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1.
Chinese Journal of Postgraduates of Medicine ; (36): 816-820, 2019.
Artigo em Chinês | WPRIM | ID: wpr-753355

RESUMO

Objective To explore the effect of enteral nutrition on tumor cell proliferation activity in rectal cancer patients with nutritional risk treated with preoperative neoadjuvant therapy. Methods Sixty-six rectal cancer patients with nutritional risk treated with preoperative neoadjuvant therapy from January 2016 to January 2018 in the Yongchuan Hospital Affiliated to Chongqing Medical University were selected. The patients were divided into experimental group (enteral nutrition combined with neoadjuvant therapy) and control group (simple adjuvant therapy) according to the random digits table method, with 33 cases in each group. The expressions of proliferating cell nuclear antigen (PCNA) and Ki-67 antigen before and after treatment were detected by immunohistochemical method; the albumin and prealbumin before and after treatment were observed, and the nutrition risk screening 2002 (NRS2002) was evaluated. Results There were no statistical differences in the expressions of PCNA and Ki-67 antigen before treatment between 2 groups (P>0.05); the expressions of PCNA and Ki-67 antigen after treatment in experimental group were significantly lower than those in control group, and there were statistical differences (P﹤0.05). There were no statistical differences in the NRS2002 score, albumin and prealbumin before treatment between 2 groups (P>0.05); the NRS2002 score after treatment in experimental group was significantly lower than that in control group: (1.58 ± 0.50) scores vs. (3.65 ± 0.72) scores, the albumin and prealbumin after treatment were significantly higher than those in control group: (35.92 ± 2.77) g/L vs. (31.12 ± 1.76) g/L and (204.58 ± 23.86) mg/L vs. (157.46 ± 18.99) mg/L, and there were statistical differences (P﹤0.01). Conclusions Enteral nutrition can reduce the proliferation activity of tumor cell in rectal cancer patients with nutritional risk treated with preoperative neoadjuvant therapy, and it can improve the nutritional status of patients.

2.
Chinese Journal of Postgraduates of Medicine ; (36): 816-820, 2019.
Artigo em Chinês | WPRIM | ID: wpr-798119

RESUMO

Objective@#To explore the effect of enteral nutrition on tumor cell proliferation activity in rectal cancer patients with nutritional risk treated with preoperative neoadjuvant therapy.@*Methods@#Sixty-six rectal cancer patients with nutritional risk treated with preoperative neoadjuvant therapy from January 2016 to January 2018 in the Yongchuan Hospital Affiliated to Chongqing Medical University were selected. The patients were divided into experimental group (enteral nutrition combined with neoadjuvant therapy) and control group (simple adjuvant therapy) according to the random digits table method, with 33 cases in each group. The expressions of proliferating cell nuclear antigen (PCNA) and Ki-67 antigen before and after treatment were detected by immunohistochemical method; the albumin and prealbumin before and after treatment were observed, and the nutrition risk screening 2002 (NRS2002) was evaluated.@*Results@#There were no statistical differences in the expressions of PCNA and Ki-67 antigen before treatment between 2 groups (P>0.05); the expressions of PCNA and Ki-67 antigen after treatment in experimental group were significantly lower than those in control group, and there were statistical differences (P<0.05). There were no statistical differences in the NRS2002 score, albumin and prealbumin before treatment between 2 groups (P>0.05); the NRS2002 score after treatment in experimental group was significantly lower than that in control group: (1.58 ± 0.50) scores vs. (3.65 ± 0.72) scores, the albumin and prealbumin after treatment were significantly higher than those in control group: (35.92 ± 2.77) g/L vs. (31.12 ± 1.76) g/L and (204.58 ± 23.86) mg/L vs. (157.46 ± 18.99) mg/L, and there were statistical differences (P<0.01).@*Conclusions@#Enteral nutrition can reduce the proliferation activity of tumor cell in rectal cancer patients with nutritional risk treated with preoperative neoadjuvant therapy, and it can improve the nutritional status of patients.

3.
Chinese Journal of Pharmacology and Toxicology ; (6): 497-502, 2014.
Artigo em Chinês | WPRIM | ID: wpr-454889

RESUMO

OBJECTlVE To investigate the myocardiaI toxicity of doxorubicin on the myocardium of rabbits and mechanism. METHODS Doxorubicin 2 mg·kg-1 was injected once a week for eight weeks. After discontinuation of doxorubicin,observation was performed for another 8 weeks. Every weekend, uItrasound examination,cardiac catheterization,angiotensinⅡ(AngⅡ)Western bIotting and pathoIogi-caI examination were performed to anaIyze eject fraction( EF),maximaI rate of rise of Ieft ventricuIar pressure(+dp/ dtmax ),AngⅡexpression IeveI,apoptosis index(AI)and the structure of the myocardium. RESULTS At the 7th injection,EF decreased( P ﹤0.05),but reached the bottom vaIue at the 8th injection. At the 3rd injection,Ieft ventricuIar +dp/ dtmax decreased( P ﹤0.05)and reached the bottom vaIue one week after withdrawaI. After that,it increased and reached a high vaIue six weeks after withd-rowaI. But it was stiII Iower than before administration. At the 2nd injection,AngⅡ expression increased (P﹤0.05). At 1 week after withdrawaI,it reached the top vaIue,but than decreased and reached a Iow vaIue six weeks after withdrowaI,but was stiII higher than before administration. At the 1st injection,AI increased( P ﹤ 0.05). At 1 week after withdrawaI,it reached the top vaIue,but then decreased and reached a Iow vaIue 5 weeks after withdrawaI. But it was stiII higher than before administration. CONCLUSlON Doxorubicin cardiac toxicity can induce an eIevated IeveI of myocardiaI AngⅡ,possibIy associated with increased aIdosterone and myocardiaI tension. Increased Ang Ⅱ may induce further myocardiaI structuraI damage and ventricuIar remodeIing through the ROS and caIcium imbaIance.

4.
Chinese Journal of Pathophysiology ; (12): 238-244, 2010.
Artigo em Chinês | WPRIM | ID: wpr-403951

RESUMO

AIM: To study the effects of metformin on the pressure overload-induced cardiac hypertrophy in rats. METHODS: Transverse aortic constriction (TAC) model of rat was made through laparotomy. One week after TAC surgery, the rats were randomly divided into 5 groups (n=8 in each group) and were administered with the corresponding drugs orally every day for 8 weeks: sham group (sham surgery, administered with 2 mL distilled water);TAC group (TAC rats, administered with 2 mL distilled water);metformin(MET) group (TAC rats, administered with MET at dose of 300 mg·kg~(-1)·d~(-1));MN group [TAC rats, administered with MET at dose of 300 mg·kg~(-1)·d~(-1) plus NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) 50 mg·kg~(-1)·d~(-1)] and L-NAME group (TAC rats, administered with L-NAME at dose of 50 mg·kg~(-1)·d~(-1)). After treated for 8 weeks, the echocardiography, hemodynamics, the ratio of heart weight to body weight (HW/BW) and histological examination of the heart were performed. The levels of myocardial AMP-activated protein kinase subunit α (AMPKα), p-AMPKα~(Thr172), endothelial nitric oxide synthase (eNOS) and p-eNOS~(Ser1177) were detected by Western blotting. Plasma and myocardial nitric oxide (NO) were detected biochemically. RESULTS: After 8 weeks treatment, the wall thickness of left ventricle, the heart weight/body weight ratio (HW/BW), and the left ventricular myocardial perivascular fibrosis and myocardial interstitial fibrosis of the animals in TAC group were significantly increased as compared to those in sham rats. Treatment with MET for 8 weeks significantly attenuated left ventricular hypertrophy and improved cardiac function in TAC rats. These effects of MET were mostly abolished by L-NAME. Molecular biology and biochemical testing revealed that the levels of left ventricular myocardial p-AMPKα~(Thr172) and p-eNOS~(Ser1177), as well as the levels of myocardial and serum NO were significantly increased in MET group. CONCLUSION: Long-term MET treatment significantly inhibits the cardiac hypertrophy and the myocardial fibrosis and improves the cardiac functions in pressure-overload rats. The anti-hypertrophic effects of MET may be mediated via activation of AMPK-eNOS signaling pathway.

5.
Journal of Sun Yat-sen University(Medical Sciences) ; (6): 190-194, 2010.
Artigo em Chinês | WPRIM | ID: wpr-402768

RESUMO

[Objective]This study was designed to investigate the effects of 5-aminoimidasole-4-carboxamide ribonucleoside (AICAR)on activity of transcription factor Forkhead O 3a(FOXO3a)and expression of ubiquitin ligase muscle atrophy F-box (MAFbx),and to explore the role of adenosine monophosphate-activated protein kinase(AMPK)on proteolysis pathways in eardiomyocytes.[Methods]The effect of AICAR on activation of AMPK was observed.Cultured neonatal rat cardiomyocytes was treated with AICAR in different concentration.Cultured cardiomyocytes were then divided into three groups:control group,AICAR group,AICAR+Compound C group.Effects of AMPK activation on phosphorylation of FOXO3a and expression of MAFbx in cardiomyocytes were detected using Western blot.[Results]①Compared with control group,activity of AMPK in cultured cardiomyocytes was increased after treatment with 0.25 mmol/L or 0.5 mmol/L AICAR for 6 h(P<0.05),and the activity of AMPK was further enhanced after treatment with 1.0 mmol/L or 2.0 mmol/L AICAR for 6 h(P<0.01).②Activation of AMPK by AICAR significantly increased the transcriptional activity of FOXO3a(P<0.01),and enhanced MAFbx protein expression in cardiomyocytes when comparing with control group(P<0.01),however,specific AMPK antagonist Compound C markedly reversed these effects induced by AICAR.[Conclusion]AMPK may regulate cardiomyocytes proteolysis by activation of FOXO3a transcription factor,and up-regulation of MAFbx protein expression.

6.
Chinese Journal of Marine Drugs ; (6)1994.
Artigo em Chinês | WPRIM | ID: wpr-584972

RESUMO

Objective To observe the effect of haishengsu preparation extracted from Tegillarca granosa on patients with NSCLC and renal cancer that lose the opportunity of operation, radical cure or large dose chemotherapy. Methods 61 cases of NSCLC and 27 cases of renal cancer patients received the haishengsu injection 2.4mg+0.9%NaCl 250ml iv once daily for a consecutive 20 days. 28 days was considered one treatment cycle and each case received 3 to 6 cycles respectively.Results In NSCLC patients,2 cases completely remitted (CR), 28 cases of partially remitted (PR) with the total effective rate of 49.18%. Curative effects in cases with initial treatment, IIIb stage, adenocarcinoma or high behavior condition were higher than those of cases with retreatment, Ⅳ stage, squamous carcinoma, or low behavior condition respectively (P

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