Vascular Network Structure Research Articles

Clinical analysis and endoscopic findings of early esophageal cancer

Objective To research the characteristics of early esophageal cancer's endoscopy and its clini-cal diagnosis. Methods Retrospective analyze the clinical symptoms and endoscopy performance of the 24 cases of early esophageal cancer which were confirmed by opemtion. Results Unaided eye observing of 24 cases of early e-acphageal cancer:diameter of pathological changes within 1.0 cm,there are four cases of the surface rough,turbidity,vascular fuzzy texture, congestive mucosa, small pieces of rotten to the core, around the realm of clear, easy bleeding by touch of three cases. Mucosa focal irregular plaquelike erosion or superficial helcosis of five cases Mucosa mild uplift,smooth surface or erosion, with slightly different colors of 10 cases ( including one case of pelypoid change) Mucosa fo-cal wormhole-like change, a slight hollow, moss-covered, rubeosis or bleeding lesions after water rinse, irregular and clear borders of two cases, pathology report: one case of small cell carcinoma,one case of adenocarcinoma (cardia),High-level intraepithelial neoplasia transformation nine cases, one case of poorly differentiated adenocarcinoma, 12 ca-ses of squamous cell carcinoma. Conculsion Endoscopic early esophageal cancer for the mainfeatures of the mucous membrane color changes, mucosal thickening, transparency and mucosal vascular network st ructure changes, and mu-cosal rough, nodules, plaques, erosion and uplift superficial, shallow depression and other patterns chang, GeneraUe-sions were confined or isolated like chang, irregular, and the mucous membrane around the borderclear. Clinicalofte misdiagnosed, missed diagnosis, early diagnosis to have significant value. Key words: Esophageal neoplasms; Gastroscopy

Endothelial Signals Modulate Hepatocyte Apicobasal Polarization in Zebrafish

Emerging evidence indicates that paracrine signals from endothelial cells play a role in tissue differentiation and organ formation [1-3]. Here, we identify a novel role for endothelial cells in modulating hepatocyte polarization during liver organogenesis. We find that in zebrafish, the apical domain of the hepatocytes predicts the location of the intrahepatic biliary network. The refinement of hepatocyte polarization coincides with the invasion of endothelial cells into the liver, and these endothelial cells migrate along the maturing basal surface of the hepatocytes. Using genetic, pharmacological, and transplantation experiments, we provide evidence that endothelial cells influence the polarization of the adjacent hepatocytes. This influence of endothelial cells on hepatocytes is mediated at least in part by the cell-surface protein Heart of glass and contributes to the establishment of coordinately aligned hepatocyte apical membranes and evenly spaced intrahepatic conduits.

HMG‐CoA reductase inhibitors improve microvascular outcomes in the metabolic syndrome independent of plasma cholesterol profile

The obese Zucker rat (OZR) is afflicted with moderate hypercholesterolemia (HC), and previous studies suggest that vascular dysfunction in OZR is associated with chronic loss of nitric oxide (NO) bioavailability and chronic elevation in inflammation, also associated with HC. As such, we evaluated the impact of anti-HC therapy on vascular outcomes in OZR, and effects on inflammation and NO bioavailability. OZR were treated with gemfibrozil, probucol, atorvastatin or simvastatin for 10 weeks. Subsequently, plasma/vascular samples were collected for biochemical/molecular analyses, while vascular reactivity and network structure were assessed. All therapies were effective in reducing cholesterol, though only statins improved indices of NO bioavailability. Similarly, statins caused modest improvements to wall mechanics, these agents strongly attenuated microvascular rarefaction in OZR, and improved active hyperemia in gastrocnemius. Additionally, statin therapy reduced inflammatory state in OZR, such that most measured markers of inflammation were correlated with improved microvascular outcome. However, using discriminant analyses, plasma IL-10, RANTES, IL-1β and IL-4 were determined to be the strongest contributors to differences between groups. These results provide a framework for targeted investigation into mechanistic determinants of poor vascular outcomes in the metabolic syndrome.

Flexor digitorum profundus tendon to bone tunnel repair: A vascularization and histologic study in canines

Recent in vivo canine studies have shown incomplete restoration of the flexor digitorum profundus (FDP) insertion site after transection and repair to the cortical surface of the distal phalanx. Previous biomechanical analyses of tendon to bone surface repair have suggested that repair site gap formation of greater than 3 mm occurs frequently under physiologic loads. A recent ex vivo investigation into a novel repair of the FDP tendon into a bone tunnel in the distal phalanx showed improved tensile properties with a decrease in repair site gap formation. Time-zero data, however, do not always accurately reflect in vivo responses. The repair response of the FDP tendon when placed in an osseous compartment is not known. The purpose of this study was to analyze the histologic and vascular anatomic properties of the FDP insertion site after transection and repair in a bone tunnel within the distal phalanx. Twenty-six FDP tendon to bone repairs were performed in 13 adult mongrel dogs after insertion site transection. The tendons were repaired in a bone tunnel in the distal phalanx. Vascular analysis of the tendon and repair site was performed by using a modified Spalteholtz technique and routine hematoxylin-eosin staining was used to assess histologic properties of the repair. In normal specimens the vascular analysis showed that there was a distal network of vessels extending 1- to 2-cm proximal to the FDP insertion site. At 10 days after repair the distal tendon segment tendon remained avascular. By 21 days after repair there was proximal migration of an unorganized reticular network of tendon surface vessels with sparse intratendinous communications. At 6 weeks after repair the structure of the distal tendon vascular network resembled that of normals. The vascular response of the tendon within the bone tunnel followed a similar time frame. Histologic analysis showed an inflammatory reaction in the bone tunnel leading to a progressive degradation of that portion of the FDP tendon that resided in the tunnel. Tendon necrosis was not seen. The FDP tendon, after insertion site transection and repair in a bone tunnel, undergoes a process of neovascularization and revascularization over a period of 6 weeks. There is a progressive loss of tendon parenchyma within the bone tunnel and the suture tracks appeared to serve as conduits for the ingrowth of inflammatory tissue. Restoration of the normal 4-zone tendon-bone interface was not seen. Although ex vivo biomechanical assessment of tendon repair in a bone tunnel appears promising, the repair response in vivo may not be favorable for tendon to bone healing. The progressive tendon degeneration that was observed here may have detrimental effects on repair site tensile properties, increasing the potential for early failure.

A New Approach to the Study of Skin Vascularization

There are several methods of quantifying the vascularization of tissues, including the skin, but they are imprecise in terms of quantification of the complexity and structure of vascular networks. Fractal analysis can quantify the complexity of any structure existing in nature by using fractional dimension. This study makes a case for this approach by demonstrating the fractal structure of the skin vascular network in the mouse. The skin was removed from the posterior face of the thigh, which is supplied by a musculocutaneous perforator system. Twenty arterial vascular networks were investigated by image analysis and the fractal dimension was determined by the box counting method. Statistical analysis revealed an average mean of fractal dimension D = 1.256 (SD = 0.086), indicating low to intermediate complexity with a narrow distribution of results. D should logically fluctuate within a certain limit, depending on the anatomical structure investigated and its physiological function. These results demonstrate the ability of fractal analysis to quantify the vascular pattern of the skin. Fractal analysis opens a new field of investigation in the study of vascularization patterns and possible vascular modification by different physiological or pathological conditions (flap-delay techniques, tobacco use, diabetes mellitus, classification of diabetic retinopathies).

Vascular remodeling in the growth hormone transgenic mouse.

Using mice transgenic for the growth hormone gene (TGHM), we have studied the effects of a systemic elevation of growth hormone on vascular growth with the aim of investigating the role of vascular mass changes in producing hypertension. In contrast to human acromegaly or gigantism, there was no elevation of blood pressure in TGHM, but there were significant increases in vascular wall mass. In accordance with a presumably increased perfusion of larger organs, the medial cross-sectional areas of thoracic aorta and mesenteric resistance vessels were greater in the TGHM. These differences could be normalized in the aorta by body weight and in the mesenteric vessel by small intestine weight. Furthermore, the brain was not significantly heavier in the TGHM, and their carotid and cerebral vessels also were not larger. Wall-to-lumen ratios were similar in the aorta, carotid, and middle cerebral arteries suggesting that wall stress was the controlling factor in wall thickness. Surprisingly, the mesenteric vessels had increased wall-to-lumen ratio, which was similar to that seen in hypertensive vascular remodeling but in a normotensive animal. In an attempt to explain this finding it was noted that the pattern of mesenteric vascular networks and even organized structure within the vessel wall itself appeared to be fixed, perhaps by genetic mechanisms. Thus, vascular network structure may be a potentially limiting factor in the ability of the vessel wall to remodel and may have been responsible for the greater wall-to-lumen ratio in TGHM mesenteric vessels. A similar situation in human acromegaly or gigantism could result in a circulation marginally able to correct for other demands on blood flow resulting in about one third of cases being hypertensive.