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H K Hahn

Publications and source records attributed to H K Hahn.

At least 19 recordsLinked to original sources
PubMed2005

[MR-based methods of the functional imaging of the central nervous system].

This review presents the basic principles of functional imaging of the central nervous system utilizing magnetic resonance imaging. The focus is set on visualization of different functional aspects of the brain and related pathologies. Additionally, clinical cases are presented to illustrate the applications of functional imaging techniques in the clinical setting. The relevant physics and physiology of contrast-enhanced and non-contrast-enhanced methods are discussed. The two main functional MR techniques requiring contrast-enhancement are dynamic T1- and T2*-MRI to image perfusion. Based on different pharmacokinetic models of contrast enhancement diagnostic applications for neurology and radio-oncology are discussed. The functional non-contrast enhanced imaging techniques are based on "blood oxygenation level dependent (BOLD)-fMRI and arterial spin labeling (ASL) technique. They have gained clinical impact particularly in the fields of psychiatry and neurosurgery.

Animals↗
PubMed2004

A hybrid approach to the skull stripping problem in MRI.

We present a novel skull-stripping algorithm based on a hybrid approach that combines watershed algorithms and deformable surface models. Our method takes advantage of the robustness of the former as well as the surface information available to the latter. The algorithm first localizes a single white matter voxel in a T1-weighted MRI image, and uses it to create a global minimum in the white matter before applying a watershed algorithm with a preflooding height. The watershed algorithm builds an initial estimate of the brain volume based on the three-dimensional connectivity of the white matter. This first step is robust, and performs well in the presence of intensity nonuniformities and noise, but may erode parts of the cortex that abut bright nonbrain structures such as the eye sockets, or may remove parts of the cerebellum. To correct these inaccuracies, a surface deformation process fits a smooth surface to the masked volume, allowing the incorporation of geometric constraints into the skull-stripping procedure. A statistical atlas, generated from a set of accurately segmented brains, is used to validate and potentially correct the segmentation, and the MRI intensity values are locally re-estimated at the boundary of the brain. Finally, a high-resolution surface deformation is performed that accurately matches the outer boundary of the brain, resulting in a robust and automated procedure. Studies by our group and others outperform other publicly available skull-stripping tools.

Algorithms↗
PubMed2004

A reliable and efficient method for cerebral ventricular volumetry in pediatric neuroimaging.

OBJECTIVES: Cerebral ventricular volume has the potential to become an important parameter in quantitative neurological diagnosis. However, no accepted methodology for routine clinical use exists to date. We sought a robust, reproducible, and fast technique to evaluate cerebral ventricular volume in young children. METHODS: We describe a novel volumetric methodology to segment and visualize intracerebral fluid spaces and to quantify ventricular volumes. The method is based on broadly available T1 weighted volumetric magnetic resonance (MR) imaging, an interactive watershed transform, and a fully automated histogram analysis. We evaluated this volumetric methodology with 34 clinical volumetric MR datasets from non-sedated children (age 6-7 y) with a history of prematurity and low birth weight (< or = 1500 g) obtained during a prospective study. RESULTS: The methodology, with adaptation for small ventricular size, was capable of evaluating all 34 of the pediatric datasets for cerebral ventricular volume. The method was a) robust for normal and pathological anatomy, b) reproducible, c) fast with less than five minutes for image analysis, and d) equally applicable to children and adults. CONCLUSIONS: Clinical brain ventricular volume calculations in non-sedated children can be performed using routine MR imaging besides efficient three-dimensional segmentation and histogram analysis with results that are robust and reproducible.

Algorithms↗
PubMed1986

Interaction between marginal zinc deficiency and chronic alcoholism: pancreatic structure and function in rats in vitro.

The present study was done to determine interaction of ethanol and marginal zinc nutriture on morphology and function of rat pancreas. Sprague-Dawley rats were maintained on Wayne Rodent-Blox ad libitum; marginal zinc-deficient diet plus ethanol ad libitum and pair fed with animals fed marginal zinc-deficient liquid diet and zinc-supplemented liquid diet with ethanol for 33 (+/- 1 SEM) days. Body, pancreas, liver, heart, and kidney weights were determined, and studies of pancreatic DNA, RNA, total proteins and newly labeled proteins, amylase, lipase, trypsinogen, and chymotrypsinogen were done on pancreatic lobules in vitro. Ethanol feeding independent of the zinc content of the diet caused a decrease in zinc content of the liver, body weight, liver and pancreas weight, pancreatic DNA, total protein, and amylase concentration and an increase in lipase and trypsinogen concentrations and in secretion of amylase and lipase. Interaction of the marginal zinc diet and ethanol feeding resulted in a decreased synthesis of RNA and secretion of newly synthesized protein and an increase in secretion of serine proteases. Morphological studies revealed a reduction in the number of zymogen granules in animals fed low levels of zinc, also with an accumulation of lipid droplets when the diet contained ethanol. These studies confirmed our previous observations of specific injury to the pancreas due to marginal zinc nutriture or to ethanol, independent of each other. Marginal zinc nutriture in concert with ethanol resulted in impaired RNA synthesis and secretion of nascent proteins and increased secretion of serine proteases. These data indicate that altered zinc metabolism induced by ethanol per se may contribute to ethanol-induced disturbance of pancreatic function.

Alcoholism↗
PubMed1984

Effects of zinc deficiency on ethanol metabolism and alcohol and aldehyde dehydrogenase activities.

Alcohol dehydrogenase, low Km and high Km mitochondrial and microsomal aldehyde dehydrogenase, and in vivo ethanol elimination rates were determined in five groups of male Sprague-Dawley rats given liquid diets, as follows: control (C), control plus 5% ethanol (CE), pair-fed control and zinc-deficient (PC-ZnD), zinc-deficient (ZnD), and zinc-deficient plus 5% ethanol (ZnDE). Rats fed CE had decreased liver and serum zinc content. The animals given ZnD diets had an even more dramatic decrease in their tissue zinc concentrations and displayed marked growth retardation. The in vivo blood ethanol elimination rate was increased in animals fed ethanol, and this increase was accompanied by increased alcohol and aldehyde dehydrogenase activities. There was a significant decrease in the ethanol elimination rate in rats given ZnD and ZnDE diets. Alcohol dehydrogenase activities in rats with deficient zinc levels also were decreased, and there were no changes in acetaldehyde dehydrogenase activities. Our results suggest that the metabolism of ethanol to acetaldehyde is impaired in zinc deficiency, but acetaldehyde to acetate conversion appears normal.

Alcohol Dehydrogenase↗
PubMed1983

Impaired ethanol metabolism with advancing age.

Ethanol metabolism as a function of age was assessed in male Sprague-Dawley rats. The ethanol metabolic rates decreased linearly with advancing age. It was also observed that a linear decrease in hepatic alcohol dehydrogenase activity occurred as a function of age. The decreased enzyme activity could be the biochemical mechanism underlying changes in ethanol metabolism. Impaired ethanol metabolism may produce increased pharmacologic effects in older subjects due to increased blood ethanol levels.

Aging↗
PubMed1980

Enhanced lipid peroxidation in liver microsomes of zinc-deficient rats.

The clinical association of decreased serum and hepatic zinc in patients with cirrhosis of the liver presumably arising from excess ethanol ingestion prompted a study of the activities of zinc and alcohol in experimental animals. The purpose of this study was to determine the effect of zinc deficiency upon lipid peroxidation in the liver. The effect of ethanol and zinc deficiency on lipid peroxidation was also evaluated. Rats were used in the experimental design, one group received a control diet, and one was maintained on a zinc-deficient diet. One-half of each group also received 3.85 g ethanol per kilogram body weight daily. Lipid peroxidation in vivo was determined by estimation of diene conjugation of microsomal lipids. The in vitro lipid peroxidation potential was measured by the generation of malonic dialdehyde by enzymatic as well as nonenzymatic reactions. Analysis of this data indicated that increased hepatic microsomal lipid peroxidation was associated with zinc deficiency whether using in vivo or in vitro indices of measurement. Review of the data from individual animals indicated that the lowest levels of serum zinc were associated with increased hepatic content of phospholipids. The degree of lipid peroxidation in the zinc deficient animals was not increased by ingestion of alcohol.

Animals↗
PubMed1979

Trace elements in human nutrition.

Clinical recognition of the role of trace elements in human nutrition is increasing. Heretofore, many clinicians felt that the development of deficiency states was not likely except in very extreme conditions because the presence of trace elements in nature was so ubiquitous. The increased use of total parenteral nutrition seems to have made this viewpoint untenable. The recognition of additional genetic diseases of trace element metabolism such as Menkes' kinky hair syndrome and acrodermatitis enteropathica has also served to focus clinical attention on trace elements. As time passes, no doubt, additional diseases of trace element metabolism will be recognized.

Aging↗
PubMed1979

Serum levels of selenium, calcium, copper magnesium, manganese and zinc in various human diseases.

Serum selenium as well as serum zinc, copper, magnesium, calcium and manganese were investigated in a control group of adult males and in 11 groups of patients in various disease states. Not only the change of each trace element but also the possible association between elements was studied in the various groups. All patients were fasting when sampled and studied only after the acute phase of the disease was corrected. Trace metal determinations were performed by atomic absorption spectrophometry (Mg, Ca, Cu, Zn) and by neutron activation analysis (Se, Mn). All patients showed low serum zinc when compared to controls. Cirrhotic patients had a low serum selenium level as well as low calcium, magnesium and zinc. Emphysemia and cancer patients had an elevated serum copper concentration while copper and manganese levels were elevated in congestive heart failure, infection and pschoses. To our knowledge this is the first time low serum selenium values have been demonstrated to be associated with the low serum zinc, calcium and magnesium levels found in cirrhotic patients.

Adult↗
PubMed1979

Trace element composition of ascitic fluid.

The relationship between trace elements in the serum and ascites of the cirrhotic patient was investigated because there is an interchange of protein, particularly albumin, between serum and ascitic fluid. To study this relationship, serum and ascitic fluid were obtained from 13 patients with biopsy-proved Laennec's cirrhosis. The trace element content of the ascitic fluid studied was less (22% to 73%) than that in serum. Protein fractions were all decreased in ascitic fluid compared with serum. Levels of zinc, calcium, copper, selenium in ascitic fluid correlated well with the ascitic fluid protein fractions. Thus, the trace element composition of ascitic fluid differed appreciably from that of serum, and seemed to correlate with the protein composition of the ascitic fluid in the case of zinc, copper, calcium, and selenium.

Aged↗
PubMed1978

Effects of phenobarbital administration on levels of physiological antioxidants in rat liver.

Administration of phenobarbital to rats over a period of 5 days was shown to increase hepatic lipid peroxidation concomitant with induction of cytochrome P-450 and cytochrome c reductase. The purpose of this study was to determine whether the increase in lipid peroxidation was due to a lowering in hepatic antioxidants. The results show that increased lipid peroxidation was not due to a decreased level of antioxidants since the fat-soluble antioxidants were unchanged and ascorbate, a water-soluble antioxidant, was elevated. The relationship of the increase in hepatic ascorbate to enhanced lipid peroxidation is discussed.

Animals↗
PubMed1975

Serum and tissue enzyme activity and trace-element content in response to zinc deficiency in the pig.

Zinc deficiency is associated with poor growth and development. It has been postulated that a deficiency of the various zinc metalloenzymes results from the lack of dietary zinc. From present study, an examination of some aspects of this postulate, we conclude the following about zinc deficiency in pigs: (1) Of the tissues studied, it results im diminished zinc content only in liver, kidney, and pancreas. (2) It is associated with tissue abnormalities of various trace elements other than zinc. (3) Histochemical enzyme assays are satisfactory for qualitative but not quantitative determination of zinc metalloenzymes. (4) Deficiency of various tissue zinc metalloenzymes is difficult to demonstrate, even in severe zinc deficiency. (5) It is associated with decreased activity of hepatic leucine aminopeptidase and ornithine transcarbamylase, and decreased serum cholesterol concentrations. Our findings are consistent with the postulate that alterations in a number of trace elements may occur in the entity called zinc deficiency.

Animals↗
PubMed1975

Tissue trace element and enzyme content in pigs fed a low manganese diet. I. Arelationship between manganese and selenium.

Pigs received a diet containing 0.59 p.p.m. Mn. Control pigs received the samequantity of the same diet which was supplemented with 22 p.p.m. of Mn. At the end of6 weeks, pigs fed the low Mn diet had a diminution in tissue Mn levels as well as a diminution in tissue Se content. Tissue levels of Zn, Cu, Ca, and Mg were notaffected by the dietary regimen. Indicative of the fact that experimental animals were probably Mn-deficient was a statistically significant decrease in hepatic arginaseactivity that could be enhanced by the addition of Mn. These studies represent the first experimental evidence that there may be a specific interaction between tissue Se and Mn. Tissue Se levels were decreased to a statistically significant degree in all tissues studied except the kidney in the Mn-deficient animals.

Alkaline Phosphatase↗