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1.
Chinese Mental Health Journal ; (12): 677-684, 2017.
Article in Chinese | WPRIM | ID: wpr-668295

ABSTRACT

This paper discusses cancer clinic benefit from distress screening through searching literatures within 15 years in the database of Pubmed,Medline,and CNKI,describes pros and cons of the frequently-used distress screening measurements in cancer clinical daily work,summarizes current situation,and makes suggestions about cancer distress screening in China

2.
Acta Academiae Medicinae Sinicae ; (6): 399-403, 2016.
Article in English | WPRIM | ID: wpr-277966

ABSTRACT

Objective To investigate the changes of regulatory T cells (Tregs) and whether Tregs can modulate the distribution of macrophage subtypes in visceral adipose tissue in the early stage of obesity.Methods After C57BL/6 mice obesity models were successfully established,metabolic parameters and numbers of Tregs and M1/M2 macrophage were measured at 4,10,and 20 weeks.The changes of metabolic parameters and adipose tissue inflammation in obesity mice after rapamycin intervention were evaluated. Results The early-stage obesity models were successfully established.Compared with normal diet mice,high fat diet mice had significantly higher epididymal adipose tissue mass and serum leptin levels(P<0.05).However,there was no statistical difference in blood glucose and insulin levels between these two groups(All P>0.05). Macrophages infiltration in adipose tissue in high fat diet mice gradually increased with time,coincident with decrease in Treg numbers. Increased numbers of Treg,improved metabolic parameters,and decreased ratio of M1/M2 can be seen after rapamycin intervention in mice.Conclusion The decrease of Tregs in the early stage of obesity may contribute to abnormal distribution of macrophage subtypes in visceral adipose.


Subject(s)
Animals , Mice , Blood Glucose , Diet, High-Fat , Inflammation , Intra-Abdominal Fat , Cell Biology , Leptin , Blood , Macrophages , Cell Biology , Mice, Inbred C57BL , Mice, Obese , Obesity , Allergy and Immunology , T-Lymphocytes, Regulatory , Cell Biology
3.
Acta Academiae Medicinae Sinicae ; (6): 614-619, 2014.
Article in English | WPRIM | ID: wpr-329774

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effect of high-fat or high-glucose diet on obesity and visceral adipose tissue in C57BL/6 mice.</p><p><b>METHODS</b>Four-week-old C57BL/6 mice were allocated into normal diet group,high-fat diet group,and high-glucose diet group according to the random number table until 20 weeks old. Body weight,epididymal adipose tissue weight,blood leptin,fat infiltration in liver,M1/M2 macrophage subtypes,and monocyte chemoattractant protein-1 mRNA in epididymal adipose tissues were measured.</p><p><b>RESULTS</b>Compared with normal diet group,body weight,epididymal adipose tissue weight,and leptin concentration in high fat diet group at 20 weeks were significantly increased (P < 0.05),and oil red O staining showed more prominent adipocyte infiltration in liver in high-fat diet group than those in normal diet and high-glucose diet group. However,no apparent differences were seen in high-glucose diet group at 20 weeks in terms of body weight,epididymal adipose tissue weight and leptin concentration. In high-fat diet group,the macrophages infiltration in epididymal adipose tissue increased with time and the percentage of M2 macrophage decreased in high-fat diet group than that in high-glucose diet group(P<0.05). Compared with normal diet group,monocyte chemoattractant protein-1 mRNA expression increased significantly in high-fat diet group(P<0.05). In high-glucose group,however,no significant differences were discerned (P > 0.05).</p><p><b>CONCLUSION</b>High-fat diet,rather than 60% high glucose diet,will lead to obesity and macrophage infiltration in adipose tissues.</p>


Subject(s)
Animals , Mice , Adipocytes , Adipose Tissue , Body Weight , Chemokine CCL2 , Genetics , Metabolism , Diet, High-Fat , Methods , Glucose , Intra-Abdominal Fat , Leptin , Macrophages , Mice, Inbred C57BL , Obesity , RNA, Messenger
4.
Acta Pharmaceutica Sinica ; (12): 146-152, 2011.
Article in Chinese | WPRIM | ID: wpr-348984

ABSTRACT

In view of gemcitabine resistance has limited clinical activity of gemcitabine as a cellulotoxic drug in pancreatic cancer patients, this study is designed to investigate the effect of emodin on the sensitivity of pancreatic cancer to gemcitabine as well as its mechanism. After gemcitabine-resistant pancreatic cancer cell line (SW1990/GZ) was established by escalating doses of gemcitabine serially in pancreatic cancer cell line (SW1990). The cellular proliferation was detected by cell counting kit-8 (CCK-8) assay. Flow cytometry (FCM) was used to determine apoptosis of pancreatic cancer cells. The activity of NF-kappaB in pancreatic cancer cells was measured by electrophoretic mobility shift assay (EMSA). Western blotting was used to detect the protein expression of Bcl-2 and Survivin in SW1990/GZ cells. Metastatic model simulating human pancreatic cancer was established by orthotopic implantation of histologically intact human tumor tissue into pancreatic wall of nude mice. Also, immunohistochemistry was used to detect the positive expression of Ki-67, NF-kappaB, Bcl-2 and Survivin in the tumors. The results show that pretreatment of cells with emodin followed by gemcitabine induced a higher percentage of growth inhibition and apoptosis of pancreatic cancer cells than that of gemcitabine alone. In addition to in vitro results, emodin in combination with gemcitabine is much more effective as an antitumor agent compared to either agent alone in the orthotopic tumor model. Further study showed that the emodin with or without gemcitabine significantly down-regulates NF-kappaB and its regulated molecules such as Bcl-2 and Survivin proteins both in vitro and in vivo. It is concluded that inactivation of NF-kappaB signaling pathway by emodin resulting in the chemosensitization of pancreatic cancer to gemcitabine, which is likely to be an important and novel strategy for the treatment of pancreatic cancer.


Subject(s)
Animals , Female , Humans , Mice , Antimetabolites, Antineoplastic , Pharmacology , Apoptosis , Cell Line, Tumor , Cell Proliferation , Deoxycytidine , Pharmacology , Drug Resistance, Neoplasm , Emodin , Pharmacology , Inhibitor of Apoptosis Proteins , Metabolism , Ki-67 Antigen , Metabolism , Mice, Inbred BALB C , Mice, Nude , NF-kappa B , Metabolism , Neoplasm Transplantation , Pancreatic Neoplasms , Metabolism , Pathology , Proto-Oncogene Proteins , Metabolism , Proto-Oncogene Proteins c-bcl-2 , Repressor Proteins , Metabolism , Tumor Burden
5.
Chinese Journal of Contemporary Pediatrics ; (12): 433-435, 2010.
Article in Chinese | WPRIM | ID: wpr-347578

ABSTRACT

<p><b>OBJECTIVE</b>To summarize the etiology and treatment of gynecomastia in male children.</p><p><b>METHODS</b>The clinical data of 38 boys with gynecomastia at ages of 2-14 years were retrospectively studied.</p><p><b>RESULTS</b>In the 38 cases, 17 cases were identified as adolescent breast hyperplasia, 2 cases were relevant to primary disease, 4 cases were caused by ingestion of drugs containing hormone, and 15 cases did not show identifiable causes and were diagnosed as idiopathic gynecomastia. For the 3 children with breast development in B3 stage, oral rupixiao was administered (1.34 g, tid) for one month. For 16 children at ages of over 12 years with breast development in B2 stage and with obvious clinical symptoms, oral rupixiao was administered (1.34 g, tid) for 3-5 days. The other patients did not receive drug treatment. In a one month to one year follow-up, most of the patients recovered well.</p><p><b>CONCLUSIONS</b>The etiology of gynecomastia in male children includes adolescent breast hyperplasia, ingestion of drugs containing hormone and secondary causes. Most gynecomastia can be attributed to physiological reasons. Only a few children with obvious clinical symptoms need drug treatment.</p>


Subject(s)
Adolescent , Child , Child, Preschool , Humans , Male , Gynecomastia , Therapeutics , Retrospective Studies
6.
China Biotechnology ; (12)2006.
Article in Chinese | WPRIM | ID: wpr-686096

ABSTRACT

Objective:Establish mass-scale purification technology of cell-derived influenza virus. Methods: A microcarrier-based process was used to produce human influenza virus in serum free-adapted Vero cells. The virus was purified in a sequence of downstream processing steps including inactivation, clarification, anion exchange chromatography, affinity chromatography and size-exclusion chromatography. Results: The recovery of HA reached 102%. 95.3% total protein, including 99.77% host cell protein, and 99.99% host cell DNA were removed during downstream processing. Conclusion: Providing a high effective purification technology for cell-derived influenza virus.

7.
Journal of Central South University(Medical Sciences) ; (12): 36-51, 2006.
Article in Chinese | WPRIM | ID: wpr-813771

ABSTRACT

OBJECTIVE@#To investigate the lymphangiogenesis and location of tumor lymphatic vessels induced by vascular endothelial growth factor C (VEGF-C) in primary breast cancer.@*METHODS@#The expression of VEGF-C mRNA in 89 cases of primary breast cancer was detected by in situ hybridization, and lymphatic vessels with vascular endothelial growth factor receptor-3 (VEGFR-3) were labeled by immunohistochemistry SP method.@*RESULTS@#VEGF-C mRNA expressed in 49 of all 89 cases of primary breast cancer, and the expression rate was 55.06%. The expression of VEGF-C mRNA was positively correlated with lymphatic vessel density (LVD) and axillary lymph node metastasis, LVD and the rate of axillary lymph node metastasis were significantly higher in VEGF-C mRNA positive group than those in the negative group (both P < 0.05). Different levels of lymphangiogenesis took place in all cases of breast cancer, but it was mainly located in tumor stroma, and apparently mature lymphatic vessels were not found in cancer nests. LVD was positive related with the clinical stage and axillary lymph node metastasis in breast cancer; the clinical stage, the LVD, the axillary lymph node metastasis in positive group were higher than those in the negative group (P < 0.05).@*CONCLUSION@#The expression of VEGF-C mRNA is positively correlated with lymphangiogenesis and axillary lymph node metastasis in primary breast cancer. Lymphangiogenesis induced by VEGF-C predominantly takes place in the tumor stroma tissue, and mature lymphatic vessels are not found in cancer nests.


Subject(s)
Adult , Aged , Female , Humans , Middle Aged , Breast Neoplasms , Metabolism , Pathology , Lymphangiogenesis , Lymphatic Metastasis , RNA, Messenger , Genetics , Vascular Endothelial Growth Factor C , Genetics , Vascular Endothelial Growth Factor Receptor-3 , Metabolism
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