molecules and cytokines are take part in the process of the deterioration of T2DM and the occurrence of vascular disease.

Objective To observe the effect of heat stress-induced burst out of reactive oxygen on neuronal apoptosis and investigate pathogenesis of brain damage caused by severe heat stroke.Methods Neurons heat stress model is set up.Control group were incubated at 37 ℃,5%CO2 ,While heat stress group of cells were incubated at 43 ℃for 2 h,then all the cells were further incubated at 37 ℃for different time as indicated.The amounts of ROS were assayed by DCFH staining at 0 h,0.5 h,1 h,2 h after heat stress.Apoptosis was analyzed by flow cytometry using Annexin V-FITC/PI staining and expression of caspase-3 were determined by westen blotat 0 h、3 h、6 h、12 h after heat stress.In addition,MnTMPyP is the specificscavengers of ROS,which effect on apoptosis is also studied at 12 h after heat stress.Results Compared with control group,amounts of ROS was significant increased at 0 h after heat stress,the burst out of it was at 2 h after heat stress (P<0.05 ).Apoptosis was induced at 3h after heat stress ,it was significant increased at 12 h after heat stress (43.2%,P<0.05 ).The expression of caspase-3 was also significant increased at 12 h after heat stress (P<0.05 ),and its trend was consistent with apoptosis rate trend.In addition,the scavengers MnTMPyP significantly decreased the apoptosis (47.42% to 18.45%, P<0.05 )and expression of caspase-3 at 12 h after heat stress.Conclusions An upstream signaling molecules,ROS could mediate heat stress-induced neuronal apoptosis,but its intermediate mechanism needs for further studies.

Objective To analyze the immune state and discuss the effects of immunoregulation therapy of combined use of ulinastatin and thymosin ?1 in the treatment of posttraumatic sepsis. Methods Forty-eight patients with posttraumatic sepsis admitted to ICU during Oct. 2005 to Oct. 2007 were included and randomly divided into treatment group and control group (24 each). Patients in control group received conventional SSC treatment, while those in treatment group received conventional SSC treatment plus immunoregulation therapy with a combination of ulinastatin and thymosin ?1. Peripheral blood CD14+ monocyte HLA-DR expression was detected by flow cytometry to determine the innate immunity of posttraumatic septic patients on day 1, 5, 7 and 28 (or death), and serum levels of IL-6 and IL-10 were assessed by ELISA to evaluate the nonspecific immunity at day 1 and 28 (or death). APACHE Ⅱ scores were recorded on day 1, 5, 7 and 28 (or dearth). Ten healthy volunteers were enrolled as healthy controls. Results At admission the expression of CD14+ monocyte HLA-DR was lower than 30% in 9 posttraumatic septic patients. The expression levels of CD14+ monocyte HLA-DR in the patients in treatment group were much higher than those in control group (P0.05). Before treatment, no significant difference existed in APACHE Ⅱ scores between treatment group and control group, while this score in the patients in treatment group was much lower than that in control group on day 5, 7 and 28 (P0.05). Conclusions There is immunosuppression in some posttraumatic patients with somplication of sepsis. All these patients manifest exaggerated nonspecific immunity at the early stage, and then manifest immunodepression as sepsis progresses. The immunoregulation effects of a combination of ulinastatin and thymosin may facilitate the balance of pro-inflammatory and anti-inflammatory media, thus ameliorating septic symptoms. No improvement in 28 day mortality has been seen, probably due to limited number of patients in present study.

Objective Since integrons play an important role in the spread of antibiotic resistance genes in bacteria,the characterization of a new resistance gene cassette in class 1 integron positive strains of E.coli was analyzed. Methods The presence and genetic content of class 1 integron were examined by PCR and sequencing.The sequence was analyzed by using some bioinformatics softwares.Results 5 class 1 integron positive strains were amplified by primers of in-F and in-B which were set for amplifying the region of antibiotics resistance genes.Among the 5 strains,an amplicon of 1009 bp was yielded.Sequencing analysis revealed that amplicon of 1009 bp harbored a 780 bp ORF.Further analysis with bioinformatics software showed that it was 99.6% and 99.5% identical to the known aadA23 and aadA21 cassette,and was just 66.4% identical to the known aadA5 cassette.It was conferring resistant to spectinomycin and streptomycin,and was given a new name aadA23b.Conclusions Multi-drug resistance genes has been proved changeable in E.coli clinical strains.The result not only stressed the need for continuing surveillance of antibiotic resistance in the molecular level,but also the need caring for genetic variation of drug resistance gene cassettes.