Original Article
A Selective Cyclooxygenase-2
Inhibitor Prevents Inflammation-
related Squamous Cell Carcinogenesis
of the Forestomach Via Duodenogastric Reflux in Rats
Masaru Oba,MD,PhD1,Koichi Miwa,MD,PhD1,T akashi Fujimura,MD,PhD1,Shinichi Harada,PhD2,
Shozo Sasaki,MD,PhD1,Katsunobu Oyama,MD,PhD1,T etsuo Ohta,MD,PhD1,and
T akanori Hattori,MD,PhD3
BACKGROUND:Duodenal reflux causes inflammation-related squamous cell carcinogenesis in the forestom-ach of rats without any carcinogens.The aim of this study was to investigate the efficacy of a selective cyclo-oxygenase(COX)-2inhibitor,meloxicam,in preventing this carcinogenesis.METHODS:A series of188rats underwent a surgical duodenogastric reflux procedure and were divided into2groups.One group was given commercial chow(control group),and the other was given experimental chow containing meloxicam(0.3 mg/kg body weight/day)(meloxicam group).The animals were sequentially sacrificed at Weeks20,30,40, 50,and60after surgery.The forestomach was examined for the presence of carcinoma,the incidence of reflux-related morphological changes,COX-2expression,and its activity.RESULTS:At Week60,squamous cell carcinoma developed in8of21animals(38%)in the control group,but none of20(0%)in the meloxicam group(P<.05).In addition,basal cell dysplasia developed in19of21(90%)animals in the control group,but only4of20(20%)in the meloxicam group(P<.01).COX-2immunoreactivity was predominantly detected in macrophages in the epithelial https://www.doczj.com/doc/b91257358.html,pared with nonsurgical rats,RNA expression of COX-2in the ep-ithelium was up-regulated,reaching peak at an early stage of Week20in both groups(P<.005).The expression of microsomal prostaglandin E synthase-1was lower in the meloxicam group than in the control group.PGE2production was significantly suppressed throughout the experiment in the meloxicam group compared with the control group(P<.005).CONCLUSIONS:Meloxicam was effective in preventing reflux-induced squamous cell carcinogenesis via an inflamed squamous epithelium.Cancer2009;115:454--64.
V C2009American Cancer Society.
KEY WORDS:duodenogastric reflux,COX-2,forestomach,squamous carcinogenesis,chemoprevention.
Duodenogastric reflux(DGR)most commonly occurs after stomach surgery(eg,gastrectomy,pylo-roplasty,gastrojejunostomy),but it is also a physiologic event in some people who have not been surgically
Corresponding author:Takashi Fujimura,MD,PhD,Gastroenterological Surgery,Department of Oncology,Division of Cancer Medicine, Graduate School of Medical Science,Kanazawa University,13-1Takara-machi,Kanazawa920-8641,Japan;tphuji@surg2.m.kanazawa-u.ac.jp 1Gastroenterological Surgery,Department of Oncology,Division of Cancer Medicine,Graduate School of Medical Science,Kanazawa University,Kanazawa,Ja-pan;2Center for Biomedical Research and Education,Graduate School of Medical Science,Kanazawa University,Kanazawa,Japan;3Department of Pathology, Shiga University of Medical Science,Ohtsu,Japan
Received:May13,2008;Revised:July25,2008;Accepted:July29,2008
Published online:December28,2008,V C2008American Cancer Society
DOI:10.1002/cncr.23990,https://www.doczj.com/doc/b91257358.html,
treated.Chronic reflux of duodenal contents into the fore-gut lumen is thought to be directly linked with pathoge-nesis,such as some gastric lesions,Barrett esophagus,and esophageal adenocarcinoma(ADC).1Conversely,esopha-geal squamous cell carcinoma(SCC)has a multifactorial etiology involving several environmental,dietary,and other genetic factors.Although reflux symptoms are not associated as a risk for esophageal SCC,in contrast to esophageal ADC,2great interest has focused on chronic acid and alkaline reflux as another factor associated with an increased risk for laryngeal SCC through inflamma-tion.3,4It is possible that the DGR may reach the proxi-mal segment of the esophagus and then also the larynx. Duodenal reflux containing bile,pancreatic juice,and du-odenal secretions have the potential to initiate foregut car-cinogenesis in experimental models.We previously demonstrated in rats that reflux of duodenal contents causes carcinogenesis in the forestomach and the esopha-gus without any carcinogens.5,6The histological spectrum of these carcinomas includes ADC,SCC,and adenosqua-mous carcinoma.Our experimental results showed a close association between an inflamed squamous epithelium and the genesis of SCC in duodenal reflux models. Inflammation-related squamous cell carcinogenesis in the absence of carcinogens should be investigated and prevented.
Cyclooxygenase(COX)is the rate-limiting enzyme in the conversion of arachidonic acid to intermediate prostaglandin H2(PGH2),and terminal prostaglandin E2 (PGE2)synthase(PGES)catalyzes isomerization of PGH2 to PGE2.COX has2isoforms,of which COX-1is consid-ered a housekeeping gene,whereas COX-2is an induci-ble,immediate-early gene,and its role has been related to inflammation,reproduction,and carcinogenesis.Clinical, genetic,and biochemical evidence has suggested that COX-2and PGE2produced via a COX-2dependent pathway play a crucial role in tumorigenesis.7-13Recently, 3different forms of PGES have been identified:cytosolic PGES(cPGES)and two types of microsomal PGES (mPGES-1and mPGES-2).14-16Among them,mPGES-1has received much attention,as this enzyme is colocal-ized and functionally coupled with COX-2in marked preference to COX-1.
Expression of COX-2is elevated in a variety of human carcinomas,including esophageal or laryngeal SCC,but little is known about possible links between du-odenal reflux-induced squamous cell carcinogenesis and COX-2expression.17-21It also remains unclear exactly how COX-2expression interacts with carcinogenesis through inflammation.To elucidate the role of COX-2in squamous cell carcinogenesis,we performed an operation on rats to make all duodenal contents flow back into the forestomach,an anatomical extension of the esophagus composed of a squamous epithelium that is histologically identical to that of the esophagus.
Epidemiologic studies indicate that chronic intake of traditional nonsteroidal anti-inflammatory drugs (NSAIDs)is associated with reduced risk of malignancies, especially in the digestive tract.22Several COX-2inhibi-tors were reported to suppress the development of gastro-intestinal malignancies,such as Barrett esophageal cancer, gastric cancer,and colorectal cancer,using experimental animals.23Some studies indicate that COX-independent pathways are also important in the cancer preventive properties of NSAIDs or COX-2inhibitors.24,25In this study,we focused on PGE2production via a COX-2 dependent pathway.
The primary aim was to explore how COX-2expres-sion is associated with DGR-induced squamous cell carci-nogenesis.In addition,we assessed the efficacy of a selective COX-2inhibitor,meloxicam,in protecting against carcinogenesis through inflammation in the ab-sence of carcinogens.
MATERIALS AND METHODS
Animals
Eight-week-old male F344rats were purchased from Charles River Japan Inc.(Kanagawa,Japan)and housed3 per cage on wood-chip bedding in our animal center under controlled conditions:23?1 C room tempera-ture,55%?5%humidity,20times/hour air change,and a12-hour light/dark cycle.Standard solid chow(CRF-1; Charles River)and tap water were available ad libitum before and up to1week after surgical intervention.The rats were allowed to acclimatize for2weeks before surgical intervention.A total of200rats were operated on to give a total of188surviving rats that could be randomized1 week postoperatively.An additional10rats were followed without any intervention to obtain normal tissue.Animals Reflux-induced Squamous Carcinogenesis/Oba et al
were not treated with any known carcinogen throughout the experiments.
Surgical Procedures
After fasting for24hours,animals were anesthetized by inhalation with diethyl ether during operation.The rat forestomach carcinogenesis by DGR model established by Miwa et al5was used.Briefly,a midline laparotomy was performed,and the ligament of Treitz was identified.The upper jejunum was transected about3cm anal from its or-igin,and the proximal end was closed with sutures.The cut distal end was connected to the greater curvature of the forestomach by end-to-side anastomosis.All duodenal contents flowed back into the forestomach through the pylorus.The rats were given water and commercial chow in the24hours after surgery.All procedures used in this experiment were conducted in accordance with Kanazawa University Graduate School of Medical Science’s Guide-lines for the Care and Use of Research Animals.
Study Design and Drug Administration
A series of188rats were randomized into2groups1week postoperatively.The control group(n?99)was given commercial rat chow(CRF-1).The meloxicam group (n?89)was given experimental rat chow premixed with meloxicam(0.3mg/kg body weight[bw]/day).Meloxicam was obtained from Boehringer Ingelheim GmbH(Ingel-heim,Germany).An additional10rats were followed without any intervention and were kept on regular rat chow to obtain normal tissue.The rats were examined daily for the duration of this study.Rats were weighed pre-operatively,every4weeks postoperatively,and just before sacrifice.Rats in each group were sacrificed at Weeks20, 30,40,50,and60postoperatively to evaluate the end-points,as outlined in the Statistical Analysis section.Dos-age selection of the selective COX-2inhibitor,meloxicam, was based on in vivo studies performed in rats to evaluate the safety risk in therapeutic use in human medicine.In a chronic toxicity study with oral administration over a pe-riod of12months in rats,adverse side effects and organ-damaging effects were not found at a dose of less than0.8 mg/kg bw.26In the present study,a daily dose of0.3mg/ kg bw of meloxicam was administered to rats as a chemo-preventive agent with adequate safety.Tissue Preparation
The entire stomach was resected along with the esopha-gus,duodenum,and anastomosed portion of the jejunum,and opened along the greater curvature longitu-dinally.Representative forestomach tissues included abnormal lesions that were immediately stored in RNA-later Reagent(Ambion,Austin,Tex)below room temper-ature for analysis of COX-2and mPGES-1mRNA expression.To analyze PGE2production,the tissue sam-ples were snap-frozen and stored atà80 C.As a normal control,rats without surgical intervention in Week60 were used.In a comparison of the rats treated with or without meloxicam,the samples of7randomly selected rats from each group in Weeks20,30,40,50,and60after the operation were used.The remaining forestomach was fixed in10%buffered formalin for24hours and then cut into stepwise longitudinal strips2mm wide along the lesser curvature at nonanastomosed regions and perpen-dicular to the anastomotic line at anastomosed regions. The tissues were embedded in paraffin and sectioned into serial4-l m slices for hematoxylin and eosin staining and immunohistochemistry.
Histopathological Criteria
The pathological changes in the forestomach were catego-rized into the following3lesions.
Basal cell hyperplasia(BCH):The basal layer in the squamous epithelium simply thickens and occupies >15%of the epithelial layer(Fig.1a).
Basal cell dysplasia(DYS):The epithelial layer is composed of dysplastic squamous cells that have large and polymorphic nuclei,deeply stained chromatin,and increased numbers of mitotic figures.Squamous dysplasia may involve the lamina propria of the epithelium,but does not invade the submucosal layer(Fig.1b).
SCC:Carcinoma is defined as an epithelial growth with cellular and structural atypism,invading into the submucosal layer(Fig.1c).
Immunohistochemical Analysis
Localization of COX-2protein was determined by immu-nohistochemical staining using specific antibodies.The DAKO EnVision system(Dako Cytomation Japan Co. Ltd.,Kyoto,Japan)was used with autoclave acceleration. After blocking of endogenous peroxidase,deparaffinized
Original Article
sections covered with a protein block and serum-free (Dako)were incubated overnight at 4 C with individual primary antibodies:antimouse COX-2(1:50,mouse monoclonal;BD Transduction Laboratories,San Jose,Calif).Sections were treated with a secondary biotinylated antibody (Dako).3,30-diaminobenzidine tetrahydro-chloride was used as the chromogen,and the sections were counterstained with hematoxylin.
Expression Assay of COX-2,mPGES-1mRNA by Semiquantitative Reverse
Transcriptase-Polymerase Chain Reaction The tissue samples were soaked into RNA later Reagent and stored at à80 C.RNA later maintains high RNA mo-lecular integrity in long-term storage once the tissue has been suspended in it.27,28Purification of total RNA from the stabilized tissue was subsequently carried out using an RNeasy Mini Kit (QIAGEN,Chatsworth,Calif),follow-ing the protocol for isolation of total RNA from animal tissues.Methods of disruption and homogenization using the Mixer Mill MM 300(QIAGEN)are given.Ethanol was then added to the lysate,creating conditions that pro-moted selective binding of RNA to the RNeasy silica-gel membrane.The sample was then applied to the RNeasy mini column.Total RNA bound to the membrane,and contaminants were efficiently washed away.Total RNA was eluted with RNase-free water.In addition,to remove the residual genomic DNA,all isolated RNA was treated with an RNase-Free DNase Set (QIAGEN),as described in the manufacturer’s instructions.Reverse transcription (RT)of RNA (1l g)was performed using TaqMan reverse transcription reagents (Applied Biosystems,Foster City,Calif).The reaction was performed in the presence of a 1?RT buffer,5.5mM MgCl 2,500l M each 20deoxynucleoside-S 0triphosphate mixture,2.5l M ran-dom hexamers,and 0.4U/l L RNase inhibitor.Then,1.25U/l L MultiScribe Reverse Transcriptase (Applied Biosystems)was prepared and a first strand cDNA was synthesized using an ABI 9700(Applied Biosystems)ther-mal cycler.Thermal cycling conditions were made up of a primer incubation step (25 C for 10minutes),an RT step (48 C for 30minutes),and reverse transcriptase inactiva-tion (95 C for 5minutes).Polymerase chain reaction (PCR)primers and TaqMan MGB hydrolysis probes for COX-2and mPGES-1genes,except glyceraldehyde-3-phosphate dehydrogenase (GAPDH),used the same sequences as described previously.29The primer and probe sequences of the specific genes for real-time quanti-tative PCR were as follows.COX-2gene:forward primer,50-CATGATCTACCCTCCCCACG-30;reverse
primer,
FIGURE 1.Histological findings in the forestomach resulting from duodenogastric reflux are shown:(a)basal cell hyper-plasia (H &E;original magnification,?40);(b)basal cell dys-plasia (H &E;original magnification,?40);(c)squamous cell carcinoma (SCC;H &E;original magnification,?100).SCC observed here are foci of the poorly differentiated type.
Reflux-induced Squamous Carcinogenesis/Oba et al
50-CAGACCAAAGACTTCCTGCCC-30;probe,50-CCT GAGCACCTGCGGTTCGCTG-30;and mPGES-1gene:forward primer,50-GCGAACTGGGC CAGAA CA-30;reverse primer,50-GGCCTACCTGGG CAAAA TG-30;probe,50-CCCCGGAGCGAATGCG TGG-30.Predeveloped rodent GAPDH primers and probe sets were purchased from Applied Biosystems.All TaqMan MGB hydrolysis probes except the GAPDH probe con-sisted of a gene-specific oligonucleotide dually labeled with a6-FAM reporter dye at the50end and a tetramethyl-6-car-boxyrhodamine(TAMRA)quencher dye at the30end.The rodent GAPDH probe was labeled with VIC reporter dye at the50end and a TAMRA quencher dye at the30end.Real time PCR was performed on an ABI PRISM7700 Sequence Detection System(Applied Biosystems).Each PCR was performed in a total volume of25l L,containing 2l L cDNA,1?TaqMan Universal PCR Master Mix (Applied Biosystems),200nM forward and reverse primers, 100nM TaqMan MGB probe,and nuclease-free water to complete.The thermal cycling conditions were as follows: 50 C for2minutes and95 C for10minutes,followed by 40cycles at95 C for15seconds and60 C for1minute. The quantification of the real-time PCR results was per-formed as described in User Bulletin#2of the ABI PRISM 7700Sequence Detection System(Applied Biosystems) using the Comparative C T Method.
Measurement of PGE2Production
Each tissue sample frozen atà80 C was weighed and ho-mogenized using a Polytron homogenizer PT-MR2100 (Kinematica AG,Littau,Switzerland)in0.5mL of ho-mogenization buffer(0.1M phosphate,pH7.4,contain-ing1mM ethylenediamine tetraacetic acid and10l M indomethacin)to100mg tissue.Then,2volumes of ace-tone were added to the samples and vigorously spun.The samples were incubated at room temperature for5 minutes,and centrifuged at1500g for10minutes to remove precipitated proteins.The supernatant was trans-ferred into a clean tube,and dried to remove the acetone using a gentle stream of nitrogen.One mL of1.0M ace-tate buffer,pH7.4,was added to dissolve samples,and immediately affinity purified with an SPE cartridge(Cay-man Chemical,Ann Arbor,Mich).The samples were assayed using a PGE2EIA kit(Cayman Chemical),according to the manufacturer’s instructions.PGE2levels were shown as pg/mg of tissue.
Statistical Analysis
Rat weights and serious complications,including death, were recorded.Fisher exact test was used for statistical analy-sis of the incidence of histopathological changes.COX-2 and mPGES-1mRNA expression and PGE2levels were expressed as mean?standard deviation.Mann-Whitney U test was used to compare between each group(eg,nonsurgi-cal intervention group and surgical intervention group,con-trol group and meloxicam group).Data management and statistical analysis were performed using Stat View5.0soft-ware(SAS Institute Inc.,Cary,NC).Differences were con-sidered significant when the P value was<.05. RESULTS
General Observations
Of200rats,12died due to the surgery itself within1 week,and an additional36rats(24in the control group and12in the meloxicam group)died of complications such as reflux esophagitis in23,gastric stasis in7,and unknown causes in6.Thus,the effective number of exam-ined animals was75in the control group and77in the meloxicam group.There was no significant difference in postoperative weight gain or mortality between the2 groups.
Macroscopic Findings
In Week60,the squamous epithelium of the forestomach showed gyrus-like mucosal thickening and nodular lesions in the control group,whereas that of the meloxicam group showed a smooth and glistening surface without thicken-ing(Fig.2).
Histopathological Changes
The incidence of histopathological changes in the forest-omach is summarized in the Table1.DGR-associated morphologic changes were markedly reduced by meloxi-cam treatment,as shown in Figure3.
Original Article
SCC
SCC developed in the control group at Weeks 40,50,and 60.The incidence was 15%,25%,and 38%,respectively,whereas no SCC was observed in the meloxicam group.The incidence of SCC at Week 60between the 2groups was significantly different (P <.05).The development of SCC was inhibited by meloxicam treatment.DYS
DYS was observed from Week 20and sequentially increased to 90%at Week 60in the control group.In the meloxicam group,the incidence of DYS was lower than in the control group at any point and statistically lower at Weeks 50and 60(P <
.01).
FIGURE 2.Macroscopic appearance of the entire stomach in a control rat (a),is compared with that in a meloxicam-treated rat (b).Rats were autopsied 60weeks after the operation.
Table 1.Incidence of Pathological Findings in the Forestomach
Postoperative Weeks Group No.
Incidence (%)
BCH
DYS
SCC
20Control 1010(100)5(50)0(0)Meloxicam 107(70)2(40)0(0)30Control 1515(100)8(53)0(0)Meloxicam 2012(60)*5(40)0(0)40Control 1313(100)9(70)2(15)Meloxicam 137(54)*4(31)0(0)50Control 1616(100)13(81)4(25)Meloxicam 147(50)*4(29)y 0(0)60
Control 2121(100)19(90)8(38)Meloxicam 207(35)*
4(20)y
0(0)z
Data show number of rats with percentages in parentheses.Statistical significance was assessed by Fisher exact test.BCH indicates basal cell hyperplasia;DYS,basal cell dysplasia;SCC,squamous cell carcinoma.*P <.05for BCH in meloxicam-treated rats versus in control rats.y P <.01for DYS in meloxicam-treated rats versus in control rats.z P <.05for SCC in meloxicam-treated rats versus in control rats.
Reflux-induced Squamous Carcinogenesis/Oba et al
FIGURE 3.Histopathological findings at the junction of the forestomach-glandular stomach are shown.(a)Duodenogastric reflux-induced morphologic changes were observed in control rats (H &E;original magnification,?20).(b)Chemopreventive effi-cacy of meloxicam against the histological changes 60weeks after the operation is shown (H &E;original magnification,?20).
Original Article
BCH
The incidence of BCH between the 2groups was signifi-cantly different at Weeks 30,40,50,and 60(P <.05)Localization of COX-2Protein
Every animal that suffered from DGR demonstrated COX-2protein expression in the forestomach.Immunor-eactivity for COX-2was predominantly detected in infil-trating mononuclear cells such as macrophages and fibroblasts in the mucosal stroma (Fig.4).However,the neoplastic cells seen in the experiment were negative for COX-2protein.
RNA Expression of COX-2and mPGES-1The COX-2mRNA level of the DGR mucosa was more significantly up-regulated compared with that in the intact mucosa without surgical intervention (P <.005).The COX-2mRNA expression in both groups increased,peak-ing at an early stage of Week 20.There was no effect on the induction of mRNA level because of meloxicam treatment (Fig.5a).The expression of mPGES-1mRNA was posi-tively correlated with that of COX-2mRNA in the control group.In the meloxicam group,the level of mPGES-1decreased during the course of the study and was signifi-cantly suppressed compared with that in the control group in the early phase of Week 20(P <.01)(Fig.5b).Induction of PGE 2Production
The PGE 2production in the DGR mucosa was markedly increased in the control animals compared with the nonsur-gical rats (P <.005).The levels of PGE 2in the meloxicam group were significantly lower than those in the control group throughout the experiment (P <.005)(Fig.5c).
DISCUSSION
The present study has confirmed the conclusion previ-ously reported that prolonged exposure to duodenal reflux contents induced SCC surrounded by an inflamed squa-mous epithelium with features of basal cell hyperplasia and regenerative thickening in the forestomach and esophagus of rats.5,6Repeated mucosal damage because of DGR finally induces SCC,which follows a process of ini-tial BCH and subsequent DYS.In this study,duodenal regurgitation into the forestomach was not involved in the genesis of the columnar-lined epithelium (CLE)or ADC,in contrast to the pathogenesis in
several
FIGURE 4.Immunohistochemical staining is shown for cyclooxygenase (COX-2)in the forestomach (original magnification,?100).COX-2protein was predominantly detected in the inflammatory mononuclear cells,such as macrophages and myofibro-blasts,in the mucosal stroma.
Reflux-induced Squamous Carcinogenesis/Oba et al
duodenoesophageal reflux models.6,30,31Miwa et al sug-gested that the incidence of CLE might be dependent on the amounts of duodenal contents into the esophagus.By using gastroduodenoesophageal reflux models,ADC within CLE always occurred in the lower esophagus near the anastomotic line,where more is regurgitated,and SCC surrounded by chronic squamous esophagitis was observed distant from the site of anastomosis.6Barrett esophagus appeared to arise in the regenerative process in response to severely chronic inflammation through exces-sive reflux.In this study,the large capacity of the forest-omach and the buffer effect of gastric juice in the presence of the glandular stomach may have decreased the degree of reflux injury to the squamous epithelium.Although it is widely accepted in humans that duodenal contents re-gurgitation is closely linked to Barrett esophagus and to the development of esophageal ADC,esophageal SCC is not reported to be related to reflux,but is strongly associ-ated with tobacco smoking and alcohol consumption.Gastroesophageal reflux does not appear to be an inde-pendent risk factor for esophageal SCC,but may enhance the acknowledged risk factors such as tobacco smoking and alcohol consumption,which have a refluxogenic effect due to upper and/or lower esophageal sphincter relaxation and esophageal peristalsis dysfunction.
With regard to forestomach carcinogenesis in rats,SCC has been induced by N -nitroso compounds that are well known as genotoxic carcinogens such as N -methyl-N 0-nitrosoguanidine and N -methylnitrosourethane.32Recently,Kodama et al reported induction of SCC in dia-betic rats after a single intravascular dose of the nongeno-toxic chemical,alloxan.33Our established DGR rat model is more physiologic,without any known carcino-gen exposure,and the pathogenesis of prolonged DGR closely resembles human reflux diseases.
COX-2is well established as playing an important role in the tumorigenesis of a variety of human carcino-mas and their precursor lesions,and specific inhibition of COX-2activity suppresses tumor growth in several ani-mal models of foregut carcinogenesis.30,31,34,35However,no study has been published to report on possible links between reflux-induced squamous cell carcinogenesis and COX-2expression.Moreover,there has been no report regarding the preventative effect of selective COX-2inhibitors on the development of experimental squamous cell carcinogenesis.The present study demonstrated
that
FIGURE 5.mRNA levels of (Top )cyclooxygenase (COX)-2and (Middle )microsomal prostaglandin E 2(PGE 2)synthase (mPGES)-1were measured by semiquantitative reverse tran-scriptase-polymerase chain reaction in the forestomach mu-cosa.Relative quantity levels in control rats compared with those in meloxicam-treated rats are presented as the mean ?standard deviation (SD).*P <.005versus nonsurgical rats;**P <.01between the 2groups (Mann-Whitney U test).(Bottom )PGE 2induction because of duodenogastric reflux in the forestomach mucosa and the effect of meloxicam are shown.PGE 2levels in control rats compared with those in meloxicam-treated rats are presented as the mean ?SD.*P <.005versus nonsurgical rats;**P <.005between the 2groups (Mann-Whitney U test).W indicates weeks.
Original Article
DGR induced a BCH-DYS-SCC sequence in the forest-omach through inflammation.At Week60,we encoun-tered DYS in90%and SCC in38%of the control group, but in20%and0%,respectively,of the meloxicam group. Immunoreactivity for COX-2protein was predominantly positive for macrophages and fibroblasts in the mucosal stroma,but was negative for neoplastic epithelial cells in the animal study.It is possible that stromal mononuclear cells such as macrophages play a key role in inflammation-related squamous cell carcinogenesis associated with COX-2expression.
Through these sequential events in our experi-ment,COX-2was up-regulated,accompanied by PGE2 production at an early phase.Some investigators also suggested that COX-2may be involved in the early stage of squamous cell carcinogenesis of the esophagus.21,36 In addition,the COX-2/mPGES-1pathway seemed to have a strong involvement with the carcinogenesis because of duodenal reflux.Jang et al demonstrated that mRNA levels of COX-2and mPGES-1are highly increased in esophageal squamous cell dysplasia and Barrett metaplasia induced by duodenal reflux contents in rat.37The formation of DYS or CLE is regarded as an early stage in carcinogenesis and is an irreversible change.31,38The persistent inflammation because of du-odenal reflux may promote the process from DYS to SCC or CLE to ADC.Therefore,earlier administration of a selective COX-2inhibitor could be more effective in preventing this carcinogenesis.
In addition to being COX-dependent targets against carcinogenesis,COX-2inhibitors appear to have their own,more or less specific,COX-independent anticarci-nogenic mechanisms.Many studies have shown that cele-coxib exerts its anticarcinogenic effects in various cancer cell lines by central inhibition of phosphoinositide-dependent kinase1and its downstream substrate protein kinase B,leading to the inhibition of cell cycle progression and induction of apoptosis.25Recently,Liu et al demon-strated in esophageal SCC in in vivo studies that meloxi-cam induced apoptosis through the mechanisms of inhibiting the pathway of nuclear factor-kappaB down-stream regulation of COX-2.39In this study,we focused on PGE2via the COX-2/mPGES-1-dependent pathway as the agent against carcinogenesis.The finding that meloxicam suppressed PGE2production suggested che-moprevention against squamous cell carcinogenesis.
In conclusion,a specific COX-2inhibitor,meloxi-cam,significantly reduced a series of inflammatory changes caused by duodenal reflux and inhibited the de-velopment of DYS and SCC.Meloxicam is effective in preventing DGR-induced squamous cell carcinogenesis in the absence of carcinogen exposure.DGR up-regulated mucosal PGE2production,indicating that the COX-2/ mPGES-1pathway contributed to the inflammation-related carcinogenesis in a relatively early event.The DGR animal model is useful to elucidate the importance of enhanced COX-2expression and its activity in the pro-cess of carcinogenesis because of inflammation.A selective COX-2inhibitor could be a chemopreventive agent against squamous cell carcinogenesis.
References
1.Miwa K,Hattori T,Miyazaki I.Duodenogastric reflux and
foregut carcinogenesis.Cancer.1995;75:1426-1432.
https://www.doczj.com/doc/b91257358.html,gergren J,Bergstrom R,Lindgren A,et al.Symptomatic
gastroesophageal reflux as a risk factor for esophageal ade-nocarcinoma.N Engl J Med.1999;340:825-831.
3.Galli J,Cammarota G,Calo L,et al.The role of acid and
alkaline reflux in laryngeal squamous cell https://www.doczj.com/doc/b91257358.html,ryn-goscope.2002;112:1861-1865.
4.Cammarota G,Galli J,Cianci R,et al.Association of
laryngeal cancer with previous gastric resection.Ann Surg.
2004;240:817-824.
5.Miwa K,Segawa M,Takano Y,et al.Induction of oeso-
phageal and forestomach carcinomas in rats by reflux of duodenal contents.Br J Cancer.1994;70:185-189.
6.Miwa K,Sahara H,Segawa M,et al.Reflux of duodenal or
gastro-duodenal contents induces esophageal carcinoma in rats.Int J Cancer.1996;67:269-274.
7.Tsujii M,DuBois RN.Alterations in cellular adhesion and
apoptosis in epithelial cells overexpressing prostaglandin en-doperoxide synthase2.Cell.1995;83:493-501.
8.Oshima M,Dinchuk JE,Kargman SL,et al.Suppression
of intestinal polyposis in Apcá716knockout mice by inhibi-tion of cyclooxygenase2(COX-2).Cell.1996;87:803-809.
9.Williams CS,Mann M,DuBois RN.The role of cyclooxy-
genases in inflammation,cancer,and development.Onco-gene.1999;18:7908-7916.
10.Sheng H,Shao J,Washington MK,et al.Prostaglandin E2
increases growth and motility of colorectal carcinoma cells.
J Biol Chem.2001;276:18075-18081.
11.Pai R,Soreghan B,Szabo IL,et al.Prostaglandin E2trans-
activates EGF receptor:a novel mechanism for promoting colon cancer growth and gastrointestinal hypertrophy.Nat Med.2002;8:289-293.
Reflux-induced Squamous Carcinogenesis/Oba et al
12.Seno H,Oshima M,Ishikawa T,et al.Cyclooxygenase-2
and Prostaglandin E2receptor EP2-dependent angiogenesis in Apcá716mouse intestinal polyps.Cancer Res.2002;62: 506-511.
13.Buchanan FG,Wang D,Bargiacchi F,et al.Prostaglandin
E2regulates cell migration via the intracellular activation of the epidermal growth factor receptor.J Biol Chem.
2003;278:35451-35457.
14.Murakami M,Naraba H,Tanioka T,et al.Regulation of
prostaglandin E2biosynthesis by inducible membrane-associ-ated prostaglandin E2synthase that acts in concert with cyclo-oxygenase-2.J Biol Chem.2000;275:32783-32792.
15.Tanioka T,Nakatani Y,Semmyo N,et al.Molecular identifi-
cation of cytosolic prostaglandin E2synthase that is function-ally coupled with cyclooxygenase-1in immediate prostaglandin E2biosynthesis.J Biol Chem.2000;275:32775-32782.
16.Tanikawa N,Ohmiya Y,Ohkubo H,et al.Identification
and characterization of a novel type of membrane-associated prostaglandin E synthase.Biochem Biophys Res Commun.
2002;291:884-889.
17.Sano H,Kawahito Y,Wilder RL,et al.Expression of cyclo-
genase-1and-2in human colorectal cancer.Cancer Res.
1995;55:3785-3789.
18.Ristimaki A,Honkanen N,Jankala H,et al.Expression of
cyclooxygenase-2in human gastric carcinoma.Cancer Res.
1997;57:1276-1280.
19.Wolff H,Saukkonen K,Anttila S,et al.Expression of
cyclooxygenase-2in human lung carcinoma.Cancer Res.
1998;58:4997-5001.
20.Hwang D,Scollard D,Byrne J,et al.Expression of cyclo-
oxygenase-1and cyclooxygenase-2in human breast cancer.
J Natl Cancer Inst.1998;90:455-460.
21.Shamma A,Yamamoto H,Doki Y,et al.Up-regulation of
cyclooxygenase-2in squamous carcinogenesis of the esopha-gus.Clin Cancer Res.2000;6:1229-1238.
22.Thun MJ,Henley SJ,Patrono C.Nonsteroidal anti-
inflammatory drugs as anticancer agents:mechanistic,phar-macologic,and clinical issues.J Natl Cancer Inst.2002;
94:252-266.
23.Fujimura T,Ohta T,Oyama K,et al.Role of cyclooxygen-
ase-2in the carcinogenesis of gastrointestinal tract cancers:
a review and report of personal experience.World J Gastro-
enterol.2006;7:1336-1345.
24.Soh J-W,Weinstein IB.Role of COX-independent targets
of NSAIDs and related compounds in cancer prevention and treatment.In:de Dannenberg AJ,DuBois RN,eds.
COX-2:Progress in Experimental Tumor Research.Vol
37.Basel,Switzerland:Karger;2003:261-283.
25.Grosch S,Maier TJ,Schiffmann S,et al.Cyclooxygenase-
2(COX-2)-independent anticarcinogenic effects of
selective COX-2inhibitors.J Natl Cancer Inst.2006;98: 736-747.
26.Yabe T,Honma M,Katsuki S,et al.Oral toxicity studies
of meloxicam in rats.Oyo Yakuri/Pharmacometrics.
1997;53:29-49.
27.Florell SR,Coffin CM,Holden JA,et al.Preservation of
RNA for functional genomic studies:a multidisciplinary tumor bank protocol.Mod Pathol.2001;14:116-128.
28.Ellis M,Davis N,Coop A,et al.Development and validation of
a method for using breast core needle biopsies for gene expres-
sion microarray analyses.Clin Cancer Res.2002;8:1155-1166.
29.Claveau D,Sirinyan M,Guay J,et al.Microsomal prosta-
glandin esynthase-1is a major terminalsynthase that is selectively up-regulated during cyclooxygenase-2-dependent prostaglandin E2production in the rat adjuvant-induced ar-thritis model.J Immunol.2003;170:4738-4744.
30.Buttar NS,Wang KK,Leontovich O,et al.Chemopreven-
tion of esophageal adenocarcinoma by COX-2inhibitors in an animal model of Barrett’s esophagus.Gastroenterology.
2002;122:1101-1112.
31.Oyama K,Fujimura T,Ninomiya I,et al.A COX-2inhib-
itor prevents esophageal inflammation-metaplasia-adenocar-cinoma sequence in rats.Carcinogenesis.2005;26:565-570.
32.Kaneko M,Morimura K,Nishikawa T,et al.Different
genetic alterations in rat forestomach tumors induced by genotoxic and nongenotoxic carcinogens.Carcinogenesis.
2002;23:1729-1735.
33.Kodama Y,Ozaki K,Sano T,et al.Induction of squamous
cell carcinoma of forestomach in diabetic rats by single alloxan treatment.Cancer Sci.2006;97:1023-1030.
34.Nam KT,Hahm K-B,Oh S-Y,et al.The selective cycloox-
ygenase-2inhibitor nimesulide prevents Helicobacter pylori-associated gastric cancer development in a mouse model.
Clin Cancer Res.2004;10:8105-8113.
35.Hu PJ,Yu J,Zeng ZR,et al.Chemoprevention of gastric
cancer by celecoxib in rats.Gut.2004;53:195-200.
36.Zhi H,Wang L,Zhang J,et al.Significance of COX-2
expression in human esophageal squamous cell carcinoma.
Carcinogenesis.2006;27:1214-1221.
37.Jang TJ,Min SK,Bae JD,et al.Expression of cyclooxygen-
ase2,microsomal prostaglandin E synthase1,and EP receptor is increased in rat oesophageal squamous cell dys-plasia and Barrett’s metaplasia induced by duodenal con-tents reflux.Gut.2004;53:27-33.
38.Nishijima K,Miwa K,Miyashita T,et al.Impact of the
biliary diversion procedure on carcinogenesis in Barrett’s esophagus surgically induced by duodenoesophageal reflux in rats.Ann Surg.2004;240:57-67.
39.Liu JF,Zhang SW,Jamieson GG,et al.The effects of a
COX-2inhibitor meloxicam on squamous cell carcinoma of the esophagus in vivo.Int J Cancer.2009;122:1639-1644.
Original Article
习题1 选择题 (1) 一运动质点在某瞬时位于矢径),(y x r 的端点处，其速度大小为 (A)dt dr (B)dt r d (C)dt r d | | (D) 22)()(dt dy dt dx + [答案：D] (2) 一质点作直线运动，某时刻的瞬时速度s m v /2=，瞬时加速度2 /2s m a -=，则一秒钟后质点的速度 (A)等于零 (B)等于-2m/s (C)等于2m/s (D)不能确定。 [答案：D] (3) 一质点沿半径为R 的圆周作匀速率运动，每t 秒转一圈，在2t 时间间隔中，其平均速度大小和平均速率大小分别为 (A) t R t R ππ2, 2 (B) t R π2,0 (C) 0,0 (D) 0,2t R π [答案：B] 填空题 (1) 一质点，以1 -?s m π的匀速率作半径为5m 的圆周运动，则该质点在5s 内，位移的大小是 ；经过的路程是 。 [答案： 10m ； 5πm] (2) 一质点沿x 方向运动，其加速度随时间的变化关系为a=3+2t (SI)，如果初始时刻质点的速度v 0为5m·s -1，则当t 为3s 时，质点的速度v= 。 [答案： 23m·s -1 ] (3) 轮船在水上以相对于水的速度1V 航行，水流速度为2V ，一人相对于甲板以速度3V 行走。如人相对于岸静止，则1V 、2V 和3V 的关系是 。 [答案： 0321=++V V V ]
一个物体能否被看作质点，你认为主要由以下三个因素中哪个因素决定： (1) 物体的大小和形状； (2) 物体的内部结构； (3) 所研究问题的性质。 解：只有当物体的尺寸远小于其运动范围时才可忽略其大小的影响，因此主要由所研究问题的性质决定。 下面几个质点运动学方程，哪个是匀变速直线运动？ （1）x=4t-3；（2）x=-4t 3+3t 2+6；（3）x=-2t 2+8t+4；（4）x=2/t 2-4/t 。 给出这个匀变速直线运动在t=3s 时的速度和加速度，并说明该时刻运动是加速的还是减速的。（x 单位为m ，t 单位为s ） 解：匀变速直线运动即加速度为不等于零的常数时的运动。加速度又是位移对时间的两阶导数。于是可得（3）为匀变速直线运动。 其速度和加速度表达式分别为 2 2484 dx v t dt d x a dt = =+== t=3s 时的速度和加速度分别为v =20m/s ，a =4m/s 2。因加速度为正所以是加速的。 在以下几种运动中，质点的切向加速度、法向加速度以及加速度哪些为零哪些不为零？ (1) 匀速直线运动；(2) 匀速曲线运动；(3) 变速直线运动；(4) 变速曲线运动。 解：(1) 质点作匀速直线运动时，其切向加速度、法向加速度及加速度均为零； (2) 质点作匀速曲线运动时，其切向加速度为零，法向加速度和加速度均不为零； (3) 质点作变速直线运动时，其法向加速度为零，切向加速度和加速度均不为零； (4) 质点作变速曲线运动时，其切向加速度、法向加速度及加速度均不为零。 ｜r ?｜与r ? 有无不同?t d d r 和d d r t 有无不同? t d d v 和t d d v 有无不同?其不同在哪里?试举例说明． 解：（1）r ?是位移的模，?r 是位矢的模的增量，即r ?12r r -=，12r r r -=?； （2） t d d r 是速度的模，即t d d r ==v t s d d . t r d d 只是速度在径向上的分量. ∵有r r ?r =（式中r ?叫做单位矢），则 t ?r ?t r t d d d d d d r r r += 式中 t r d d 就是速度在径向上的分量，
变电所母线桥的动稳定校验 随着用电负荷的快速增长，许多变电所都对主变进行了增容，并对相关设备进行了调换和校验，但往往会忽视主变母线桥的动稳定校验，事实上此项工作非常重要。当主变增容后，由于阻抗发生了变化，短路电流将会增大许多，一旦发生短路，产生的电动力有可能会对母线桥产生破坏。特别是户内母线桥由于安装时受地理位置的限制，绝缘子间的跨距较长，受到破坏的可能性更大，所以应加强此项工作。 下面以我局35kV/10kv胡店变电所#2主变增容为例来谈谈如何进行主变母线桥的动稳定校验和校验中应注意的问题。 1短路电流计算 图1为胡店变电所的系统主接线图。(略) 已知#1主变容量为10000kVA，短路电压为7.42%，#2主变容量为12500kVA，短路电压为7.48%(增容前短路电压为7.73%)。 取系统基准容量为100MVA，则#1主变短路电压标么值 X1＝7.42/100×100×1000/10000＝0.742， #2主变短路电压标么值 X2＝7.48/100×100×1000/12500＝0.5984 胡店变电所最大运行方式系统到35kV母线上的电抗标么值为0.2778。 ∴#1主变与#2主变的并联电抗为： X12=X1×X2/(X1+X2)＝0.33125； 最大运行方式下系统到10kV母线上的组合电抗为： X＝0.2778+0.33125＝0.60875
∴10kV母线上的三相短路电流为：Id=100000/0.60875*√3*10.5，冲击电流：I sh=2.55I =23032.875A。 d 2动稳定校验 (1)10kV母线桥的动稳定校验： 进行母线桥动稳定校验应注意以下两点： ①电动力的计算，经过对外边相所受的力，中间相所受的力以及三相和二相电动力进行比较，三相短路时中间相所受的力最大，所以计算时必须以此为依据。 ②母线及其支架都具有弹性和质量，组成一弹性系统，所以应计算应力系数，计及共振的影响。根据以上两点，校验过程如下： 已知母线桥为8×80mm2的铝排，相间中心线间距离为210mm，先计算应力系数： ∵频率系数N f＝3.56，弹性模量E＝7×10.7 Pa，单位长度铝排质量M＝1.568kg/m，绝缘子间跨距2m，则一阶固有频率: f’=(N f/L2)*√(EI/M)=110Hz 查表可得动态应力系数β＝1.3。 ∴单位长度铝排所受的电动力为： f ph＝1.73×10-7I sh2/a×β＝568.1N/m ∵三相铝排水平布置，∴截面系数W＝bh2/6＝85333mm3，根据铝排的最大应力可确定绝缘子间允许的最大跨距为： L MAX=√10*σal*W/ f ph=3.24m ∵胡店变主变母线桥绝缘子间最大跨距为2m，小于绝缘子间的最大允许跨距。
习题1 1.1选择题 (1) 一运动质点在某瞬时位于矢径),(y x r 的端点处，其速度大小为 (A)dt dr (B)dt r d (C)dt r d | | (D) 22)()(dt dy dt dx + [答案：D] (2) 一质点作直线运动，某时刻的瞬时速度s m v /2=，瞬时加速度2 /2s m a -=，则一秒钟后质点的速度 (A)等于零 (B)等于-2m/s (C)等于2m/s (D)不能确定。 [答案：D] (3) 一质点沿半径为R 的圆周作匀速率运动，每t 秒转一圈，在2t 时间间隔中，其平均速度大小和平均速率大小分别为 (A) t R t R ππ2, 2 (B) t R π2,0 (C) 0,0 (D) 0,2t R π [答案：B] 1.2填空题 (1) 一质点，以1 -?s m π的匀速率作半径为5m 的圆周运动，则该质点在5s 内，位移的大小是 ；经过的路程是 。 [答案： 10m ； 5πm] (2) 一质点沿x 方向运动，其加速度随时间的变化关系为a=3+2t (SI)，如果初始时刻质点的速度v 0为5m·s -1，则当t 为3s 时，质点的速度v= 。 [答案： 23m·s -1 ] (3) 轮船在水上以相对于水的速度1V 航行，水流速度为2V ，一人相对于甲板以速度3V 行走。如人相对于岸静止，则1V 、2V 和3V 的关系是 。 [答案： 0321=++V V V ]
1.3 一个物体能否被看作质点，你认为主要由以下三个因素中哪个因素决定： (1) 物体的大小和形状； (2) 物体的内部结构； (3) 所研究问题的性质。 解：只有当物体的尺寸远小于其运动范围时才可忽略其大小的影响，因此主要由所研究问题的性质决定。 1.4 下面几个质点运动学方程，哪个是匀变速直线运动？ （1）x=4t-3；（2）x=-4t 3+3t 2+6；（3）x=-2t 2+8t+4；（4）x=2/t 2-4/t 。 给出这个匀变速直线运动在t=3s 时的速度和加速度，并说明该时刻运动是加速的还是减速的。（x 单位为m ，t 单位为s ） 解：匀变速直线运动即加速度为不等于零的常数时的运动。加速度又是位移对时间的两阶导数。于是可得（3）为匀变速直线运动。 其速度和加速度表达式分别为 2 2484 dx v t dt d x a dt = =+== t=3s 时的速度和加速度分别为v =20m/s ，a =4m/s 2。因加速度为正所以是加速的。 1.5 在以下几种运动中，质点的切向加速度、法向加速度以及加速度哪些为零哪些不为零？ (1) 匀速直线运动；(2) 匀速曲线运动；(3) 变速直线运动；(4) 变速曲线运动。 解：(1) 质点作匀速直线运动时，其切向加速度、法向加速度及加速度均为零； (2) 质点作匀速曲线运动时，其切向加速度为零，法向加速度和加速度均不为零； (3) 质点作变速直线运动时，其法向加速度为零，切向加速度和加速度均不为零； (4) 质点作变速曲线运动时，其切向加速度、法向加速度及加速度均不为零。 1.6 ｜r ?｜与r ? 有无不同?t d d r 和d d r t 有无不同? t d d v 和t d d v 有无不同?其不同在哪里?试举例说明． 解：（1）r ?是位移的模，?r 是位矢的模的增量，即r ?12r r -=，12r r r -=?； （2） t d d r 是速度的模，即t d d r ==v t s d d . t r d d 只是速度在径向上的分量. ∵有r r ?r =（式中r ?叫做单位矢），则 t ?r ?t r t d d d d d d r r r += 式中 t r d d 就是速度在径向上的分量，
电力电子技术期末考试 试题及答案 Coca-cola standardization office【ZZ5AB-ZZSYT-ZZ2C-ZZ682T-ZZT18】
电力电子技术试题 第1章电力电子器件 1.电力电子器件一般工作在__开关__状态。 2.在通常情况下，电力电子器件功率损耗主要为__通态损耗__，而当器件开关频率较高时，功率损耗主要为__开关损耗__。 3.电力电子器件组成的系统，一般由__控制电路__、_驱动电路_、_主电路_三部分组成，由于电路中存在电压和电流的过冲，往往需添加_保护电路__。 4.按内部电子和空穴两种载流子参与导电的情况，电力电子器件可分为_单极型器件_、_双极型器件_、_复合型器件_三类。 5.电力二极管的工作特性可概括为_承受正向电压导通，承受反相电压截止_。 6.电力二极管的主要类型有_普通二极管_、_快恢复二极管_、_肖特基二极管_。 7.肖特基二极管的开关损耗_小于_快恢复二极管的开关损耗。 8.晶闸管的基本工作特性可概括为__正向电压门极有触发则导通、反向电压则截止__。 9.对同一晶闸管，维持电流IH与擎住电流IL在数值大小上有IL__大于__IH 。 10.晶闸管断态不重复电压UDSM与转折电压Ubo数值大小上应为，UDSM_大于__Ubo。 11.逆导晶闸管是将_二极管_与晶闸管_反并联_（如何连接）在同一管芯上的功率集成器件。 的__多元集成__结构是为了便于实现门极控制关断而设计的。 的漏极伏安特性中的三个区域与GTR共发射极接法时的输出特性中的三个区域有对应关系，其中前者的截止区对应后者的_截止区_、前者的饱和区对应后者的__放大区__、前者的非饱和区对应后者的_饱和区__。 14.电力MOSFET的通态电阻具有__正__温度系数。 的开启电压UGE（th）随温度升高而_略有下降__，开关速度__小于__电力MOSFET 。 16.按照驱动电路加在电力电子器件控制端和公共端之间的性质，可将电力电子器件分为_电压驱动型_和_电流驱动型_两类。 的通态压降在1/2或1/3额定电流以下区段具有__负___温度系数，在1/2或1/3额定电流以上区段具有__正___温度系数。 18.在如下器件：电力二极管（Power Diode）、晶闸管（SCR）、门极可关断晶闸管（GTO）、电力晶体管（GTR）、电力场效应管（电力MOSFET）、绝缘栅双极型晶体管（IGBT）中，属于不可控器件的是_电力二极管__，属于半控型器件的是__晶闸管_，属于全控型器件的是_GTO 、GTR 、电力
母线电动力及动热稳定性计算 1 目的和范围 本文档为电气产品的母线电动力、动稳定、热稳定计算指导文件，作为产品结构设计安全指导文件的方案设计阶段指导文件，用于母线电动力、动稳定性、热稳定性计算的选型指导。 2 参加文件 表1 3 术语和缩略语 表2 4 母线电动力、动稳定、热稳定计算 4.1 载流导体的电动力计算 4.1.1 同一平面内圆细导体上的电动力计算
? 当同一平面内导体1l 和2l 分别流过1I 和2I 电流时（见图1），导体1l 上的电动力计 算 h F K I I 4210 π μ= 式中 F ——导体1l 上的电动力（N ） 0μ——真空磁导率，m H 60104.0-?=πμ； 1I 、2I ——流过导体1l 和2l 的电流（A ）； h K ——回路系数，见表1。 图1 圆细导体上的电动力 表1 回路系数h K 表 两导体相互位置及示意图 h K 平 行 21l l = ∞=1l 时，a l K h 2= ∞≠1l 时，?? ? ???-+=l a l a a l K h 2)(12 21l l ≠ 22 2) ()(1l a m l a l a K h ++-+= 22)()1(l a m +-- l a m =
? 当导体1l 和2l 分别流过1I 和2I 电流时，沿1l 导体任意单位长度上各点的电动力计 算 f 124K f I I d μ= π 式中 f ——1l 导体任意单位长度上的电动力（m N ）； f K ——与同一平面内两导体的长度和相互位置有关的系数，见表2。 表2 f K 系数表
4.1.2 两平行矩形截面导体上的电动力计算 两矩形导体（母线）在b ＜＜a ，且b ＞＞h 的情况下，其单位长度上的电动力F 的 计算见表3。 当矩形导体的b 与a 和h 的尺寸相比不可忽略时，可按下式计算 712 210x L F I I K a -=? 式中 F -两导体相互作用的电动力，N ； L -母线支承点间的距离，m ； a -导体间距，m ； 1I 、2I -流过两个矩形母线的电流，A ； x K -导体截面形状系数； 表3 两矩形导体单位长度上的电动力 4.1.3 三相母线短路时的电动力计算
《电力电子技术》试卷1答案 一、填空（每空1分，36分） 1、请在正确的空格内标出下面元件的简称： 电力晶体管GTR；可关断晶闸管GTO；功率场效应晶体管MOSFET；绝缘栅双极型晶体管IGBT；IGBT是MOSFET和GTR的复合管。 2、晶闸管对触发脉冲的要求是要有足够的驱动功率、触发脉冲前沿要陡幅值要高和触发脉冲要与晶闸管阳极电压同步。 3、多个晶闸管相并联时必须考虑均流的问题，解决的方法是串专用均流电抗器。 4、在电流型逆变器中，输出电压波形为正弦波，输出电流波形为方波。 5、型号为KS100-8的元件表示双向晶闸管晶闸管、它的额定电压为800V伏、额定有效电流为100A。 6、180°导电型三相桥式逆变电路，晶闸管换相是在同一桥臂上的上、下二个元件之间进行；而120o导电型三相桥式逆变电路，晶闸管换相是在不同桥臂上的元件之间进行的。 7、当温度降低时，晶闸管的触发电流会增加、正反向漏电流会下降；当温度升高时，晶闸管的触发电流会下降、正反向漏电流会增加。 8、在有环流逆变系统中，环流指的是只流经逆变电源、逆变桥而不流经负载的电流。环流可在电路中加电抗器来限制。为了减小环流一般采控用控制角α大于β的工作方式。 9、常用的过电流保护措施有快速熔断器、串进线电抗器、接入直流快速开关、控制快速移相使输出电压下降。（写出四种即可） 10、双向晶闸管的触发方式有Ⅰ+、Ⅰ-、Ⅲ＋、Ⅲ-四种。 二、判断题,（每题1分，10分）（对√、错×） 1、在半控桥整流带大电感负载不加续流二极管电路中，电路出故障时会出现失 控现象。（√） 2、在用两组反并联晶闸管的可逆系统，使直流电动机实现四象限运行时，其中 一组逆变器工作在整流状态，那么另一组就工作在逆变状态。（×） 3、晶闸管串联使用时，必须注意均流问题。（×） 4、逆变角太大会造成逆变失败。（×） 5、并联谐振逆变器必须是略呈电容性电路。（√） 6、给晶闸管加上正向阳极电压它就会导通。（×） 7、有源逆变指的是把直流电能转变成交流电能送给负载。（×） 8、在单相全控桥整流电路中，晶闸管的额定电压应取U2。（×） 9、在三相半波可控整流电路中，电路输出电压波形的脉动频率为300Hz。（×） 10、变频调速实际上是改变电动机内旋转磁场的速度达到改变输出转速的目的。 （√） 三、选择题（每题3分，15分）
筠连县分水岭煤业有限责任公司 井 下 高 压 电 缆 热 稳 定 性 校 验 计 算 书 巡司二煤矿 编制：机电科 筠连县分水岭煤业有限责任公司
井下高压电缆热稳定校验计算书 一、概述： 根据《煤矿安全规程》第453条及456条之规定，对我矿入井高压电缆进行热稳定校验。 二、确定供电方式 我矿高压供电采用分列运行供电方式，地面变电所、井下变电所均采用单母线分段分列供电方式运行，各种主要负荷分接于不同母线段。 三、井下高压电缆明细： 矿上有两趟主进线，引至巡司变电站不同母线段，一趟931线，另一趟925线。井下中央变电所由地面配电房10KV输入。 入井一回路：MYJV22-8.7/10KV 3*50mm2--800m(10KV) 入井二回路：MYJV22-8.7/10KV 3*50mm2--800m(10KV) 四、校验计算 1、井下入井回路高压电缆热稳定性校验 已知条件：该条高压电缆型号为，MYJV22-8.7/10KV 3*50mm2 ,800m，电缆长度为800m=0.8km。 （1）计算电网阻抗 查附表一，短路电流的周期分量稳定性为 电抗：X=0.072*0.8=0.0576Ω； 电阻：R=0.407*0.8=0.3256 Ω； (2)三相短路电流的计算
A Z I 5.174693305 .0310000 3v 3=?== ∞ （3）电缆热稳定校验 由于断路器的燃弧时间及固有动作时间之和约为t=0.05S; 查附表二得热稳定计算系数取K=142; 故电缆最小热值稳定截面为 23mm 51.2705.0142/5.17469t )/(min ===∞）（K I S Smin<50mm 2 故选用 MYJV 22 -8.7/10KV 3*50 电缆热稳定校验合格，符合要求。 附表一：三相电缆在工作温度时的阻抗值（Ω/Km ） 电缆截面S （mm 2 ） 4 6 10 16 2 5 35 50 70 95 120 150 185 240 交联聚乙烯 R 4.988 3.325 2.035 1.272 0.814 0.581 0.407 0.291 0.214 0.169 0.136 0.11 0.085 X 0.093 0.093 0.087 0.082 0.075 0.072 0.072 0.069 0.069 0.069 0.07 0.07 0.07 附表二 不同绝缘导体的热稳定计算系数 绝缘材料 芯线起始温度（° C ） 芯线最高允许温度（°C ） 系数K 聚氯乙烯 70 160 115（114） 普通橡胶 75 200 131 乙丙橡胶 90 250 143（142） 油浸纸绝缘 80 160 107 交联聚乙烯 90 250 142
习题1 1.1选择题 (1) 一运动质点在某瞬时位于矢径),(y x r 的端点处，其速度大小为 (A)dt dr (B)dt r d (C)dt r d | | (D) 22)()(dt dy dt dx + [答案：D] (2) 一质点作直线运动，某时刻的瞬时速度s m v /2=，瞬时加速度2 /2s m a -=，则 一秒钟后质点的速度 (A)等于零 (B)等于-2m/s (C)等于2m/s (D)不能确定。 [答案：D] (3) 一质点沿半径为R 的圆周作匀速率运动，每t 秒转一圈，在2t 时间间隔中，其平均速度大小和平均速率大小分别为 (A) t R t R ππ2, 2 (B) t R π2,0 (C) 0,0 (D) 0,2t R π [答案：B] 1.2填空题 (1) 一质点，以1 -?s m π的匀速率作半径为5m 的圆周运动，则该质点在5s 内，位移的大小是 ；经过的路程是 。 [答案： 10m ； 5πm] (2) 一质点沿x 方向运动，其加速度随时间的变化关系为a=3+2t (SI)，如果初始时刻质点的 速度v 0为5m ·s -1 ，则当t 为3s 时，质点的速度v= 。 [答案： 23m ·s -1 ] (3) 轮船在水上以相对于水的速度1V 航行，水流速度为2V ，一人相对于甲板以速度3V 行走。如人相对于岸静止，则1V 、2V 和3V 的关系是 。 [答案： 0321=++V V V ]
1.3 一个物体能否被看作质点，你认为主要由以下三个因素中哪个因素决定： (1) 物体的大小和形状； (2) 物体的内部结构； (3) 所研究问题的性质。 解：只有当物体的尺寸远小于其运动范围时才可忽略其大小的影响，因此主要由所研究问题的性质决定。 1.4 下面几个质点运动学方程，哪个是匀变速直线运动？ （1）x=4t-3；（2）x=-4t 3+3t 2+6；（3）x=-2t 2+8t+4；（4）x=2/t 2 -4/t 。 给出这个匀变速直线运动在t=3s 时的速度和加速度，并说明该时刻运动是加速的还是减速的。（x 单位为m ，t 单位为s ） 解：匀变速直线运动即加速度为不等于零的常数时的运动。加速度又是位移对时间的两阶导数。于是可得（3）为匀变速直线运动。 其速度和加速度表达式分别为 2 2484 dx v t dt d x a dt = =+== t=3s 时的速度和加速度分别为v =20m/s ，a =4m/s 2 。因加速度为正所以是加速的。 1.5 在以下几种运动中，质点的切向加速度、法向加速度以及加速度哪些为零哪些不为零？ (1) 匀速直线运动；(2) 匀速曲线运动；(3) 变速直线运动；(4) 变速曲线运动。 解：(1) 质点作匀速直线运动时，其切向加速度、法向加速度及加速度均为零； (2) 质点作匀速曲线运动时，其切向加速度为零，法向加速度和加速度均不为零； (3) 质点作变速直线运动时，其法向加速度为零，切向加速度和加速度均不为零； (4) 质点作变速曲线运动时，其切向加速度、法向加速度及加速度均不为零。 1.6 ｜r ?｜与r ? 有无不同?t d d r 和d d r t 有无不同? t d d v 和t d d v 有无不同?其不同在哪里?试举例说明． 解：（1）r ?是位移的模，?r 是位矢的模的增量，即r ?12r r -=，12r r r -=?； （2） t d d r 是速度的模，即t d d r ==v t s d d . t r d d 只是速度在径向上的分量. ∵有r r ?r =（式中r ?叫做单位矢），则 t ?r ?t r t d d d d d d r r r += 式中 t r d d 就是速度在径向上的分量，
电力电子技术答案 2-1与信息电子电路中的二极管相比，电力二极管具有怎样的结构特点才使得其具有耐受高压和大电流的能力？ 答：1.电力二极管大都采用垂直导电结构，使得硅片中通过电流的有效面积增大，显著提高了二极管的通流能力。 2.电力二极管在P 区和N 区之间多了一层低掺杂N 区，也称漂移区。低掺杂N 区由于掺杂浓度低而接近于无掺杂的纯半导体材料即本征半导体，由于掺杂浓度低，低掺杂N 区就可以承受很高的电压而不被击穿。 2-2. 使晶闸管导通的条件是什么？ 答：使晶闸管导通的条件是：晶闸管承受正向阳极电压，并在门极施加触发电流（脉冲）。或：uAK>0且uGK>0。 2-3. 维持晶闸管导通的条件是什么？怎样才能使晶闸管由导通变为关断？ 答：维持晶闸管导通的条件是使晶闸管的电流大于能保持晶闸管导通的最小电流，即维持电流。 要使晶闸管由导通变为关断， 可利用外加电压和外电路的作用使流过晶闸管的电流降 到接近于零的某一数值以下，即降到维持电流以下，便可使导通的晶闸管关断。 2-4图2-27中阴影部分为晶闸管处于通态区间的电流波形，各波形的电流最大值均为I m ，试计算各波形的电流平均值I d1、I d2、I d3与电流有效值I 、I 、I 。 πππ4 π4 π2 5π4a) b)c) 图1-43 图2-27 晶闸管导电波形 解：a) I d1= π21?π πωω4 )(sin t td I m =π2m I (122+)≈0.2717 I m I 1= ?π πωωπ 4 2 )()sin (21 t d t I m =2m I π 2143+≈0.4767 I m b) I d2 = π1?π πωω4)(sin t td I m =π m I ( 12 2 +)≈0.5434 I m I 2 = ? π π ωωπ 4 2) ()sin (1 t d t I m = 2 2m I π 21 43+ ≈0.6741I m c) I d3=π21?2 )(π ωt d I m =41 I m I 3 =? 2 2 ) (21π ωπt d I m = 2 1 I m 2-5上题中如果不考虑安全裕量,问100A 的晶阐管能送出的平均电流I d1、I d2、I d3各为多少?这时，相应的电流最大值I m1、I m2、 I m3各为多少? 解：额定电流I T(AV)=100A 的晶闸管，允许的电流有效值I=157A,由上题计算结果知 a) I m1≈4767.0I ≈329.35， I d1≈0.2717 I m1≈89.48 b) I m2≈ 6741 .0I ≈232.90, I d2≈0.5434 I m2≈126.56 c) I m3=2 I = 314, I d3= 4 1 I m3=78.5 2-6 GTO 和普通晶闸管同为PNPN 结构,为什么GTO 能够自关断,而普通晶闸管不能? 答：GTO 和普通晶阐管同为PNPN 结构，由P1N1P2和N1P2N2构成两个晶体管V1、V2，分别具有共基极电流增益 1α和2α， 由普通晶阐管的分析可得， 121=+αα是器件临界导通的条件。1 21＞αα+两个等效晶体管过饱和而导通；
井下高压开关、供电电缆动热稳定性校验 一、-350中央变电所开关断路器开断能力及电缆热稳定性校验 1 23 G 35kV 2 Uz%=7.5△P N.T =12kW △P N.T =3.11kW S N.T =8MVA 6kV S1点三相短路电流计算： 35kV 变压器阻抗： 2 22.1. u %7.5 6.30.37()1001008z N T N T U Z S ?===Ω? 35kV 变压器电阻：2 22.1.22. 6.30.0120.007()8 N T N T N T U R P S =?=?=Ω 35kV 变压器电抗：10.37()X = ==Ω 电缆电抗：02(x )0.415000.08780 0.66()1000 1000i L X ??+?== =Ω∑ 电缆电阻：02(x )0.11815000.118780 0.27()1000 1000 i L R ??+?== =Ω∑ 总阻抗： 21.370.66) 1.06( Z ==Ω S1点三相短路电流：(3)1 3.43()d I KA === S2点三相短路电流计算： S2点所用电缆为MY-3×70+1×25，长400米，变压器容量为500KV A ，查表的：(2)2d I =2.5KA
S2点三相短路电流：32 d d =2.88I I KA = 1、架空线路、入井电缆的热稳定性校验。已知供电负荷为3128.02KV A ，电压为6KV ，需用系数0.62，功率因数cos 0.78φ=，架空线路长度1.5km ，电缆长度780m (1)按经济电流密度选择电缆，计算容量为 3128.020.62 2486.37cos 0.78 kp S KVA φ?= ==。 电缆的长时工作电流Ig 为239.25 Ig === A 按长时允许电流校验电缆截面查煤矿供电表5-15得MYJV42-3×185-6/6截面长时允许电流为479A/6kV 、大于239.25A 符合要求。 (2)按电压损失校验，配电线路允许电压损失5%得 60000.1300Uy V ?=?=，线路的实际电压损失 109.1L U COS DS φφ?====，U ?小于300V 电压损失满足要求 (3)热稳定性条件校验，短路电流的周期分量稳定性为 电缆最小允许热稳定截面积： 3 2min d =S I mm 其中：i t ----断路器分断时间，一般取0.25s ； C----电缆热稳定系数，一般取100，环境温度35℃，电缆温升不超过120℃时，铜芯电缆聚乙烯电缆熔化温度为130℃，电
1.试求出圆柱坐标系的尺度系数，并由此导出圆柱坐标系中的导热微分方程。 2 .一无限大平板，初始温度为T 0；τ>0时，在x = 0表面处绝热；在x = L 表面以对流方式向温度为t f 的流体换热。试用分离变量法求出τ>0时平板的温度分布（常物性）。（需求出特征函数、超越方程的具体形式，范数（模）可用积分形式表示）。（15分） , 3.简述近似解析解——积分法中热层厚度δ的概念。 答：近似解析解：既有分析解的特征：得到的结果具有解析函数形式，又有近似解的特征：结果只能近似满足导热解问题。在有限的时间内，边界温度 的变化对于区域温度场的影响只是在某一有限的范围内，把这个有限的范围定义为热层厚度δ。 4.与单相固体导热相比，相变导热有什么特点 答：相变导热包含了相变和导热两种物理过程。相变导热的特点是 1.固、液两相之间存在着 移动的交界面。 2.两相交界面有潜热的释放（或吸收） | 对流部分（所需量和符号自己设定） 1 推导极坐标系下二维稳态导热微分方程。 2 已知绕流平板流动附面层微分方程为 y u y u V x u u 22??=??+??ν 取相似变量为： x u y νη∞ = x u f νψ∞= 写出问题的数学模型并求问题的相似解。 3 已知绕流平板流动换热的附面层能量积分方程为： ?=∞?? =-δ00)(y y t a dy t t u dx d 当Pr<<1时，写出问题的数学模型并求问题的近似积分解及平均Nu （取三次多项式）。 4 ] O x
5写出常热流圆管内热充分发展流动和换热问题的数学模型并求出速度和温度分布及Nu x.辐射 1．请推导出具有n个表面的净热流法壁面间辐射换热求解公式，并简要说明应用任一种数值方法的求解过程。 2．试推导介质辐射传递方程的微分形式和积分形式，要求表述出各个步骤和结果中各个相关量的含义。 3．根据光谱辐射强度表示下面各量：1）光谱定向辐射力；2）定向辐射力；3）光谱辐射力；4）辐射力；5）辐射热流量。要求写清各量的符号、单位。 4．说明下列术语（可用数学表达式）（每题4分） a)光学厚度 b)漫有色表面 c)? d)兰贝特余弦定律 e)光谱散射相函数 f)定向“灰”入射辐射
《电力电子技术》试卷 一．填空（共15分，1分/空） 1.电力电子技术通常可分为（）技术和（）技术两个分支。 2.按驱动电路信号的性质可以将电力电子器件分为（）型器件和（）型器件两类，晶闸管属于其中的（）型器件。 3.晶闸管单相桥式全控整流电路带反电动势负载E时（变压器二次侧电压有效值为U ，忽略主电路 2 各部分的电感），与电阻负载时相比，晶闸管提前了电角度δ停止导电，δ称为（）角，数量关系为δ=（）。 4.三相桥式全控整流电路的触发方式有（）触发和（）触发两种，常用的是（）触发。 5.三相半波可控整流电路按联接方式可分为（）组和（）组两种。 6.在特定场合下，同一套整流电路即可工作在（）状态，又可工作在（）状态，故简称变流电路。 7.控制角α与逆变角β之间的关系为（）。 二．单选（共10分，2分/题） 1．采用（）是电力电子装置中最有效、应用最广的一种过电流保护措施。 A.直流断路器 B. 快速熔断器 C.过电流继电器 2．晶闸管属于（）。 A.不可控器件 B. 全控器件 C.半控器件 3．单相全控桥式整流电路，带阻感负载（L足够大）时的移相范围是（）。 A．180O B.90O C.120O 4．对三相全控桥中共阴极组的三个晶闸管来说，正常工作时触发脉冲相位应依次差（）度。 A.60 B. 180 C. 120 5．把交流电变成直流电的是（）。 A. 逆变电路 B.整流电路 C.斩波电路 三．多选（共10分，2分/题） 1．电力电子器件一般具有的特征有。 A.所能处理电功率的大小是其最重要的参数 B.一般工作在开关状态 C.一般需要信息电子电路来控制 D.不仅讲究散热设计，工作时一般还需接散热器 2．下列电路中，不存在变压器直流磁化问题的有。 A.单相全控桥整流电路 B.单相全波可控整流电路 C.三相全控桥整流电路 D.三相半波可控整流电路 3．使晶闸管关断的方法有。 A.给门极施加反压 B.去掉阳极的正向电压 C.增大回路阻抗 D.给阳极施加反压 4．逆变失败的原因有。 A.触发电路不可靠 B.晶闸管发生故障 C.交流电源发生故障 D.换相裕量角不足 5．变压器漏抗对整流电路的影响有。 A.输出电压平均值降低 B.整流电路的工作状态增多 C.晶闸管的di/dt减小 D.换相时晶闸管电压出现缺口 四．判断（共5分,1分/题） 1.三相全控桥式整流电路带电阻负载时的移相范围是150O。（） 2.晶闸管是一种四层三端器件。（）
*作品编号：DG13485201600078972981* 创作者：玫霸* 筠连县分水岭煤业有限责任公司 井 下 高 压 电 缆 热 稳 定 性 校 验 计 算 书 巡司二煤矿
编制：机电科 筠连县分水岭煤业有限责任公司 井下高压电缆热稳定校验计算书 一、概述： 根据《煤矿安全规程》第453条及456条之规定，对我矿入井高压电缆进行热稳定校验。 二、确定供电方式 我矿高压供电采用分列运行供电方式，地面变电所、井下变电所均采用单母线分段分列供电方式运行，各种主要负荷分接于不同母线段。 三、井下高压电缆明细： 矿上有两趟主进线，引至巡司变电站不同母线段，一趟931线，另一趟925线。井下中央变电所由地面配电房10KV输入。 入井一回路：MYJV22-8.7/10KV 3*50mm2--800m(10KV) 入井二回路：MYJV22-8.7/10KV 3*50mm2--800m(10KV) 四、校验计算 1、井下入井回路高压电缆热稳定性校验 已知条件：该条高压电缆型号为，MYJV22-8.7/10KV 3*50mm2 ,800m，电缆长度为800m=0.8km。 （1）计算电网阻抗 查附表一，短路电流的周期分量稳定性为
电抗：X=0.072*0.8=0.0576Ω； 电阻：R=0.407*0.8=0.3256 Ω； (2)三相短路电流的计算 （3）电缆热稳定校验 由于断路器的燃弧时间及固有动作时间之和约为t=0.05S; 查附表二得热稳定计算系数取K=142; 故电缆最小热值稳定截面为 Smin<50mm2故选用 MYJV22 -8.7/10KV 3*50 电缆热稳定校验合格，符合要求。 附表一：三相电缆在工作温度时的阻抗值（Ω/Km）
20××－20××学年第一学期期末考试 《电力电子技术》试卷(A) （时间90分钟 满分100分） （适用于 ××学院 ××级 ××专业学生） 一、 填空题（30分,每空1分）。 1．如下器件：电力二极管（Power Diode ）、晶闸管（SCR ）、门极可关断晶闸管（GTO ）、电力晶体管（GTR ）、电力场效应管（电力MOSFET ）、绝缘栅双极型晶体管（IGBT ）中，属于不可控器件的是________，属于半控型器件的是________，属于全控型器件的是________；属于单极型电力电子器件的有________，属于双极型器件的有________，属于复合型电力电子器件得有 ________；在可控的器件中，容量最大的是________，工作频率最高的是________，属于电压驱动的是________，属于电流驱动的是________。（只写简称） 2．单相桥式全控整流电路中，带纯电阻负载时，α角移相范围为 _，单个晶闸管所承受的最大正向电压和反向电压分别为 和 ；带阻感负载时，α角移相范围为 ，单个晶闸管所承受的最大正向电压和反向电压分别为 和 。 3．直流斩波电路中最基本的两种电路是 和 。 4．升降压斩波电路呈现升压状态时，占空比取值范围是__ _。 5．与CuK 斩波电路电压的输入输出关系相同的有 、 和 。 6．当采用6脉波三相桥式电路且电网频率为50Hz 时，单相交交变频电路的输出上限频率约为 。 7．三相交交变频电路主要有两种接线方式，即 _和 。 8．矩阵式变频电路是近年来出现的一种新颖的变频电路。它采用的开关器件是 ；控制方式是 。 9．逆变器按直流侧提供的电源的性质来分，可分为 型逆变器和 型逆变器。 10．把电网频率的交流电直接变换成可调频率的交流电的变流电路称为 。 二、简答题（18分,每题6分）。 1．逆变电路多重化的目的是什么？如何实现？串联多重和并联多重逆变电路各应用于什么场合？ 2．交流调压电路和交流调功电路有什么异同？ 3．功率因数校正电路的作用是什么？有哪些校正方法？其基本原理是什么？ 三、计算题（40分，1题20分，2题10分，3题10分）。 1．一单相交流调压器，电源为工频220V ，阻感串联作为负载，其中R=0.5Ω，L=2mH 。 试求：①开通角α的变化范围；②负载电流的最大有效值；③最大输出功率及此时电源侧的功率因数；④当2πα＝时，晶闸管电流有效值，晶闸管导通角和电源侧功率因数。 2．.三相桥式电压型逆变电路，工作在180°导电方式，U d =200V 。试求输出相电压的基波幅值U UN1m 和有效值U UN1、输出线电压的基波幅值U UV1m 和有效值U UV1、输出线电压中7次谐波的有效值U UV7。 3 ．如图所示降压斩波电路E=100V ，L 值极大，R=0.5Ω，E m =10V ，采用脉宽调制控制方式，T=20μs ，当t on =5μs 时，计算输出电压平均值U o ，输出电流平均值
电力电子技术试题 第1章 电力电子器件 1.电力电子器件一般工作在__开关__状态。 2.在通常情况下，电力电子器件功率损耗主要为__通态损耗__，而当器件开关频率较高时，功率损耗主要为__开关损耗__。 3.电力电子器件组成的系统，一般由__控制电路__、_驱动电路_、 _主电路_三部分组成，由于电路中存在电压和电流的过冲，往往需添加_保护电路__。 4.按内部电子和空穴两种载流子参与导电的情况，电力电子器件可分为_单极型器件_ 、 _双极型器件_ 、_复合型器件_三类。 5.电力二极管的工作特性可概括为_承受正向电压导通，承受反相电压截止_。 6.电力二极管的主要类型有_普通二极管_、_快恢复二极管_、 _肖特基二极管_。 7.肖特基二极管的开关损耗_小于_快恢复二极管的开关损耗。 8.晶闸管的基本工作特性可概括为 __正向电压门极有触发则导通、反向电压则截止__ 。 9.对同一晶闸管，维持电流IH 与擎住电流I L 在数值大小上有I L __大于__IH 。 10.晶闸管断态不重复电压UDSM 与转折电压Ubo 数值大小上应为，UDSM _大于__Ubo 。 11.逆导晶闸管是将_二极管_与晶闸管_反并联_（如何连接）在同一管芯上的功率集成器件。 12.GTO 的__多元集成__结构是为了便于实现门极控制关断而设计的。 13.MOSFET 的漏极伏安特性中的三个区域与GTR 共发射极接法时的输出特性中的三个区域有对应关系，其中前者的截止区对应后者的_截止区_、前者的饱和区对应后者的__放大区__、前者的非饱和区对应后者的_饱和区__。 14.电力MOSFET 的通态电阻具有__正__温度系数。 15.IGBT 的开启电压UGE （th ）随温度升高而_略有下降__，开关速度__小于__电力MOSFET 。 16.按照驱动电路加在电力电子器件控制端和公共端之间的性质，可将电力电子器件分为_电压驱动型_和_电流驱动型_两类。 17.IGBT 的通态压降在1/2或1/3额定电流以下区段具有__负___温度系数， 在1/2或1/3额定电流以上区段具有__正___温度系数。 18.在如下器件：电力二极管（Power Diode ）、晶闸管（SCR ）、门极可关断晶闸管（GTO ）、电力晶体管（GTR ）、电力场效应管（电力MOSFET ）、绝缘栅双极型晶体管（IGBT ）中，属于不可控器件的是_电力二极管__，属于半控型器件的是__晶闸管_，属于全控型器件的是_ GTO 、GTR 、电力MOSFET 、IGBT _；属于单极型电力电子器件的有_电力MOSFET _，属于双极型器件的有_电力二极管、晶闸管、GTO 、GTR _，属于复合型电力电子器件得有 __ IGBT _；在可控的器件中，容量最大的是_晶闸管_，工作频率最高的是_电力MOSFET ，属于电压驱动的是电力MOSFET 、IGBT _，属于电流驱动的是_晶闸管、GTO 、GTR _。 第2章 整流电路 1.电阻负载的特点是_电压和电流成正比且波形相同_，在单相半波可控整流电阻性负载电路中，晶闸管控制角α的最大移相范围是_0-180O _。 2.阻感负载的特点是_流过电感的电流不能突变，在单相半波可控整流带阻感负载并联续流二极管的电路中，晶闸管控制角α的最大移相范围是__0-180O _ ， 2__，续流二极管承受的最大反向电压为2_（设U 2为相电压有效值）。 3.单相桥式全控整流电路中，带纯电阻负载时，α角移相范围为__0-180O _，单个晶闸管所承受的最大正向电压和反向电压分别为22 和2；带 阻感负载时，α角移相范围为_0-90O _，单个晶闸管所承受的最大正向电压和反向电压分别为2_和2_；带反电动势负载时，欲使电阻上的电流不出 现断续现象，可在主电路中直流输出侧串联一个_平波电抗器_。 4.单相全控桥反电动势负载电路中，当控制角α大于不导电角δ时，晶闸管的导通角θ =_π-α-δ_; 当控制角α小于不导电角 δ 时，晶闸管的导通角 θ =_π-2δ_。 5.电阻性负载三相半波可控整流电路中，晶闸管所承受的最大正向电压UFm 2_，晶闸管控制角α的最大移相范围是_0-150o _，使负载电流连续的条 件为__o 30≤α__(U2为相电压有效值)。 6.三相半波可控整流电路中的三个晶闸管的触发脉冲相位按相序依次互差_120o _，当它带阻感负载时，α的移相范围为__0-90o _。 7.三相桥式全控整流电路带电阻负载工作中，共阴极组中处于通态的晶闸管对应的是_最高__的相电压，而共阳极组中处于导通的晶闸管对应的是_最低_的相电压；这种电路 α 角的移相范围是_0-120o _，u d 波形连续的条件是_o 60≤α_。 8.对于三相半波可控整流电路，换相重迭角的影响，将使用输出电压平均值__下降_。 9.电容滤波单相不可控整流带电阻负载电路中，空载时，输出电压为2_，随负载加重Ud 逐渐趋近于_0.9 U 2_，通常设计时，应取RC ≥_1.5-2.5_T ，此 时输出电压为Ud ≈__1.2_U 2(U 2为相电压有效值，T 为交流电源的周期)。 10.电容滤波三相不可控整流带电阻负载电路中，电流 id 断续和连续的临界条件是_=RC ω。 11.实际工作中，整流电路输出的电压是周期性的非正弦函数，当 α 从0°～90°变化时，整流输出的电压ud 的谐波幅值随 α 的增大而 _增大_，当 α 从90°～180°变化时，整流输出的电压 ud 的谐波幅值随 α 的增大而_减小_。