Laser-heated needle for biopsy tract ablation: In vivo study of rabbit liver biopsy

PurposeTo investigate the efficacy of a newly-developed laser-heated core biopsy needle in the thermal ablation of biopsy tract to reduce hemorrhage after biopsy using in vivo rabbit’s liver model.Materials and methodsFive male New Zealand White rabbits weighed between 1.5 and 4.0 kg were anesthetized and their livers were exposed. 18 liver biopsies were performed under control group (without tract ablation, n = 9) and study group (with tract ablation, n = 9) settings. The needle insertion depth (~3 cm) and rate of retraction (~3 mm/s) were fixed in all the experiments. For tract ablation, three different needle temperatures (100, 120 and 150 °C) were compared. The blood loss at each biopsy site was measured by weighing the gauze pads before and after blood absorption. The rabbits were euthanized immediately and the liver specimens were stained with hematoxylin-eosin (H&E) for further histopathological examination (HPE).ResultsThe average blood loss in the study group was reduced significantly (p < 0.05) compared to the control group. The highest percentage of bleeding reduction was observed at the needle temperature of 150 °C (93.8%), followed by 120 °C (85.8%) and 100 °C (84.2%). The HPE results show that the laser-heated core biopsy needle was able to cause lateral coagulative necrosis up to 14 mm diameter along the ablation tract.ConclusionThe laser-heated core biopsy needle reduced hemorrhage up to 93.8% and induced homogenous coagulative necrosis along the ablation tract in the rabbits’ livers. This could potentially reduce the risk of tumor seeding in clinical settings.     

Infection intensity of gastrointestinal nematodosis and coccidiosis of sheep raised under three types of feeding and management regims in Ningxia Hui Autonomous Region, China

By using faecal egg counting, larvae culturing, coccidian oocysts identifying, the present study was conducted to determine infection intensity of nematodosis and coccidosis of young sheep (6–12 months) raised under three types of feeding and management regims namely, confinement system (2 farms, n = 30), semiconfinement system (2 farms, n = 30) and grazing system (2 farms, n = 30) in Ningxia Hui Autonomous Region (NHAR) in China. The mean egg counts of gastrointestinal nematodes were zero in confinement system, 63 EPG in semiconfinement system and 263 EPG in grazing system, while the mean coccidian oocyst counts (oocysts per gram of faeces, OPG) of each regim were 3784, 1713 and 687, respectively. Gastrointestinal parasite loads of sheep were attributed to low EPG (zero EPG) in confinement, moderate EPG in semiconfinement and high EPG in grazing regim, respectively, which in turn resulted in high OPG in confinement, moderate OPG in semiconfinement and low OPG in grazing regim, respectively. The infection rate of nematodes of sheep was zero in confinement, 43.33% in semiconfinement and 96.67% in grazing regim, while the infection rate of coccidia was 100%, 96.67% and 86.67%, respectively. The nematodes of sheep in grazing regim were, in the order of prevalence: Ostertagia (Teladorsagia) (80.00%), Marshallagia (66.67%), Nematodirus (63.33%), Trichostrongylus (43.33%), Haemonchus contortus (43.33%), and Chabertia (16.67%), while in semiconfinement regim were, in the same order of prevalence: 43.33%, 10.00%, 40.00%, 20%, 20% and 0%, respectively. Seven species of Eimeria were recognized in the three management regims. Their prevalence rates were E. parva (85.56%), E. ahsata (70.00%), E. ovinoidalis (34.44%), E. intricata (21.11%), E. crandallis (20.00%), E. granulosa (18.89%), and E. faurei (5.56%). These results may provide a further understanding of the factors associated with parasite epizootiology under different feeding and management regims.     

Modulation of malaria-induced immunopathology by concurrent gastrointestinal nematode infection in mice

We investigated malaria-associated pathology in mice co-infected with Heligmosomoides polygyrus (Hp) and Plasmodium chabaudi AS (Pc). Despite higher peak parasitemia, co-infected wild-type (WT) C57BL/6 mice displayed similar body weight losses, malarial anaemia, and tissue damage but less severe hypothermia and hypoglycaemia, and earlier reticulocytosis than Pc-infected WT mice. Co-infected STAT6^−/− mice, deficient in nematode-induced Th2 responses, experienced similar peak parasitemias and generally suffered malaria-associated pathology to a similar degree as co-infected WT mice. These data indicate a complex relationship amongst helminths, malaria and host immune responses resulting in modulation of some but not all aspects of malaria-associated pathology.     

A temporal shift in regulatory networks and pathways in the bovine small intestine during Cooperia oncophora infection

Cooperia oncophora is an important parasitic nematode of cattle with a wide distribution in temperate areas. Twenty Holstein nematode-naïve bull calves were experimentally infected with approximately 100,000 infective L3s and infection was allowed to progress for 7, 14, 28, 42 days, respectively. This experiment was conducted to identify putative recognition and inflammatory pathways in the host-parasite relationship. Gene expression profiles of the small intestine were compared using a high-density bovine 60 mer oligo microarray. A total of 310 genes were differentially expressed during the course of infection. The pathways and regulatory networks significantly impacted by the infection were analysed. A total of 22 canonical pathways and nine regulatory networks were significantly affected during infection. During the early phase of the infection (7 days p.i.), parasites suppressed the acute phase response and the complement system of the host. At 14 days p.i., three out of the six pathways impacted were related with retinoid X receptor (RXR) functions. At 28 days p.i., the effects on RXR were less evident. The host response shifted to lipid metabolism and signalling, especially eicosanoid production and signalling, suggesting that eicosanoid-mediated inflammation might be a major host defence mechanism. By 42 days p.i., the pathways impacted involved glycosphingolipid biosynthesis and transforming growth factor β (TGFβ signalling. The expression of cadherin-like 26 (CDH26) was strongly up-regulated starting at 14 days p.i. and peaked at 28 days p.i. The extent of its expression is positively correlated with the infiltration of eosinophils (R = 0.82) and coincides with the number of adult parasites in the tissue. CDH26 demonstrated an expression profile similar to two other cell adhesion molecules involved in recognition of carbohydrates on foreign organisms, collectin and galectin, suggesting that it may serve as a pattern recognition molecule for C. oncophora. These results provide a potential molecular roadmap for future studies aimed at defining host immune responses and understanding protective immunity against gastrointestinal nematodes.     

PBL联合CBL教学方法在胃肠外科临床见习教学中的应用

目的:探讨PBL联合CBL教学模式在医学生胃肠外科见习教学中的应用效果.方法:选取50名2008级胃肠外科见习医学生作为研究对象,将其随机分成两组:实验组采用PBL联合CBL教学模式,对照组则仅采用传统LBL教学模式.通过出科考核及问卷调查两种方式评价胃肠外科见习教学效果.结果:显示PBL+ CBL组的考试成绩要明显优于LBL组,差异有统计学意义(P＜ 0.05),并且见习后的问卷调查结果提示学生对PBL+ CBL的教学模式满意度较高.结论:我们的研究结果表明PBL+ CBL双轨教学模式受到学生欢迎,在提高学生理论知识水平方面比LBL模式更为有效.     

Expression pattern of the homeotic gene Bapx1 during early chick gastrointestinal tract development

Regulation of the Bone Morphogenetic Protein (BMP) signaling pathway is essential for the normal development of vertebrate gastrointestinal (GI) tract, but also for the differentiation of the digestive mesenchymal layer into smooth muscles and submucosal layer. Different studies demonstrated that Bapx1 (for bagpipe homeobox homolog 1) negatively regulates the BMP pathway, but its precise expression pattern during the development and the differentiation of the GI tract mesenchyme actually remains to be examined. Here, we present the spatio-temporal expression profile of Bapx1 in the chick GI tract. We show that Bapx1 is first expressed in the undifferentiated mesenchyme of the gizzard and the colon. After the differentiation of the digestive mesenchyme, we found Bapx1 strongly expressed in the gizzard smooth muscle and in the submucosa layer of the colon. This expression pattern provides new insights into the roles of Bapx1 during the regionalization of the GI tract and the differentiation of the digestive mesenchyme of the colon and the stomach.     

Isolation of Primary Myofibroblasts from Mouse and Human Colon Tissue

The myofibroblast is a stromal cell of the gastrointestinal (GI) tract that has been gaining considerable attention for its critical role in many GI functions. While several myofibroblast cell lines are commercially available to study these cells in vitro, research results from a cell line exposed to experimental cell culture conditions have inherent limitations due to the overly reductionist nature of the work. Use of primary myofibroblasts offers a great advantage in terms of confirming experimental findings identified in a cell line. Isolation of primary myofibroblasts from an animal model allows for the study of myofibroblasts under conditions that more closely mimic the disease state being studied. Isolation of primary myofibroblasts from human colon tissue provides arguably the most relevant experimental data, since the cells come directly from patients with the underlying disease. We describe a well-established technique that can be utilized to isolate primary myofibroblasts from both mouse and human colon tissue. These isolated cells have been characterized to be alpha-smooth muscle actin and vimentin-positive, and desmin-negative, consistent with subepithelial intestinal myofibroblasts. Primary myofibroblast cells can be grown in cell culture and used for experimental purposes over a limited number of passages.     

The Citrobacter rodentium Mouse Model: Studying Pathogen and Host Contributions to Infectious Colitis

This protocol outlines the steps required to produce a robust model of infectious disease and colitis, as well as the methods used to characterize Citrobacter rodentium infection in mice. C. rodentium is a gram negative, murine specific bacterial pathogen that is closely related to the clinically important human pathogens enteropathogenic E. coli and enterohemorrhagic E. coli. Upon infection with C. rodentium, immunocompetent mice suffer from modest and transient weight loss and diarrhea. Histologically, intestinal crypt elongation, immune cell infiltration, and goblet cell depletion are observed. Clearance of infection is achieved after 3 to 4 weeks. Measurement of intestinal epithelial barrier integrity, bacterial load, and histological damage at different time points after infection, allow the characterization of mouse strains susceptible to infection.The virulence mechanisms by which bacterial pathogens colonize the intestinal tract of their hosts, as well as specific host responses that defend against such infections are poorly understood. Therefore the C. rodentium model of enteric bacterial infection serves as a valuable tool to aid in our understanding of these processes. Enteric bacteria have also been linked to Inflammatory Bowel Diseases (IBDs). It has been hypothesized that the maladaptive chronic inflammatory responses seen in IBD patients develop in genetically susceptible individuals following abnormal exposure of the intestinal mucosal immune system to enteric bacteria. Therefore, the study of models of infectious colitis offers significant potential for defining potentially pathogenic host responses to enteric bacteria. C. rodentium induced colitis is one such rare model that allows for the analysis of host responses to enteric bacteria, furthering our understanding of potential mechanisms of IBD pathogenesis; essential in the development of novel preventative and therapeutic treatments.     

Balancing on the crest – Evidence for disruption of the enteric ganglia via inappropriate lineage segregation and consequences for gastrointestinal function

Normal enteric nervous system (ENS) development relies on numerous factors, including appropriate migration, proliferation, differentiation, and maturation of neural crest (NC) derivatives. Incomplete rostral to caudal migration of enteric neural crest-derived progenitors (ENPs) down the gut is at least partially responsible for the absence of enteric ganglia that is a hallmark feature of Hirschsprung disease (HSCR). The thought that ganglia proximal to aganglionosis are normal has guided surgical procedures for HSCR patients. However, chronic gastrointestinal dysfunction suffered by a subset of patients after surgery as well as studies in HSCR mouse models suggest that aberrant NC segregation and differentiation may be occurring in ganglionated regions of the intestine. Studies in mouse models that possess enteric ganglia throughout the length of the intestine (non-HSCR) have also found that certain genetic alterations affect neural crest lineage balance and interestingly many of these mutants also have functional gastrointestinal (GI) defects. It is possible that many GI disorders can be explained in part by imbalances in NC-derived lineages. Here we review studies evaluating ENS defects in HSCR and non-HSCR mouse models, concluding with clinical implications while highlighting areas requiring further study.