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Biomedical subjects

H Kaji

Publications and source records attributed to H Kaji.

At least 235 records · Page 13Linked to original sources

Biochemical correlates of hypnoanalgesia in arthritic pain patients.

Self-reported levels of pain, anxiety, and depression, and plasma levels of beta-endorphin, epinephrine, norepinephrine, dopamine, and serotonin were measured in 19 arthritic pain patients before and after hypnosis designed to produce pain reduction. Correlations were found between levels of pain, anxiety, and depression. Anxiety and depression were negatively related to plasma norepinephrine levels. Dopamine levels were positively correlated with both depression and epinephrine levels and negatively correlated with levels of serotonin. Serotonin levels were positively correlated with levels of beta-endorphin and negatively correlated to epinephrine. Following hypnotherapy, there were clinically and statistically significant decreases in pain, anxiety, and depression and increases in beta-endorphin-like immunoreactive material.

Adult↗

Amino acid sequence of derivatives of newborn rat epidermal thiol proteinase inhibitor.

Three different forms of thiol proteinase inhibitor (TPI) were isolated from newborn rat epidermis, in which two forms, TPI-1 and TPI-2, inhibited a proteinase activity, but another newly detected one (designated as TPI-3), showed no inhibitory effect. The complete amino acid sequence of TPI-2 and the sequence of the first seventeen residues from the NH2-terminus of TPI-3 were determined. The sequence shows that TPI-2 lacks in the first six (or four) residues from the NH2-terminus of intact inhibitor, TPI-1, whereas TPI-3 is devoid of its fifteen amino acid residues. These results indicate a high and specific susceptibility of TPI to proteolysis. Most significantly, the NH2-terminal region of TPI appears to be essential for inhibition of proteinase activity.

Amino Acid Sequence↗

Stimulatory effect of peptide histidine isoleucine amide 1-27 on prolactin release in the rat.

Intravenous injection of pure peptide histidine isoleucine amide 1-27 (PHI) resulted in a prompt and significant increase of plasma prolactin (PRL) in conscious freely-moving male rats. Using a perifusion system of rat anterior pituitary tissues in vitro, effluent PRL levels were also increased by 10(-8)-10(-7) M PHI. A PRL releasing potency of PHI was almost similar with that of vasoactive intestinal polypeptide (VIP) or TRH both in vivo and in vitro. Coupled with the recent immunocytochemical studies showing the dense network of PHI immunoreactive fibers around the hypophysial portal vessels, PHI might be another candidate for PRL releasing factor.

Animals↗

Deficiency of erythrocyte superoxide dismutase and catalase activities in patients with malignant lymphoma and acute myeloid leukemia.

The activity of erythrocyte superoxide dismutase (SOD) and catalase was determined in 38 patients with lung cancers (n = 15), malignant lymphoma (n = 11) and acute myeloid leukemia (n = 12). The patients with malignant lymphoma and acute myeloid leukemia showed a significant decrease in both enzyme activities (P less than 0.01) while the patients with lung cancer (9 squamous cell carcinomas and 6 small cell carcinomas) showed normal values of SOD and catalase activities. Furthermore, the patients with malignant lymphoma and acute myeloid leukemia, in remission, but not treated with anticancer drugs, also showed a significant decrease in SOD and catalase activity. These observations therefore indicate that a deficiency of erythrocyte SOD and catalase activities is caused by cancer and varies with the type of the cancer.

Acatalasia↗

Noradrenergic modulation of human pancreatic growth hormone-releasing factor (hpGHRF1-44)-induced growth hormone release in conscious male rabbits: involvement of endogenous somatostatin.

To clarify the role of noradrenergic neurons in the regulation of GH secretion, the effects of iv administered noradrenergic antagonists were investigated in freely moving, conscious male rabbits. During a 6-h observation period (1030-1630 h), control rabbits manifested pulsatile GH secretion with surges between 1030-1200 and 1415-1630 h. Phenoxybenzamine, (POB), an alpha-adrenergic blocker (5 mg/kg, twice), abolished the episodic GH surges; propranolol, a beta-adrenergic blocker (2.5 mg/kg, twice), did not. The bolus injection (1 or 10 micrograms) of synthetic human pancreatic GH-releasing factor (hpGHRF) with 44 amino acid residues (hpGHRF1-44) resulted in significant rises in the plasma GH of control animals. The plasma GH responses to hpGHRF1-44 were significantly larger in propranolol-treated than control rabbits. In contrast, POB completely suppressed the hpGHRF1-44-induced GH release. The injection of antisomatostatin (SRIF) serum into POB-treated rabbits did not yield a disinhibition of the episodic GH surges but restored the plasma GH rises after hpGHRF1-44 injection. These results indicate that noradrenaline++ plays an important role in regulating GH secretion in the rabbit. We propose that alpha-noradrenergic blockade suppresses GH release not only by inhibiting the release of hypothalamic GHRF but also by stimulating the secretion of SRIF and that beta-noradrenergic blockade enhances GH release by inhibiting the release of SRIF from the hypothalamus.

Animals↗

Stimulation of growth hormone by vasoactive intestinal polypeptide in acromegaly.

Vasoactive intestinal polypeptide (VIP) was administered as an iv bolus of 1 micrograms/kg BW to 8 acromegalic patients and in doses of 0.5 and 1 microgram/kg BW to 15 normal volunteers. Both systolic and diastolic blood pressures decreased, and pulse rate increased transiently after VIP injection. VIP stimulated PRL release from the anterior pituitary in normal subjects. Plasma PRL responses to VIP in women were dose dependent and larger than those in men. On the other hand, plasma GH levels rose markedly after VIP injection in all 6 patients with untreated acromegaly. In 2 patients studied after transsphenoidal microadenomectomy, there was no plasma GH response to VIP. In 2 other patients with inactive acromegaly as well as in normal subjects, VIP failed to affect plasma GH levels. In all 6 patients with active acromegaly, LRH (1-2 micrograms/kg BW, iv) did not increase plasma GH levels, but TRH (5-10 micrograms/kg BW, iv) caused significant increases in plasma GH, the magnitude of which was not similar to that of increases seen after VIP injection. Paradoxical GH responses to TRH were not observed in patients in the inactive phase after transsphenoidal surgery. These findings suggest that VIP stimulates GH release in vivo in acromegalic patients. A VIP test as well as a TRH test offer promise as simple and reliable techniques to evaluate the activity of acromegaly, particularly after transsphenoidal surgery.

Acromegaly↗

Prolactin secretion from human prolactinomas perifused in vitro: effect of TRH, prostaglandin E1, theophylline, dopamine and dopamine receptor blockers.

To clarify the functional characteristics of prolactin (Prl)-producing adenoma cells, the effect of TRH, prostaglandin E1 (PGE1), theophylline, dopamine and dopaminergic antagonists on Prl secretion was examined in vitro in perifused pituitary adenoma tissues obtained at surgery from 8 patients with prolactinoma. Perifusion with TRH at a concentration of 10(-6) to 10(-5) M resulted in a significant increase in effluent Prl levels in 3 of the 8 adenoma tissues. In the remaining 5 adenomas, TRH produced no effect on Prl release in vitro. On the other hand, PGE1 (10(-5) M) stimulated Prl secretion in 2 of the 4 adenomas examined. Addition of theophylline (5.5 mM) caused a marked increase of effluent Prl levels in all 8 prolactinomas regardless of the reactivity to TRH or PGE1. Dopamine (5 X 10(-7) M) suppressed Prl secretion from adenoma tissue in 5 of 7 patients tested but had no effect in the remaining two adenomas. When perifused simultaneously with dopamine, sulpiride (D2-selective dopamine receptor blocker, 5 X 10(-7) M) blocked the inhibitory effect of dopamine on Prl release in 3 of the 4 dopamine-sensitive prolactinomas. In one adenoma responsive to dopamine but resistant to sulpiride, YM-09151-2 (relatively specific D1-dopamine receptor blocker, 5 X 10(-7) M) antagonized the dopaminergic inhibition of Prl release. When perifused alone, neither sulpiride nor YM-09151-2 affected Prl release from any of the adenoma tissues tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Investigating the myopathic effects of 6-mercaptopurine on developing skeletal muscle cells in vitro.

6-Mercaptopurine (6-MP) is an adenine antagonist which has been shown to cause skeletal muscle atrophy in neonatal rats. To investigate the effects of 6-MP on developing muscles, pure populations of myoblasts and myotubes in vitro were treated with 6-MP (5-50 micrograms/ml). The viability and protein content of myotubes, but not myoblasts, was decreased by 6-MP. Microscopic examination of the 6-MP-treated (50 micrograms/ml) myotubes demonstrated that severe degenerative changes had occurred, including extensive necrosis, inhibition of myotube formation, and the appearance of intracellular vacuoles. However, 6-MP treatment decreased the incorporation of radiolabeled leucine and thymidine by myoblasts, but not myotubes. These findings indicate that 6-MP exerted a selective toxicity on myotubes but not myoblasts.

Animals↗

Release of vasoactive intestinal polypeptide into the cerebrospinal fluid of the fourth ventricle of the rat: involvement of cholinergic mechanism.

Vasoactive intestinal polypeptide (VIP) is found abundantly in the cerebrospinal fluid (CSF). In order to clarify its source in the brain and the control mechanism of its release, cerebral ventricles of urethane-anesthetized male rats were locally perfused with the artificial CSF at a constant rate of 120 microliters/min by means of a push-pull cannula and immunoreactive VIP was continuously measured in the effluents obtained at 10 min intervals. The perfusion with veratridine, a depolarizing agent, at a rate of 5 x 10(-4) M/min, caused a significant (P less than 0.01) increase in the effluent VIP levels when the tip of a cannula was placed in the fourth ventricle but not when it was in the third or the lateral ventricle. The release of VIP into the fourth ventricle was also significantly (P less than 0.05) enhanced by the perfusion with acetylcholine (ACh) at a dose of 3.66 x 10(-5) to 1.83 x 10(-4) M/min. A simultaneous perfusion of hexamethonium (1.9 x 10(-4) M/min) blocked ACh-induced VIP release. These results indicate that VIP is released into the CSF from the wall of the fourth ventricle by a mechanism possibly involving nicotine-sensitive cholinergic pathways.

Acetylcholine↗

The influence of insulin in the cell cycle of human aging cells.

Normal human IMR 90 fibroblasts at population doubling levels (PDL) 28 approximately 33 had an increased incorporation of 3H-thymidine into DNA when the cells were pretreated with physiologic concentrations of insulin (5 approximately 10 ng/ml) prior to re-initiation of the cell cycle. Insulin stimulation was not observed with fibroblasts at PDL 50 nor with SV40 virus transformed cells. In all cells treated with supra-physiologic concentrations of insulin (1000 approximately 6000 ng/ml) prior to the re-initiation of cell cycle, the incorporation of thymidine into DNA was greatly diminished. Autoradiographic studies of the effect of insulin suggest that a larger fraction of cells was found to enter S phase than untreated cultures. This effect was evident in younger cells rather than senescent cells.

Autoradiography↗

Human pancreatic growth hormone-releasing factor stimulates release of growth hormone in conscious unrestrained male rabbits.

The effect on GH secretion of GH-releasing factor (GRF), a 44-amino acid peptide recently isolated from a human pancreatic tumor (hpGRF), was examined in conscious male rabbits. During a 6-h period (1030-1630 h) of the control study individual rabbits exhibited pulsatile GH release with a surge at 1030-1200 h, a trough at 1200-1400 h, and a second peak at 1400-1630 h. Intravenous bolus injections of 1 and 10 micrograms hpGRF caused significant and dose-related increases in plasma GH during both the period of the trough (1300 h) and the surge (1530 h), although the GH responses were obviously higher during the latter than the former period. Passive immunization with anti-somatostatin (SRIF) sheep serum resulted in a prompt increase in plasma GH immediately after an injection of the antiserum. When 0.1, 1, and 10 micrograms hpGRF were successively injected iv at 1215, 1345, and 1515 h, respectively, maximum levels of plasma GH after hpGRF in anti-SRIF sheep serum-treated rabbits were significantly higher than in animals given normal sheep serum. The plasma GH responses to 10 micrograms hpGRF, given iv only once at 1515 h in normal sheep serum-treated animals, were not different from those to 10 micrograms hpGRF injected at 1515 h after the prior administration either of the smaller hpGRF dose (0.1 micrograms, 1215 h; 1 microgram, 1345 h), nor of the large dose (10 micrograms, 1100 h). These findings suggest the following: 1) that the secretion of GH is pulsatile in conscious, unrestrained male rabbits; 2) that hpGRF is a potent secretagogue for GH release in rabbits as well as other species; 3) that the magnitude of plasma GH response to hpGRF is different according to timing of the injection during the course of pulsatile GH secretion but is not influenced by the prior administration of hpGRF (no priming effect); and 4) that the responsiveness of plasma GH to hpGRF is affected by circulating endogenous SRIF.

Animals↗

Nutritional aspect of methionine isomers studied by pulmonary exhalation of dimethyl sulfide and urinary excretion of alpha-keto-gamma-methiolbutyrate in humans.

With the view of evaluating the relative utilization of methionine isomers, the pulmonary exhalation of dimethyl sulfide and methyl mercaptan and the urinary excretion of alpha-keto-gamma-methiolbutyrate were studied in normal healthy subjects following oral or intravenous administration of L- or D-isomer of methionine. Dimethyl sulfide concentration in the expired alveolar gas (mean +/- SD) before methionine loading was 2.1 +/- 1.4 ng/dl (N = 23). Maximum concentrations of dimethyl sulfide in oral methionine loading tests were: 56.0 +/- 24.9 ng/dl (D-2g) (n = 4), 66.0 +/- 42.1 (D-1g) (N = 6) and 4.6 +/- 2.6 (L-2g) (N = 4); and in intravenous loading tests: 60.0 +/- 19.9 (D-Ig) (N = 4) and 4.2 +/- 2.1 (L-2g) (N = 3), respectively. The changes in methyl mercaptan in the expired alveolar gas were small and were disproportional to the changes in dimethyl sulfide following administration of both isomers. Preloading concentration of alpha-keto-gamma-methiolbutyrate in urine was 0.15 +/- 0.10 microgram/mg Creatinine (mean +/- SD) (N = 5). Postloading values during the initial two hours were 578 and 156 micrograms/mg Creatinine following 3g of D- and 0.20 and 29.7 micrograms/mg Creatinine following 3g of L-methionine ingestion. In view of the results obtained, significant amounts of D-methionine seem to be metabolized through the transaminative pathway of methionine metabolism.

Adult↗