Hyperdense MCA resolved after tPA.
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Fibrinolytic Agents↗
Biomedical subjects
J W Tsao
Publications and source records attributed to J W Tsao.
Diagnostic dilemma. Emphysematous cystitis.
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Aged↗
Radial artery mycotic pseudoaneurysm: an unusual complication of catheterization.
Radial artery pseudoaneurysms are rare, and those that become infected are rarer still. We present the case of a patient who developed a radial artery pseudoaneurysm as a late complication of arterial catheterization. Blood cultures were positive for Staphylococcus aureus, and a pulsatile mass, with associated tissue necrosis, was palpable over the radial artery. The diagnosis was confirmed by gray-scale and color Doppler sonography, which showed a partially thrombosed pseudoaneurysm and turbulent flow in the pseudoaneurysm and native artery.
Aged↗
Altered brain metabolism in the C57BL/Wld mouse strain detected by magnetic resonance spectroscopy: association with delayed Wallerian degeneration?
In the C57BL/Wld(s) (Wld) mouse strain, both PNS and CNS axonal disintegration during Wallerian degeneration is dramatically slowed, with isolated axons being able to conduct compound action potentials (CAPs) for several weeks post-transection. The ability to conduct a CAP signifies the presence of an intact plasma membrane, normal ion gradients, and functioning ion channels. In neurons, ion homeostasis is primarily regulated by the Na(+)-K(+)-ATPase, which utilizes approximately 50% of neuronal energy output. To investigate the possibility that the Wld mutation prolongs axonal degeneration by conferring a more favorable energetic status to neurons or alters metabolism, we used 31P and 1H magnetic resonance spectroscopy (MRS) to compare the cerebral and muscle energy metabolism, membrane phospholipid contents, and water-soluble metabolites of Wld and wild-type (C57BL/6J [6J], and BALB/c) mouse strains. We first demonstrate that, with advancing age, transected Wld CNS nerves degenerate faster, paralleling previous findings in the PNS. We found significantly decreased phosphocreatine and phosphomonoester concentrations in the brains of Wld mice at 1- and 2-months of age compared to both 6J and BALB/c mice, but we failed to find differences in the adenylate (ATP, ADP, or AMP) or phospholipid concentrations. In another excitable tissue, skeletal muscle, no differences in energy-containing metabolites were detected. High resolution 1H MRS indicated that at 1 month of age, Wld brains have cytosolic levels of glutamate and phosphocholine that are significantly decreased, relative to total N-acetyl aspartate content. Our results demonstrate that delayed Wallerian degeneration in the C57BL/Wld mouse strain is associated with altered cerebral metabolism, although these changes may be secondary to the mutation.
Action Potentials↗
Temperature modulation reveals three distinct stages of Wallerian degeneration.
After peripheral nerve transection, axons distal to the cut site rapidly degenerate, a process termed Wallerian degeneration. In wild-type mice the compound action potential (CAP) disappears by 3 d. Previous studies have demonstrated that cold temperatures and lower extracellular calcium ion (Ca2+) concentrations can slow the rate of Wallerian degeneration. We have incubated isolated sciatic nerve segments from wild-type and C57BL/Wld mice (which carry a gene slowing Wallerian degeneration) in vitro at 25 and 37 degrees C. At 25 degrees C we found that the degeneration rate of wild-type axons was slowed dramatically, with the CAP preserved up to 7 d post-transection. In contrast, at 37 degrees C the CAPs were minimal at 2 d. When the temperature of wild-type nerves was raised to 37 degrees C after 24-72 hr at 25 degrees C, degeneration occurred within the subsequent 24 hr. Wld nerves, too, were preserved longer at 25 degrees C but, on return to 37 degrees C, degenerated promptly. Cooling the nerve within 12 hr after axotomy enhanced axonal preservation. Neither wild-type nor Wld nerves showed different degeneration rates when they were incubated with 250 microM or 5 or 10 mM extracellular Ca2+ for 1-2 d, suggesting that an abrupt increase in intracellular Ca2+ occurs at the time of axonal destruction. Wallerian degeneration, thus, appears to progress through three distinct stages. Initiation occurs at the time of injury with subsequent temperature-dependent and -independent phases. Nerves appear to remain intact and are able to exclude Ca2+ from entering until an as yet unknown process finally increases axolemmal permeability.
Animals↗
Images in clinical medicine. Indinavir crystalluria.
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Abdominal Pain↗
Mycotic aneurysm presenting as Pancoast's syndrome in an injection drug user.
Injection drug users frequently present to emergency departments with fever. A careful history and physical examination with attention to anatomic localization of symptoms and signs are often necessary to unmask unusual underlying medical conditions. We report a case of a woman with recent injection drug use who presented with fever, a palpable neck mass, and Pancoast's syndrome. She had been seen recently at the ED of another hospital and discharged with oral antibiotics for presumed cellulitis. A mycotic aneurysm of the subclavian artery causing Pancoast's syndrome was later diagnosed by using computed tomography and angiography. A high index of suspicion for anatomically localized infective processes should always be maintained with febrile injection drug users.
Adult↗
Persistence of neuromuscular junctions after axotomy in mice with slow Wallerian degeneration (C57BL/WldS).
The present study was undertaken to examine the fate of neuromuscular junctions in C57BL/WldS mice (formerly known as OLA mice) after nerve injury. When a peripheral nerve is injured, the distal axons normally degenerate within 1-3 days. For motor axons, an early event is deterioration of motor nerve terminals at neuromuscular junctions. Previously, the vulnerability of motor terminals has been attributed either to a 'signal' originating at the site of nerve injury and transported rapidly to the terminals or to their continual requirement for essential maintenance factors synthesized in the motor neuron cell body and supplied to the terminals by fast axonal transport. Mice of the WldS strain have normal axoplasmic transport but show an abnormally slow rate of axon and myelin degeneration. Structure and function are retained in the axons of distal nerve stumps for several days or even weeks after nerve injury in these mice. The results of the present study show that WldS neuromuscular junctions are also preserved and continue to release neurotransmitter and recycle synaptic vesicle membrane for at least 3 days and in some cases up to 2 weeks after nerve injury. Varying the site of the nerve lesion delayed degeneration by approximately 1-2 days per centimetre of distal nerve remaining. These findings suggest that the mechanisms of nerve terminal degeneration after injury are more complex than can be accounted for simply by the failure of motor neuron cell bodies to supply their terminals with essential maintenance factors. Rather, the data support the view that nerve section normally activates cellular components or processes already present, but latent, in motor nerve endings, and that in WldS mice either the trigger or the cellular response is abnormal.
Aging↗
Radiation-induced reductions in macrophage recruitment have only slight effects on myelin degeneration in sectioned peripheral nerves of mice.
Macrophage recruitment into the distal nerve stump of the cut or crushed sciatic or saphenous nerves of C57BL/6J mice was reduced by prior whole body irradiation. This procedure was successful in keeping the numbers of cells stained with the mouse macrophage-specific antibody F4/80 to the levels found in unsectioned nerves. Quantitative image analysis of immunostained sections showed that the rate of loss of myelin basic protein was identical in nerves from irradiated and unirradiated mice up to 5 days but thereafter was slower in macrophage-deprived nerves. Similar analysis of semithin sections stained with toluidine blue detected more undegenerated myelin in the nerves from irradiated mice 10 days after operation. Quantitative counts made from electron micrographs of the sectioned nerves at 7 days also showed slightly less extensive myelin breakdown in the nerves from irradiated mice. Complete removal of myelin from some Schwann cells can occur without macrophages, but macrophages accelerate the removal of myelin in the later stages of Wallerian degeneration. It is concluded that there are two phases to the breakdown of myelin in peripheral nerves undergoing Wallerian degeneration: an initial stage entirely dependent on the activity of Schwann cells and a later stage dependent on both Schwann cells and the presence of macrophages.
Animals↗
Loss of the compound action potential: an electrophysiological, biochemical and morphological study of early events in axonal degeneration in the C57BL/Ola mouse.
In the C57BL/Ola (Ola) mouse strain there is a marked slowing of axonal disintegration during Wallerian degeneration. The locus of the mutation controlling this phenomenon (slow Wallerian degeneration--Wlds) has been mapped to chromosome 4, and its protective effect decreases with advancing age. Using biochemical, electrophysiological and histological techniques, the present study was undertaken to determine whether neurofilament phosphorylation and stability are altered or whether calcium-activated proteases are absent in the sciatic nerves of Ola mice. A compound action potential was detectable only when neurofilaments were present and normal axonal architecture was seen. In 1-month-old Ola mice, compound action potentials and neurofilaments were still detectable at 21 days post-transection, whereas both were undetectable by 2 days in BALB/c and C57BL/6J (6J) mice of the same age. Neurofilament levels declined faster with advancing Ola age, confirming previous results, whereas degeneration slowed in ageing BALB/c and 6J mice. In vitro and in vivo degeneration rates were comparable in BALB/c and 6J nerves. Ola nerves, however, showed more rapid decline in vitro than in vivo. Ola and BALB/c nerves frozen and then thawed and incubated in the presence of calcium ions and the ionophore A23187 were not resistant to degradation by intrinsic proteases. Even when a compound action potential could no longer be elicited, however, a majority of nerves still had > 50% of myelinated and unmyelinated axons whose electron microscopic profiles appeared normal. Thus, it appears that the first event in Wallerian degeneration in the Ola mouse is a change at the plasma membrane--a transected nerve becomes unable to conduct a compound action potential.(ABSTRACT TRUNCATED AT 250 WORDS)
Action Potentials↗
The Effectiveness of the Gene Which Slows the Rate of Wallerian Degeneration in C57BL/Ola Mice Declines With Age.
The rate of Wallerian degeneration is unusually slow in severed axons of mice of the C57BL/Ola strain. Within mice of that strain we have now found that the rate of degeneration increases with the age of the animal. In 4-week-old mice nerve stimulation evokes muscle contractions even 5 days after sciatic nerve section and compound action potentials can be recorded in the distal nerve stump up to 3 weeks after section. In 1-year-old animals no action potentials can be excited 5 days after nerve section. Heterozygous mice carrying only one copy of the dominant gene show the same age-related decline in viability of the distal nerve stump after axotomy, and the rate of decline is no greater than for homozygous mice. The more rapid rate of degeneration of severed axons of mice of the C57BL/6J strain was affected in the opposite way by age, degeneration occurring more slowly in older animals.
Journal Article↗
Studies on frequency-dependent attenuation in the normal liver and spleen and in liver diseases, using the spectral-shift zero-crossing method.
This report presents results of studies using the spectral-shift zero-crossing method to measure frequency-dependent attenuation (FDA) in normal liver and spleen and in diseased liver. We developed a new system for attenuation analysis that calculated FDA in dB/cm/MHz according to the following equation: (formula: see text). Data are collected from the region of interest on the scan image. Graphite-gel phantoms of known attenuation value are used to create a high degree of accuracy in this new system. Mean attenuation of normal livers was 0.55 +/- 0.05 dB/cm/MHz, while that of normal spleen was 0.37 +/- 0.06 dB/cm/MHz. No correlation between FDA and age could be seen. FDA was 0.81 +/- 0.17 dB/cm/MHz in fatty liver, 0.63 +/- 0.13 dB/cm/MHz in liver cirrhosis, and 0.64 +/- 0.12 dB/cm/MHz in chronic hepatitis. These values are higher than those obtained from normal liver, while tumor masses in the liver (hepatocellular carcinoma, hepatoblastoma, hemangioma) and diffuse infiltration by malignant lymphoma produced lower than normal values, averaging 0.38 +/- 0.08 dB/cm/MHz.
Adolescent↗
Retardation of calcification of bovine pericardium used in bioprosthetic heart valves by phosphocitrate and a synthetic analogue.
The purpose of this study was to determine if phosphocitrate (PC), a naturally occurring inhibitor of calcification, and its synthetic analogue, N-sulpho-2-amino tricarballylate (SAT), administered either by daily injection or local delivery via Alzet osmotic minipump, could inhibit calcification of glutaraldehyde-preserved bovine pericardium used in bioprosthetic heart valves, subcutaneously implanted in rats. Local drug delivery, but not systemic administration, was effective. PC, administered by Alzet minipump (12 mg.kg-1.day-1), inhibited calcification significantly (tissue calcium = 5 +/- 2 micrograms/mg dry tissue, mean +/- SEM), compared with untreated or saline-treated controls (89 +/- 9 and 49 +/- 9 micrograms/mg, respectively). SAT, administered by the same route at both the same and a higher molar dosage, was less potent (tissue calcium = 26 +/- 9 micrograms/mg and 17 +/- 5 micrograms/mg, respectively). PC and SAT therapy were not associated with adverse effects. We conclude that locally administered PC and SAT can inhibit intrinsic calcification of bovine pericardium, with PC being more potent.
Animals↗
Calcification of bovine pericardium used in cardiac valve bioprostheses. Implications for the mechanisms of bioprosthetic tissue mineralization.
Calcification of bioprosthetic heart valves fabricated from glutaraldehyde-pretreated bovine pericardium has not been investigated. The objectives of this study were to characterize pericardium before and after glutaraldehyde pretreatment and to study the pathophysiology of mineralization of glutaraldehyde-preserved pericardium. Pericardial protein was approximately 90% collagen, predominantly Type I. Glutaraldehyde incorporation was complete following 24 hours' incubation (151 X 10(-9) mol/mg). Bovine pericardium pretreated in buffered 0.6% glutaraldehyde, implanted subcutaneously in young rats for 24 hours to 112 days, was analyzed chemically (calcium and phosphorus) and morphologically. Mineralization, detected at 48 hours' implantation, was initially associated with pericardial connective tissue cells and later also collagen. Mean calcium content was 114 micrograms/mg at 21 days and 199 micrograms/mg at 112 days. The morphologic features and the kinetics and degree of mineral accumulation in glutaraldehyde-pretreated bovine pericardium were strikingly similar to those previously determined for porcine aortic valve. These results predict that calcification will critically limit the late durability of clinical pericardial bioprostheses and suggest generalized mechanisms of bioprosthetic tissue mineralization which are probably dependent on modification of implant microstructure by glutaraldehyde pretreatment.
Amino Acids↗