Biomedical subjects
Publications and source records attributed to J Kang.
In a crossover study of seven term neonates who had neuroimaging studies, chloral hydrate (75 mg/kg administered orally) was more efficacious (p<0.05) but similar with regard to toxic effects than midazolam (0.2 mg/kg administered intravenously). Thus newer drugs are not necessarily better, and monitoring is essential even after a single oral sedative dose.
When nasal augmentation is performed with implants fashioned from a piece of solid silicone block or commercially available prefabricated implants, the precise sculpturing of the ventral surface of the implant in order to conform to the convex contour of the nose is often difficult to achieve, increasing the possibility for malposition and extrusion. We devised two methods of making soft silicone elastomer implants from nasal cast models obtained from alginate impressions of patients' noses: type I, in which the implant is made from the curing of silicone adhesive that is spread on both sides of the sheet blueprint placed on the cast model, and type II, in which the implant is made only from the curing of silicone adhesive. Because these custom-made implants have a ventral surface of exact concave contour conforming to the convex surface of the nasal framework, they blend in nicely with the various configurations of the existing nasal framework and thus minimize malposition and extrusion. These implants also avoid having a prototype nose for everyone and are more cost-effective than commercially available implants.
1. Postnatal development of a large conductance Ca(2+)-activated K+ channel (BK channel) was investigated in neocortical infragranular pyramidal neurons with inside-out and outside-out patchclamp configurations. Neurons were acutely isolated from slices of 1- to 28-day-old rats (P1-P28) by using a vibrating glass probe after preincubation with low concentrations of enzymes. Patch membrane area was estimated by measuring membrane capacitance. The density, distribution, voltage dependence, Ca2+ sensitivity, kinetics, and pharmacological properties of BK channels were examined in neurons from animals of different ages. 2. In somata, the density of BK channels was 0.056 +/- 0.011/ micron 2 in P1 neurons and 0.312 +/- 0.008/micron 2 in P28 neurons. There was an abrupt increase between P5 and P7 at a rate of approximately 0.042/ micron 2/day. Before P5 and after P7, the density of BK channels also increased but at slower rates. 3. The density of BK channels in proximal apical dendrites underwent a similar developmental sequence. There was a relatively large increase between P5 and P7 with a rate of approximately 0.021/ micron 2/day, and after P7, channel density increased more slowly (approximately 0.002/microns 2/day). In P1 neurons, channel density in apical dendrites was 0.039 +/- 0.008/micron 2, which was close to that in somata, whereas in P28 neurons, channel density (0.134 +/- 0.008/micron 2) was less than one-half of that in somata. 4. The distribution of BK channels was different in immature and mature neurons. In somata of P1 neurons, BK channels were distributed singly without evidence of clustering, whereas in P28 neurons BK channels were clustered in groups of approximately 4. 5. BK channels in both P1 and P14 neurons showed a steep increase in the probability of opening (Po) as intracellular Ca2+ concentration was raised from 50 to 100 nM, especially at positive membrane potentials. The Ca2+ dependence, as measured by the [Ca2+]i that provided half-maximal Po at a variety of membrane potentials, was not different in patches from P1 and P14 neurons. On the other hand, the voltage dependence of BK channels shifted during ontogeny such that Po was larger at negative potentials in P14 than in P1 neurons. 6. The voltage dependence of P1 BK channels was bimodally distributed with 57% of channels exhibiting an "immature" pattern consisting of a more positive V1/2 and a smaller change in voltage required to produce an e-fold increase in Po. Immature type P1 BK channels showed a longer mean closed time at negative membrane potentials than either P14 or "mature" P1 BK channels. 7. No postnatal developmental changes in pharmacological properties of BK channels were observed. In both mature and immature neurons, BK channels were partially inhibited by 30 or 100 nM charybdotoxin (ChTX) and fully blocked by 1 microM ChTX. The IC50 for ChTX was 100 nM, indicating that BK channels in neocortical pyramidal neurons are much less sensitive to ChTX than those in muscle cells and sympathetic ganglion neurons. BK channels were also inhibited by 0.5 mM tetraethylammonium chloride (TEA) and 50 microM trifluoperazine. 8. These data indicate that functional somatic and dendritic BK channels are inserted into neuronal membranes during neocortical development, with an especially rapid increment in density occurring around P5-P7. These changes, which occur at a time when other voltage-gated ion channels are known to be increasing in density, contribute to the development of neocortical excitability.
1. The properties of large conductance Ca(2+)-activated K+ channels (BK channels) were investigaed in neocortical infragranular pyramidal neurons by the use of inside-out patch recordings. Neurons were acutely isolated from slices of newborn to 28-day-old rats (P0-P28) by using minimal protease exposure followed by trituration with a vibrating glass probe. Two types of BK channels, slow-gating and fast-gating, were observed in immature neurons (P0-P5), whereas only slow-gating BK were found in more mature neurons. Fast-gating BK channels differed in conductance, voltage dependence, and kinetics from the slow-gating ones. 2. The properties of fast-gating channels included a conductance of 145 +/- 12.9 (SE) pS; frequent openings with short mean open times that were relatively voltage-independent, mean closed times that showed a voltage-dependent increase, a voltage-dependent decrease in open probability (Po). The properties of slow-gating channels contrasted with those of the fast-gating ones, in that the former had a conductance of 181 +/- 3.9 pS, longer mean open times that showed a voltage-dependent increase, mean closed times that showed a marked voltage-dependent decrease, a voltage-dependent increase in Po, and slight inward rectification. The significance of these developmental variations in channel properties is discussed.
OBJECTIVE: The primary purpose of this study was to evaluate the acute effect of exercise of differing intensity on plasma glucose and insulin responses to an oral glucose challenge. RESEARCH DESIGN AND METHODS: Six obese men and six obese men with NIDDM of similar age, weight, percentage body fat, and VO2peak participated in the study. Each subject underwent two 7-day exercise programs in a counterbalanced order at 2-week intervals. During each 7-day exercise period, the subjects cycled every day at a power output corresponding to 50% VO2peak for 70 min or 70% VO2peak for 50 min. Muscle glycogen utilization was estimated during exercise on day 7 using a [3H]glucose infusion technique in conjunction with indirect calorimetry. During the day before and after each 7-day exercise period, a 3-h oral glucose tolerance test (OGTT) was administered after a 12-h overnight fast. RESULTS: The average caloric expenditure did not differ between exercise at 50 and 70% VO2peak in both obese and obese NIDDM subjects. However, the carbohydrate oxidation was higher (P < 0.05) during exercise at 70 than 50% VO2peak in obese subjects (77 +/- 5 vs. 68 +/- 6 g) and obese NIDDM subjects (70 +/- 4 vs. 58 +/- 6 g). Muscle glycogen utilization was also higher (P < 0.05) during exercise at 70 than 50% VO2peak in obese subjects (59 +/- 9 vs. 30 +/- 7 g) and in obese NIDDM subjects (48 +/- 5 vs. 24 +/- 5 g). In obese subjects, plasma glucose response area during the OGTT did not change after 7 days of exercise at either 50 or 70% VO2peak. Plasma insulin response area during the OGTT also did not change after 7 days of exercise at 50% VO2peak. However, plasma insulin response area was reduced (P < 0.05) after 7 days of exercise at 70% VO2peak (9,644 +/- 1,783 vs 7,538 +/- 1,522 microU.ml-1.180 min-1). In obese NIDDM subjects, both plasma glucose and insulin response areas during the OGTT did not decrease after 7 days of exercise at either 50 or 70% VO2peak. CONCLUSIONS: It is concluded that the exercise-induced improvement in insulin sensitivity is influenced by exercise intensity in obese individuals. The improved insulin sensitivity after 7 days of exercise at 70% VO2peak in obese individuals may be related to greater muscle glycogen utilization during exercise. The lack of improvement in glucose tolerance and insulin sensitivity after 7 days of exercise at either 50 or 70% VO2peak in obese NIDDM patients may be due to the fact that the NIDDM patients selected in the present study were relatively hypoinsulinemic.
This investigation examined the effect of carbohydrate substrate availability on ratings of perceived exertion (RPE) during cycling at moderate intensity to exhaustion and the relation between submaximal endurance performance and RPE obtained following 2 hr. of cycling at moderate intensity. Seven male cyclists performed two exercise trials at power output corresponding to 70% of their peak oxygen uptake until exhaustion. Subjects ingested either a 6% glucose/sucrose solution at the rate of 0.6 g.kg-1 (Body Weight).hr.-1 or an equal volume of artificially flavored placebo every 20 min. throughout the exercise trials. RPE for the legs, chest, and over-all body, and oxygen consumption, expired ventilation, carbohydrate oxidation rate, and blood concentrations of glucose, glycerol, and lactate were measured every 20 min. throughout exercise and at exercise termination. Statistical analysis of these dependent variables indicates that (1) an exercise-induced decrease in blood-borne carbohydrate substrate intensifies leg and over-all perceptions of exertion during the later stages of prolonged cycling at 70% VO2peak. (2) Factors other than availability of blood-borne carbohydrate substrate may influence perceptual intensity at exhaustion. (3) Ratings of perceived exertion for the legs and over-all body obtained after 2 hr. of cycling at moderate intensity may be useful in predicting submaximal endurance performance.
This investigation examined the validity of the Borg 15-category Ratings of Perceived Exertion (RPE) scale during semirecumbent exercise in 32 degrees C water. 9 men undertook 12 8-min. trials at 3 power outputs and 4 pedal-crank rates. The power output was distributed between the arms (20%) and legs (80%). RPEs were measured for the arms, legs, chest, and over-all body. Correlation coefficients for RPE expressed as a function of power output and gross metabolic efficiency (MEG) ranged from .56 to .83 and .54 to .70, respectively, for each pedal-crank rate. Validity coefficients were greatest at those pedal-crank rates having the highest MEG. The Borg 15-category RPE scale is valid for use during semirecumbent exercise in water.
BACKGROUND: Tamoxifen, a nonsteroidal estrogen agonist-antagonist, is used in the treatment of breast cancer. CASE: A postmenopausal woman, aged 73, while being treated with Tamoxifen, developed continuous growth of her myomatous uterus, became symptomatic and required surgery. CONCLUSION: Tamoxifen at a dose of 40 mg/d has been associated with endometrial carcinoma. The growth of myomas seen with Tamoxifen in this patient seems to be a result of its direct agonist properties.
The authors experienced a case of idiopathic spinal cord herniation with duplicated dura mater. A 63-year-old woman presented right dominant slowly progressive spastic paraplegia and dissociated sensory disturbance. Magnetic resonance imaging (MRI) demonstrated an enlarged dorsal arachnoid space associated with an apparently focally narrowed thoracic cord. The cord was kinked towards the anterior and closely applied to vertebral body at the level of Th3-4. Computed tomographic myelography (CTM) revealed homogeneous filling at dorsal arachnoid space immediately after injection and no defects. At operation multilocular arachnoid cyst and duplicated dura mater was respectively observed dorsally, and ventrally. From defected area of the inner layer, a ventral part of the spinal cord was incarcerated between the two dural layers. After rejection of arachnoid cyst and inner layer was performed, the patient recovered neurologically. Idiopathic spinal cord herniation is a rare disease that shows slowly progressive myelopathy at middle age. The herniations were observed at ventral thoracic cord in all reported cases. The mechanism of this disease is still uncertain. But at least three successive factors seem to be necessary for formation of herniation, 1) abnormal structure of the dura mater such as defect, diverticulum and duplication; 2) adhesion between the cord and the destructive dura mater, and 3) continuous cerebrospinal fluid (CSF) pressure pushing the cord outward from subdural space. In the thoracic spine, mobility is limited compared with the cervical and lumbar spine, and because of physiological curvature the cord situates rather ventrally. For these reasons the incidence of adhesion might be higher at ventral thoracic spine. Although neuroradiological imagings especially MRI and CTM were useful, operative findings were necessary for definitive diagnosis in many reported cases. Considering the effectiveness of surgical treatment, study of the ventral side of the cord should be important to avoid misdiagnosis.
A 48-year-old woman complained of fever, headache and nausea in October, 1994. Because polymerase chain reaction (PCR) was positive for mycobacterium tuberculosis in her cerebrospinal fluid, she was administered anti-tuberculous drugs. Steroid hormone was also administered for her symptoms of intracranial hypertension. However, multiple intracerebral masses appeared on CT and MRI 2 months later, and have increased in number and size. Cessation of the steroid hormone was impossible as her intracranial hypertension had been deteriorated. She was transferred to our clinic on October 23, 1995. On neurological examination she was drowsy and showed papilledema, weakness of bilateral lower extremities, left cerebellar sign, and bilateral Babinski's reflexes. Enhanced CT and MRI revealed multi-locular lesions in the right fronto-temporal, left temporal and left cerebellar regions. On November 7, 1995 she was operated on. Right fronto-temporal and left cerebellar masses were partially removed. Pathological examination and PCR of the surgical specimens demonstrated tuberculoma. Postoperatively, her consciousness disturbance improved and the residual tuberculomas decreased in size under the influence of anti-tuberculous drugs and cessation of the use of steroid hormone. Recently, tuberculosis is common neither in Japan nor in Western countries. Intracerebral tuberculoma is also very rare. The tuberculosis in our patient with multiple intracerebral tuberculomas resistant to antituberculous drugs was thought to have been induced by decreased resistance to the infection due to the administration of the steroid hormone.
In 1974 Drachman and his colleagues first raised the possibility of beneficial effect of glucocorticoid in an uncontrolled trial of Duchenne muscular dystrophy (DMD) patients. In contrast, Siegel et al. could not find any significant effect of glucocorticoid in a controlled study. There then followed notable absence in formal trials until Brooke et al. published interesting results in a trial of prednisone in 1987. This was subsequently followed by a series of short term, randomized, double-blind, controlled trials. These studies demonstrated that glucocorticoid could slow the rate of decline of muscle strength. We also investigated the effect of glucocorticoid in 10 DMD patients taking a dosage of prednisolone 1 mg/kg on alternate day. Seven patients of those maintained activities of daily living after 48 weeks of treatment, but the benefits did not last over 192 weeks in any patient. Glucocorticoid therapy may be a valuable option in DMD patients because that no effective medical treatment is currently available. It does significantly slow the progress of disease for at least 3 years. Benefits must be weighed against expected side effects from glucocorticoid. Further studies are needed to establish optimal treatment schedules using prednisolone and develop therapeutic agents with fewer side-effects. The mechanism of beneficial effect of glucocorticoid is unknown.
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Two models have been considered to account for the differentiation of gamma delta and alpha beta T cells from a common hematopoietic progenitor cell. In one model, progenitor cells commit to a lineage before T cell receptor (TCR) rearrangement occurs. In the other model, progenitor cells first undergo rearrangement of TCR gamma, delta, or both genes, and cells that succeed in generating a functional receptor commit to the gamma delta lineage, while those that do not proceed to attempt complete beta and subsequently alpha gene rearrangements. A prediction of the latter model is that TCR gamma rearrangements present in alpha beta T cells will be nonproductive. We tested this hypothesis by examining V gamma 2-J gamma 1C gamma 1 rearrangements, which are commonly found in alpha beta T cells. The results indicate that V gamma 2-J gamma 1C gamma 1 rearrangements in purified alpha beta T cell populations are almost all nonproductive. The low frequency of productive rearrangements of V gamma 2 in alpha beta T cells is apparently not due to a property of the rearrangement machinery, because a transgenic rearrangement substrate, in which the V gamma 2 gene harbored a frame-shift mutation that prevents expression at the protein level, was often rearranged in a productive configuration in alpha beta T cells. The results suggest that progenitor cells which undergo productive rearrangement of their endogenous V gamma 2 gene are selectively excluded from the alpha beta T cell lineage.
A 59-year-old woman with dissection of the thoracic aorta and a fusiform aneurysm of the abdominal aorta without evidence of Marfan's syndrome underwent aneurysmorrhaphy with a bifurcated expanded polytetrafluoroethylene graft. Histological specimens of the aneurysmal wall revealed the presence of idiopathic cystic medial necrosis. As typical findings of idiopathic cystic medial necrosis in the aortic wall are very rare except in cases of Marfan's syndrome, the present case is reported and the implications of this condition are discussed.
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This investigation determined whether carbohydrate ingestion during prolonged moderate-intensity exercise enhanced endurance performance when the exercise was preceded by carbohydrate supercompensation. Seven male trained cyclists performed two trials at an initial power output corresponding to 71 +/- 1% of their peak oxygen consumption. During the trials, subjects ingested either a 6% glucose/sucrose (C) solution or an equal volume of artificially flavored and sweetened placebo (P) every 20 min throughout exercise. Both C and P were preceded by a 6-day carbohydrate supercompensation procedure in which subjects undertook a depletion-taper exercise sequence in conjunction with a moderate- and high-carbohydrate diet regimen. Statistical analysis of time to exhaustion, plasma glucose concentration, carbohydrate oxidation rate, fat oxidation rate, and plasma glycerol concentration indicated that in spite of a carbohydrate supercompensation procedure administered prior to exercise, carbohydrate ingestion during exercise can exert an additional ergogenic effect by preventing a decline in blood glucose levels and maintaining carbohydrate oxidation during the later stages of moderate-intensity exercise.
Angiotensin II (ANG II) stimulates the delayed rectifier K+ current (IK) in neurons cultured from rat hypothalamus and brain stem via AT2 receptors, and this effect involves activation of a Gi protein and protein phosphatase 2A (PP2A). However, there was no evidence that the AT2 receptor involved in this response was the same as the recently cloned AT2 receptor. In the present study, intracellular injection of a 22-amino acid peptide (PEP-22) corresponding to the putative third intracellular loop of the cloned AT2 receptor elicited an increase in IK in cultured neurons that was similar to the effect produced by ANG II. Furthermore, this effect of PEP-22 was abolished by pertussis toxin (200 ng/ml, 24 h) pretreatment and also by superfusion of the PP2A inhibitor okadaic acid (10 nM), suggesting the involvement of Gi protein and PP2A, respectively. Intracellular injection of a random peptide or normal pipette solution did not affect neuronal IK. This is direct evidence to link the cloned AT2 receptor to a defined response elicited by ANG II.