Microvascular circulation of the ascending colon in healthy horses was studied using microangiography, light microscopy, and scanning electron microscopy. The pelvic flexure with 30 cm of ventral and dorsal colon attached was removed from 14 adult horses immediately after horses were euthanatized. The lumen was flushed with warm water, and this section of the ascending colon was placed in a 37-C bath of isotonic NaCl. In sections from 8 horses, colic vessels were perfused with a radio-opaque medium for microangiography. After angiographic evaluation, tissue sections were prepared for light microscopic observation, using standard histologic methods. In sections from 6 horses, injection replicas were made by perfusing the vessels with 2 types of plastics. The results of microangiography, light microscopy, and scanning electron microscopy of vascular replicas were correlated, providing acomprehensive documentation of the microvasculature of the ascending colon at the pelvic flexure. Arteries branched from mesenteric colic vessels approximately every 2 cm toward the colonic tissue. Immediately after branching, arterial vessels formed an anastomotic plexus, the colonic rete. However, each branch from the colic vessel eventually continued into the colonic tissue. A second set of vessels originated from the colonic rete and supplied the mesenteric lymph nodes. Arterial vessels penetrated the tunica muscularis into the sub-mucosa 3 to 4 cm toward the antimesenteric border forming a submucosal vascular network. From the submucosal arterioles, branching took place at right angles to supply the mucosal capillaries. Capillaries surrounded the colonic glands and anastomosed at the luminal surface, forming a superficial luminal honeycomb-appearing vascular plexus. Venules, sparsely distributed, drained the superficial plexus. Arterial venous anastomoses were not observed within the mucosa.

The purpose of this study was to investigate the protective effect of hydrogen-rich saline (HRS) against liver ischaemia-reperfusion combined resection injury. Eighteen miniature pigs were randomly divided into three groups: a sham operated group (sham group, laparoscopic liver ischaemia-reperfusion combined resection injury group (IRI group), and a hydrogen-rich saline intervention group (IRI + HRS group). Samples of hepatic tissue and serum were collected at the time of reperfusion and then 3 h, 1 d, and 3 d post reperfusion. Liver function, oxidative stress, autophagy-related mRNA genes, and protein expression were evaluated. Changes in cell and tissue ultrastructure were examined by transmission electron microscopy. Compared with the sham group, the level of autophagy of hepatocytes increased in the IRI and IRI + HRS groups, corresponding to high oxidative stress and severe liver function injury. Liver function, antioxidant content, autophagy levels, and liver injury were improved after intervention with HRS in the IRI + HRS group compared with the IRI group. Intervention with hydrogen-rich saline could exert a protective effect against liver ischaemia-reperfusion combined resection injury through the reduction of oxidative stress and hepatocyte autophagy.

Introduction: The functions and mechanisms of prion proteins (PrPC) are currently unknown, but most experts believe that deformed or pathogenic prion proteins (PrPSᶜ) originate from PrPC, and that there may be plural main sites for the conversion of normal PrPC into PrPSᶜ. In order to better understand the mechanism of PrPC transformation to PrPSᶜ, the most important step is to determine the replacement or substitution site. Material and Methods: BALB/c mice were challenged with prion RML strain and from 90 days post-challenge (dpc) mice were sacrificed weekly until all of them had been at 160 dpc. The ultra-structure and pathological changes of the brain of experimental mice were observed and recorded by transmission electron microscopy. Results: There were a large number of pathogen-like particles aggregated in the myelin sheath of the brain nerves, followed by delamination, hyperplasia, swelling, disintegration, phagocytic vacuolation, and other pathological lesions in the myelin sheath. The aggregated particles did not overflow from the myelin in unstained samples. The phenomenon of particle aggregation persisted all through the disease course, and was the earliest observed pathological change. Conclusion: It was deduced that the myelin sheath and lipid rafts in brain nerves, including axons and dendrites, were the main sites for the conversion of PrPC to PrPSᶜ, and the PrPSᶜ should be formed directly by the conversion of protein conformation without the involvement of nucleic acids.

Sixteen white Wistar female rats were divided into two equal groups. Experimental group received per os 40 mg/kg b.w. of L-arginine, every other day for 2 weeks and were decapitated after 3 weeks of the experiment. Control rats received in the same manner 2 ml of distilled water and were decapitated after 3 weeks of the experiment. The renal lesions observed under electron microscope were of focal character and concerned only the experimental group. The tubules with necrotic cells were observed among normal tubules or single normal epithelial cells of the tubular wall. The boundaries between epithelial cells of the tubule wall were blurred. The mitochondria indicated abnormal structure. Numerous lysosomes and peroxysomes with dark, homogenous content were observed. The rough endoplasmic reticulum had widened channels and was focally completely destroyed. The nucleus of damaged cells was most commonly located in one of the cell poles; its shape was changed and visibly smaller than the nuclei of normal cells. Condensation and peripherally located chromatin were noticed. The lesions observed were characteristic for apoptotic cells.

The study investigated the effect of various doses of carbendazim on the morphology of the magnum of the Japanese quail. No morphological changes were observed in the magnum in birds treated with carbendazim at doses of 25 mg/kg and 100 mg/kg bodyweight. A carbendazim dose of 400 mg/kg bodyweight was the lowest dose which caused morphological changes in the magnum. Histologically, carbendazim caused pyknosis and glandular atrophy in the magnum mucosa. Carbendazim also caused significant decreases in the height of the mucosal folds, epithelial height, glandular width and glandular luminal diameter at 400 mg/kg and 800 mg/kg (p < 0.05). At ultrastructural level, dose-dependent deciliation was observed. Pyknotic nuclei, dilated cisternae of rough endoplasmic reticulum, swollen mitochondria, numerous vacuoles and lysosomes in the luminal and glandular epithelia were identified. The observed degenerative changes could be due to cytoskeletal disruption caused by carbendazim toxicity. Degeneration of the luminal and glandular cells in the magnum pose a potential threat to the egg production and reproduction of exposed birds.

Injury due to burning is known to impact on coagulation and haemostasis by disturbing the coagulation cascade and is also associated with impaired fibrinolysis. Also, venous thrombosis, pulmonary embolism and hypercoagulability are common during thermal injury. Using a Wistar albino rat model, we investigated in this study whether burn injury affects the ultrastructure of the fibrin networks. A typical fibrin network will contain mostly major, thick fibres with minor, thin fibres distributed amongst them. We found that the clot architecture changes after burn injury, showing more prominent minor, thin fibres in a netted appearance. Also, the clot showed areas of matted fibrin. We suggest that the thrombotic events associated with burn injury are due to the thickened and netlike areas formed when thrombin activates the coagulation cascade. This is due to impaired fibrinolysis activities, causing the resulting fibrin clots not to be successfully disseminated. Small fragments of these netted, clumped areas may therefore break loose and lead to thrombotic events after burn injuries. The current study therefore provided morphological evidence for thrombotic events associated with burn injury.