Objective To study the variation of uterine artery hemodynamics indexes of patients treated with laparoscopic myomectomy during perioperative period.Methods 78 patients with hysteromyoma were selected as research object,and they were divided into the control group(open surgery group) 39 cases and the observation group (laparoscopic surgery group) 39 cases based on the surgery method,then the Vmax,Vmin,PI and RI of all levels uterine artery of two groups before and after the surgery at tenth and thirtieth day were detected and compared.Results The change range of Vmax,Vmin,PI and RI of all levels uterine artery of observation group after the surgery at tenth and thirtieth day were all bigger than those of control group (all P ＜ 0.05),there were all significant differences.Conclusion The change of uterine artery hemodynamics indexes of patients treated with laparoscopic myomectomy during perioperative period is obvious,and it reflects that the stress degree of organism is smaller.

Objective:Clonidine,by activating peripheral?-adrenoceptors,produces transient pressor response after i.v. injection in anesthetized animals.Moxonidine,with at least 40-fold higher affinity to I_1-imidazoline receptors than to?_2-adreno- ceptors,produces also a transient pressor response.This work was designed to investigate whether I_1-imidazoline receptors are involved in this pressor effect of moxonidine.Methods:Female spontaneously hypertensive rats(SHRs,aged 14-16 weeks) were anesthetized with urethane.To observe the transient pressor responses,moxonidine 0.1,0.3,1.0 mg/kg(intravenous, i.v.),2.0?g(intracerebroventricular,i.c.v.)and 1.0,10.0 mg/kg(intragastric,i.g.)were administrated in different groups of rats.To evaluate the roles of?_1-adrenoceptors,?_2-adrenoceptors and I_1-imidazoline receptors in the transient pressor responses to moxonidine,prazosin(10.0?g/kg),yohimbine(2.0 mg/kg),phentolamine(0.2 mg/kg),idazoxan(1.0 mg/kg) or yohimbine+idazoxan(2.0 mg/kg+1.0 mg/kg)were intravenously given to the animals before moxonidine 0.3 mg/kg (i.v.).Results:It was found that i.v.moxonidine produced a greater pressor response than clonidine when producing a similar reduction of blood pressure.This effect of moxonidine was not influenced by prazosin,but was partly inhibited by yohimbine, phentolamine or idazoxan,and completely blocked by the combination of yohimbine and idzaxon.Neither i.c.v.injection nor i.g.administration of moxonidine induced transient pressor responses.Conclusion:The transient pressor response of i.v.mox- onidine is mediated by both peripheral I_1-imidazoline receptors and?_2-adrenoceptors.

Asbestos ; adverse effects ; Humans ; Mesothelioma ; chemically induced ; diagnosis ; Peritoneal Neoplasms ; chemically induced ; diagnosis

Adult ; Bis(Chloromethyl) Ether ; poisoning ; Humans ; Lung Neoplasms ; chemically induced ; Male ; Middle Aged ; Occupational Diseases ; chemically induced

Objective To study the antagonistic effects of selenium and germanium (Se-Ge) in combination on the kidney damage induced by fluoride in rats.Methods Fifty SD rats were randomly divided into 5 groups,the control group (distilled water),fluoride group (NaF,100 mg/L),fluoride plus selenium group (100 mg/L NaF + 20 mg/L Na2SeO3),fluoride plus germanium group(100 mg/L NaF + 2 000 mg/L Ge-132) and fluoride plus selenium and germanium group(100 mg/L NaF+ 20 mg/L Na2SeO3+ 2 000 mg/L Ge-132),10 in each group (males and females were in the same number).The administration was conducted through gavage for 90 days.After 90 days of treatment,the kidneys were collected and the organ coefficients were calculated,MDA contents,SOD and GSH-Px activities in the tissue were determined and the histopathological examination was done.Results Fluoride decreased the organ coefficient of kidney,Se and/or Ge showed an obvious antagonism to fluoride,administration in combination was more efficient than singly.Na2SeO3 and/or Ge-132 had an antagonistic effect to fluoride in the increase of lipid peroxide(MDA) and decrease of the activity of glutathione peroxidase(GSH-Px),superoxide dismutase(SOD).Na2SeO3 and/or Ge132 could prevent the pathologic damage caused by fluoride in the kidneys.Conclusion Na2SeO3 and Ge-132 in combination has an obvious antagonistic effect on fluoride-induced kidney damage.

BACKGROUND: MyoD gene is one of family members of muscle transcription factors. Transfection MyoD gene can switch on the procedure of differentiation of muscles, and transit non-muscle cells into muscle cells.The MyoD gene only expresses in skeletal muscles. Based on the same contractive structure in myocardial cells and skeletal muscle cells, it is imagined that the conversion from exogenous MyoD gene-induced fibroblast in local myocardium into skeletal muscle cells that had contractive function may become another method in the treatment of congestive heart failure on clinic.OBJECTIVE: To construct and identify a recombinant adenoviral vector carrying MyoD gene for further studies on the recovery function of MyoD gene in myocardial injury.DESIGN: Single sample experiment.SETTING: Department of Cardiology, First Affiliated Hospital, Nanjing Medical University.MATERIALS: The experiment was conducted at the Laboratory of Microbiology and Immunology, Nanjing Medical University between September 2004 and September 2005. MyoD gene and non-replicating form expressive vector of adenovirus were taken as research materials.METHODS: MyoD cDNA fragments were extracted from plasmids pEMSV-MyoD with polymerase chain reaction (PCR), and PCR was used to clone the whole-length gene of MyoD. After adding CACC sequence at 5' end, MyoD gene was cloned by orient topology into transfer ventor, pENTR/D-TOPO. Objective gene was transferred into adenoviral expression vector DNA via pENTR/D-TOPO vector. The recombinant adenoviral vectors transfected into HEK293A cells by using lipofectamine were packaged and amplified.MAIN OUTCOME MEASURES: Evaluation of PCR and DNA sequencing were used for confirming the size of segment and correctness of rank of MyoD cDNA and detecting the titre of virus.RESULTS: MyoD recombinant adenovirus contained target segment with precise length confirmed by PCR and DNA sequence that was correct. The titre of virus was 1.3×1011 pfu/mL.CONCLUSION: The recombinant adenoviral vector carrying MyoD gene is constructed successfully.

Objective To investigate the pulmonary microvascular responsiveness of diabetic animals to sepsis and the potential mechanism of NO system.Methods Sixty-four Wistar rats of clean grade were randomly (random number) divided into 4 groups,namely normal control group (group A,n =16),diabetes group (group B,n =16),sepsis group (group C,n =16),diabetes and sepsis group (group D,n =16).Diabetic mellitus model was made in rats with injection of streptozotocin,STZ (65 mg/kg).Successful model was defined as the blood glucose value≥ 16.67 mmol/L 48 hours after injection of STZ.All animals were fed 4 weeks before initiation of next experiment.The sepsis model was established by intravenous injection of LPS (10 mg/kg) in rats.RT-PCR was used to determine the mRNA expression of Tie-2 in rats'blood.The ratio of dry/wet of lung tissue and the extravasation of Evans blue dye into the lung were detected.Quantitation of NO in lung tissue and serum was measured by using Griess method.RT-PCR was also used for determination of iNOS,eNOS,DDAH2 mRNA expressions in lung tissue.Data were analyzed with ANONA and LSD method for comparison between groups,and P ＜ 0.05 was considered statistically significant.Results Compared with septic group.,the diabetic rats with sepsis group demonstrated higher expression of Tie-2 mRNA in blood (19.72 ± 0.70) vs.(3.99 ± 0.92),P =0.00,lower ratio of dry/wet in lung tissue (0.19 ±0.01) vs.(0.22 ±0.01),P =0.000,higher permeability of Evans blue dye into lung tissue (3.76 ± 0.77) vs.(1.74 ± 0.24),P =0.000.Serum NO level was lower in group D than that in group C (123.13 ±4.24) vs.(188.30 ±5.18),P =0.000,however,NO levels in lung tissue of both group D and group C were higher than that in control group (53.62 ± 6.70),(23.63± 3.92) vs.(10.37 ± 1.29),P =0.00,and NO level in group D was higher in 2 times than that in group C (P =0.00).However,there were no differences in eNOS expression among groups A,B and C,but the difference in eNOS expression was present between group D with lower expression and group A,that lower in group D (0.07 ±0.02) vs.(0.38 ±0.05),P=0.017.Compared with group C,the expression of iNOS was higher in group D (80.23 ±2.49),(32.48±5.37) vs.(1.74±0.23),P=0.00),and the expression of DDAH2 was lower in group D (0.49 ±0.13),(7.26 ±0.50) vs.(11.96 ±0.55).Conclusions Diabetic rats with sepsis enhanced endothelial cell damages.Diabetes deteriorates the regulatory activity of NO system,suggesting the potential mechanism of the worsened damages of EC in diabetic sepsis host.

Objective This study was designed to explore the influence about apoptosis of STI571 on NB4.Methods After NB4 cells were treated with STI571 in different concentration(0.5,1.0,5.0umol/L)at indicated time(24h,48h,72h)(1)morphological observation:To determine cell morphology by light microscope.(2)MTT assay:Inhibition of proliferation was measured with a colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-dipheny tetrazolium bromide(MYa3 assay.(3)Flow cytometric analysis:The expression of survivin and smac were measured on NB4 by FCM.Results Morphological observation showed characteristic apoptosis changes.MTT assay showed that STI at (0.5,1.0,5.0 μmol/L) range for 24 h,48 h and 72 h can markedly inhibit the proliferation of NB4 cells in a dose-dependent manner as well as a time-dependent manner(P＜0.05).FCM showed the expression of survivin decrease and smac increase.Conclusion STI571 In Vitro inhibits proliferation of NB4.

Soft-tissue deformation is one of the important research directions in virtual surgery. Mass-spring model and finite-element model are the two most important modeling technology of the soft tissue modeling. It is very important for the current soft-tissue deformation modelling to analysize, to summarize the main idea, the influence factors and the modeling route of the two kinds of modeling methods and then to give comprehensive review.
Computer Simulation ; Humans ; Models, Biological ; Surgery, Computer-Assisted ; methods ; User-Computer Interface

Objective To explore molecular mechanisms of apoptosis induced by STI571 in human acute promyelocytie 1eukemia cell lines NB4.nethods The expression of Annexin-V,Fas,Caspase-3 and bcl-2 in NB4 cells were detected by FCM after the treatment of STI571 at(0.5,1.0,5.0 μmol/L)ranging for 24 h,48 h and 72 h.Results With the increasing dose of STI571,the expression of bcl-2,Caspase-3,Annexin-V,Fas in NB4 changed from(10.22±0.62)declining to (5.82±0.52),from(42.21±1.02)ascending to(52.35±0.83),from(25.A2±1.21)ascending to(37.84±0.63),from(18.21±0.81)to(21.41±1.02)respectively.With the dealing time increasing(24,48,72 h),the expression of bcl-2,Caspase-3,Annexin-V,Fas in NB4,changed from (5.81±0.52)declining to(2.51±0.43),from(52.31±0.83)ascending to(69.51±1.12),from(37.81±0.93)ascending to(78.62±0.83),from(23.41±0.73)to(26.53±1.02)respectively.Conclusion STI571 can enhance the apoptosis program to Ni4 in a time-dependence and dose-dependence manner,but no change to Fas was observed.