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B E Park

Publications and source records attributed to B E Park.

9 recordsLinked to original sources
PubMed2001

Potential role of leptin in angiogenesis: leptin induces endothelial cell proliferation and expression of matrix metalloproteinases in vivo and in vitro.

Leptin, the product of ob gene, is an endocrine hormone that regulates adipose tissue mass. Recently, leptin has been found to generate a growth signal involving a tyrosine kinase-dependent intracellular pathway and promote angiogenic processes via activation of leptin receptor (Ob-R) in endothelial cells. However, it is not clear how leptin functions to promote multi-step processes involved in the neovascularization at the atherosclerotic plaque. We have examined the expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) and Ob-R in human atherosclerotic lesions, leptin-mediated angiogenesis in vivo and in vitro. Immunohistochemical analysis of human atherosclerotic aorta revealed an increased expression of Ob-R in the intima of neorevascularized regions and of both MMPs and TIMPs predominantly in the endothelial lining of intimal neovessels and macrophages/foam cells. In the rat corneal angiogenesis assay, leptin elicited a comparable sensitivity of angiogenic activity to those of vascular endothelial growth factor (VEGF). The immunohistological analysis of the leptin-treated rat cornea showed definitive rises in Ob-R, MMPs and TIMPs expression as well as those of VEGF receptor (VEGFR-1). Leptin (10-40 ng/ml) induced proliferation of the human umbilical vein endothelial cells (HUVECs) and elevation of MMP-2, MMP-9, TIMP-1, and TIMP-2 expression in a dose-dependent manner. Leptin also induced increases of MMP-2, MMP-9, TIMP-1, and Up-regulated the human coronary artery smooth muscle cells (HCASMCs). These findings suggest that leptin, a hormone with pluralistic properties including a mitogenic activity on vascular endothelial cells, plays a role in matrix remodeling by regulating the expression of MMPs and TIMPs. Taken together, our findings further provide evidences for leptin's role as an angiogenesis inducer in the normal organ (rat cornea) and in aberrant vasculature under duress like atherosclerosis.

Animals↗
PubMed2001

Hemodynamic effects on atherosclerosis-prone coronary artery: wall shear stress/rate distribution and impedance phase angle in coronary and aortic circulation.

The objective of the present study was to evaluate the hemodynamic characteristics of an atherosclerosis-prone coronary artery compared to the aorta. We describe three- dimensional spatial patterns of wall shear stress (WSS) according to the impedance phase angle in pulsatile coronary and aorta models using in vivo hemodynamic parameters and computed numerical simulations both qualitatively and quantitatively. Angiography of coronary arteries and aortas were done to obtain a standard model of vascular geometry. Simultaneously to the physiologic studies, flow-velocity and pressure profiles from in vivo data of the intravascular Doppler and pressure wire studies allowed us to include in vitro numerical simulations. Hemodynamic variables, such as flow-velocity, pressure and WSS in the coronary and aorta models were calculated taking into account the effects of vessel compliance and phase angle between pressure and flow waveforms. We found that there were spatial fluctuations of WSS and in the recirculation areas at the curved outer wall surface of the coronary artery. The mean WSS of the calculated negative phase angle increased in the coronary artery model over that in the aorta model and the phase angle effect was most prominent on the calculated amplitude of WSS of the coronary artery. This study suggests that the rheologic property of coronary circulation, such as the fluctuation of WSS/WSR induces several hemodynamic characteristics. A separation of flow-velocity, a difference in phase between pressure conductance and blood flow and prominent temporal and/or spatial oscillatory fluctuations of the shear forces as a function of pulsatile flow might be important factors in atherogenesis and progression of atherosclerosis.

Adult↗
PubMed1994

A brave new world?

Explore the source record for details and available documents.

Ethics, Medical↗
PubMed1979

Increased pulmonary vascular permeability follows intracranial hypertension in sheep.

After reviewing the characteristics of neurogenic pulmonary edema, Theodore and Robin suggested that it was probably due to rupture of lung vessels by marked but transitory pulmonary hypertension. In this study, we have determined the effects of increased intracranial pressure in a sheep model in which we could measure the flow rate and protein content of lung lymph, and thus detect changes in pulmonary vascular permeability. We found that increasing intracranial pressure to amounts near systemic arterial pressure produced a 3-fold increase in the flow of protein-rich lymph, which indicates increased lung vascular permeability. The high permeability often developed, and always persisted, without extraordinary increases in pulmonary vascular pressure. We conclude that increased lung vascular permeability may follow intracranial hypertension and that extreme pulmonary hypertension is not a prerequisite. Our data do not permit us to exclude barotrauma to exchanging vessels as a cause of capillary damage, but do suggest that other factors, perhaps local release of permeability mediators, may be involved.

Animals↗
PubMed1979

Spontaneous subarachnoid hemorrhage complicated by communicating hydrocephalus: epsilon amino caproic acid as a possible predisposing factor.

An increased incidence of communicating hydrocephalus following subarachnoid hemorrhage has been observed on the neurosurgical service at Vanderbilt University Hospital during the past four years. This increase parallels the time interval during which epsilon amino caproic acid (Amicar) has been used in the preoperative regimen for intracranial aneurysms to prevent recurrent hemorrhage. Radiographic studies of 48 patients with subarachnoid hemorrhage not receiving Amicar were compared with 46 similar patients treated with this antifibrinolytic agent. In the series not treated with Amicar, a 17% incidence of dilated lateral ventricles was found, with 10% of the series being symptomatic from their hydrocephalus. A total of 43% of patients in the group treated with Amicar demonstrated dilated ventricles, with 31% of the group clinically symptomatic. Mechanisms of action of Amicar possibly implicated in this increased incidence of hydrocephalus are discussed.

Adult↗
PubMed1976

Nonketotic hyperglycemic hyperosmolar coma. Report of neurosurgical cases with a review of mechanisms and treatment.

Seventy-eight critically ill patients who died while on the neurosurgical service were studied retrospectively to establish the prevalence of nonketotic hyperglycemic hyperosmolar coma (NHHC). All the patients had been comatose before death, and all underwent necropsy. Criteria for the diagnosis of NHHC included moderate-to-severe hyperglycemia with glucosuria, absence of significant acetonuria, hyperosmolarity with dehydration, and neurological dysfunction. This study revealed seven cases of unequivocal NHHC (9%), and six of hyperosmolarity but with incomplete records. Five of the seven confirmed cases of NHHC demonstrated no evidence of cerebral edema transtentorial herniation, or brain-stem damage, and showed central nervous system (CNS) lesions compatible with survival. Fatal complications of this syndrome, such as acute renal failure, terminal arrhythmias, and vascular accidents, both cerebral and systemic, were common in this series. The mechanism of coma in NHHC is believed related to shifts of free water from the cerebral extravascular space to the hypertonic intravascular space, with subsequent intracellular dehydration, accumulation of metabolic products of glucose, and brain shrinkage. It is uncertain whether injury to specific areas in the CNS is a predisposing factor to the development of NHHC. Factors documented to be significant in its development include nonspecific stress to primary illnesses, hyperosmolar tube feedings, dehydration, diabetes and mannitol, Dilantin, or steroid administration.

Adolescent↗
PubMed1975

Pathogenesis of pigment and spheroid formation in Hallervorden-Spatz syndrome and related disorders.

In a case of Hallervorden-Spatz syndrome, neuromelanin was found in neurons and, extracellularly, in the globus pallidus and pars reticulata of the substantia nigra. Some cells of pars compacta contained Lewey bodies. We propose that neuromelanin is formed by a metal-catalyzed pseudoperoxidation of lipofuscin, involving increased amounts of iron and copper in the affected regions. A similar mechanism of spheroid formation, often associated with neuromelanin, may result from pathologic accumulations of lipid peroxides during fatty acid oxidation of myelin. We suggest that neuromelanin is a late stage in the metabolism on intraneuronal and extraneuronal lipopigments. Discrepancies among the histochemical features of the pigment in different cases may be explained by differences in amounts of lipofuscin, neuromelanin, and their precursors. We propose relation of peroxidation to the pathogenesis of some related degenerative diseases.

Adult↗
PubMed1975

Closed head injury complicated by nonketotic hyperglycemic hyperosmolar coma.

A case of nonketotic hyperglycemic hyperosmolar coma occurring in a patient with closed head injury and basilar skull fracture is reported. The metabolic abnormality masqueraded as a progression of central transtentorial herniation due to cerebral edema. It is suggested that the development of this complication is related to various predisposing factors normally employed in cases of critically ill, neurologically compromised patients. The anatomic lesions found at autopsy were considered inappropriate as a cause of death; the occurrence of central transtentorial herniation three days before death had been reversed. An awareness of this syndrome is emphasized in considering patients receiving steroids, mannitol, tube feedings, Dilantin, and dehydrative measures as part of their care.

Adult↗