However, cell inactivation was not significantly observed at concentrations of 10 6 , 10 7 cfu/ml even after an exposure of 150 min. Ultrastructural changes of treated bacteria showed deformation, rough damage and surface destruction revealed by scanning electron microscopy. Some bacterial cells showed collapsed and shrunken patterns within 60 min and severe rupture and cellular lysis after 90 min of ozone treatment. This study supports the proposed mechanism of the bacteria inactivation by ozone that caused cell membrane destruction and finally lysis reaction. Thus, the precaution of using ozone as a biocide should be used to address appropriate concentrations of bacterial contamination in water.

Living PC12 cells, a model cell type for studying neuronal function, were imaged using the negative feedback mode of a scanning electrochemical microscope (SECM). Six biocompatible redox mediators were successfully identified from a large pool of candidates and were then used for imaging PC12 cells before and after exposure to nerve growth factor (NGF). When exposed to NGF, cells differentiate into a neuron phenotype by growing narrow neurites (1-2 microm wide) that can extend > 100 microm from the cell proper. We demonstrate that carbon fiber electrodes with reduced tip diameters can be used for imaging both the cell proper and these neurites. Regions of decreased current, possibly resulting from raised features not identifiable by light microscopy, are clearly evident in the SECM images. Changes in the morphology of undifferentiated PC12 cells could be detected in real time with the SECM. After exposure to hypotonic and hypertonic solutions, reversible changes in cell height of <2 microm were measured.

The liver, which produces a large volume of lymph, has a lymphatic system which can be classified into three categories: portal, sublobular, and superficial lymphatic vessels. As little is known about the origin and pathways of sublobular lymph, this study demonstrates pathways of interstitial fluid flowing into sublobular lymphatic vessels. Livers from cats whose thoracic ducts were either ligated or non-ligated were examined by light-, transmission electron- and scanning electron-microscopy (SEM). Complete ligation of the thoracic duct caused significant dilation of the hepatic sinusoids, the space of Disse, and channels passing through the limiting plate. Sublobular interstitial space and sublobular lymphatic vessels were also expanded. The channels between hepatocytes forming the limiting plate contained collagen fibers, and connected the space of Disse with a sublobular interstitial space. The alkali-water maceration/SEM confirmed that collagen fibers traversing the layer of the limiting plate independently of blood vessels connected collagen fibers in the space of Disse with those in the sublobular space. Complete ligation of the thoracic duct also showed an accumulation of mast cells and plasma cells in the sublobular interstitial space. Our data suggest that fluid in the space of Disse flows along collagen fibers in channels traversing the limiting plate as well as those along the sinusoids and central veins that drain into sublobular veins, and enters the sublobular interstitial space to finally lead into sublobular lymphatic vessels. Our study has also shown that hepatic lymphostasis causes the accumulation of mast cells and plasma cells in the sublobular interstitial space, which may be involved in lymphangiogenesis and fibrogenesis.

No abstract

Abnormalities in insulin hormone levels leads to a hyperglycemic condition of diabetic mellitus. Hyperglycemia seriously induces organ and system destructions. The excessive accumulation of collagen fiber deposits occurs in inflammatory and reorganization processes of chronic liver diseases in type I insulin-dependent diabetes. Regarding the research objective, glabridin (GLB), an active compound of licorice, was used as a daily supplement (40 mg/kg) in order to decrease hepatocyte destruction and collagen deposition in liver tissue of diabetic animals induced by streptozotocin. A total of 40 were randomly allocated to five groups (each, n=10), control, control treated with GLB (GLB), diabetic rats (DM) injected with single dose of streptozotocin (60 mg/kg) to induce a diabetic condition, diabetic rats receiving GLB (DM+GLB; 40 mg/kg) and diabetic rats treated with glibenclamide (DM+GL; 4 mg/kg). Characteristic histopathological changes in liver cells and tissues of rats were determined by Masson's trichrome staining and transmission electron microscopy (TEM). Western blotting was used to detect the expression of the key markers, collagen type I and fibronectin proteins. The histological investigation of liver tissue of the DM group revealed that the collagen fiber deposition was increased in the periportal, pericentral and perisinusoidal spaces compared with controls. Hepatocytes appeared as small and fragmented cells in TEM examination. Collagenization of the perisinusoidal space was recently demonstrated to represent a new aspect of the microvascular abnormalities and liver fibrosis. Healthy hepatocytes with round nucleus were observed following supplementation of glabridin. In addition, collagen fiber deposition was reduced in the area adjacent to the perisinusoidal space. The expression of collagen type I and fibronectin decreased strongly following glabridin supplementation in DM+GLB rats compared with DM rats, indicating that the hepatic tissue reorganization regained its normal morphology. These findings suggest that it may be beneficial to examine the role of glabridin as a therapeutic agent in diabetes treatment in future research.