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Biomedical subjects

S Tsuzuki

Publications and source records attributed to S Tsuzuki.

At least 19 recordsLinked to original sources

Molecular cloning and characterization of genes encoding rat pancreatic cholecystokinin (CCK)-releasing peptide (monitor peptide) and pancreatic secretory trypsin inhibitor (PSTI).

The genes encoding a rat pancreatic cholecystokinin (CCK)-releasing peptide (monitor peptide) and its structurally related peptide, rat pancreatic secretory trypsin inhibitor (PSTI), have been isolated and sequenced. The two genes share extremely high sequence similarity in the 5' flanking regions, suggesting that these regions may be responsible for the characteristic coordinate expression of the two peptides.

Amino Acid Sequence

Monitor peptide gene expression is increased by exogenous CCK in the rat pancreas and in a rat pancreatic acinar cell line (AR4-2J).

Monitor peptide (CCK-releasing peptide) mRNA increased on the administration of CCK in rat pancreas and the AR4-2J pancreatic cell line. Subcutaneous injection of CCK into rats at 8 h intervals increased the level of monitor peptide mRNA in the pancreas. Concomitant injection of CCK antagonist CR-1409 strongly decreased it. The monitor peptide mRNA was also increased by CCK in AR4-2J cells and was decreased by the antagonist. These findings suggest that the plasma CCK induced by prolonged intake of a high protein diet may be responsible for the adaptative increase in the monitor peptide as well as exocrine proteases in the pancreas.

Amylases

[Treatment of aplastic anemia with antilymphocyte globulin, high-dose methylprednisolone and androgen].

Twenty-seven patients with aplastic anemia (20 severe: 7 moderate) were treated with combined immunosuppression consisting of antilymphocyte globulin (ALG: Ahlbulin, Green Cross Co., Osaka, Japan) and high-dose methylprednisolone. Danazol or meptiostane was administered concurrently for at least 3 months. Ten of 27 patients had sustained improvement in hematopoiesis within 3 months of treatment. Three patients with hematological response had a recurrence of pancytopenia 12-36 months after the combined immunosuppressive therapy. Six patients died due to fungal pneumonia (2), hepatic failure (2), interstitial pneumonitis (1) and complication following allogeneic bone marrow transplantation (1). By life table analysis, the survival rate for all patients was 76 +/- 8% at 4 years, with 70 +/- 10% survival rate for patients with severe aplastic anemia and 100% for patients with moderate aplastic anemia. The factors predicting the good response to the therapy were a longer interval from diagnosis to the therapy and higher counts of platelet and reticulocyte at admission.

Adolescent

[A case report of multiple-transfused aplastic anemia complicated by hemolysis and delayed neutrophil recovery after bone marrow transplantation].

The authors report an 18-year-old female who developed severe hemolytic reaction and delayed neutrophil recovery after bone marrow transplantation (BMT) for aplastic anemia from her HLA-identical sibling. She had received much transfusion (61 units of red blood cells including 4 units of fresh whole blood from her parents and 350 units of platelets) for 12 years before BMT. To prevent graft rejection, she received an intensified preparative regimen consisted of cyclophosphamide 200 mg/kg followed by 5 Gy total body irradiation and 5 Gy total lymphoid irradiation. Prophylaxis for GVHD was short term methotrexate and cyclosporin-A. Despite of the removal of the red cells from the marrow, marked hemolytic reaction caused by antibodies directed to rh" (E) and hr' (c) red cell antigens was observed when rh" (E) and hr' (c) positive donor erythroid began to recover. The recovery of neutrophils, especially the fraction of segmented cells was also delayed. Flow cytometry showed that the serially collected patient's sera reacted to neutrophils derived from both patient's blood on the 64th post-transplant day and the donor's blood. The reactivity was strongest in pre-BMT sera. We conclude that residual antibodies sensitized before BMT are a major cause of these hematological problems.

Adolescent

Effect of a high-protein diet on the gene expression of a trypsin-sensitive, cholecystokinin-releasing peptide (monitor peptide) in the pancreas.

The adaptation to a high protein diet of the concentration and mRNA level of a trypsin-sensitive, cholecystokinin-releasing peptide (monitor peptide), which was proposed to be the mediator of the cholecystokinin release in response to protein intake, was investigated in the rat pancreas. Adult rats were placed on one of two isocaloric diets. One group was fed a 22% casein diet (control diet) and the other a 64% casein diet (high-protein diet) for 14 days. In order to quantify the monitor peptide separately from pancreatic secretory trypsin inhibitor (PSTI-II), which is highly similar in its amino acid and mRNA nucleotide sequences to the monitor peptide but has less cholecystokinin-releasing activity, we used specific assay methods: HPLC was used for determining the monitor peptide concentration in zymogen granules and a synthetic oligonucleotide probe for determining the mRNA of the monitor peptide in the pancreas. The concentrations in the zymogen granules and the mRNA levels in the pancreas of the two peptides increased in parallel during the adaptation to the high protein diet, indicating that these two peptides were under the same control during the adaptation. The concentration and mRNA level of the monitor peptide, which were measured after 0, 3, and 14 days, increased throughout the experiment period, as did the concentration of trypsin. This suggested that the monitor peptide and trypsin may respond to similar signals during the adaptation to a high protein diet and that this apparent coordination may facilitate the adaptation of the pancreas to the diet.

Amino Acid Sequence

[Delay in red blood cell recovery after major ABO incompatible bone marrow transplantation].

In 6 of 27 patients in whom major ABO incompatible marrow was transplanted, the recovery of red blood cells (reticulocyte count greater than or equal to 1%) required more than 50 days after the transplantation. In 3 of them, more than 100 days were required. High titers of pre-transplant anti-A or anti-B agglutinin correlated with the delay in red blood cell recovery (IgM: p less than 0.01, IgG: p less than 0.05). In all of the patients whose pre-transplant IgM titers were 4 or less, and whose IgG titers were 32 or less, the red blood cells recovered within 50 days. Administration of cyclosporine did not correlate with the delay in red blood cell recovery. All the patients finally developed red cell production within 8 months without any treatment.

ABO Blood-Group System

[Crossed cerebellar diaschisis after brainstem infarction].

Metabolic depression in the cerebellar hemisphere contralateral to supratentorial stroke termed "Crossed Cerebellar Diaschisis" (CCD) was first described by Baron and coworkers and now interpreted as a transneuronal deactivation resulted from loss of excitatory afferent inputs. Among the cerebrocerebellar pathways possibly involved, the corticopontocerebellar pathway is considered to be the most important to induce CCD. According to the hypothesis that CCD results from the destruction of the corticopontocerebellar pathway, any lesion wherever located in the corticopontocerebellar pathway may induce CCD. Little is known, however, about CCD after the brainstem lesion. Our case presented here showed that a brainstem lesion actually induced CCD and that CCD resulted from transneuronal deactivation. An 80-year-old female was admitted to the neurological department of Kasugai City Hospital because of left-sided hemiparesis of sudden onset on March 19, 1989. On admission and 5 days after admission CT scan of the brain was performed, but no stroke lesion was found. Magnetic resonance imaging of the brain disclosed a localized lesion in the right peduncle and tegmentum of the midbrain. Single photon emission computerized tomography of the brain using N-isopropyl-P-(123I) iodoamphetamine (IMP) performed about a month after admission disclosed decreased blood flow in the left hemisphere of the cerebellum compared with the right one and the findings of CCD were observed.

Aged

[A case of left hand agraphia without callosal apraxia].

A 65-year-old male who had agraphia confined to the left hand was reported. The patient was admitted to the neurological department of Kasugai city Hospital because of suddenly-developed mild right-sided hemiparesis with central facial palsy. Computerized tomography of the brain was performed 2 and 14 days after admission. As a result, low-density regions were found in the left cingulate and medial frontal gyri and the trunk of the corpus callosum. Magnetic resonance imaging of the saggital plane more clearly visualized a localized infarction affecting both the trunk of the corpus callosum and its leftward outflow. Neuropsychological findings of the patient were summarized as follows. 1) He had no difficulty in any of the actual use of object, copying the manipulation of objects, and proper use of objects according to verbal commands. 2) With the eyes closed, he could correctly name the objects handed over to the right hand, while he could do only 15 out of 20 objects handed over to the left hand. However, whichever hand an object was handed to, he could explain how to use the object. 3) He could write Hiragana, Katakana, and Kanji correctly with his right hand in accordance with verbal commands, whereas with his left hand he could do only for 20% of Hiragana, 20% of Katakana, and 90% of Kanji. 4) He could copy Kanji, Hiragana, and figures with either right or left hand. 5) He could point out verbally-presented letters using letter cards whether with the right hand or with the left hand, and could also select the letter card corresponding to the letter visually-presented.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged