铝卷卷式退火粘伤问题的分析及解决措施

箱式炉卷材退火由于其成本低等优点仍是目前各大铝厂的退火主流。但铝材卷式退火易产生退火粘伤等问题。针对此问题,分析了粘伤的形成原因,并根据其不同的形貌及形成机理进行了分类阐述。同时针对因不同原因形成的退火粘伤问题给出了相应的解决措施,并且为了改进高温退火时卷材的放置方式,独创出"悬空退火"法,有效地解决了横条状粘伤问题。

铝热连轧薄板粘伤缺陷原因分析及控制措施

以铝热连轧在生产3104合金薄板为例,分析了热轧薄板层间粘伤问题属于局部板型突变引起的压力焊接现象。以现有的设备控制能力,采用变凸度控制措施,避免了弯棍力的剧烈波动,减少了板型局部凸起的形成,有效避免了层间粘伤缺陷。

阳极氧化用5052铝合金基材轧制表面质量控制浅析

分析了热连轧和冷轧过程中影响5052铝合金阳极氧化效果的主要表面缺陷,如黑条、压过划痕、粘伤、印痕和黑点等产生原因,并制定了相应的解决措施。

Theoretical Study on the Temporary Cavity Caused by a High Speed Projectile When Wounding Living Organisms

Analyzes and calculates the process of development of a temporary cavity in the muscle directly after a projectile wounds organisms at a high speed. The muscle is taken as a non compressible Voigt Kelvin viscoelastic fluid model, on the assumption of moving in a radial direction and on spherical symmetry, a theoretical model proposed using the basic equations of the non Newtonian fluid mechanics. The model can well describe the pulsation process of the temporary cavity and changes of pressure in the cavity. The calculated results are in correspondence with the experimental results. The model can be applied in the quantitative analysis of a temporary cavity.

Molecular cross-talk between Helicobacter pylori and human gastric mucosa

Helicobacter pylori (H.pylori) has co-evolved with humans to be transmitted from person to person and to colonize the stomach persistently.A well-choreographed equilibrium between the bacterial effectors and host responses permits microbial persistence and health of the host,but confers a risk for serious diseases including gastric cancer.During its long coexistence with humans,H.pylori has developed complex strategies to limit the degree and extent of gastric mucosal damage and in? ammation,as well as immune effector activity.The present editorial thus aims to introduce and comment on major advances in the rapidly developing area of H.pylori/human gastric mucosa interaction (and its pathological sequelae),which is the result of millennia of co-evolution of,and thus of reciprocal knowledge between,the pathogen and its human host.

Predictability of outcome of caustic ingestion by esophagogastroduodenoscopy in children

AIM: To assess the necessity of esophagogastroduodenoscopy (EGD) to predict the outcome of caustic ingestion in children. METHODS: The study included 206 children who underwent EGD because of ingestion of caustic substances between January 2005 and August 2010. Retrospective analysis of data of the patients was performed. RESULTS: The male/female ratio was 1.6 and mean age was 38.1 ± 28.8 mo. The caustic substances were acidic in 72 (34.9%) cases, alkaline in 56 (27.2%), liquid household bleach in 62 (30.1%), and unknown in 16 (7.8%). Fifty-seven (27.7%) patients were symptom-free. Significant clinical findings were observed in 149 (72.3%) patients. Upper gastrointestinal endoscopy findings of esophageal injury were grade 0 in 86 (41.7%) patients, grade 1 in 49 (23.8%), grade 2a in 42 (20.4%), grade 2b in 28 (13.6%), and grade 3a in 1 (0.5%) patient. 35 patients with grade 2a, 2b, and 3a injuries underwent esophageal dilation at second week of ingestion. Esophageal stricture, which necessitated a regular dilation program developed in 13 of the aforementioned 35 patients. There is no statistically significant difference in the rate of development of esophageal stricture between the patients who ingested acidic (15.3%) and alkaline (8.9%) substances (P = 0.32). Severe gastric injury was detected in 38 (18.5%) patients. The rate of development of gastric injury was significantly higher in the acidic group (14%) than in the alkaline group (2.9%) (P = 0.001). Out of 149 patients with clinical findings, 49 (32.9%) patients had no esophageal injury and 117 (78.5%) patients had no gastric lesion. Esophageal and severe gastric injuries were detected in 20 (35.1%) and 8 (14%) of patients with no clinical findings respectively. Pyloric stenosis developed in 6 patients. Pyloric obstruction improved with balloon dilation in 2 patients. Mean hospitalization time were 1.2 ± 0.5 d for grade 0 and 2.3 ± 5 d for grade 1 and 6.3 ± 6.2 d for grade 2a and 15.8 ± 18.6 d for grade 2b. It was significantly longer for patients with grade 2a and 2b injuries (P = 0.000). CONCLUSION: Endoscopy is an effective technique for determining the presence of esophageal and gastric damage and to avoid unnecessary treatment in patients with no or mild injury.

Gastric mucosal damage in water immersion stress:Mechanism and prevention with GHRP-6

AIM:To investigate the mechanism of gastric mucosal demage induced by water immersion restraint stress(WRS) and its prevention by growth hormone releasing peptide-6(GHRP-6).METHODS:Male Wistar rats were subjected to conscious or unconscious(anesthetized) WRS,simple restraint(SR),free swimming(FS),non-water fluid immersion,immersion without water contact,or rats were placed in a cage surrounded by sand.To explore the sensitivity structures that influence the stress reaction besides skin stimuli,a group the rats had their eyes occluded.Cervical bilateral trunk vagotomy or atropine injection was performed in some rats to assess the parasympathetic role in mucosal damage.Gastric mucosal lesions,acid output and heart rate variability were measured.Plasma renin,endothelin-1 and thromboxane B2 and gastric heat shock protein 70 were also assayed.GHRP-6 was injected [intraperitoneal(IP) or intracerebroventricular(ICV)] 2 h before the onset of stress to observe its potential prevention of the mucosal lesion.RESULTS:WRS for 6 h induced serious gastric mucosal lesion [lesion area,WRS 81.8 ± 6.4 mm 2 vs normal control 0.0 ± 0.0 mm 2,P < 0.01],decreased the heart rate,and increased the heart rate variability and gastric acid secretion,suggesting an increase in vagal nervecarrying stimuli.The mucosal injury was inversely correlated with water temperature(lesion area,WRS at 35 ℃ 56.4 ± 5.2 mm 2 vs WRS at 23 ℃ 81.8 ± 6.4 mm 2,P < 0.01) and was consciousness-dependent.The injury could not be prevented by eye occlusion,but could be prevented by avoiding contact of the rat body with the water by dressing it in an impermeable plastic suit.When water was replaced by vegetable oil or liquid paraffin,there were gastric lesions in the same grade of water immersion.When rat were placed in a cage surrounded by sand,there were no gastric lesions.All these data point to a remarkable importance of cutenuous information transmitted to the high neural center that by vagal nerves reaching the gastric mucosa.FS alone also induced serious gastric injury,but SR could not induce gastric injury.Bilateral vagotomy or atropine prevented the WRS-induced mucosal lesion,indicating that increased outflow from the vagal center is a decisive factor in WRS-induced gastric injury.The mucosal lesions were prevented by prior injection of GHRP-6 via IP did,but not via ICV,suggesting that the protection is peripheral,although a sudden injection is not equivalent to a physiological release and uptake,which eventually may affect the vagal center.CONCLUSION:From the central nervous system,vagal nerves carry the cutaneous stimuli brought about by the immersion restraint,an experimental model for inducing acute gastric erosions.GHRP-6 prevents the occurrence of these lesions.

Direct hemoperfusion with a polymyxin B-immobilized cartridge in intestinal warm ischemia reperfusion

AIM： To investigate the effectiveness of direct hemoperfusion with polymyxin B-immobilized fibers （DHPPMX therapy） on warm ischemia-reperfusion （I/R） injury of the small intestine.METHODS： The proximal jejunum and distal ileum of mongrel dogs were resected. Warm ischemia was performed by clamping the superior mesenteric artery （SMA） and vein （SMV） for 2 h. Blood flow to the proximal small intestine was restored 1 h after reperfusion, and the distal small intestine was used as a stoma. The experiment was discontinued 6 h after reperfusion. The dogs were divided into two groups： the DHP-PMX group （n = 6, DHP-PMX was performed for 180 min; from 10 min prior to reperfusion to 170 rain after reperfusion） and the control group （n = 5）. The rate pressure product （RPP）, SMA blood flow, mucosal tissue blood flow, and intramucosal pH （pHi） were compared between the two groups. The serum interleukin （IL）-10 levels measured 170 min after reperfusion were also compared.RESULTS： The RPP at 6 h after reperfusion was significantly higher in the PMX group than in the control group （12174 ± 1832 mmHg/min vs 8929 ± 1797 mmHg/min, P 〈 0.05）. The recovery rates of the SMA blood flow at I and 6 h after reperfusion were significantly better in the PMX group than in the control group （61%±7% vs 44% ±4%, P 〈 0.05, and 59%±5% vs 35%±5%, P 〈 0.05, respectively）. The recovery rate of the mucosal tissue blood flow and the pHi levels at 6 h after reperfusion were significantly higher in the PMX group （61%±8% vs 31%±3%, P 〈 0.05 and 7.91±0.06 vs 7.69±0.08, P 〈 0.05, respectively）. In addition, the serum IL-IO levels just before DHP-PMX removal were significantly higher in the PMX group than in the control group （1 569 ± 253 pg/mL vs 211± 40 pg/mL, P 〈 0.05）.CONCLUSION： DHP-PMX therapy reduced warm I/R injury of the small intestine. IL-10 may play a role in inhibiting I/R injury during DHP-PMX therapy.

Pathogenesis of NSAID-induced gastric damage:Importance of cyclooxygenase inhibition and gastric hypermotility

This article reviews the pathogenic mechanism of nonsteroidal anti-inflammatory drug(NSAID)-induced gastric damage,focusing on the relation between cyclooxygenase(COX) inhibition and various functional events.NSAIDs,such as indomethacin,at a dose that inhibits prostaglandin(PG) production,enhance gastric motility,resulting in an increase in mucosal permeability,neutrophil infiltration and oxyradical production,and eventually producing gastric lesions.These lesions are prevented by pretreatment with PGE 2 and antisecretory drugs,and also via an atropine-sensitive mechanism,not related to antisecretory action.Although neither rofecoxib(a selective COX-2 inhibitor) nor SC-560(a selective COX-1 inhibitor) alone damages the stomach,the combined administration of these drugs provokes gastric lesions.SC-560,but not rofecoxib,decreases prostaglandin E 2(PGE 2) production and causes gastric hypermotility and an increase in mucosal permeability.COX-2 mRNA is expressed in the stomach after administration of indomethacin and SC-560 but not rofecoxib.The up-regulation of indomethacin-induced COX-2 expression is prevented by atropine at a dose that inhibits gastric hypermotility.In addition,selective COX-2 inhibitors have deleterious influences on the stomach when COX-2 is overexpressed under various conditions,including adrenalectomy,arthritis,and Helicobacter pylori-infection.In summary,gastric hypermotility plays a primary role in the pathogenesis of NSAID-induced gastric damage,and the response,causally related with PG deficiency due to COX-1 inhibition,occurs prior to other pathogenic events such as increased mucosal permeability;and the ulcerogenic properties of NSAIDs require the inhibition of both COX-1 and COX-2,the inhibition of COX-1 upregulates COX-2 expression in association with gastric hypermotility,and PGs produced by COX-2 counteract the deleterious effect of COX-1 inhibition.

Preventive effects of geranylgeranylacetone on rat ethanolinduced gastritis

AIM:To establish a rat ethanol gastritis model,we evaluated the effects of ethanol on gastric mucosa and studied the preventive effects of geranylgeranylacetone on ethanol-induced chronic gastritis.METHODS:One hundred male Sprague-Dawley rats were randomly divided into 4 equal groups:normal control group,undergoing gastric perfusion of normal saline(NS) by gastrogavage;model control group and 2 model therapy groups that underwent gastric perfusion with ethanol(distillate spirits with 56% ethanol content) by gastrogavage for 4 wk.Low or high doses of geranylgeranylacetone were added 1 h before ethanol perfusion in the 2 model therapy groups,while the same amount of NS,instead of geranylgeranylacetone was used in that model control group.The rats were then sacrificed and stomachs were removed.The injury level of the gastric mucosa was observed by light and electron microscopy,and the levels of prostaglandin 2(PGE 2),endothelin-1(ET-1) and nitric oxide(NO) were measured by radioimmunoassay and the Griess method.RESULTS:The gastric mucosal epidermal damage score(EDS;4.5) and ulcer index(UI;12.0) of the model control group were significantly higher than that of the normal control group(0 and 0 respectively,all P = 0.000).The gastric mucosal EDS and UI of the 2 model therapy groups(EDS:2.5 and 2.0;UI:3.5 and 3.0) were significantly lower than that of the model control group(all P < 0.01).There was no statistically significant difference between the low-dose and high-dose model therapy groups.The expression value of plasma ET-1 of the model control group was higher than that of the normal control group(P < 0.01) and the 2 model therapy groups(all P < 0.01).The expression values of gastric mucosal PGE 2 and serum NO of the model control group were lower than those of the normal control group(all P < 0.05) and the 2 model therapy groups(all P < 0.05).The thickness of the gastric mucous layerand the hexosamine content in the model control group were significantly lower than that in the normal control group(all P < 0.01) and the 2 model therapy groups(all P < 0.05).Scanning and transmission electron microscopy observation showed that in the model control group,the epithelial junctions were vague,the intercellular joints disappeared and damage of the intracellular organelles were significantly worse than those in the normal control group.However,in the 2 model therapy groups,damage to the intercellular joints and organelles was ameliorate relative to the model control group.CONCLUSION:Administration of geranylgeranylacetone was correlated with a more favorable pattern of gastric mucosa damage after ethanol perfusion.The mechanism could be related to regulation of ET-1,NO and PGE 2.

MUC1 and MUC5AC mucin expression in liver fluke-associated intrahepatic cholangiocarcinoma

AIM： To investigate the expressions of MUC1 and MUC5AC in intrahepatic cholangiocarcinoma （ICC）. Association of expressions of mucins MUC1 and MUC5AC with clinical findings, metastasis, and survival of the liver fluke-associated ICC patients was determined. METHODS： The expressions of MUC1 and MUC5AC mucins were examined by immunohistochemical staining in 87 cases of histologically-proven ICC. The expressions of mucins in relationship between clinicopathological significance and prognosis of the patients were evaluated. RESULTS： Fifty-two patients （60%） exhibited both MUC1 and MUCSAC expressions, whereas 31% expressed either MUC1 or MUC5AC, and 9% expressed neither. High MUC1 immunoreactivity displayed a significant correlation wibh tumor progression as reflected by vascular invasion （P〈0.001）, whereas high expression of MUC5AC significantly correlated with neural invasion （P = 0.022） and advanced ICC stage （P = 0.008）. Patients with high expression of MUC1 had a significantly shorter survival （P = 0.0002）. According to multivariate analyses, MUC1 reactivity （P = 0.026）, histological grading and stage of tumor represented the least probability of survival. CONCLUSION： MUC1 is overexpressed in liver flukeassociated cholangiocarcinoma and relates to vascular invasion and poor prognosis, whereas MUC5AC mucin is neoexpressed and relates to neural invasion and advanced ICC stage. High MUC1 expression in tumor may be useful for predicting the poor outcome of ICC patients.

EFFECT OF ELECTROACUPUNCTURE OF "ZUSANLI" ON VIP CONTENTS OF THE PERIPHERAL BLOOD, GASTRIC MUCOSAL AND BRAIN TISSUES IN GASTRIC MUCOSAL INJURY RATS

Objective: To observe the therapeutic effect of electroacupuncture (EA) of "Zusanli"(ST 36) on vasoactive intestinal peptide (VIP) levels in the peripheral blood, gastric mucosal and brain tissues in experimental gastric injury rats. Methods: Gastric mucosal injury model was established by using cold restraining stress method. 40 Wistar rats were randomly and evenly divided into normal control group, model group, EA group and non acupoint group. VIP contents of plasma and gastric mucosal and medulla oblongata tissues were assayed using radioimmunoassay and gastric mucosal blood flow (GMBF) was measured by employing hydrogen clearing method. Results: In cold restraining stress rats, spot and strip like bleeding necrosis foci in the gastric mucous primarily in the gastric antrum could be seen clearly, GMBF and VIP contents in plasma, gastric mucous and brain tissues declined significantly (P<0.05, 0.01), while the gastric mucosal lesion index (LI) raised significantly (P<0.05) in comparison with those of normal control group. Following EA of "Zusanli" (ST 36), GMBF decreased pronouncedly, VIP contents of the plasma, bulba and gastric mucosal tissues increased strikingly in comparison with model group (P<0.01). Conclusion: EA of "Zusanli" (ST 36) possesses a protection effect on gastric mucous under stress condition and VIP is involved in the effect of EA.

Pathophysiology and prevention of postoperative peritoneal adhesions

Peritoneal adhesions represent an important clinical challenge in gastrointestinal surgery. Peritoneal adhesions are a consequence of peritoneal irritation by infection or surgical trauma, and may be considered as the pathological part of healing following any peritoneal injury, particularly due to abdominal surgery. The balance between fi brin deposition and degradation is critical in determining normal peritoneal healing or adhesion formation. Postoperative peritoneal adhesions are a major cause of morbidity resulting in multiple complications, many of which may manifest several years after the initial surgical procedure. In addition to acute small bowel obstruction, peritoneal adhesions may cause pelvic or abdominal pain, and infertility. In this paper, the authors reviewed the epidemiology, pathogenesis and various prevention strategies of adhesion formation, using Medline and PubMed search. Several preventive agents against postoperative peri-toneal adhesions have been investigated. Their role aims in activating fi brinolysis, hampering coagulation, diminishing the inflammatory response, inhibiting col-lagen synthesis or creating a barrier between adjacentwound surfaces. Their results are encouraging but most of them are contradictory and achieved mostly in animal model. Until additional fi ndings from future clinical researches, only a meticulous surgery can be recommended to reduce unnecessary morbidity and mortality rates from these untoward effects of surgery. In the current state of knowledge, pre-clinical or clini-cal studies are still necessary to evaluate the effective-ness of the several proposed prevention strategies of postoperative peritoneal adhesions.

EFFECT OF PREOPERATIVE GLUTAMINE ADMINISTRATION ON ICAM-1 EXPRESSION IN RAT LUNG INDUCED BY INTESTINAL ISCHEMIA-REPERFUSION

Objective To evaluate the effect of preoperative glutamine administration on intracellular adhesion molecule-1 （1CAM-l） expression in rat lung induced by intestinal ischemia-reperfusion（ I/R）. Methods Sprague-Dawley rats （n = 25） were randomly divided into 5 groups： sham group （sham surgery）, glutamine groups （three different doses） and control group. All groups except sham were subjected to intestinal 1/R injury, and superior mesenteric artery （SMA） occluded for 60 min followed by 90 min of reperfusion. Lung injury was evaluated with Evans blue dye concentration and histopathologic examination. The immunohistochemical expression and mRNA expression of 1CAM-1 were measured with immunohistochemical staining and RT-PCR method respectively. The level of myeloperoxidase （MPO） was also measured with biochemistry method. Results Intestinal 1/R resulted in lung injury characterized by an increase in Evans blue dye concentration, neutrophil sequestration, and obvious staining for expression of pulmonary 1CAM-l, compared with sham group. The expression of 1CAM-1 and the level of MPO in rat lung were lower in glutamine groups compared with control group. Conclusion 1-R injury increases the expression of 1CAM-1 within the lung. This may contribute to the migration, accumulation and activation of polymorphonuclear neutrophils （PAINs） after such injury. Preoperative glutamine administration attenuates rat lung injury induced by intestinal I-R, and inhibiting 1CAM-1 expression maybe one of the potential mechanisms.

Effect of nuclear factor kappa B on intercellular adhesion molecule-1 expression and neutrophil infiltration in lung injury induced by intestinal ischemia/reperfusion in rats

AIM： To investigate the role of nuclear factor kappa B （NF-κB） in the pathogenesis of lung injury induced by intestinal ischemia/reperfusion （I/R）, and its effect on intercellular adhesion molecule-1 （ICAM-1） expression and neutrophil infiltration. METHODS： Twenty-four Wistar rats were divided randomly into control, I/R and pyrrolidine dithiocarbamate （PDTC） treatment groups, n = 8 in each. I/R group and PDTC treatment group received superior mysenteric artery （SMA） occluding for 1 h and reperfusion for 2 h. PDTC group was administrated with intraperitoneal injection of 2% 100 mg/kg PDTC 1 h before surgery. Lung histology and bronchia alveolus lung fluid （BALF） protein were assayed. Serum IL-6, lung malondialdehyde （MDA） and myeloperoxidase （MPO） as well as the expression level of NF-κB and ICAM-1 were measured.RESULTS： Lung injury induced by intestinal I/R, was characterized by edema, hemorrhage and neutrophil infiltration as well as by the significant rising of BALF protein. Compared to control group, the levels of serum IL-6 and lung MDA and MPO increased significantly in I/R group （P=0.001）. Strong positive expression of NF-κB p65 and ICAM-1 was observed. After the administration of PDTC, the level of serum IL-6, lung MDA and MPO as well as NF-κB and ICAM-1 decreased significantly （P〈 0.05） when compared to I/R group.CONCLUSION： The activation of NF-κB plays an important role in the pathogenesis of lung injury induced by intestinal I/R through upregulating the neutrophil infiltration and lung ICAM-1 expression. PDTC as an inhibitor of NF-κB can prevent lung injury induced by intestinal I/R through inhibiting the activity of NF-κB.

Hemoperfusion with polymyxin B-immobilized fiber column improves liver function after ischemia-reperfusion injury

AIM： To investigate the usefulness of direct hemoperfusion with a polymyxin B-immobilized fiber column （DHP-PMX therapy） for warm hepatic ischemia-reperfusion （I/R） injury after total hepatic vascular exclusion （THVE） using a porcine model. METHODS： Eleven Mexican hairless pigs weighing 22-38 kg were subjected to THVE for 120 min and then observed for 360 min. The animals were divided into two groups randomly： the DHP-PMX group （n = 5） underwent DHP-PMX at a flow rate of 80 mL/min for 220 min （beginning 10 rain before reperfusion）, while the control group did not （n = 6）. The rate pressure product （RPP）： heart rate x end-systolic arterial blood pressure, hepatic tissue blood flow （HTBF）, portal vein blood flow （PVBF）, and serum aspartate aminotransferase （AST） levels were compared between the two groups. RESULTS： RPP and HTBF were significantly （P 〈 0.05） higher in the DHP-PMX group than in the control group 240 and 360 min after reperfusion. PVBF in the DHP-PMX group was maintained at about 70% of the flow before ischemia and differed significantly （P 〈 0.05） compared to the control group 360 min after reperfusion. The serum AST increased gradually after reperfusion in both groups, but the AST was significantly （P 〈 0.05） lower in the DHP-PMX group 360 min after reperfusion. CONCLUSION： DHP-PMX therapy reduced the hepatic warm I/R injury caused by THVE in a porcine model.

Effects of cardiopulmonary bypass on endothelial cell injury

Objective: To observe the changes of plasma concentrations of endotoxin, soluble intercellular adhesion molecule 1, tumor necrosis factor α, and urinary microalbumin in children undergoing cardiac procedure and to study the effects of cardiopulmonary bypass (CPB) on the injury or activation of endothelial cells and vascular permeability. Methods: Twenty children undergoing cardiac operation with CPB were selected in the study. Plasma concentrations of endotoxin, soluble intercellular adhesion molecule 1, tumor necrosis factor α, and urinary microalbumin were measured after anesthetic induction (baseline), bypass for 20 minutes, at the end of CPB, and at 2, 4, and 18 h after the end of CPB. Results: The plasma concentrations of endotoxin, soluble intercellular adhesion molecule 1, and urinary microalbumin began to increase at 2 h after the end of CPB, and remained higher than that of the baseline, while the concentration of tumor necrosis factor α increased only at the end CPB and at 2 h after the end of CPB. Conclusion: Cardiopulmonary bypass can induce inflammatory response, resulting in the activation or injury of vascular endothelial cells, and can increase the vascular permeability.

Creation of a rabbit model for intrauterine adhesions using electrothermal injury

The pathogenesis and therapeutic treatment of intrauterine adhesions （IUAs） remain unsolved, highlighting the need for stable and effective experimental animal models. In this study, uterine electrocoagulaUon of twenty-one female New Zealand White rabbits was carried out to establish an IUA model. As rabbits have two completely separate uterine horns, each rabbit had its own internal control： one uterine horn was given an electrothermal injury （Group A, n=21）, and the contralateral uterine horn received no treatment and served as the control （Group B, n=21）. The en- dometrial morphology, number of endometrial glands, area of endometrial fibrosis, and number of implanted fetuses were compared between the two groups. In Group A, the numbers of endometrial glands on Days 7 and 14 and the number of implanted fetuses were significantly lower than those in Group B（P〈0.05, P〈0.05, and P〈0.01, respectively）, while the ratio of the area with endometrial stromal fibrosis to the total endometrial area was significantly increased （P〈0.01）. These results suggest that this method of electrothermal injury is effective for the establishment of a rabbit lUA model between 7 and 14 d after surgery.

Stress transfer around a broken fiber in unidirectional fiber-reinforced composites considering matrix damage evolution and interface slipping

A shear-lag model is applied to study the stress transfer around a broken fiber within unidirectional fiber-reinforced composites(FRC) subjected to uniaxial tensile loading along the fiber direction.The matrix damage and interfacial debonding,which are the main failure modes,are considered in the model.The maximum stress criterion with the linear damage evolution theory is used for the matrix.The slipping friction stress is considered in the interfacial debonding region using Coulomb friction theory,in which interfacial clamping stress comes from radial residual stress and mismatch of Poisson's ratios of constituents(fiber and matrix).The stress distributions in the fiber and matrix are obtained by the shear-lag theory added with boundary conditions,which includes force continuity and displacement compatibility constraints in the broken and neighboring intact fibers.The result gives axial stress distribution in fibers and shear stress in the interface and compares the theory reasonably well with the measurement by a polarized light microscope.The relation curves between damage,debonding and ineffective region lengths with external strain loading are obtained.

Platelet-mediated adhesion facilitates leukocyte sequestration in hypoxia-reoxygenated microvessels

Leukocyte transendothelial migration and sequestration are two distinct outcomes following leukocyte adhesion to endotheli- um during ischemia-reperfusion injury, in which platelets may play a pivotal role. In the present study, we established an in vitro hypoxia-reoxygenation model to mimic ischemia-reperfusion injury and found platelet pre-incubation significantly in- creased leukocyte adhesion to endothelial cells after hyoxia-reoxygenation （over 67%）. Blockade of endothelial-cell-expressed adhesion molecules inhibited leukocyte direct adhesion to endothelial cells, while platelet-mediated leukocyte adhesion was suppressed by blockade of platelet-expressed adhesion molecules. Further experiments revealed platelets acted as a bridge to mediate leukocyte adhesion, and platelet-mediated adhesion was the predominant pattern in the presence of platelets. However, platelet pre-incubation significantly suppressed leukocyte transendothelial migration after hypoxia-reoxygenation （over 31%）, which could be aggravated by blockade of endothelial-cell-expressed adhesion molecules, but alleviated by blockade of plate- let-expressed adhesion molecules. This would indicate that platelet-mediated adhesion disrupted leukocyte transendothelial migration. An in vivo meseuteric ischemia-reperfusion model demonstrated leukocyte transfusion alone caused mild leukocyte adhesion to reperfused vessels and subsequent leukocyte infiltration, while simultaneous leukocyte and platelet transfusion led to massive leukocyte adhesion and sequestration within reperfused microvessels. Our studies revealed platelets enhanced leu- kocyte adhesion to endothelial cells, but suppressed leukocyte transendothelial migration. Overall, this leads to leukocyte se- questration in hypoxia-reoxygenated microvessels.