1.Prevalence and risk factors of chronic low back pain in puerperas after childbirth
Yingjun GUAN ; Shiyuan XU ; Yesong CHEN ; Jun JIN ; Lanlan ZHONG ; Shuang TAN
Chinese Journal of Postgraduates of Medicine 2015;38(6):432-434,439
Objective To observe the prevalence and risk factors of chronic low back pain in puerperas after childbirth.Methods Eight hundred and eighty-one puerperas were selected,among whom 459 cases had uterine-incision delivery,and 422 cases had spontaneous delivery.The age,height and weight of pregnant women,birth weight of newborn,history of preoperative low back pain,parity and mode of delivery were recorded.The rate of chronic low back pain occurring within 1 month after childbirth and continuing for 3 months was recorded by telephone.The factors with P values less than 0.05 would enter the Logistic regression analysis to screen the risk factors of chronic low back pain.Results Two hundred and fifty-nine puerperas (259/881,29.4%) appeared chronic low back pain,of whom 157 puerperas (157/459,34.2%)delivered by uterine-incision and 102 puerperas (102/422,24.2%) delivered spontaneously,and the difference was statistically significant (P < 0.01).Six hundred and fifty-eight puerperas had no history of preoperative low back pain,and 150 puerperas (150/658,22.8%) appeared newly developed chronic low back pain.Logistic regression analysis showed that mode of delivery,parity and history of preoperative low back pain were the risk factors of chronic low back pain.Condusions The rate of chronic low back pain in puerperas after childbirth is 29.4%,and the newly developed chronic low back pain is 22.8%.Uterineincision delivery,multiparity and history of preoperative low back pain are the risk factors of chronic low back pain for puerperas after childbirth.
2.Clinical observation on nimotuzumab combined with radiochemotherapy in locoregionally advanced nasopharyngeal carcinoma
Juying LIU ; Wei CHEN ; Jing WEN ; Yesong GUO ; Xuesong JIANG ; Xiuhua BIAN
Cancer Research and Clinic 2013;25(10):696-699
Objective To assess the efficacy and safety of nimotuzumab in combination with radiochemotherapy in locoregionally advanced nasopharyngeal carcinoma (NPC).Methods 42 patients with locoregionally advanced NPC were retrospectively analyzed.They all received the treatment of nimotuzumab in combination with radiochemotherapy.Intensity modulated radiationtherapy (IMRT) was applied and the prescribed radiation dose administered to the primary tumor was between 70 to 79.2 Gy in 32-37 fractions and 41-49 days.The dose administered to lymph nodes was between 65 to 76 Gy in 32-37 fractions and 41-49 days.Nimotuzumab was given weekly during irradiation.All patients received chemotherapy.Results The main adverse events were mucositis,bone marrow suppression,dermatitis and xerostomia.Grade 1 or 2 oropharyngeal mucositis occurred in 29 (69.0 %) patients,and grade 3 in 2 (4.8 %).Grade 1 or 2,3 or 4 leucopemia occurred in 25 cases (59.5 %),16 cases (38.1%),respectively,without occurrence of febrile neutropenia.There was no treatment related death.Complete response (CR) rate was 90.5 % (38/42),partial response (PR) rate was 9.5 % (4/42) and the total efficiency was 100 %.After a median follow-up of 22.5 months,the 1-year local control rate was 100 %.1-year distant metastasis-free survival rate was 92.7 %.1-year overall survival rate was 95.2 %.Conclusion Nimotuzumab combined with radiochemotherapy was efficient and safe for locoregionally advanced NPC.
3.AngiotensinⅡ up-regulates cardiomyocyte Cx43 gap expression via AT_1 receptor and ERK1/2
Yesong WANG ; Hong MA ; Yuan HU ; Wutao ZENG ; Huizhong ZHANG ; Jianwen CHEN
Chinese Journal of Pathophysiology 1986;0(01):-
AIM: To investigate the effect of angiotensinⅡon Cx43 gap junction in cultured neonatal rat cardiac myocytes and its mechanism. METHODS: The cardiomyocytes were treated with AngⅡ for 24 h, which were pretreated with valsartan or PD98059 for 60 min before AngⅡ treatment. The controls were treated with equal amount of DMSO. The Cx43 expression, synthesis and gap junction in cardiomyocytes were characterized by Western blotting, metabolic labeling and immunoprecipitation assay, and electron microscope. RESULTS: Western blotting analysis revealed that Cx43 content concentration-dependently increased in cells treated with 10 -9-10 -6 mol/L AngⅡfor 24 h. Phosphorylated extracellular signal regulated kinase (P-ERK) 1/2 activity increased in cells treated with 0.1 ?mol/L AngⅡ for 24 h (P
4.Effects of benazepril on cardiac function, free oxygen radicals, sarcoplasmic reticulum Ca~(2+)- ATPase following cardiac ischemia- reperfusion in spontaneously hypertensive rats
Yesong WANG ; Hong MA ; Jianwen CHEN ; Yuan HU ; Xiujian LAN ; Fanhua QIU
Chinese Journal of Pathophysiology 1986;0(03):-
AIM: To investigate the effects of angiotensin converting enzyme inhibitor (ACEI), benazepril(B), on cardiac function, free oxygen radicals, sarcoplasmic reticulum(SR) Ca~(2+)-ATPase following ischemia-reper-fusion in sportaneously hypertensive rats (SHRs). METHODS: Thirty 10-week-old female SHRs were randomly assigned into two groups: group SHR was control; The animal in group SHR+B was given with 10 mg/kg of benazepril perday. Another 15 Wistar rats with the same age and sex were normal control (group Wistar). After 12 weeks of pretreatment, all rats in each group were subjected to 30 min of left anterior descending coronary artery occlusion and 30 min of reperfusion. Hemodynamic parameters, left heart-to-body weight ratio(LVW/BW), myocardial malondialdehyde (MDA) concentration, superoxide dismutase (SOD) activity, and SR Ca~(2+)-ATPase activity were measured. RESULTS: Compared to group Wistar, the rats in group SHR had higher blood pressure, LVW/BW and myocardial MDA concentration, more serious left cardiac function injury and lower myocardial SOD activity and SR Ca~(2+)-ATPase activity; group SHR+B had lower myocardial MDA concentration, higher myocardial SOD activity, but no difference in blood pressure, LVW/BW, the degree of left cardiac function injury and myocardial SR Ca~(2+)-ATPase activity. CONCLUSION: Benazepril can attenuate ischemia-reperfusion-induced cardiac function injury by regression of left ventricular hypertrophy (LVH), improving SR Ca~(2+)-ATPase activity and decreasing oxygen free radicals injury in SHRs.