Objective:To evaluate the prognostic value of post-mastectomy radiation therapy (PMRT) in patients with axillary lymph node-positive breast cancer treated with breast conservation surgery and to establish the candidates for PMRT based on different pN stages and lymph node ratios (LNR). Methods:A retrospective analysis of the clinical data of the patients was conducted. The pa-tients had positive lymph nodes (n=152) between 1998 and 2007 and underwent breast conservation surgery. A comparison of the dis-ease-free survival (DFS) and overall survival (OS) rates was conducted based on LNR and pN staging and with PMRT as a prognostic factor. Results:A total of 152 cases were studied, of which 114 were pN1, 23 were pN2, and 15 were pN3. Among these cases, 114 had an LNR ranging from 0.01 to 0.20, 26 had an LNR from 0.21 to 0.65, and 12 had an LNR>0.65. Univariate analysis showed that the number of dissected lymph nodes, LNR, pN stage, estrogen and progesterone receptor status, and radiotherapy were the prognostic fac-tors for DFS and OS rates (P<0.05). Age and chemotherapy were prognostic factors only for OS rate (P<0.05). Multivariate analysis in-dicated that PMRT and LNR were independent prognostic factors of DFS and OS (P<0.05). The pN staging had no significant effect on DFS or OS (P>0.05). In the subgroup analysis, PMRT had significant effect on DFS and OS (P<0.05) in patients with pN1 and LNR<0.21. Conclusion:LNR is an independent prognostic factor in axillary lymph node-positive breast cancer patients treated with breast conservation surgery, and a candidate for PMRT should be established based on different LNR risks.

Axillary reverse mapping (ARM) is a technique used to map and preserve arm lymphatic drainage during axillary lymph node dissection (ALND) and/or sentinel lymph node dissection (SLND). As a result, the risk of arm lymphedema is reduced. ARM is an emerging technology for breast cancer surgery and currently in the clinical trial phase. In this article, related clinical trials conducted in recent years were reviewed and the displaying methods of ARM lymph nodes and lymphatic vessels were analyzed. The feasibility of retained ARM lymph nodes and lymphatic vessels was also evaluated. Furthermore, the clinical significance of ARM was evaluated in terms of the reduction of the incidence of upper extremity lymphedema after breast cancer surgery.

The neuropeptide orexins, including orexin A and orexin B, are located exclusively in hypothalamus OX1R and OX2R are receptors of orexin. OX1R is selective to orexin A while OX2R is not. The distributions of orexin neurons in human brain are the same as those of rats. Orexin was closely related with sleep and awakening behavior besides regulating the feeding behavior. Orexin-containing terminals are also found in areas modulating sleep and awakening such as the locus ceruleus, tuberomammillary nucleus, dorsal raphe, and the basal forebrain. In those areas, there are also lots of OX1R and OX2R and their precursors. Orexin neurons are extremely active during rapid wave sleep and awakening. If hypothalamus in some areas is destroyed and orexin neurons are reduced, sleep-awakening dysfunction will appear (for instance: narcolepsy).

Aim To investigate the effects of PLCε on the invasion and migration of human osteosarcoma cancer cells U2OS. Methods RNA interference ( RNAi) was used to inhibit PLCεexpression, and the proliferation of cancer cells was measured by CCK-8 assay. The migration of the cells was measured by scratch wound healing assay and migration chamber as-say. Gelatin zymography was performed to measure the MMP2 activities in U2OS cells. Results PLCε ex-pression was suppressed by siRNA. CCK-8 assay showed that PLCε had no effect on the proliferation of cancer cells. PLCε knockdown inhibited cell invasion and activities of MMP2 . Conclusion PLCε knock-down can inhibit the migration and invasion of human osteosarcoma cancer cells U2OS.

The overexpression of proto-oncogene protein c-pim-1 (Pim-1) in tumor tissue is related to the stage and prognosis.Recent studies indicate that Pim-1 plays a critical role in the proliferation and apoptosis of cells and the metastasis of tumor.Pim-1 acts as an essential factor in several signaling pathways and its expression and activation are regulated by many factors as well as affects others widely.As an influential factor in the occurrence and development of tumor,Pim-1 has been a potential target in oncotherapy.

Objective To investigate the effect of mild hypothermia combined with mitochondrial divison inhibitor 1 in mitochondrial after cerebral ischemia-reperfusion (IR).Methods Fourty male healthy Sprague-Dawley (SD) rats, weighing 280-320 g, were randomly divided into 5 groups (n=8 each): group Sham, group IR, hypothermia group (group H), Mdivi-1 group (group M) and hypothermia+Mdivi-1 group (group HM).Animal models of global cerebral IR were established by transoesophageal cardiac pacing inducing cardiac arrest followed by cardiopulmonary resuscitation (ischemia 4 min and reperfusion 6 h).The group Sham was similarly treated to group IR except the cardiac arrest and cardiopulmonary resuscitation.In groups H and HM, the core temperature was cooled down to 32-34℃ within 15 min starting from the beginning of reperfusion, and maintained for 6 h.In the other groups, the core temperature was maintained at the normal temperature.In groups M and HM, the animals were given Mdivi-1 (1.2 mg/kg) intravenously at the beginning of the reperfusion and the other groups were given the same Volume of dimethylsnlfone (DMSO).After 6 h of reperfusion, the rats were sacrificed, and bilateral hippocampi were immediately removed for determination the protein level of dynamin-related proten 1 (Drp1) and cytochrome C (Cyt-C) expression by Western blot and obsevation of the mitochondrial structure of pyramidal cell in hippocampal CA1 under electronic microscope.Results Compared with group Sham, the expression of Drp1 and Cyt-C was up-regulated in groups IR, H, M and HM (P＜0.05).Compared with group IR, the expression of Drp1 and Cyt-C was down-regulated in groups H, M and HM (P＜0.05).Compared with groups H and M, the expression of Drp1 and Cyt-C was down-regulated in group HM (P＜0.05).There was no significant difference in the expression of Drp1 and Cyt-C between groups H and M.The mitochondria were rod-shaped with clear and sound structure in group Sham, while mitochondria showed various degree of fission, swollen structures, matrix deposit, vacuoles formation and cristae collapse in other groups.The changes of group HM were relatively slight.Conclusion Mild hypothermia combined with mitochondrial divison inhibitor 1 alleviate mitochondrial damage after global cerebral IR of rats.The combined effect is better than that of any individual application.

Objective To evaluate the effect of hypothermia on the expression of dynamin?related protein 1 ( Drp1) in brain tissues during global cerebral ischemia?reperfusion ( I∕R) in rats. Methods Thirty?six healthy male Sprague?Dawley rats, weighing 280-320 g, were divided into 3 groups ( n=12 each) using a random number table: sham operation group ( group Sham ) , global cerebral I∕R group ( group I∕R) and hypothermia group ( group H) . Cardiac arrest was induced by transoesophageal cardiac pacing followed by cardiopulmonary resuscitation to establish the global cerebral I∕R model in anesthetized rats in I∕R and H groups. In group H, the body temperature ( rectal temperature) was cooled down to 32-34 ℃ within 15 min starting from the beginning of reperfusion, and maintained at this level for 6 h. At 72 h of reperfusion, neurological deficit was scored, and the rats were sacrificed, and the whole brain was removed for examination of the pathological changes in hippocampal CA1 region and for determination of nor?mal pyramidal cell count and neuronal apoptosis in hippocampal CA1 region and expression of Drp1 and cy?tochrome c (Cyt c) in hippocampal tissues (by Western blot). The apoptosis rate was calculated. Re?sults Compared with group S, the neurological deficit score and apoptosis rate were significantly in?creased, and the number of normal pyramidal cells was decreased in I∕R and H groups, the expression of Drp1 and Cyt c in hippocampal tissues was significantly up?regulated in group I∕R ( P<0.05) , and no sig?nificant change was found in the expression of Drp1 and Cyt c in hippocampal tissues in group H ( P>0.05) . Compared with group I∕R, the neurological deficit score and apoptosis rate were significantly de?creased, the number of normal pyramidal cells was increased, and the expression of Drp1 and Cyt c in hip?pocampal tissues was down?regulated in group H ( P<0.05) . Conclusion The mechanism by which hypo?thermia inhibits cell apoptosis during global cerebral I∕R may be related to down?regulation of Drp1 expres?sion in rats.

Objective:To observe influence of exercise rehabilitation combined diet guidance on cardiac function and quality of life (QOL) in patients after heart valve replacement .Methods:A total of 120 patients after heart valve replacement were selected and randomly divided into control group (n=60 ,received routine health education ) and experiment group (n=60 ,received diet guidance and exercise rehabilitation based on routine health education ) .After discharge ,patients re‐ceived outpatient follow‐up for six months ,body weight ,cardiac function and QOL on six months after surgery were fol‐lowed up and observed in two groups ,and the results were statistically compared .Results:Compared with control group six months after discharge ,there were significant rise in left ventricular ejection fraction [ (51.75 ± 9.30)% vs .(57.73 ± 6.13)% ] andoxygenmetabolicequivalent [(7.05±1.85)METsvs.(11.34±2.18)METs],andeachitemscoreofQOL and total score of QOL [ (4.98 ± 0.40) scores vs .(6.49 ± 0.53) scores] ,P<0.05 or <0.01;and significant reduction in body weight [(67.75 ± 10.67) kg vs .(61.25 ± 10.34) kg] in experiment group ,P<0.01. Conclusion:Exercise rehabili‐tation combined diet guidance can avoid rapid increase in body weight after surgery ,promote recovery of cardiac function and improve quality of life after surgery in patients with heart valvular diseases .

OBJECTIVE To investigate the effects of lead exposure on the permeability,secretion and transportation function of blood-cerebro-spinal fluid barrier (BCB)of rats in order to provide the theo-rical basis for elucidating the mechanis m of lead induced neurotoxicity.MEHTODS 60 SPF SD rats were rando mly divided into 4 groups,including a control group and three doses lead exposed groups. Rat in the lead exposure groups were given drinking water containning 0.05%,0.1 % and 0.2% lead acetate (at dose of 80,160,320 mg·kg -1 )for 8 weeks.Laser scanning confocal microscopy was uti-lized to determine the lead content in seru m,cerebrospinal fluid (CSF)and choroid plexus sa mples. Morris maze was used to test learning and me mory.Fe moral artery perfusion of Evans blue (EB)and fluorescein sodiu m (NaFI)was performed to measure BCB permeability function.Confocal laser scan-ning was applied to detect junction adhesion molecule (JAM)and occludin protein expression in choroid plexus.ELISA was used to measure the concentration of transthyretin (TTR)and leptin in seru m and CSF.RESULTS The lead content in seru m,choroid plexus and CSF significantly increased,especially the lead level in CSF.Morris water maze data showed that escape latency of rat in lead acetate 160 and 320 mg·kg -1 group were 52 ±12,(89 ±19)s,respectively,longer than that of control group 〔(28 ±7)s, P<0.05〕.The ti mes across platform of rats in lead acetate 160 and 320 mg·kg -1 group were lower than that of control group(P <0.05).The NaFI content in CSF of rats in all lead acetate exposure groups were 0.94 ±0.09,1 .02 ±0.03 and (1 .08 ±0.18)mg·L -1 ,respectively,and were higher than those of control group〔(0.74 ±0.04)mg·L -1 〕;While the EB content in CSF of rat in lead acetate 160 and 320 mg·kg -1 group were higher than the control group(P <0.05),which indicated that lead acetate exposure at low dose can lead to the increase of permeability of BCB.Laser scanning confocal micro-scope i mages showed that the JAM protein expression of choroid plexus in lead acetate 160 and 320 mg·kg -1 group were 44.9% and 42.9% of the control group.Sa me decline was seen in terms of occludin expression.The TTR content of CSF of rats in lead acetate 80 mg·kg -1 group was (32.3 ± 1 1 .7)ng·g -1 protein,lower than that of the control group,and the difference was significant.This decline was also noted in lead acetate 160 and 320 mg·kg -1 group.The data of TTR in CSF suggested that the low dose lead acetate exposure can disrupt the BCB secretion function.The leptin levels in CSF of lead acetate 160 and 320 mg·kg -1 group were lower than that in the control group (P <0.05 ). CONCLUSION Lead exposure did disrupt the permeability,transportation and secretion function of BCB.Our data suggest that BCB dysfunction might be involved in the mechanis m of lead induced neurotoxicity.

Objective:To retrospectively evaluate the prognostic risk factors of T1-2 stage breast cancer patients with one to three positive node(s) and their effects on the benefits of post-mastectomy radiation therapy (PMRT). Methods:We retrospectively analyzed 457 breast cancer patients with T1-2 stage and one to three positive axillary lymph nodes treated in our hospital between 2000 and 2002. The independent prognostic factors of the patients were calculated by the Cox proportional hazards model. The patients were fur-ther classified into high-risk and low-risk subgroups according to the risk factors to explore the benefit of PMRT on the prognosis of dif-ferent subgroups using survival analysis. Results:PMRT was not an independent beneficial factor of overall survival (OS) (HR=0.949;CI:0.435-2.074;P=0.896) or loco-regional recurrent free survival (LRRFS) (HR=0.611;CI:0.231-1.614;P=0.320) in all patients. Ex-tracapsular extension (ECE) and pathological grades were independent prognostic risk factors, and the benefits of PMRT were signifi-cantly different on the prognosis of high-risk subgroup patients (group ECE+OS:P=0.020, LRRFS:P=0.014;group GradeⅢOS:P=0.002, LRRFS:P<0.001). Meanwhile, PMRT failed to prolong the OS and LRRFS of low-risk subgroup patients (group ECE+OS:P=0.353, LRRFS:P=0.796;group GradeⅠtoⅡOS:P=0.267, LRRFS:P=0.589). Conclusion:ECE and gradeⅢwere the independent risk factors of death and loco-regional recurrence in the T1-2 breast cancer patients with one to three positive lymph node(s). PMRT was an effective adjuvant therapy to improve the prognosis of patients with high-risk factors. However, the benefit of PMRT had no sig-nificance in patients with ECE-or gradeⅠ-Ⅱ.