Search PubMed⌕ Search

Biomedical subjects

A Kishimoto

Publications and source records attributed to A Kishimoto.

At least 37 records · Page 2Linked to original sources
PubMed1994

[Anesthesiological management of a patient with primary aldosteronism complicated with hypertrophic cardiomyopathy].

A 49-year-old male with primary aldosteronism, accompanied by hypertrophic cardiomyopathy (HCM), underwent our anesthesiological management for resection of a left adrenal tumor. The preoperative examination revealed hypertension, mild nephropathy and hypokalemia. Spilnolactone treatment was discontinued 3 days before surgery. In the operating room, a Swan-Ganz catheter was inserted for monitoring hemodynamic parameters. Anesthesia was maintained with nitrous oxide-oxygen-isoflurane and vecuronium. During the surgery, prostaglandin E1 and nitroglycerin were used as vasodilators. During surgery, the patient was successfully managed, anesthesiologically. In anesthesiological management of patients with primary aldosteronism, care is needed regarding changes in blood pressure and electolyte levels during adrenalectomy. In cases where aldosteronism is accompanied by HCM, as in the present case, hemodynamic changes can cause a fatal outcome, and hence, carefulness is needed in using anesthetics and drugs which act on the circulatory system.

Adrenalectomy↗
PubMed1993

N200 component of event-related potentials in depression.

Event-related potentials (ERPs) recorded during a two-tone discrimination (oddball) task were examined in 36 drug-free depressed patients and 36 control subjects. At remission, the ERPs of 12 of the depressed patients were reexamined. In the depressed patients, although a group difference was not detected in the peak latency and amplitude of N200 to rare stimuli, the mean amplitude for the N200 latency range in the difference waves was smaller than in the control subjects. Mismatch negativity (N2a), which was elicited by rare stimuli, was reduced in amplitude; but N2b may have been evoked to frequent stimuli more in the patients than in the control subjects. Depressed subjects may have a deviance in the fully automatic cerebral mismatch process that is assumed to be related to mismatch negativity and provoke the controlled mismatch detection process (presumed to be associated with N2b) even to nontarget frequent stimuli. These findings were observed during remission; however, there was a tendency for the N2b amplitude to decrease and recover toward the level of the control subjects.

Adolescent↗
PubMed1993

[A controlled study of the prophylactic effect of mianserin and placebo in recurrent depression].

To examine the prophylactic effect of mianserin on depressive episode, 26 patients with recurrent depression were randomly allocated on a double-blind basis to treatment with either inactive placebo (PL group) or mianserin in daily dose of 20-60 mg (MIA group) for 18 months and the frequencies or durations of depressive episode during the treatment were compared between the two groups. Except for the 4 patients who dropped out, a comparison of the prophylactic effects of the two groups was performed on 9 patients of the MIA group and 13 patients of the PL group. As a result, recurrence of depressive episode occurred in 4 of 9 patients in the MIA group and in all 13 patients in the PL group during the study. The recurrence rate of the depressive episode during the period in the MIA group was always less than that in the PL group, and significant differences were observed between the two groups from the third to the 18th month of the study. Whereas the frequency and duration of the depressive episode in the MIA group during the period of the study were significantly less than those prior to the study, there was no such difference in the PL group. On the other hand, there was no significant difference in the safety between the two groups. From the result of this study, it was suggested that mianserin is effective in the prophylaxis of depressive episode in patients with recurrent depression.

Adult↗
PubMed1992

The treatment of affective disorder with carbamazepine: prophylactic synergism of lithium and carbamazepine combination.

1. In order to examine the prophylactic interaction between lithium and carbamazepine (CBZ), 18 patients who had been treated prophylactically with a combination of lithium and CBZ (combination therapy), lithium alone (Li-therapy), or CBZ alone (CBZ-therapy) were investigated in terms of episode occurrence. 2. The results revealed that the duration of symptoms and the frequency of hospitalization per year were significantly lower in the combination therapy than in both the Li-therapy and the CBZ-therapy. 3. In 7 out of 18 patients, the best prophylactic effect was obtained during combination therapy and none of the parameters measured was definitely inferior to those measured during the two single therapies. 4. During combination therapy, serum lithium level was significantly lower than during Li-therapy in the CBZ responders, and the combination of the two drugs enabled the required concentrations of lithium to be decreased. 5. It was concluded that synergistic action and a decrease in required concentrations of lithium can be expected with the combined use of lithium and CBZ, especially in responders to CBZ.

Adult↗
PubMed1991

Phosphorylation of cAMP response element-binding protein, CRE-BP1, by cAMP-dependent protein kinase and protein kinase C.

The human recombinant CRE-BP1 was phosphorylated by cAMP-dependent protein kinase and protein kinase C, in vitro. These two protein kinases modified distinct serine residues of CRE-BP1. Ser-62 downstream of a putative metal finger structure of CRE-BP1 was the phosphorylation site by cAMP-dependent protein kinase, whereas two serine residues, Ser-340 and Ser-367, located in the basic region of this protein were the major protein kinase C phosphorylation sites. It seems possible that transcriptional and DNA-binding activities of CRE-BP1 are regulated by phosphorylation with these protein kinases.

Amino Acid Sequence↗
PubMed1991

Protein kinase C in rat brain synaptosomes. Beta II-subspecies as a major isoform associated with membrane-skeleton elements.

A small fraction (approximately 5%) of protein kinase C (PKC) in the adult rat brain synaptosomes is tightly associated with Triton X-100-insoluble components (most likely membrane-skeleton elements), and is solubilized only after denaturation with sodium dodecyl sulfate. The kinase domain of this PKC can be released as a soluble form after limited proteolysis with calpain, whereas the regulatory domain which binds phorbol ester remains insoluble. The PKC in this fraction was identified as the beta II-subspecies or its related molecule. Presumably, this enzyme subspecies is responsible for the phosphorylation of a major PKC substrate protein, growth-associated protein-43, which is located in nerve endings as well as in growth cones in association with the membrane-skeleton elements.

Amino Acid Sequence↗
PubMed1991

H1 histone stimulates limited proteolysis of protein kinase C subspecies by calpain II.

Limited proteolysis of protein kinase C (PKC) subspecies with Ca2(+)-dependent neutral protease II (calpain II) was remarkably stimulated by basic polypeptides, such as H1 histone and poly-L-lysine. This stimulatory effect was observed for proteolysis of the active form of PKC, which was associated with phospholipid and diacylglycerol. The inactive form of PKC was far less susceptible to proteolysis, both in the presence and absence of the basic polypeptides. The basic polypeptides did not appear to interact with calpain II, but made the PKC molecule more susceptible to proteolysis. The relative rates of cleavage of type I (gamma), II (beta), and III (alpha) PKC were 2:2:1. The available evidence suggests that, like calpain I, calpain II may also contribute to the down-regulation or depletion of PKC.

Animals↗
PubMed1991

Phosphorylation of type II (beta) protein kinase C by casein kinase II.

Rat brain type II (beta) protein kinase C (PKC) was phosphorylated by rat lung casein kinase II (CK-II). Neither type I (gamma) nor type III (alpha) PKC was significantly phosphorylated by CK-II. CK-II incorporated 0.2-0.3 mol of phosphate into 1 mol of type II PKC. This phosphate was located at the single seryl residue (Ser-11) in the V1-variable region of the regulatory domain of the PKC molecule. A glutamic acid cluster was located at the carboxyl-terminal side of Ser-11, showing the consensus sequence for phosphorylation by CK-II. The velocity of this phosphorylation was enhanced by the addition of Ca2+, diolein, and phosphatidylserine, which are all required for the activation of PKC. Phosphorylation of casein or synthetic oligopeptides by CK-II was not affected by Ca2+, diolein, or phosphatidylserine. Available evidence suggests that CK-II phosphorylates preferentially the activated form of type II PKC. It remains unknown, however, whether this reaction has a physiological significance.

Amino Acid Sequence↗
PubMed1991

Abnormalities in event-related potentials, N100, P200, P300 and slow wave in schizophrenia.

Event-related potentials were recorded in 54 schizophrenics and 88 age-matched controls during a two-tone discrimination (odd ball) task. All the subjects were free from medication. In the schizophrenics, the mean amplitudes of the N100, P300 and Slow Wave latency ranges were decreased, and the amplitude of the P200 latency range was greater than that for the controls. These reductions and the increase were found both for the ERPs elicited by rare target stimuli and for those elicited by frequent nontarget stimuli. The peak latency of N200 to rare stimuli was more prolonged in the schizophrenics than in the controls. This finding confirms the prolongation of N200 latency that Brecher et al. (1987) found for a different visual stimuli task. Neither the N100 nor P300 latency differed between the two groups.

Adult↗
PubMed1990

Protein kinase C subspecies in estrogen receptor-positive and -negative human breast cancer cell lines.

Estrogen receptor-positive (MCF7) and -negative (BT20) human breast cancer cell lines, which are frequently used for studies on cancer chemotherapy with triphenylethylene (TPE) anti-estrogens, express at least three protein kinase C subspecies. Two of them are identified as type II PKC having the beta-sequence and type III PKC having the alpha-sequence. The other one shows typical characteristics of PKC which responds to Ca2+, phosphatidylserine and diacylglycerol, but shows kinetic properties subtly different from the previously known PKC subspecies. Immunoblot analysis has shown that this enzyme does not correspond to any of the well defined subspecies with known sequence structures. All of these PKC subspecies are similarly susceptible to the TPE antiestrogens.

Biomarkers, Tumor↗
PubMed1990

Protein kinase C during differentiation of human promyelocytic leukemia cell line, HL-60.

Protein kinase C (PKC) from human promyelocytic leukemia HL-60 cells can be resolved into three fractions (peak, a, b and c) by hydroxyapatite column chromatography. Peak a and c enzymes are indistinguishable from the brain type II PKC having beta (beta I and beta II)-sequence and type III having alpha-sequence, respectively. Peak b enzyme is a previously unidentified PKC subspecies that has enzymological properties subtly different from type I (having gamma-sequence), type II and type III PKC. Upon treatment of HL-60 cells with 1 microM retinoic acid, this peak b enzyme is decreased dramatically within 24 h, whilst peak a enzyme (beta-PKC) is increased, and peak c (alpha-PKC) enzyme is slightly decreased within 48 h. The result implies that the PKC subspecies in HL-60 cells have distinct functions during cell differentiation.

Amino Acid Sequence↗
PubMed1990

A synthetic peptide substrate for selective assay of protein kinase C.

Among various phosphate acceptor proteins and peptides so far tested, a synthetic peptide having the sequence surrounding Ser(8) of myelin basic protein, Gln-Lys-Arg-Pro-Ser(8)-Gln-Arg-Ser-Lys-Tyr-Leu, (MBP4-14), is the most specific and convenient substrate which can be used for selective assay of protein kinase C. This peptide is not phosphorylated by cyclic AMP-dependent protein kinase, casein kinases I and II, Ca2+/calmodulin-dependent protein kinase II, or phosphorylase kinase, and can be routinely used for the assay of protein kinase C with low background in the crude tissue extracts. The Km value is considerably low (7 microM) with a Vmax value of twice as much as that for H1 histone.

Amino Acid Sequence↗