Biomedical subjects

Y K Wu

Publications and source records attributed to Y K Wu.

At least 19 recordsLinked to original sources

PubMed2006

High-gain lasing and polarization switch with a distributed optical-klystron free-electron laser.

This Letter reports the first experimental results from the world's first distributed optical-klystron (DOK) free-electron laser (FEL), the DOK-1 FEL, at Duke University. The DOK-1 FEL is a hybrid system, comprised of four wigglers: two horizontal and two helical. With the DOK-1 FEL, we have obtained the highest FEL gain among all storage ring based FELs at 47.8% (+/-2.7%) per pass. We have also demonstrated that the FEL gain can be enhanced by increasing electron bunching using wigglers with a different polarization. Furthermore, we have realized controlled polarization switches of the FEL beam by a nonoptical means through the manipulation of a buncher magnet.

Journal Article↗

PubMed2005

Anomalous hollow electron beams in a storage ring.

This Letter reports the first observations of an anomalous hollow electron beam in the Duke storage ring. Created by exciting the single-bunch beam in a lattice with a negative chromaticity, the hollow beam consists of a solid core inside and a large ring outside. We report the detailed measurements of the hollow beam phenomenon, including its distinct image pattern, spectrum signature, and its evolution with time. By capturing the postinstability bursting beam, the hollow beam is a unique model system for studying the transverse instabilities, in particular, the interplay of the wakefield and the lattice nonlinearity. In addition, the hollow beam can be used as a powerful tool to study the linear and nonlinear particle dynamics in the storage ring.

Journal Article↗

PubMed2003

Explicit symplectic integrator for s-dependent static magnetic field.

This paper reports our recent work on explicit symplectic integration techniques for the charged particle motion in an s-dependent static magnetic field. Using the extended phase space, symplectic integrators can be developed for Hamiltonians with or without the paraxial approximation using either the space or time as an independent variable. This work extends the successful element-by-element tracking method for studying single-particle nonlinear dynamics to a set of s-dependent magnetic elements. Important applications of this work include the studies of the charged particle dynamics in a storage ring with various insertion devices, superconducting magnets, large aperture magnets with significant fringe fields, and solenoid magnets in the interaction region. Consequently, this work is expected to make an impact on design and optimal operation of existing and future light source rings and high energy physics accelerators.

Journal Article↗

PubMed2002

Aberrant patterns of cellular communication in diabetes-induced embryopathy. I. Membrane signalling.

OBJECTIVE: Our purpose was to investigate the role of membrane signalling in the mechanism of diabetes-induced embryopathy. METHODS: Three groups of 70-90-day-old Sprague-Dawley rats were employed in our study: group 1 was normal control rats receiving a normal diet; group 2 represented experimentally induced diabetic rats with malformed offspring (intravenous injection of 65 mg/kg streptozotocin on pregnancy day 6) and group 3 included streptozotocin-induced diabetic rats with normal offspring. Embryos were examined on day 12 under light microscopy, categorized as morphologically normal or defective, and yolk sac cells were harvested from each group. Activities of ERK1 and 2, Raf-1, JNK1 and 2 in yolk sac cells were analyzed by Western blot with primary antibodies specific to the phosphorylated kinases, respectively. RESULTS: A strong link between hyperglycemia and congenital malformations was confirmed. Key mitogen-activated protein kinases serve as syllabic intermediates: increased activities of Jun-amino-terminal kinase (JNK1 and 2) and decreased activities of extracellular signal-regulated kinase (ERK1 and 2) were observed during hyperglycemia-induced embryopathy. CONCLUSIONS: Poorly controlled maternal diabetes results in embryopathy which is mediated via a pattern of aberrant cellular communication manifested by both macroscopic and microscopic membrane injury.

Animals↗

PubMed1999

Signaling pathways and diabetic embryopathy.

Diabetic embryopathy is the leading cause of neonatal death and/or congenital malformations in infants of diabetic mothers. Because the development of the embryo critically depends on the maternal and the embryonic signaling pathways, a defective signaling mechanism between the maternal and the embryonic tissues appears to be involved in the etiology of diabetic embryopathy. Analyses of the recent studies from different laboratories suggest a "multifactorial" basis for diabetic embryopathy. These studies suggest that a wide variety of signal-transducers converge towards the regulation of elcosanoid signaling pathway which appears to be the critical pathway involved in diabetic embryopathy. The characterization of the regulatory components of this pathway is likely to identify the signaling loci susceptible for the therapeutic intervention.

Arachidonic Acid↗

PubMed1998

Microstructure investigations of ball milled materials.

HREM and FEG TEM were emphasized and extensively used to follow the most subtle changes in the structure and composition of ball-milled Cu, Fe-Cu, and thermally decomposed Fe60Cu40. Some significant results are obtained and summarized as follows: HREM shows that the deformation of ball-milled copper proceeds mainly by twinning and shear bands (SBs) formation. The nano-grains formed during ball milling (BM) contain a high density of dislocations. The grain boundaries (GBs) of nanocrystalline (NC) Cu prepared by BM are ordered, curved, and strained, but disordering, lattice distortion, and nanovoids in local regions were frequently observed. Nanoscale composition analysis on mechanically alloyed Fe16Cu84 shows that the average Fe content in both the interior of grains and the GBs is close to the designed composition, which proves that a supersaturated solid solution has really formed. However, the Fe content is rather inhomogeneous between the larger and smaller grains, which infers the inhomogeneous mixing of Fe and Cu during mechanical alloying (MA). NC structure and the mechanical force-enhanced fast diffusion are the reasons of the formation of supersaturated solid solutions in immiscible systems with positive enthalpy of mixing. HREM observations carried out with the thermally decomposed Fe60Cu40 solid solution show that the Nishiyama (N-W) or Kurdyumov-Sachs (K-S) orientation relationships exist between alpha-Fe and Cu. Energy dispersive X-ray spectra (EDXS) results show that the Cu content in these alpha-Fe grains reaches as high as 9.5 at.% even after heating to 1,400 degrees C, which is even higher than the maximum solubility of Cu in gamma-Fe at 1,094 degrees C.

Alloys↗

PubMed1998

Dietary myo-inositol therapy in hyperglycemia-induced embryopathy.

Dysmorphogenesis in diabetic mothers occurs more frequently than in the general population. This phenomenon is believed to be caused by the teratogenic effects of metabolic fuel mixtures with associated membrane injury and aberrations in the biochemical constituents. The present experiment was designed to determine: 1) if hyperglycemia-induced membrane injury is associated with intracellular and/or extracellular lipid disturbances; 2) if supplemental myo-inositol therapy prevents hyperglycemia-induced embryopathy; 3) if a correlation exists between dietary myo-inositol, serum and tissue levels of myo-inositol, and conceptus development; and 4) the cellular content of arachidonic acid following myo-inositol supplementation. Sixty-five female Sprague-Dawley rats were mated, and divided into three groups. One group was nondiabetic normal controls, and two groups had diabetes experimentally induced with streptozotocin. Of the diabetic groups, one received a normal diet, while the other received a myo-inositol-supplemented diet during the period of organogenesis. Blood samples were collected on days 0 and 12 of pregnancy. Embryos and yolk sacs were analyzed for myo-inositol and arachidonic acid levels, using mass spectrochromatography. Dietary myo-inositol supplementation of diabetic mothers resulted in a significant decrease in the incidence of neural tube defects when compared with diabetics not receiving supplements (9.5 vs. 20.4%; P < 0.05). This protective effect was incomplete, based on the incidence observed in the nondiabetic controls (9.5 vs. 3.8%; P < 0.05). The myo-inositol embryonic tissue levels in the diabetic group which had been fed a regular diet without supplementation were significantly lower than in the nondiabetic group. Dietary therapy successfully restored myo-inositol levels in the yolk sacs, as suggested by similar tissue levels in diabetics receiving myo-inositol supplementation and normal controls (18.7 +/- 1.3 vs. 19.1 +/- 2.0 ng/mg; P = ns). Dietary therapy, however, failed to restore myo-inositol levels in the embryos, suggesting hyperglycemia-induced faulty transport of nutrients from the yolk sac to the embryo. No correlation was noted between maternal blood levels of myo-inositol, with or without supplementation, and the clinical outcome. Tissue arachidonic acid levels were markedly reduced in the conceptuses of diabetic mothers with (0.4 +/- 0.1 micrograms/mg) or without (0.25 +/- 0.08 micrograms/mg) myo-inositol supplementation when compared to the nondiabetic controls (3.33 +/- 0.24 micrograms/mg). These data demonstrate that diabetes-induced embryopathy is associated with a deficiency state in both myo-inositol and arachidonic acid. The myo-inositol deficiency is not demonstrated at the serum level, but rather at the tissue level, suggesting a paracrine action. Dietary supplementation of myo-inositol is associated with an increase in tissue myo-inositol levels and a decrease in malformations. This therapy holds promise for use as a dietary prophylaxis against diabetic embryopathy.

Animals↗

PubMed1998

Determinants of lethality from suicidal pesticide poisoning in metropolitan HsinChu.

Acute pesticide poisoning is a global health problem, especially in developing countries. Although Taiwan has quickly industrialized during the last several decades, pesticide use is still prevalent in the agricultural sector. We reviewed 187 consecutive hospitalized cases of the Provincial HsinChu Hospital from January 1989 through December 1995 to explore the determinants of acute pesticide poisoning in Metropolitan HsinChu. The annual incidence rate of acute pesticide poisoning was 3.2/100,000 with an overall fatality rate of 23% which was more severe than the rates found in developed countries. The major agents involved were organophosphates, and the major cause of poisoning was suicide. Alcohol abuse, history of major medical illnesses, and history of suicide were significantly associated with suicidal poisoning; quarrel was the immediate risk factor. Causes of poisoning (suicide vs non-suicide) and selection of the pesticides were major determinants of lethality. More stringent legislation and enforcement regarding the sale and distribution of extremely toxic pesticides are needed to reduce fatalities due to acute pesticide poisoning.

Adolescent↗

PubMed1997

Free radical scavenging enzymes in fetal dysmorphogenesis among offspring of diabetic rats.

Recent studies have suggested that the fetal dysmorphogenesis in diabetic pregnancies is associated with an increase in embryonic oxygen-free radicals. This excess of oxygen-free radicals may result from either overproduction or decreased clearance by the enzymatic scavenging mechanism. However, there are no in vivo data on the activity of embryonic oxygen-free radical scavenging enzymes. The purpose of the current study is to investigate whether this increase in embryonic oxygen-free radicals is the result of a change in the activity of the fetal oxygen-free radical scavenging/antioxidant enzymes during pregnancy complicated by maternal diabetes in an in vivo rat model. Thirty-six Sprague-Dawley rats were randomly assigned to one of two study groups: nondiabetic control and an untreated diabetic group. On day 12, fetuses were examined for crown-rump lengths, somite numbers, and external anomalies. The activity of fetal oxygen-free radical scavenging enzymes, including superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT), were determined. The untreated diabetic group of rats had a significantly higher mean blood glucose level than that of the nondiabetic controls and also a significantly lower weight gain, higher resorption rate, smaller embryonic size with lower total protein content, and a approximately 6-fold increase in the rate of fetal neural tube defects compared to the nondiabetic controls. Superoxide dismutase activity was significantly reduced in the embryos with neural tube defects regardless of maternal diabetic status (2.25 +/- 0.83 vs. 1.17 +/- 0.04 u/mg protein; P < 0.05). Glutathione peroxidase and catalase activity were significantly reduced in malformed versus normal-formed embryos of nondiabetic mothers (GPX-2.68 +/- 1.15 vs. 4.46 +/- 1.12 mu/mg protein, CAT -1.67 +/- 0.53 vs 2.49 +/- 0.61 u/mg protein respectively; P < 0.01). However, overall catalase activity was increased in embryos of diabetic mothers as compared to controls. Two-way analysis of variance identified fetal malformations as the variance associated with reduced fetal SOD activity, whereas maternal diabetes was associated with the increase in fetal catalase activity. Neither neural tube defect nor maternal diabetes was found to be the variable affecting fetal GPX activity, Fetal oxygen-free radical scavenging enzymes respond differently to the adverse environment created by maternal diabetes during pregnancy. Defects in embryonic SOD and catalase activity, regardless of maternal diabetic status, may reduce the ability of the fetus to clear free oxygen radicals, thereby exposing it to an increased oxidative load that may cause fetal dysmorphogenesis. The diabetic state of the mothers did not decrease embryonic activity of any of the scavenging enzymes. Therefore, although excess oxidative load, as observed in diabetes, may cause tissue injury and embryopathy, the mechanism does not appear to be a diabetes-induced reduction in the action of the scavenging enzymes.

Abnormalities, Drug-Induced↗

PubMed1997

Dietary intake of myo-inositol and neural tube defects in offspring of diabetic rats.

OBJECTIVE: Embryopathy in diabetic mothers occurs at a rate four to five times higher than that observed in the general population. The current investigation was undertaken to assess the use of dietary myo-inositol supplementation as a pharmacologic prophylaxis to obviate the teratogenic effects of hyperglycemia in an in vivo study. STUDY DESIGN: Seventy Sprague-Dawley rats were mated and after conception were randomly divided into five groups: one group was nondiabetic normal controls and four groups had diabetes experimentally induced with streptozotocin. Of the diabetic groups, one received the usual diet, whereas the others received, respectively, 0.08, 0.16, and 0.5 mg/day supplemental myo-inositol orally. RESULTS: With the myo-inositol supplementation (0.08 mg/day), the incidence of neural tube defects was significantly reduced from 20.4% to 9.5% (p < 0.01). The most effective dosage of myo-inositol was 0.08 mg/day. Increasing the dose of myo-inositol beyond that level did not significantly reduce the rate of neural tube defects. However, the resorption rate was increased to 29.8%. CONCLUSION: These data demonstrate that myo-inositol supplementation reduces the incidence of diabetic embryopathy and may serve as a pharmacologic prophylaxis against diabetes-induced congenital malformations.

Animals↗

PubMed1997

Prevention of diabetic embryopathy in offspring of diabetic rats with use of a cocktail of deficient substrates and an antioxidant.

OBJECTIVE: The current study sought to determine whether a dietary cocktail of deficient substrates and antioxidant could reduce the incidence of diabetic embryopathy to the background rate in an in vivo rat model. STUDY DESIGN: Sprague-Dawley rats 70 to 90 days old were assigned to one of eight groups: two control groups (groups 1 and 2) and six diabetic groups (groups 3 to 8). One group of controls (group 2) received an oral supplemental cocktail of vitamin E ((alpha-tocopherol, 400 mg/day), safflower oil (arachidonic acid, 1 ml/day), and myo-inositol 0.08 mg per day. Four other diabetic groups (groups 5 to 8) received the cocktail in varying strengths. One diabetic group (group 3) received a normal diet only without insulin or cocktail, whereas another diabetic group (group 4) received insulin but no cocktail supplementation. On day 6 of gestation diabetes was induced in groups 3 to 8 with intravenous streptozotocin (65 mg/kg), and maternal glucose levels were monitored. Animals were killed on day 12; embryos were examined for size, somite number, and evidence of malformations and were biochemically evaluated for vitamin E and myo-inositol levels and superoxide dismutase activity. RESULTS: The diabetic groups had a significantly higher (p < 0.05) mean blood glucose level than controls did. The insulin-treated group 4 had glucose levels that were comparable to those of controls. The unsupplemented diabetic group 3 had a neural tube defect rate of 23.7% versus 4.04% in controls and 3.55% in insulin-treated diabetics (p < 0.05). The rate of neural tube defects was significantly reduced to the background level in animals receiving half-strength cocktail or stronger doses (groups 6 to 8) compared with the diabetic unsupplemented controls (group 3). Diabetic animals in group 5 receiving only quarter-strength cocktail did not demonstrate a significant reduction in the malformation rate. Serum myo-inositol levels were not significantly different among the groups. However, serum levels of vitamin E were significantly higher in diabetics receiving half-strength cocktail than in nondiabetic controls, diabetics receiving no supplements, and diabetics receiving quarter-strength cocktail. Superoxide dismutase activity was also significantly increased in diabetic animals receiving supplementation versus animals not receiving the same, and the increases in vitamin E and superoxide dismutase were significantly correlated (r = 0.66, p < 0.05). CONCLUSION: These data demonstrate that a cocktail containing deficient substrates and an antioxidant in varying strengths reduces the malformation rate to background in offspring of diabetic rats.

Animals↗

PubMed1996

Image segmentation and bright contrast spot localization of the high resolution atomic image.

Some basic quantitative analysis techniques of digitized high resolution atomic image are developed in this paper. We describe how to divide the atomic image into small independent areas with special structure information by the valley mesh segmentation method. The procedure is with regard to the bright contrast spot segmentation of atomic images. We suggest several ways for bright contrast spot localization in images. Calculation routines for peak detection and weighted local position average methods for this purpose are given.

Microscopy, Electron↗

PubMed1996

Multifactorial basis of the syndrome of diabetic embryopathy.

OBJECTIVE: The aim of the current paper is to explore the multifactorial basis of diabetes-induced embryopathy. METHOD: A review of the literature regarding congenital malformations was undertaken to elucidate new advances in our understanding of diabetic embryopathy. Data from both clinical and experimental studies were collected and analyzed. RESULTS: Numerous investigators have demonstrated that hyperglycemia and other metabolic fuels produce teratogenic effects during organogenesis. However, the exact mechanism(s) involved have not been completely elucidated. We and others have shown that aberrant metabolic fuels including hyperglycemia and hyperketonemia are teratogenic and that these effects occur via the yolk sac which appears to be the target site of injury. Other proposed etiologic factors include nutrient deficient states in membrane lipids such as arachidonic acid and myo-inositol as well as the generation of excess free oxygen radicals. This review highlights the multiple theories that have been proposed and summarizes the experimental and clinical data which support a multifactorial basis. CONCLUSIONS: Evidence suggests that although the teratogenic process in the diabetic pregnancy is multifactorial, it may operate via a common pathway. Prevention of malformations in offspring of diabetic rats is achieved by glycemic control during organogenesis. Similar results may be obtained in a hyperglycemic state, provided there is restoration of essential fatty acid/phospholipid deficiency state and normalization of excess free radicals which may be achieved through dietary supplementation of polyunsaturated fatty acids, myoinositol, or antioxidants. The latter approach offers great promise as an adjunct to periconceptional glycemic control and as a dietary prophylaxis against the syndrome of diabetic embryopathy.

Animals↗

PubMed1996

Synchronization of the factors critical for diabetic teratogenesis: an in vitro model.

OBJECTIVE: Our goal was to determine the relationship between critical factors and conditions such as gestational age and exposure time to elevated glucose levels in diabetic embryopathy. STUDY DESIGN: A postimplantation rat embryo culture was used as a model for investigation. The effect of various factors on embryonic development was studied. Experiments were conducted with increasing glucose concentrations (150 to 905 mg/dl, n = 186), at various gestational ages (10 to 12 days, n = 169), and for varying durations of exposure (30 to 180 minutes, n = 169). Gross morphologic characteristics of the yolk sac and embryo were assessed. RESULTS: Embryopathy was induced by hyperglycemia in a dose-related fashion: a 20% rate at two times control glucose concentration, almost a 50% rate at four times control, and approximately a 100% abnormality rate at more than six times control. A critical window in gestational age, days 10 to 11, and a minimum exposure time to hyperglycemia of 2 hours were necessary to induce teratogenesis. CONCLUSIONS: Diabetic teratogenesis occurs in a dose-related fashion and requires a minimum exposure time and critical gestational age. Only synchronization of these critical conditions induces embryonic maldevelopment. Furthermore, nonsynchronized aberrant conditions may result in apparently normal embryonic development.

Animals↗

PubMed1996

Dietary vitamin E prophylaxis and diabetic embryopathy: morphologic and biochemical analysis.

OBJECTIVE: In this study we sought to determine whether dietary supplementation with vitamin E, a known antioxidant, would reduce the incidence of diabetic embryopathy in an in vivo rat model. STUDY DESIGN: Eighty-day-old Sprague-Dawley rats were assigned to one of five groups: two control groups (groups 1 and 2) and three diabetic groups (groups 3, 4, and 5). One group of controls (group 2) and one group of diabetic rats (group 4) received dietary supplements of vitamin E (440 mg/day). The other three groups (groups 1, 3, and 5) received a normal diet only. Group 5 received insulin therapy to control glucose levels. On day 6 of gestation diabetes was induced in groups 3, 4, and 5 with streptozotocin (65 mg/kg). Animals were killed on day 12; embryos were examined for size, protein content, evidence of malformations, and superoxide dismutase activity. RESULTS: In both groups (groups 3 and 4) of diabetic rats the mean blood glucose level than was significantly higher in controls. Insulin-treated animals (group 5) had glucose levels that were comparable to those of controls. The unsupplemented diabetic group had a neural tube defect rate of 21.48% +/- 9.6% (percentage of neural tube defects per rat) and a resorption rate of 21.37% +/- 20.39% (percentage of resorptions per rat) as compared with rates in the supplemented diabetic group of 6.92% +/- 4.08% and 2.17% +/- 3.74%, respectively (p < 0.01). Groups 1, 2, and 5 had similar neural tube defect rates (6.63% +/- 5.0%, 5.01% +/- 4.87%, and 3.55% +/- 5.92%, respectively. Vitamin E levels, measured by high-performance liquid chromatography, were significantly higher in maternal serum and embryos in the supplemented groups (p < 0.001) than in controls. Superoxide dismutase activity was reduced in the diabetes groups and was not affected by vitamin E therapy. CONCLUSIONS: Supplementation with the antioxidant vitamin E confers a significant protective effect against diabetic embryopathy and may potentially serve as a dietary prophylaxis in the future. We postulate that this protective effect is mediated by a reduction in the oxidative load induced by hyperglycemia.

Animals↗

PubMed1996

Dietary polyunsaturated fatty acid prevents malformations in offspring of diabetic rats.

OBJECTIVE: The purpose of the current study was to determine whether a dietary source of arachidonic acid could serve as a pharmacologic prophylaxis to obviate the teratogenic effects of hyperglycemia. STUDY DESIGN: Eighty-day-old Sprague-Dawley rats were mated, and after conception were randomly allocated to five groups: two groups were nondiabetic normal controls and three groups had diabetes experimentally induced with streptozocin. Of the two control groups, one was fed a normal diet (group 1) and the other group (group 2) received a normal diet and 1.0 ml of safflower oil, a polyunsaturated fatty acid known to increase serum arachidonic acid levels. In the three diabetic groups (groups 3, 4, and 5) glucose levels were allowed to remain > 350 mg/dl by withholding daily insulin therapy. Group 3 received a normal diet without supplementation; group 4 received a normal diet plus normal saline solution sham feedings, whereas group 5 received a normal diet supplemented with 1.0 ml of safflower oil. The oral agents (normal saline solution and polyunsaturated fatty acid) were administered with a tuberculin syringe. RESULTS: Diabetic rats not receiving insulin therapy and receiving normal diets produced offspring with malformation rates of 20% compared with control rates of 4.8%. Supplemental normal saline solution or safflower oil given orally to controls did not alter the growth or malformation rates. These rates were similarly unaffected in the diabetic rats receiving oral supplementation of normal saline solution. However, with safflower oil supplementation to diabetic rats the incidence of neural tube defects was decreased from 20.0% to 7.6% (p < 0.0001). An inverse relationship was observed between the malformation rate and the serum arachidonic acid level: 17.83 (SD 5.84 micrograms/ml) in the nondiabetic controls, with a malformation rate of 4.8%, versus 14.18 (SD 2.58 micrograms/ml) in the diabetic rats, with a malformation rate of 20.0% (p < 0.05). With safflower oil supplementation serum levels of arachidonic increased from 14.18 +/- 2.58 micrograms/ml to 19.99 +/- 7.99 micrograms/ml (p < 0.05); this was associated with a concomitant decline in the malformation rate. CONCLUSION: These data demonstrate that diabetic embryopathy is associated with a deficiency state in essential fatty acid, corroborating our previous in vitro findings. Furthermore, the use of a dietary polyunsaturated fatty acid that specifically increases arachidonic levels significantly reduced the incidence of diabetic embryopathy. These findings may serve as a basis for developing strategies of pharmacologic prophylaxis against diabetes-induced congenital malformations.

Animals↗

PubMed1996

Choledochal cyst in neonates.

Common bile duct cyst, or choledochal cyst is known to be an uncommon cause of neonatal jaundice. It is usually associated with distal biliary tract obstruction and presents a clinical picture that is indistinguishable from biliary atresia. We report two cases of neonatal choledochal cyst encountered from 1992 to 1994. The infants were free from perinatal insult and presented with prolonged jaundice. In both cases, antenatal ultrasonography was unremarkable. Biochemical examinations revealed elevated levels of serum transaminases, alkaline phosphatase and direct bilirubin. Abdominal sonograms disclosed a cystic mass close to the gall-bladder. Intrahepatic duct dilation was noted in one patient. Hepatobiliary scintigraphy demonstrated accumulation of the radionuclide in the porta hepatis without subsequent intestinal activity. Cystic dilatation of the common bile duct with distal obstruction was noted during surgery. Both infants underwent cyst excision with Roux-en-Y hepaticojejunostomy and cholecystectomy. Liver biopsy in one infant showed mild proliferation of the interlobular bile duct and mild portal fibrosis. The postoperative course was uneventful. We conclude that early detection and treatment of choledochal cyst in neonates are important for preventing serious complications of biliary obstruction.

Choledochal Cyst↗

PubMed1994

Creep of a poly(etherurethane urea) in an oxidative environment.

The creep behavior of a PEUU without added stabilizers was examined in H2O2/CoCl2, an environment that simulates the biodegradation of this polymer. Creep in the control environments, air, water, and H2O2, was logarithmic with time as is characteristic of primary or viscoelastic creep. At short times, creep in H2O2/CoCl2 followed the same time dependency as creep in H2O2; however, at longer times an acceleration in the creep rate was observed. Creep in H2O2/CoCl2 was satisfactorily described by addition of a linear time term to the creep equation with an induction time, ti. The induction time was extended by stress-induced crystallization of the soft segments, but was reduced by an increase in H2O2 concentration. Oxidative degradation of the PEUU soft segments was detected by infrared and GPC analysis at times less than ti. This led to the speculation that an initial "precursor" layer was created at the surface by chain cleavage. Microcracking in a subsequent stage was postulated to be responsible for the observed effect on the creep behavior.

Biocompatible Materials↗