Antineoplastic Agents, Phytogenic ; therapeutic use ; Camptothecin ; analogs & derivatives ; therapeutic use ; Humans ; Neoadjuvant Therapy ; Neoplasm Staging ; Rectal Neoplasms ; drug therapy ; pathology ; Remission Induction

Animals ; Environment ; Female ; Male ; Maze Learning ; physiology ; Memory ; physiology ; Microarray Analysis ; Rats ; Rats, Sprague-Dawley ; Weaning

Objective To review our clinical experiences in the treatment of big area burn accompanying in-halation injury to explore the optimal preventive measures and therapy. Methods To analyze the clinical cases con-ducted of 20 such admitted the big area burn aeeornpanying inhalation injury from 2004 to 2007. Results 18 patients (90%) were cured and 2 patients(2%) died. Conclusion The curative rate of big area burn accompanied by inha-lation injury can be enhanced by combining various treatments,including early treat,early presentive tracheotomy,ap-propriate tracheobronchial lavage,and clear traeheoobronchial secretion.

Adult ; Axilla ; Breast Neoplasms ; pathology ; surgery ; Carcinoma, Ductal, Breast ; pathology ; secondary ; surgery ; Carcinoma, Intraductal, Noninfiltrating ; pathology ; secondary ; surgery ; False Negative Reactions ; Female ; Humans ; Lymph Node Excision ; Lymph Nodes ; pathology ; surgery ; Lymphatic Metastasis ; Mastectomy ; methods ; Reproducibility of Results ; Sentinel Lymph Node Biopsy ; methods ; Technetium Tc 99m Sulfur Colloid

BacKground:Fanconi anemia( FA)pathway as a DNA crossIink damage repair pathway pIays an important roIe in maintaining genome stabiIity. In recent years,FA pathway was wideIy studied in DNA damage and cancer pathogenesis. Aims:To investigate the interaction between RAD18 and FANCD2 protein in human coIorectaI cancer ceII Iine SW480. Methods:Antigen-antibody compIex was co-precipitated by immunoprecipitation. Expressions of rabbit anti-human FANCD2 and RAD18 protein in antigen-antibody compIexes were detected by Western bIotting. The pIasmids of GST-RAD18 and GST were transferred into BL21 ceIIs and induced to express the target proteins. TotaI proteins of the ceII was extracted and GST-beads were used to conjugate the GST-RAD18 protein,and then incubated with the SW480 ceII Iysates, and Western bIotting was performed with the addition of rabbit anti-human FANCD2 antibodies. Results:RAD18 protein was detected in the antigen-antibody compIex from immunoprecipitation by using anti-FANCD2 antibody,and FANCD2 protein was detected by using anti-RAD18 antibody. FANCD2 protein was aIso detected by using anti-GST-RAD18 antibody. GST-RAD18 protein used as bait protein couId capture the FANCD2 protein in SW480 ceIIs. Conclusions:There is an interaction between RAD18 and FANCD2 protein in SW480 ceIIs,and aIso an interaction between GST-RAD18 and FANCD2 protein.

Objective To study helper T lymphocyte cell(Th)1/Th2 imbalance in rats′ model of asthma and the modulation of lentinan(LNT) on the airway inflammation and Th1/Th2 imbalance.Methods Thirty male SD rats were randomly divided into control,asthma and LNT groups.In the experiment,the rat model of asthma was established by the ovalbumin(OVA) challenge methods.Eosinophils(Eos) number and differentiated cell number in bronchoalveolar lavage fluid(BALF) were counted by different count fluids.The levels of IL-4 and IFN-? in BALF were measured by sandwich enzyme linked immunosorbent assay(ELISA).Results 1.The Eos count in BALF and the ratio of eosinophils to the total cell number(Eos%) of asthma group were significantly higher than those of the control group(t=21.94,12.81 Pa

Objective To investigate the protective effects of hyperbaric oxygen(HBO)against brain dam- age from hypoxic ischemia(HIBD)in neonatal rats.Methods One hundred and seventeen 7-day-old Sprague- Dawley rats were randomly divided into 4 groups:a control group(n=32),a hypoxic ischemia brain damage group (HIBD group,n=30),a hyperbaric air group(HBA group,n=27),and a hyperbaric oxygen group(HBO group, n=28).The HIBD model was established by permanent occlusion of the left common carotid artery followed by expo- sure to a mixture of 8% oxygen/92% nitrogen for 2 h(at 37℃).HBO therapy was administered to the HBO group after the hypoxia exposure once a day for 7 d,as was HBA therapy to the HBA group.Apoptotic cells in the cortex and hippocampus(A_(CH)cells)were measured using TUNEL at 9 d after birth,and the ratios of left and right cerebral hemisphere weight(R_(L/R))and rate of weight gain(GRW)were recorded 14 d after birth.A radial arm maze acquisi- tion test(RAMAT)was administered at 30 to 35 days.Lastly,the neuron density in the CA_1 subfield of the rats' hip- pocampi(ND_(CAI)was measured with Nissl staining.Results R_(L/R)and GRW in the HIBD group were significantly lower than in the control group(P＜0.01),while R_(L/R)was increased in the HBO and HBA groups,especially in the HBO group(P＜0.01),although there was no significant difference in GRW between the groups.Compared with the control group,A_(CH)cells were increased and ND_(CAI)was decreased in the HIBD group(P＜0.01),while A_(CH)cells were decreased and ND_(CAI)was elevated in the HBO group in comparison with the HIBD group(P＜0.01).There was no change in A_(CH)cells or ND_(CAI)in the HBA group.The RAMAT results for the HIBD group,including the time to find the arms baited with water,average times of working errors and reference memory errors,were significantly high- er than those of the control group,while these values for the HBO group were obviously lower than for the HIBD group,and there was no change for the HBA group(P＞0.05).Conclusion HBO therapy might increase the re- covery of learning and memory function by attenuating HIBD in neonatal rats.

Objective The effect of lead exposure on children is consistently associated with intellectual and other neurologic deficits.However the exact mechanism by which Pb~(2+) exerts toxic effects on developmental central nervous system remains unknown.Our group has found by gene-chip test that the expression of metabotropic glutamate receptor subtype 5 (mGluR5) mRNA was changed by lead exposure.The present study aimed to examine the effects of different level of lead exposure on the expression of mCluR5 in gestation and lactation.Methods Sprague-Dawley rats were exposed to lead acetate during gestation and lactation.Three concentrations of 0.05%,0.2%,and 0.5% lead acetate were applied and considered as low,middle and high exposure group respectively.The Pb levels of blood and hippocampus of pups were analyzed at weaning to evaluate the actual lead content at the end of the exposure.The impact of lead exposure on the expression of mGluR5 mRNA and protein in hippocampal tissue of pups was investigated by quantitative real-time polymerase chain reaction (PCR) and Western blot.The potential role of the expression of mGluR5 mRNA and protein in lead neurotoxicity were discussed.Results The levels of lead in blood and hippocampus from lead-exposed rats were significantly higher than those in the controls and positively related to the degree of lead exposure.The results of real-time PCR and Western blot showed that exposure to lead acetate decreased the expression of mCluR5 mRNA and protein with a dose-dependent manner.Conclusions Hippocampal mGluR5 might be involved in lead-induced neurotoxicity.

AIM: To investigate whether grafting neural stem cells (NSCs) improves the impaired cognitive deficits and spatial recognition after ischemic-hypoxic brain damage (HIBD) in neonatal rats. METHODS: Non-immunosuppressed 7-day-old SD rats were used as research subject and randomly divided into 3 groups: (1) sham group (n=10); (2) HIBD group (n=11); (3) transplant group (n=13). (2) and (3) were anesthetized and subjected to a hypoxic/ischemic injury obtained by combination of left carotid ligation and exposure to 8% oxygen for 2 h. At 3 days post injury, hypoxic-ischemic brain damaged animals were re-anesthetized and randomized to receive stereotactic injection of NSCs prelabeling with BrdU or control media into the hippocampus in the ipsilateral hemisphere. Cognitive (i.e., learning) deficits were assessed at 2 to 4 weeks after transplantation. At the end of the behavioral tests, the animals were killed and evaluated for NSC survival and histopathological analysis. RESULTS: Transplant group showed significantly improved cognitive function in selected tests as compared with HIBD group during the 4-week observation period. They took less time than HIBD group in finding the 3 arms baited with water and had a decreased number of working and reference memory errors in radial maze acquisition tests. Histological analysis showed that transplanted NSCs attenuated CA1 cell loss after HIBD, and NSCs survived for as long as 4 weeks after transplantation and were detected in the hippocampus. CONCLUSION: These data suggest that transplanted NSCs attenuate brain damage and cognitive dysfunction after hypoxic-ischemic brain damage. This approach warrants continued investigation in light of potential therapeutic uses.

AIM: To discuss the mechanism of hyperbaric oxygen(HBO) therapy by assessing the changes of neural stem cells(NSCs),after hypoxic-ischemic brain damage(HIBD) in neonatal rats.METHODS: Seven-day-old SD rat pups were randomly divided into 4 groups: control group(CON,n=16),HIBD group(n=16),hyperbaric air group(HBA,n=16),and HBO group(n=16).The HIBD model was produced by permanent occlusion of left common carotid artery and was exposed to a mixture of 8% oxygen and 92% nitrogen for 2 h(at 37 ℃).HBA and HBO treatment was administered by placing pups in a chamber(2 ATA for 1 h) 1 h after hypoxia exposure and performed once daily for 7 days.BrdU immunohistochemistry was used to assess how the insult had affected NSCs in the SVZ of the lateral ventricle and DG of the hippocampus.The NSCs from the ipsilateral SVZs were isolated at 3 weeks recovery from hypoxia-ischemia(HI).The number of spheres was then counted as an index of the number of NSCs residing within the SVZ.RESULTS: At 3 week survival,the SVZ of HIBD group was smaller and markedly less cellular than control group.BrdU-positive cells were dramatically decreased in the SVZ and DG of the affected hemisphere(P