Liver transplantation from non-heart-beating donors: liver procurement without in situ portal flush.
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Biomedical subjects
Publications and source records attributed to M Uchiyama.
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In order to clarify the relationship between sleep-wake and core body temperature rhythms in the delayed sleep phase syndrome (DSPS), we conducted simultaneous monitoring of these rhythms in seven patients with DSPS and nine healthy control subjects for 6-10 days during their conventional sleep-wake schedules. The sleep onset and offset times were determined visually from sleep logs, and the temperature data were fitted to 24-hour cosinor curves by the least squares method. The sleep onset and offset times and temperature nadir were delayed significantly in patients with DSPS compared with the control subjects (p = 0.01, 0.003 and 0.02, respectively). We also found that sleep length and the temperature nadir to sleep offset interval were significantly longer in the DSPS than the control group (p = 0.03 and 0.02, respectively). The latter finding suggests that the inability of the patients with DSPS to normally phase-advance their circadian rhythm may be a consequence of masking of the advance portion of their phase-response curve by the last hours of their prolonged sleep episodes.
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Serum carnitine concentrations are known to decrease in patients on regular hemodialysis and to increase in chronic renal failure. However, there is little information available concerning serum levels of carnitine in different glomerular diseases in patients whose renal functions have not yet deteriorated. In this study, we measured serum carnitine concentrations in 40 pediatric patients with idiopathic nephrotic syndrome, IgA nephropathy, non-IgA glomerulonephritis, focal segmental glomerular sclerosis, and normal controls. The results showed that there were no significant differences in the serum-free and total carnitine concentrations (S-FCC and S-TCC, respectively) between patients with different glomerular diseases and the controls. Of interest was the statistically weak correlations of both S-TCC and S-FCC with BUN in these patients, despite their normal renal functions. The ratio of S-FCC to S-TCC was significantly higher as compared with that of the controls. These findings suggest that serum carnitine concentrations are not affected by the types of glomerular lesions and that serum levels of carnitine depend mostly on the glomerular excretory capacity of urea nitrogens, even when the renal functions have not yet deteriorated. The increase in the ratio of S-FCC to S-TCC may be an early reflection of changes in the serum carnitine profiles of these patients.
We previously reported the characteristics of a murine monoclonal antibody (TO73) against the multidrug-resistant (MDR) human leukemic cell line. In the present study, we have studied the clinical significance of TO73 by examining its reactivity with primary and relapsed leukemic cells. Of 20 patients with primary leukemia and 15 patients with relapsed leukemia, none and four cases, respectively, reacted with TO73 (p < 0.05). Furthermore, three of the four positive cases were also positive for P-glycoprotein. These results indicate that TO73 preferentially reacts with leukemic cells resistant to chemotherapy and may be a new marker for refractory leukemia.
A comparative study of 201Tl and 99mTc-MIBI was performed in 39 breast tumors. 201Tl scintigraphy was carried out in 24 breast tumors and 99mTc-MIBI scintigraphy in 15. The sensitivity of 201Tl for malignant tumors was 100% (22/22), but specificity was 0% (0/2). On 99mTc-MIBI scintigraphy, the sensitivity for the malignant tumors was 83.3% (10/12) and specificity was 100% (3/3). 99Tc-MIBI might be more useful for the diagnosis of breast tumors, because the tumor/background ratio of 99mTc-MIBI was significantly higher than that of 201Tl. In addition, 201Tl scintigraphy and 99mTc-MIBI scintigraphy showed the same degree of accuracy (93.3%) in diagnosis of lymph node reached. Moreover, when either US and 201Tl or 99mTc-MIBI scintigraphy was positive for lymph node metastasis, accuracy of detection of lymph node metastasis became 94.4%. A combined study of US and scintigraphy might improve the accuracy for diagnosis of lymph node metastasis.
Strontium-89 chloride is widely available in the U.S. and Europe for patients afflicted by bone metastasis associated with pain. 89Sr is a pure beta-emitter and it is thought to be difficult to estimate its distribution externally. We tried to image the distribution of 89Sr uptake with bremsstrahlung from beta-minus decay of 89Sr by using Nal scintillation camera. Pronounced 89Sr depositions in the bone metastatic sites were imaged in the energy windows from 50 keV to 150 keV bremsstrahlung. The distribution of these depositions corresponded to 99mTc-HMDP image may be suspected to the effectiveness of this therapy. The identification of 89Sr distribution might be useful in evaluating the bone marrow radiation dose too.
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OBJECTIVE: To clarify possible associations of decay-accelerating factor (DAF, CD55), expressed on circulating lymphocyte subsets and other hematologic cells, with corresponding cytopenias observed in primary Sjögren's syndrome (SS). METHODS: DAF expression on peripheral blood (PB) cells was determined in 21 patients with SS and 11 healthy controls by single or 2 color flow cytometry. RESULTS: In the PB from SS patients, anemia, monocytopenia, neutropenia, and lymphocytopenia were observed. Compared to the controls, the percentages of DAF-negative cells were higher in CD4+ and CD8+ T cell subsets from SS patients, but the expression of DAF was similar in the other PB cells, including CD19+ B cells, CD56+ NK cells, monocytes, granulocytes, and erythrocytes. The percentages of DAF-negative cells among the CD4+ and CD8+ cells were positively correlated in SS patients, but the numbers of cells in both subsets were decreased in those patients being treated with prednisolone. However, these proportional changes are thought to reflect a decrease in the numbers of DAF-positive CD4+ and CD8+ cells, because the absolute numbers of circulating DAF-positive CD4+ and CD8+ cells, but not DAF-negative cells, were significantly decreased in SS patients. In addition, DAF-negative cells were detectable in both CD45RA+ (naive) and CD45RO+ (memory) T cells from healthy individuals, and the expression of DAF was remarkably increased in both subsets after in-vitro activation with concanavalin-A. CONCLUSION: DAF-negative cells are proportionally increased among circulating CD4+ and CD8+ T cells in SS patients, although such changes are due to decreased numbers of DAF-positive cells within each subset. When considering previous observations, the DAF-negative CD4+ and CD8+ cells probably belong to activated T cell subsets in both SS patients and controls. However, the patterns of DAF expression seemed to be different between activated T cells recognized in the PB, and those induced by in vitro-stimulation.
Modulation by acetylcholine, VIP, clonidine, omega-conotoxin and Mg2+ of the relaxant response to electrical and chemical stimulation of nitroxidergic nerves, in which nitric oxide (NO) acts as a neurotransmitter, was investigated in isolated canine cerebral arteries. Acetylcholine attenuated the response, the inhibition being reversed by atropine; however, physostigmine failed to reduce the response. VIP in submaximal doses did not alter the neurally induced relaxation. The same was true with clonidine, morphine and naloxane. Treatment with omega-conotoxin depressed the response to electrical nerve stimulation but did not influence the nicotine-induced relaxation. Mg2+ inhibited the relaxation caused by nerve stimulation and Ca2+ reversed the response. It is concluded that activation of prejunctional muscarinic receptors seems to inhibit the synthesis of release of NO from nerve terminals but endogenous acetylcholine from cholinergic nerve does not play a role in inhibiting the nitroxidergic nerve function. Prejunctional VIP, alpha 2, adrenergic and opioid receptors are not likely to participate in the regulation of nerve function. Ca2+ responsible for NO synthase activation would be produced into nerve terminals via N-type Ca2+ channels when electrically stimulated and via non-N-, non-L-type channels when stimulated by nicotine. Mg2+ and Ca2+ counteract in the neurally induced relaxation, although the underlying mechanism was not determined.
Erythrocyte ouabain maximum binding (Vmax level) represents the number of molecules of Na-K ATPase on the erythrocyte membrane. Erythrocyte Vmax levels and sodium potassium concentrations were studied in 38 mature and 57 premature infants, including 40 very low birth weight infants, 41 children and 16 adults, in order to clarify the development of erythrocyte Na-K ATPase related to mineral balance and thermogenesis. Vmax levels were the highest (22.9 +/- 8.9 nmol/l cells) for premature infants; correlated negatively with gestational age (r = -0.77, P < 0.01). Vmax levels correlated positively with the ratio of erythrocyte potassium to sodium concentration (IC-K/Na) at < 20 nmol/l cells of Vmax levels (r = 0.72, P < 0.01), but not at > or = 20 nmol/l cells (r = 0.23). Vmax levels in very low birth weight infants, especially < 28 weeks postconception, decreased gradually with postnatal days. Ln(Vmax) levels correlated negatively with postconceptional age (r = -0.75, P < 0.01). Under 28 weeks postconception, Vmax levels were high, but not correlated with IC-K/Na. It is probable that individual Na-K ATPase molecules may be less active, and the large numbers of Na-K ATPase molecules may compensate for the individual lower activity.
To clarify the effect of vitamin B12 on the human circadian clock, five healthy male adults participated in two constant routine procedures, 2 or 3 weeks apart. In one, subjects received intravenous saline injections (placebo trial) and in the other, intravenous injections of methylcobalamin (MB12) (drug trial). Intravenous administration of MB12 increased rectal temperature in the later hours of the daytime during the constant routine. The activity did not change between treatments in any period during the constant routine. During the later hours of the constant routine, alertness assessed with visual analog scale was higher in the drug trial than in the placebo trial. The period in which drug treatment produced greater alertness almost coincided with that in which MB12 elevated rectal temperature. These results may provide evidence of an effect of vitamin B12 on the circadian clock.
Using dephosphorylated neurofilament (NF) proteins as substrates, the kinase with a higher activity for the dephosphorylated NF-H than the phosphorylated form of NF-H was searched for in the porcine brain extract. Most NF-H kinase activity in the brain extract pelleted with microtubules. The NF-H kinase purified from a high salt extract of the microtubule pellets was composed of cdk5 and a 26 kDa protein, a fragment of the 35 kDa regulatory subunit of cdk5. In contrast to the association of the active kinase with microtubules, each of uncomplexed cdk5 and the 35 kDa regulatory subunit was differently distributed in the supernatant fraction and the pellet, respectively, by ultracentrifugation of the brain extract. Dephosphorylated forms of NF-H and NF-M became reactive to antibodies recognizing in vivo phosphorylation sites (SMI31, 34, and 36, JJ31 and 51) by phosphorylation with cdk5/p26. cdk5/p26 showed similar enzymatic properties to p34cdc2/cyclin B kinase; the substrate specificity and inhibition by a p34cdc2 kinase specific inhibitor, butyrolactone I. However, p34cdc2/cyclin B kinase was distinguished from cdk5/p26 by its binding to p13suc1 protein and by its reactivity to anti-p34cdc2 antibodies. In spite of similar enzymatic properties of cdk5/p26 and p34cdc2/cyclin B kinase, cdk5/p26 did not display M-phase promoting activity when assayed with a cell-free system of Xenopus egg extract.
A neonate with a large cervical mass was transferred to our hospital at 4 days of age. A computed tomography scan showed a contrast-enhanced solid mass with multiple cystic elements and fine calcification. Ultrasonography also revealed a predominantly solid mass with calcification, containing multiple cysts. These studies suggested a teratoma, but could not rule out a hemangioma. The tumor was removed on the 12th day of life. A pathological study revealed an immature teratoma that demonstrated fetal type cartilage and an immature neural tube. The operative complete removal of a cervical teratoma in neonates is recommended as soon as possible. The management of a pediatric cervical teratoma should also be similar to that of a sacrococcygeal teratoma. The incidence of cervical teratoma in all pediatric teratomas ranges from 2.3%-9.3% in the West, and from 1.6%-8.3% in Japan.
UNLABELLED: One of the causes of early onset hyperkalaemia in very low birth weight infants is presumed to be the dysfunction of K+ transport across the cell membrane. Sodium-potassium adenosine triphosphatase(Na(+)-K+ ATPase) is known to play a major role in K+ transport. We compared the concentrations of erythrocyte Na(+)-K+ ATPase (Vmax levels) for hyperkalaemic and normokalaemic infants of matched gestational age. In hyperkalaemic infants, the highest levels of Vmax were reached at 24-48 h after birth, but in normokalaemic infants, there were no significant changes in Vmax levels during the 1st week after birth. At 12-72 h after birth, erythrocyte K+ concentrations for hyperkalaemic infants were higher than those of normokalaemic infants. For both groups of infants, the highest levels of plasma K+ during the 1st week after birth showed a positive correlation with those of Vmax. CONCLUSION: Na(+)-K+ ATPase on the cell membrane is activated to compensate for hyperkalaemia; however, when this compensation is incomplete, hyperkalaemia occurs.
Serum lipid profiles and the effects of thyroid hormone on them were studied in infants with congenital hypothyroidism. Serum total cholesterol, high-density lipoprotein cholesterol (HDLC), and low-density lipoprotein cholesterol levels were increased in infants with hypothyroidism;L-thyroxine therapy decreased the HDLC levels, leading to a reduction in serum concentrations of total cholesterol. It appears that thyroid hormone suppresses circulating HDLC, although the mechanism was not discovered in this study.