Whether or not muscle hypertrophy induced by physical exercise will result in the increase in thenumber of muscle fibres is a question much debated in recent years. But little has been done so farin studying the effect of short and long term weight training on the changes in the number of muscle fibres in the human body. As an attempt to find out this effect, a research has been madeon 29 male subjects. Nine young trainees at spare-time sports schools were put through a weightliftingprogramme consisting of three hours of work a day, six days a week for 10 weeks. Before and afterthe 10-week period, the cross section of the musculus vastus lateralis was measured with computedtomography scanning (CT); maximal voluntary isometric torques of knee extension were alsomeasured; muscle biopsies were taken from the vastus lateralis to distinguish between muscle fibresof type I and type II and to find out their distribution and their average areas; and the number ofmuscle fibres was calculated by a formula. The results were compared with those obtained from thecontrol group of 13 persons and a group of seven weightlifters of national ranking. It was found thatthe 10 weeks of weight training did not result in the increase in the number of muscle fibres althoughit caused some change in the maximal torque; and that although long-term training resulted insignificant changes in the maximal torque and the area of muscle fibres, there was no significantdifference in the number of muscle fibres between the elite group on the one hand and the controlgroup and the group of trainees who had gone through 10 weeks of training on the other. Thesefindings supported Soviet scholars' idea that to respond to load stress, animals depend on bothhypertrophy and hyperplasia in the muscle while man relies on hypertrophy alone. They alsosuggested the need for further studies on this subject.

Objective To observe the imaging features of primary hepatic endocrine carcinoma. Methods Three patients with primary hepatic endocrine carcinoma proven pathologically were retrospectively analyzed. Results Single liver lesion was detected in all 3 patients, 2 in right and 1 in left lobe of liver. The maximum diameter of the masses was 4.8 cm, 6.7 cm and 10.0 cm, respectively. The masses were all solid with different extent of low density. The solid part enhanced greatly in contrast enhanced CT scanning, while the non-solid part did not. The bigger lesions pushed the vascular to move aside in 2 patients. Enhanced and circuitous vascular was observed in 1 lesion. Slightly low signal was noticed on MR T1WI , while high signal was found on T2WI and DWI. Conclusion CT and MR can show specific features of primary hepatic endocrine carcinoma, i.e. usually single solid mass with various low densities inside and the solid part enhancing dramatically.

Objective Severe acute respiratory syndrome is recently emerged infectious disease caused by a novel coronavirus, but its immmunopathological mechanism has not yet been fully elucidated. Method We established the SARS animel model and investigated changes in plasma inflammatoy cytokines monkeys and rats. 8 monkeys with PCR and antibody positive were detected. Serum levels of inflammatory cytokines interleukin(IL)-6,IL-10,Th-1 cytokine,interferon(INF)-? and tumor necrosis factor(TNF)-? were measured by enzyme-linked immunosorbent assays(ELISA).Result The concentration of IL-10 and TNF-?were not significantly different in model and control group.IL-6 showed marked elevation of at least 10 days, and there was a positive relationship between the level of IL-6 and pulmonary pathological changes. The INF-? level decreased. Conclusion The result of sera level of SARS animal model avoid the disturbance of anti-viral drug and corticosteroid, it suggest that there are different immunoregulatory events during SARS and may contribute to our understanding of the pathogenesis.

Objective: To study the pharmadynanics and acute-toxicity of Sanyuzhitongjiegu Pills Methods: Hot plate, body-twisted, in flammation caused by dimethyl benzene, cotton ball method, fracture-healed hare and hemorrheology were applied. Results: Sanyuzhitongjiegu Pills could markedly reduce the twisting times of mice and prolong the initiate of pain caused by heat irritation, inhibit mice's ear swelling caused by dimethyl benzene, diminish the weight of rat's myoidem, promote the healing of experimental fracture, reduce the sticky property of whole blood and improve hemorrheology. The maximum of dosage for mice is 10g?kg -1 , all of them survived for 7 day. Conclusion: Shayuzhitong Pills have effect on pain-killing, anti-inflammation, promotion of fracture healing, regulation of blood, remove of stagnant, The Pills have little toxicity.

Objective To investigate the dynamic changes and its significance of inflammatory factors in cervical secretions and prior cervical tissues after cervical conical resection.Methods Women who received prior cervical conization during December 2013 and December 2015 in this hospital were selected,then the cervical tissue and secretion were collected regular interval after the conization.The expression of tumor necrosis factor-α(TNF),interleukin 6 (IL-6) and high mobility group protein 1 (HMGB1) were quantitative detected and analyzed.The expression and infiltration of inflammatory cell were detected by HE and immunohistochemical staining.Results The expression of TNF-α,IL-6 and HMGB1 in cervical tissues and secretions increased gradually after priorcervical conization,which reached the peak at 1 to 2 weeks after priorcervical conization,and then gradually decreased,the differences were statistically significant when compared with the preoperative control group (P＜0.05).The inflammatory cell infiltration and the inflammatory response were most severe at 1st week after the conization.The expression of TNF-α,IL 6 and HMGB1 was at 1st week after the conization were significantly higher than that of the 4thweek group.Conclusion The cervical inflammatory were most severe after the prior cervical conization about 1-2weeks,and the hysterectomy should be avoided at this stage.

OBJECTIVE: To explore the clinical characteristics and therapies for esophageal perforation complicated with lethal massive hemorrhage caused by esophageal foreign body. METHOD: To retrospective analysis the treatment of massive hemorrhage at the carotid artery or aorta caused by esophageal foreign body in forty seven patients, Foreign body characters, surgical approaches, and postsurgical management were summarized. RESULT: Among 24 patients with cervical esophageal foreign body, the object was removed either by esophagoscopy or through lateral cervical incision. After controlling carotid artery hemorrhage and repairing Fistula of artery from cervical incision, 19 patients survived. For the 23 patients with thoracic esophageal foreign body accompanied with aorta hemorrhea, thoracotomy was performed to remove the foreign body and repair the aortic fistula. Only 3 of these 23 patients recovered from the emergent surgery, other 20 patients died. CONCLUSION For the patients with esophageal foreign body inducing large vessel impingement, the most reliable therapeutic method is surgical repairing of arterial perforation and extraction of the foreign body via cervical or thoracic incision. Carotid ligation should be considered in patients with recurrent carotid hemorrhage. For the patient with mediastinitis, esophageal exclusion is recommended to prevent infection and to promote healing of aortic perforation after aortic fistula repairing.
Adult ; Esophageal Perforation ; etiology ; surgery ; Esophagus ; Female ; Follow-Up Studies ; Foreign Bodies ; complications ; Hemorrhage ; etiology ; surgery ; Humans ; Male ; Middle Aged ; Retrospective Studies

Objective To investigate the effect of gut bacteria under chronic colitis on the progression of hepatoma in mice.Methods 22 hepatitis B virus (HBV) -transgenic mice ( male, 8 weeks) were randomly divided into two groups, one group (n =10) was fed the drinking water containing 2% dextran sodium sulphate(DSS)to induce chronic colitis and the control group(n =12)was fed with normal drinking water.In order to investigate the effect of gut microbes, 7 male HBV-transgenic mice(8 weeks, with no detectable hepatoma under microscopy) were cohoused with 4 mice with hepatoma for 16 weeks.Results No significant liver cell damage was observed in the group of the mice fed with 2% DSS-containing drinking water.By the 22 -week old,9 of the 10 mice(90.0%) fed with 2% DSS-containing drinking water, 2 of the 12 mice(16.7%) fed with normal drinking had hepatoma.Both the hepatoma incidence and the tumor numbers in the group of mice fed with DSS-containing water were significantly higher than that in the controls (P =0.002 and P =0.028respetively).Compared to controls, the bacteria family Prevotella (P =0.022) and Anaeroplasma (P =0.014) reduced significantly in the mice with induced chronic colitis.All the mice (n =7) cohoused with the mice with hepatoma had the liver tumor developed at 24 -week-old.Conclusion Alterations of gut bacteria under chronic colitis may promote the development of liver cancer.

Objective:To explore the effect of microRNA (miRNA)-3126-5p on the proliferation and migration of colorectal cancer cells by inhibiting the expression of LIM and SH3 protein 1 ( LASP1). Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression levels of miR-3126-5p in colorectal cancer cell lines (HT-29, HCT116, LoVo, SW480) and normal intestinal mucosal epithelial cells (HIEC). The cell line with the lowest expression level was selected as the experimental object. The experiment was divided into 2 groups: the negative control group (transfected with miR-NC) and the miR-3126-5p group (transfected with miR-3126-5p). Cells of each group were collected 48h after transfection. qRT-PCR method was used to detect the expression level of miR-3126-5p in each group. The MTS method and the scratch healing experiment were used to detect the proliferation level and migration ability of the cells in each group. The bioinformatics software microRNA.org and the dual-luciferase reporter gene experiment were used to predict and verify the target genes of miR-3126-5p, respectively. qRT-PCR and Western blot were used to detect the expression levels of target genes in each group of cells. Measurement data were expressed as mean±standard deviation ( Mean± SD), t test was used for comparison between two groups, and one-way analysis of variance was used for comparison between multiple groups. Results:Compared with normal intestinal mucosal epithelial cells (HIEC), the expression level of colorectal cancer cell line miR-3126-5p was significantly reduced ( P<0.05), and the cell line with the lowest expression level was HCT116 cells ( P<0.01). The expression of miR-3126-5p in HCT116 cells in the negative control group and miR-3126-5p group were (1.05±0.16) and (7.91±1.26) respectively, and the difference was statistically significant ( t=5.40, P<0.01). Compared with the negative control group, the proliferation ability of HCT116 cells in the miR-3126-5p group was significantly reduced ( t=4.52, P<0.05), and the migration ability was significantly reduced ( P<0.01). microRNA.org shows that miR-3126-5p has complementary binding sites with LIM and SH3 protein 1 ( LASP1) gene mRNA. miR-3126-5p can target LASP1 mRNA ( P<0.01). Compared with the negative control group, the expression of LASP1 gene in HCT116 cells of the miR-3126-5p group was significantly reduced ( t=4.56, P<0.01). Conclusion:The expression of miR-3126-5p in colorectal cancer cell lines is low, and miR-3126-5p can reduce the proliferation and migration ability of colorectal cancer HCT116 cells by inhibiting the expression of the target gene LASP1.

Objective:To investigate the effect of long non-coding RNA (lncRNA) HAGLR on the proliferation and migration of gastric cancer cells by inhibiting the expression of microRNA (miRNA, miR)-93-5p.Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of HAGLR in gastric cancer cell lines (HS-746T, BGC823, SGC7901, MGC803) and normal gastric mucosal epithelial cells (GES-1). Selected the cell line with the lowest HAGLR expression and transfected with the negative control plasmid (negative control group) or HAGLR-high-expression plasmid (HAGLR group) respectively. The MTS method and the scratch healing test were used to detect the proliferation and migration ability of the cells after transfection. The bioinformatics software miRcode database was used to predict the target gene of HAGLR, and the dual luciferase reporter gene experiment was used to verify the binding of HAGLR to the target gene. qRT-PCR was used to detect the expression of the target gene. Western blot was used to detect the expression of Hippo signaling pathway. The software SPSS 21.0 was used to conduct statistical analysis. The t test was used for comparison between two groups, and the one-way analysis of variance was used for comparison between multiple groups. Results:Compared with GES-1 cells, the expression level of HAGLR in gastric cancer cell lines was lower (all P<0.05), and the cell line with the lowest HAGLR expression was SGC7901 cells ( P<0.01). The HAGLR expression in SGC7901 cells in the HAGLR group and the negative control group were 1.03±0.13 and 9.75±1.10, respectively. The expression level of HAGLR in the negative control group was significantly lower than that in the HAGLR group ( t=7.87, P<0.01). Compared with the negative control group, the absorbance of SGC7901 cells in the HAGLR group was significantly reduced ( P<0.05), and the scratch healing rate was significantly reduced ( P<0.01). The miRcode database showd that HAGLR and miR-93-5p have complementary binding sites. The dual luciferase reporter gene experiment showed that HAGLR can complement miR-93-5p ( P<0.01). Compared with the negative control group, the expression of miR-93-5p in SGC7901 cells in the HAGLR group was significantly reduced ( P<0.01), and the expression of Hippo signaling pathway protein was significantly reduced (all P<0.01). Conclusions:HAGLR is low expressed in gastric cancer cell lines. HAGLR inhibits the proliferation and migration of gastric cancer SGC7901 cells by negatively regulating miR-93-5p.