Effect of lansoprazole on gastric ulceration in rats

AIM:To investigate the effect of lansoprazole on gastric ulceration in rats. METHODS:Using the gastric ulcer model induced by hemorrhagic shock, restraint water-immersion stress and pylorus-ligature, the protective effect of lansoprazole (iv) on gastric ulceration was observed. RESULTS:Pretreatment with lansoprazole (7.5-60 mg/kg) significantly inhibited the formation of gastric ulcer in the three models in a dose-dependent manner. The autiulcer efficacy of lansoprazole was similar to that of omeprazole in the equal dose, but stronger than that of omeprazole for ulcer induced by water-immersion stress.CONCLUSION:The intravenously administered lansoprazole inhibited formation of experimental gastric ulcer in rats.     

Grid keratotomy as a treatment for superficial nonhealing corneal ulcers in 10 horses

OBJECTIVE: To describe the clinical symptoms of 10 cases of superficial nonhealing corneal ulcers in horses and to evaluate the results of grid keratotomy in these patients. DESIGN: Retrospective study. ANIMALS: Ten horses with superficial nonhealing corneal ulceration in one eye. PROCEDURE: The signalment, history and clinical symptoms are reported of 10 patients with superficial nonhealing corneal ulcers during the period from August 2003 to February 2005. Grid keratotomy was performed in all cases. In addition, the surgical procedure of grid keratotomy and response to therapy are described. RESULTS: Horses generally responded well to grid keratotomy (eight cases healed after one grid keratotomy and one horse healed after a second grid keratotomy; one case was not available for follow-up). Only 2/10 had discomfort after treatment and only 2/9 had some degree of scarring after treatment. The healing time, which was known in seven cases, averaged 8.4 days (+/- SD 4). CONCLUSIONS AND CLINICAL RELEVANCE: Grid keratotomy is an appropriate option for treatment of superficial nonhealing corneal ulcers in horses. The procedure is simple to perform. It generally induces a rapid and uncomplicated healing of the cornea. Only in a limited number of cases does a small amount of scarring occur.     

Superficial, nonhealing corneal ulcers in horses: 23 cases (1989-2003)

Objective To characterize superficial, nonhealing corneal ulcers in the horse and to assess the affect of age, breed, sex, inciting cause of the ulcer, and treatment on healing time of these ulcers. Design Retrospective study. Animals Twenty‐three horses with superficial, nonhealing corneal ulcerations. Procedure Medical records from 1989 to 2003 of horses diagnosed with superficial, nonhealing corneal ulcers were reviewed. Signalment, duration of clinical signs, ophthalmic abnormalities, treatment and response to treatment were recorded. Horses were treated, in addition to medical therapy, using debridement, debridement and grid keratotomy, superficial keratectomy, and superficial keratectomy with conjunctival graft placement. Results Mean age ± SD of horses was 13.7 ± 5.8 years. The mean time of presence of the corneal ulceration was 38.9 ± 21.3 days. Mean time to complete re‐epithelialization of the corneal ulcers after treatment was 20 ± 14.7 days. Horses treated with debridement alone, grid keratotomy and superficial keratectomy healed in a mean time of 15.3 ± 14.6 days, 16 ± 12.6 days, and 22.8 ± 6.7 days, respectively. Conclusions and clinical relevance Horses treated with a single debridement at initial evaluation healed in a significantly shorter time period than horses treated with grid keratotomy or superficial keratectomy. The latter two procedures may be beneficial in the treatment of nonhealing ulceration in horses, but the results of this study suggest that these procedures should only be performed following failure of the ulcer to heal after epithelial debridement.     

Cataract phacofragmentation in horses

Cataract surgeries were carried out in fifty-one eyes of 36 horses over a 15-year period. Cataracts were removed using phacofragmentation and aspiration. Useful vision was restored after surgery in 30 horses. One year after surgery 16 of the 19 horses for which follow up information was available were still visual with several still being used as working horses. At 5-6 years after surgery three horses were still visual. The most frequent intraoperative complication was tearing of the posterior lens capsule. The most frequent postoperative problem was superficial corneal ulceration. Four eyes in three horses developed postoperative infectious endophthalmitis resulting in blindness.     

斑点叉尾鮰暴发性出血溃疡症的病理学研究

【目的】探究两起斑点叉尾鮰Ietalurus punetaus暴发性体表出血溃疡症的发病病因和病理特征。【方法】利用湿片法对鳃组织和体表黏液进行压片,观察寄生虫寄生情况。从发病鱼的肝脏、脾脏和肾脏中分离病原菌,检测细菌感染情况;利用PCR法检测患病斑点叉尾鮰的肝、脾、肾混合组织匀浆中斑点叉尾鮰病毒(Channel catfish virus,CCV)的携带情况。运用组织病理学方法观察病鱼的病理损伤特点,综合分析并推测该病的致病原因。【结果】该出血溃疡症的靶器官主要为脾脏、肾脏、肝胰脏、肠道以及皮肤肌肉。主要表现为严重的血管反应,实质细胞可见肿胀、变性、坏死;而胃、脑和心脏病变较轻,仅有轻微的炎症;鳃丝、眼球和鳔等未见明显病变。所有的患病个体均出现中度至重度出血性坏死性脾炎、中度肾炎、轻度至中度坏死性肝胰腺炎和肠炎。患病斑点叉尾鮰体内未检测到寄生虫、细菌以及CCV。【结论】综合病理学、细菌学和病毒学检测结果,推测此次斑点叉尾鮰暴发性疾病由某种非CCV的病毒感染所致,温度应激可能是引发该病的条件诱因。     

灰额刺尾鱼溃疡病病原分离及鉴定

从灰额刺尾鱼(Acanthurus glaucopareius)体表溃烂处及内脏器官中分离到5株较强致病力的菌株,经过人工感染健康鱼证实该菌株是致病菌。对该病原菌进行了形态、生理生化反应测试,结果显示为溶藻弧菌(Vibrioalginolyticus)。应用细菌16S rDNA的通用引物对该菌基因组DNA进行PCR扩增、克隆测序,得到1条长度为1 392 bp的核苷酸序列,该序列与溶藻弧菌(登录号GQ455008)的16S rDNA基因序列同源性达99%,进一步确定该致病菌为溶藻弧菌。药敏试验结果表明,该菌株对痢特灵、氟哌酸、环丙沙星等药物敏感,对甲氧胺嘧啶、氨苄青霉素、阿米卡星、青霉素等药物耐药。研究亮点:通过系统的病原学试验研究,证实了灰额刺尾鱼溃疡病的病原为溶藻弧菌,并验证了该病原菌的药物敏感性等特性,以及对该病的病症、病因及临床治疗方法进行了分析,这些结论尚属首次报道,为灰额刺尾鱼溃疡病以及其他海水观赏鱼同类疾病的临床诊断和防治技术提供科学依据。     

Expression of Wnt1 and LGR5 in gastric mucosa with stress ulcer after TBI in rats

AIM To investigate the expression of Wnt1 and LGR5 in gastric mucosa with stress ulcer after traumatic brain injury （TBI） in rats, and to study the relationship between Wnt1/LGR5 expression and stress ulcer after TBI. METHODS Healthy 7-week-old male SD rats （n=30） were randomly divided into 3 groups： sham operation （sham） group, mild TBI （mTBI） group, and severe TBI （sTBI） group. The mTBI and sTBI were induced by electronic cortical contusion impactor. Neurological severity score （NSS） was calculated 24 and 48 h after modeling. Mucosal blood flow in gastric fundus, greater curvature, pylorus and cardia of anesthetized rats 48 h after injury was measured by Doppler flowmeter. All rats were sacrificed, and their gastric tissues were harvested after 48 h and then stained with hematoxylin and eosin. The protein expression of Wnt1 and LGR5 was analyzed by Western blot and immunohistochemistry. RESULTS Compared with sham group, the NSS in mTBI group and sTBI group was significantly increased （P<0.01）. Compared with sham group, the gastric mucosal blood flow of the rats after TBI was significantly decreased （P<0.01）, and the decrease in sTBI group was more significant than that in mTBI group （P<0.05）. The protein expression of Wnt1 and LGR5 in mTBI group was significantly higher than that in sham group （P<0.05）, and that in sTBI group was significantly higher than that in mTBI group （P<0.05）. Normal glandular gastric tissue was observed, and no abnormal change was found in sham group, while the infiltration of inflammatory cells in gastric lamina propria, mucosa and submucosa was obvious in mTBI group and sTBI group. CONCLUSION Traumatic brain injury activates Wnt1 and LGR5 expression to induce inflammatory changes in gastric mucosa, and then induces stress ulcer. This results provides experimental basis for the pathogenesis and treatment of stress ulcer after trauma.