Objective To explore the severity of toxicity reaction after treated by the sequential chemoradio-therapy,alternate chemoradiotherapy or concurrent chemoradiotherapy in limited -stage small cell lung cancer. Methods 63 cases of limited -stage small cell lung cancer were reviewed,according to the chemoradiotherapy order,all cases were divided into:sequential chemoradiotherapy 15 cases,alternate chemoradiotherapy 25 cases, concurrent chemoradiotherapy 23 cases.The correlation of the factors(leukocypenia,gastrointestinal reaction,pneumo-nia,esophagitis)with different treatment groups after treated in 2 months,4 months,6 months were analyzed.Results Three groups of all the factors treated in 2 months had no significant change(χ2 =0.275,0.051,0.513,1.215, 0.051,0.231,all P >0.05).In 4 months the cases of sequential chemoradiotherapy >or =2 myelosuppression,the gastrointestinal reaction,the pneumonia and the esophagitis were 33.3%,33.3%,0.0%,0.0%;In the cases of alternate chemoradiotherapy >or =2 myelosuppression,the gastrointestinal reaction,the pneumonia and the esophagitis were 16.0%,4.0%,16.0%,0.0%;In the cases of concurrent chemoradiotherapy >or =2 myelosuppression,the gastroin-testinal reaction,the pneumonia and the esophagitis were 52.2%,34.8%,34.8%,4.3%;>or =2 myelosuppres-sion,each level gastrointestinal reaction and the pneumonia of the three groups treated were statistically significant (χ2 =7.054,9.702,7.947,6.145,7.373,all P <0.05).In 6 months the cases of sequential chemoradiotherapy >or =2 myelosuppression,the gastrointestinal reaction,the pneumonia and the esophagitis were 26.7%,13.3%,13.3%, 0.0%;In the cases of alternate chemoradiotherapy >or =2 myelosuppression,the gastrointestinal reaction,the pneu-monia and the esophagitis were 40.0%,56.0%,12.0%,0.0%;In the cases of concurrent chemoradiotherapy >or =2 myelosuppression,the gastrointestinal reaction,the pneumonia and the esophagitis were 69.6%,65.2%,43.5%,0.0%;each level myelosuppression,>or =2 gastrointestinal reaction and the pneumonia of the three groups treated were statistically significant(χ2 =6.174,7.663,10.544,6.286,all P <0.05).Conclusion Leukopenia and gastrointestinal reaction are closely related with chemotherapy,chemoradiotherapy results in the worsen of myelosuppression.Pneumonia and esophagitis are closely related with chemotherapy,chemoradiotherapy result in the worsen of radiation pneumonitis.

Objective:To investigate levels of autophagy in T cells and B cell of patients with systemic lupus erythematosus ( SLE) and its clinical significance.Methods: 68 SLE patients without treatment within 4 weeks were enrolled in this study.We accessed the levels of autophagy in T cells and B cells of 23 healthy controls and 68 patients before and after treatment by flow cytometry,and analyzed their correlations with serum levels of C3 and anti-dsDNA antibodies,SLEDAI score,et al.Results: Before treatment,a significantly increased levels of LC3-Ⅱ was observed in SLE patients than healthy controls, the active group ( SLEDAI score≥10) was significantly higher than the stable group(SLEDAI score<10),and the newly diagnosed group was significantly higher than the recurrent group(all P<0.05).While the levels of LC3-Ⅱ was decreased in B lymphocytes in SLE patients,the active group was significantly lower than stable group,and the active group was significantly lower than the newly diagnosed group(all P<0.05). Correlation analysis found that,a positively correlation was observed for the levels of LC3-Ⅱwith SLEDAI score in T lymphocyte( rs=0.289,P<0.05),and the levels of C3 were positively correlated the levels of LC3-Ⅱ in B lymphocyte(rs=0.371,P<0.01).After treatment for five days, levels of autophagy in T lymphocytes of SLE patients with good prognosis ( SLEDAI score decreased ≥4 ) significantly decreased(P<0.05).Also,three days after treatment,levels of autophagy in B lymphocytes of SLE patients with good prognosis were increased significantly ( P<0.05 ) .However, SLE patients with poor prognosis had no such difference ( P>0.05 ) . Conclusion:Levels of autophagy in T and B lymphocytes of SLE patients are abnormal compared to healthy controls,and these changes are associated with disease activity.Also,these changes are expected to be the indicators of disease activity and potential therapeutic targets in SLE.

ObjectiveTo investigate the mechanism and effect of Qingfei Paidu decoction on transient receptor potential vanilloid-1/Transient receptor potential ankyrin1 （TRPV1/TRPA1） based on heat-sensitive channel and inflammatory response. MethodAccording to body weight， 80 8-week-old C57BL/6 mice were randomly divided into the normal group， model group， dexamethasone group （5 mg·kg^-1）， and low-dose， medium-dose， and high-dose groups of Qingfei Paidu decoction （14.865， 29.73， 59.46 g·kg^-1）， with 12 mice in each group. In addition to the normal group， the other groups were administered 20 μL （1×10^-3 g·kg^-1） to each mouse by airway infusion to establish the acute lung injury （ALI） model. In the administration group， the drug was given 1 h after modeling and again after an interval of 24 h. The lung tissue was taken 36 h after modeling. Double lung wet/dry weight ratio（W/D）， hematoxylin-eosin （HE） staining， enzyme-linked immunosorbent assay （ELISA）， and Western blot were used to observe and detect the pathological changes of lung tissue， expression levels of inflammatory cytokine tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6）， and expressions of TRPV1 and TRPA1 proteins in heat-sensitive channel， nuclear factor kappa-B （NF-κB）， inhibitor of NF-κB （IκBα） in inflammatory pathway， and phosphorylated proteins. The phosphorylated protein/total protein ratio was calculated. ResultCompared with that in the normal group， the lung tissue of mice in the model group was seriously damaged， and pulmonary capillary permeability increased. Alveolar capillary congestion and dilation destroyed the complete structure of the alveolar， and the alveolar wall thickened. A large number of inflammatory cells and red blood cells were infiltrated， and pulmonary edema was significantly aggravated. The expressions of TNF-α， IL-6， TRPV1， TRPA1， phosphorylated NF-κB p65/NF-κB p65， and phosphorylated IκBα/IκBα were significantly increased （P<0.01）， and the whole lung W/D was significantly increased （P<0.01）. Compared with the model group， the dexamethasone group and low-dose， medium-dose， and high-dose groups of Qingfei Paidu decoction could significantly improve pulmonary edema. TNF-α， IL-6， TRPV1， TRPA1， lung tissue NF-κB p65， and IκBα phosphorylated protein/total protein ratio decreased significantly （P<0.05， P<0.01）. The whole lung W/D also decreased significantly （P<0.05， P<0.01）. ConclusionQingfei Paidu decoction has anti-inflammatory and protective effects on LPS-ALI mice， which can effectively reduce inflammation， induce diuresis， and alleviate edema. Its mechanism may be related to the regulation of the expression of TRPA1 and TRPV1 and the inhibition of the activation of the NF-κB pathway.

Objective To investigate the expression of UHRF1 protein in breast cancer and adjacent normal tissues, and its relationship with local recurrence. Methods Immunohistochemistry (IHC) was applied to detect the expression of UHRF1 protein in 69 specimens of breast cancer and 33 specimens of corresponding adjacent normal tissues; Chi-square test was used to analyze the relationship between UHRF1 protein expression and clinical factors. Results The positive rate expression of UHRF1 protein in breast cancer was 55.1 % (38/69), and UHRF1 protein expression was not found in adjacent normal tissues. The positive expression rate of UHRF1 protein in stage III was higher than that in stageⅠ-Ⅱ[68.4%(26/38) vs. 38.7 % (12/31), P< 0.05]. The positive expression rate of cancer tissue in breast cancer patients with chest wall recurrence after radiotherapy within 1 year was higher than that in patients without recurrence [83.3 %(10/12) vs. 49.1 % (28/57), P< 0.05], and UHRF1 protein expression of patients in different age and Herb-2 had no statistical significance (P> 0.05). Conclusions The positive expression rate of UHRF1 protein is obviously higher than that in adjacent normal tissue. Besides, UHRF1 protein is related to the stage and chest wall of local recurrence after radiotherapy.

Objective To construct cecropin A-thanatin combinant gene engineering antimicrobial peptide gene CA(1-7)-T(4-19) for expression in Pichia pastoris.Methods The combinant antimicrobial peptide gene was artificially synthesized via gene splicing by overlap extension (SOE).The gene was cloned into the pPICZαA vector and transformed into Pichia pastoris X-33 by electroporation.The positive clones obtained by the screening of bleomycin resistance were induced by methanol ,and the antibacterial activity of the products was detected and the antimicrobial spectrum was established.Results The combinant peptide gene CA (1-7)-T (4-19) was successfully cloned on the carrier pPICZαA.The identification results were consistent with the pre-designed gene sequence.The combinant peptide gene was expressed under the induction of methanol ,and the minimum inhibitory concentration of 76 strains of Gram-egative and Gram-positive pathogenic bacteria isolated from the clinic was obtained ,and the minimum inhibitory concentration was up to 5 μg/mL.Conclusion A combinant genetic engineering antimicrobial peptide with antibacterial activity was obtained successfully and it had obvious inhibition effect on clinical common multidrug-resistant strains.

Celiac trunk is a wide and short ventral branch. It originates from the anterior abdominal artery at the level of L1 vertebra, and divides into three branches: the left gastric, common hepatic and splenic arteries, supplying the upper abdominal organs such as stomach, liver, spleen, pancreas, and duodenum. However, there are many types of branches variations. The branches of celiac trunk are classified into several types. We establish a classification of variation type according to the origin of left gastric, common hepatic and splenic arteries, which includes hepatogastrosplenic trunk type, hepatosplenic trunk type, hepatogastric trunk type, gastrosplenic trunk type, and the others include hepatosplenomesentery trunk type, hepatogastrospleno-mesentery trunk type, hepatogastrosplenocolonic trunk type, hepatogastrosplenopancreatic trunk type, gastrospenic trunk plus hepatomesentery trunk type, hepatogastrosplenoic left liver trunk type, hepatogastro-splenopancreatoduodenal trunk type, hepatogastric trunk plus hepatosplenic trunk type. Development of celiac trunk variation type was introduced based on the classification of Lipshutz, Adachi, Michels and Zhang Nianjia. Mastering the types of branches variations is necessary for us to perform the upper abdominal operations safely and effectively.
Celiac Artery ; abnormalities ; Humans

Celiac trunk is a wide and short ventral branch. It originates from the anterior abdominal artery at the level of L1 vertebra, and divides into three branches: the left gastric, common hepatic and splenic arteries, supplying the upper abdominal organs such as stomach, liver, spleen, pancreas, and duodenum. However, there are many types of branches variations. The branches of celiac trunk are classified into several types. We establish a classification of variation type according to the origin of left gastric, common hepatic and splenic arteries, which includes hepatogastrosplenic trunk type, hepatosplenic trunk type, hepatogastric trunk type, gastrosplenic trunk type, and the others include hepatosplenomesentery trunk type, hepatogastrospleno-mesentery trunk type, hepatogastrosplenocolonic trunk type, hepatogastrosplenopancreatic trunk type , gastrospenic trunk plus hepatomesentery trunk type, hepatogastrospl enoic left liver trunk type, hepatogastro-splenopancreatoduodenal trunk type, hepatogastric trunk plus hepatosplenic trunk type. Development of celiac trunk variation type was introduced based on the classification of Lipshutz, Adachi, Michels and Zhang Nianjia. Mastering the types of branches variations is necessary for us to perform the upper abdominal operations safely and effectively.

Celiac trunk is a wide and short ventral branch. It originates from the anterior abdominal artery at the level of L1 vertebra, and divides into three branches: the left gastric, common hepatic and splenic arteries, supplying the upper abdominal organs such as stomach, liver, spleen, pancreas, and duodenum. However, there are many types of branches variations. The branches of celiac trunk are classified into several types. We establish a classification of variation type according to the origin of left gastric, common hepatic and splenic arteries, which includes hepatogastrosplenic trunk type, hepatosplenic trunk type, hepatogastric trunk type, gastrosplenic trunk type, and the others include hepatosplenomesentery trunk type, hepatogastrospleno-mesentery trunk type, hepatogastrosplenocolonic trunk type, hepatogastrosplenopancreatic trunk type , gastrospenic trunk plus hepatomesentery trunk type, hepatogastrospl enoic left liver trunk type, hepatogastro-splenopancreatoduodenal trunk type, hepatogastric trunk plus hepatosplenic trunk type. Development of celiac trunk variation type was introduced based on the classification of Lipshutz, Adachi, Michels and Zhang Nianjia. Mastering the types of branches variations is necessary for us to perform the upper abdominal operations safely and effectively.

ObjectiveTo investigate the mechanism of Renshentang， recorded in Synopsis of Golden Chamber， in the treatment of atherosclerosis （AS） based on the autophagic effect of transient receptor potential vanilloid subtype 1 （TRPV1） on arterial smooth muscle. MethodFourteen SPF-grade 8-week-old male C57BL/6J mice were assigned to the normal group and 70 8-week-old apolipoprotein E knockout （ApoE^-/-） mice were assigned to the experimental group. The AS model was induced by a high-fat diet in the mice in the experimental group for eight weeks. The model mice were then randomly divided into model group， low-， medium-， and high-dose Renshentang groups （2.715， 5.43， and 10.68 g·kg^-1·d^-1）， and simvastatin group （0.02 g·kg^-1·d^-1）. Drug treatment lasted eight weeks. Serum was taken and serum total cholesterol （CHO）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， and high-density lipoprotein cholesterol （HDL-C） levels were measured by assay kits to observe the changes in lipid levels in mice. The aorta was stained with hematoxylin-eosin （HE） to observe the overall pathology of the aortic root and oil red O staining was used to detect the lipid deposition in the aortic plaque and calculate the percentage of the aortic root area to the lumen area. The protein expression of TRPV1， adenylate-activated protein kinase （AMPK）， phosphorylated AMPK （p-AMPK）， autophagy effector-1 （Beclin-1）， and microtubule-associated protein 1 light chain 3 （LC3Ⅱ） in mouse aortic tissues was determined by Western blot. ResultCompared with the normal group， the model group showed increased serum CHO， TG， and LDL-C levels， decreased HDL-C， and increased aortic root plaque area （P<0.01）. Compared with the model group， the Renshentang groups showed decreased levels of CHO， TG， and LDL-C in serum （P<0.05， P<0.01）， especially in the low- and medium-dose Renshentang groups （P<0.01）. Compared with the normal group， the simvastatin group and the Renshentang groups showed reduced aortic root plaque area （P<0.05）， especially in the high-dose Renshentang group （P<0.01）. Compared with the normal group， the model group showed decreased relative expression levels of TRPV1， p-AMPK/AMPK， Beclin-1， and LC3Ⅱ/LC3Ⅰ（P<0.05， P<0.01）. Compared with the model group， the medium- and high-dose Renshentang groups showed increased relative expression levels of TRPV1， p-AMPK/AMPK， Beclin-1， and LC3Ⅱ/LC3Ⅰ（P<0.05，P<0.01）. ConclusionThe anti-AS effect of Renshentang recorded in Synopsis of Golden Chamber may be achieved by up-regulating TRPV1 expression to restore the level of autophagy mediated by AMPK.

ObjectiveTo observe the therapeutic effect and underlying mechanism of Linggui Zhugantang on lipopolysaccharide （LPS）-induced acute lung injury （ALI） in mice. MethodSeventy-two 7-week-old C57BL/6 mice of SPF grade were randomly divided into a normal group， a model group， a dexamethasone group （5 mg·kg^-1）， and high-， medium-， and low-dose Linggui Zhugantang groups （9.36， 4.68，2.34 g·kg^-1）， with 12 mice in each group. Except for the normal group， the remaining groups underwent intranasal instillation of LPS （50 μg per mouse） for the induction of the ALI model. The treatment groups received oral administration for 7 days prior to modeling. After 12 hours of modeling， mouse lung tissues were taken to measure the wet/dry weight ratio （W/D）. Hematoxylin-eosin （HE） staining was performed to observe the pathological morphological changes in lung tissues. Bronchoalveolar lavage fluid （BALF） was collected for total cell count using a cell counter， and Wright-Giemsa staining was conducted to classify and quantify inflammatory cells （neutrophils and macrophages）. Enzyme-linked immunosorbent assay （ELISA） was used to determine the expression levels of inflammatory cytokines tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in BALF. Western blot analysis was performed to detect the expression of nuclear factor-κB （NF-κB） inhibitory protein α （IκBα）， NF-κB p65， and their phosphorylated proteins， and the ratio of phosphorylated protein/total protein was calculated. ResultCompared with the normal group， the model group exhibited severe lung tissue damage， disrupted alveolar structure， thickened alveolar walls， infiltration of extensive inflammatory cells and red blood cells， and significantly aggravated lung edema （P<0.01）. The total cell count， inflammatory cell count， expression levels of IL-6， and TNF-α in BALF， as well as NF-κB p65 and phosphorylated IκBα in lung tissues， were significantly upregulated in the model group （P<0.01）. Compared with the model group， high-， medium-， and low-dose Linggui Zhugantang groups， as well as the dexamethasone group， showed improved lung injury， reduced lung edema （P<0.01）， downregulated total cell count， neutrophil count， expression levels of IL-6 and TNF-α in BALF， and NF-κB p65 and phosphorylated IκBα in lung tissues （P<0.01）， and reduced macrophage count （P<0.05）. ConclusionLinggui Zhugantang has anti-inflammatory and protective effects on LPS-induced ALI in mice， effectively reducing inflammation and promoting diuresis and edema elimination. Its mechanism may be related to the inhibition of NF-κB pathway activation.