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Biomedical subjects

T Sugimoto

Publications and source records attributed to T Sugimoto.

At least 613 records · Page 34Linked to original sources

[Mitral valve replacement and right ventricular outflow repair for hypertrophic obstructive cardiomyopathy].

A 44-year-old male with hypertrophic obstructive cardiomyopathy (HOCM) was operated on. He was in NYHA class III with a chief complaint of exertional dyspnea refractory to medical treatment. Echocardiography showed asymmetric septal hypertrophy and systolic anterior movement of the mitral valve, which caused obstruction of the left ventricular outflow tract. It also showed obstruction of the right ventricular outflow tract due to septal hypertrophy. Cardiac catheterization showed a systolic pressure gradient of 70 mmHg at the LV outflow tract and that of 30 mmHg at the RV outflow tract. He underwent mitral valve replacement and patch enlargement of the RV outflow tract. Postoperative course was uneventful. Postoperative catheterization showed a remarkable decrease of pressure gradient to 10 mmHg at the both outflow tracts.

Adult↗

[Change of mitral regurgitation before and after myocardial revascularization--is mitral repair required for ischemic mitral regurgitation?].

In twenty seven patients, intraoperative change of ischemic mitral regurgitation before and after coronary artery bypass grafting (CABG) was assessed using transesophageal echocardiography. The size of mitral regurgitation (MR) was determined by the area of MR color flow on the doppler echocardiogram. After CABG, MR area decreased in 20 patients (average: 3.7 cm2-->1.5 cm2), unchanged in one patient and increased in 6 patients (average: 17 cm2-->2.9 cm2). The change of MR area corresponded with the change of mitral annular diameter in 23 patients but uncorresponded in 2 patients. MR areas correlated exponentially with mitral annular diameters and the fair linear relation was observed between the postoperative to preoperative ratio of MR area and the postoperative increase in mitral annular diameter with the correlation of r = 0.81. When the larger MR area or mitral annular diameter before CABG was observed, the larger MR area after CABG remained, but annular diameter before CABG had more effect on postoperative MR area. No significant correlation was found between MR area and infarcted region, revascularized region, segmental wall motion etc. In conclusion, when the moderate or marked mitral annular dilatation was found in association with prominent ischemic mitral regurgitation, mitral annuloplasty with CABG should be considered.

Adult↗

[Surgical treatment of incomplete endocardial cushion defect in elderly patients].

We experienced 5 surgical cases of incomplete endocardial cushion defect who were 50 years old or older. Preoperatively, 3 cases were in New York Heart Association (NYHA) class II and 2 in class III. Catheterization study showed that systolic pulmonary arterial pressure was 24 to 48 (average; 38) mmHg and pulmonary-to-systemic flow ratio was 3.4 to 8.1 (average; 5.2). Left ventriculography showed mitral valve regurgitation (grade I-1 cases, grade II-3, grade III-1) with cleft and goose neck sign in all cases. Single atrium and patent foramen ovalis were associated in each one case. At operation, suture of mitral cleft and patch closure of ostium primum defect from mitral valve side were performed. Postoperatively, NYHA class, cardiomegaly, pulmonary arterial pressure and mitral regurgitation improved remarkably in all patients. During the follow-up period from 18 to 126 months (average; 57), right bundle branch block and supraventricular arrhythmia in electrocardiogram disappeared in 3 of 4 and 4 of 5 cases, respectively. Surgical treatment and postoperative course of incomplete ECD were reviewed in over-50-year-old patients, in reference to 17 surgical cases in Japan.

Electrocardiography↗

[Clinical studies of factors influencing acute tubular necrosis after kidney transplantation].

It is known that the earlier the graft begins functioning after cadaver kidney transplantation, the better the graft survival rate and function will be. In order to examine the possibility of shortening the period of acute tubular necrosis (AIN), we retrospectively studied the effect of several factors on the duration of postoperative hemodialysis. The subjects were 27 patients on whom a cadaver kidney transplantation was performed during a 6-year period from July 1, 1986. The mean duration of postoperative hemodialysis was 14.0 days in 26 out of the 27 patients. The remaining patient showed a primary non-functioning kidney. A significant correlation was observed between the anastomosis time and the duration of postoperative hemodialysis. No significant correlations were noted between the duration of postoperative hemodialysis and the age of the donor, renal function during the 24 hours preceding nephrectomy, or cold ischemic time. Moreover, no significant difference was observed in the duration of postoperative hemodialysis between patients using a roller pump for perfusion and patients who did not. The duration of postoperative hemodialysis was significantly shorter in patients using UW solution than in patients using Euro-Collins solution. Graft survival rate 6 months and one year after transplantation was 88.9% and 83.3%, respectively in the EC group, and 100% and 100%, respectively, in the UW group. It was concluded from these results that a short anastomosis time is essential in order to shorten the period of ATN after cadaver kidney transplantation, and that UW solution is effective in shortening the duration of postoperative hemodialysis and improving the graft survival rate thereafter.

Adenosine↗

[Immunohistochemical localization of herpes simplex virus type 1 in experimental retinitis--2. The brain, contralateral optic nerve and retina].

Unilateral intravitreal inoculation of herpes simplex virus type 1 (HSV) induced bilateral retinitis and encephalitis in rats. In a previous paper, we demonstrated immunohistochemical localization of HSV in the ipsilateral retina. In this paper, we report immunohistochemical localization of antigen to HSV in the brain and opposite eye. HSV was found in the optic chiasm, and bilaterally in the suprachiasmatic nuclei, lateral geniculate nuclei, superior colliculus, pretectum, and visual cortex. HSV was also found in the retinal ganglion cells, neural cells in the inner nuclear layer, and Müller cells in the opposite eye. We demonstrated HSV infection in the retina of the opposite eye via the optic nerve, visual pathway, and nuclei, but not through the blood stream.

Animals↗

Exocrine pancreatic ductograms in insulin-dependent diabetes mellitus.

OBJECTIVES: To examine the prevalence of abnormal pancreatic ductograms in patients with insulin-dependent diabetes mellitus (IDDM) and to determine the clinical characteristics of those patients. METHODS: Pancreatic exocrine morphology was studied by endoscopic retrograde pancreatography (ERP) in 43 patients with IDDM, 12 patients with islet cell antibody (ICA)-positive non-insulin-dependent diabetes mellitus (NIDDM), and 22 patients with ICA-negative NIDDM. RESULTS: ERP revealed a significantly higher prevalence of abnormal pancreatic ducts (dilation and stenosis, tortuosity, obstruction, and intraductal calculi) in the patients with IDDM (17/43, 40%) than in the patients with ICA-negative NIDDM (2/22, 9%, p = 0.018). IDDM patients who slowly progressed to insulin dependency more than 13 months after the onset of diabetes had a higher frequency of abnormal pancreatic ducts (13/22, 59%) than those who needed insulin therapy within 12 months after the onset (4/21, 19%, p = 0.016). There was no difference in duration of diabetes between the two groups. ICA-positive NIDDM patients also had a higher frequency of abnormal pancreatic ducts (7/12, 58%) than ICA-negative NIDDM patients (2/22, 9%, p = 0.0074). CONCLUSIONS: These results indicate that a high proportion of IDDM patients who have prolonged histories of non-insulin dependency with ICA suffer pancreatic exocrine impairment. A similarity between IDDM with a slowly progressive clinical course and fibrocalculous pancreatic diabetes seen in tropical countries also was suggested.

Autoantibodies↗

[Morphological changes of Kock pouch investigated by autopsy two years nine months postoperatively].

A 62-year-old male patient consulted us because of gross hematuria and was diagnosed as having a bladder tumor. Total cystectomy was performed and a Koch pouch was utilized. Two years and nine months later, he died as a result of recurrence of bladder tumor and pathological autopsy was performed. A microscopic section of the reservoir mucosa showed a reduction in the number of crypts and an increase in the number of goblet cells. These morphological changes seemed to be caused by chronic exposure to urine, but have a favorable effect upon metabolic alterations following the utilization of the Kock pouch.

Humans↗

Synthesis and hydrolysis of cyclic ADP-ribose by human leukocyte antigen CD38 and inhibition of the hydrolysis by ATP.

Cyclic ADP-ribose (cADPR) has been recently shown to be generated in pancreatic beta-cells by glucose stimulation, serving as a second messenger for Ca2+ mobilization in the endoplasmic reticulum in the process of insulin secretion (Takasawa, S., Nata, K., Yonekura, H., and Okamoto, H. (1993) Science 259, 370-373). In the present study, we isolated a cDNA for CD38, which has been reported to be a human leukocyte antigen, from a human insulinoma and expressed the cDNA in COS-7 cells. CD38 expression was observed in the plasma membrane and the microsome fractions of the COS-7 cells. When we incubated the plasma membrane fraction with NAD+ and analyzed the reaction products by high pressure liquid chromatography, the formation of cADPR was observed in addition to the ADP-ribose (ADPR) formation. When the plasma membrane fraction was incubated with cADPR, cADPR was converted to ADPR stoichiometrically. These results suggest that CD38 has both cADPR-forming and -hydrolyzing activities. Moreover, we found that ATP (2-10 mM), generated in the glucose metabolism in beta-cells, inhibited the cADPR-hydrolyzing activity, resulting in the increased formation of cADPR. These findings indicate a role for CD38 in the synthesis and hydrolysis of cADPR in the process of insulin secretion in pancreatic beta-cells.

ADP-ribosyl Cyclase↗

Calretinin-immunoreactivity in trigeminal neurons innervating the nasal mucosa of the rat.

Trigeminal primary neuronal cell bodies were labeled by retrograde transport of Fluoro-gold (FG) from the nasal mucosa of rats. The trigeminal ganglion containing the labeled cell bodies were processed for double stain for calretinin- and tachykinin-immunoreactivities (CR- and TK-irs). Except for a few contralateral cells, all the cells that innervated the nasal mucosa (NM cells) were confined to the ophthalmo-maxillary division of the trigeminal ganglion ipsilateral to the FG application. In the dorsal two-thirds of the ganglion, NM cells formed a cluster in the rostromedial part of ophthalmo-maxillary division (the rostromedial cluster). In the ventral third, the number of cells in the rostromedial cluster markedly decreased. Instead, numerous NM cells were found in the caudolateral part of the ophthalmo-maxillary division (the caudoventrolateral cluster). CR- and TK-irs were detected in 18% and 54% of overall population of NM cells, respectively. Virtually all of CR-immunoreactive (-ir) NM cells coexpressed TK. Although the proportion of TK-ir cells, irrespective of CR-ir, was similar for both clusters, CR-ir cells were more frequent in the caudoventrolateral cluster than in the rostromedial cluster. In the dorsal 1/3 of the ganglion where all the NM cells belonged to the rostromedial cluster, only 8.4% exhibited CR-ir. On the other hand, as much as 30.1% of NM cells expressed CR-ir in the ventral 1/3 where most NM cells were found in the caudoventrolateral cluster. Trigeminal cell bodies innervating the cornea and conjunctivum were located in the rostromedial part of the ophthalmo-maxillary division.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The human cot proto-oncogene encodes two protein serine/threonine kinases with different transforming activities by alternative initiation of translation.

The cot gene is an oncogene encoding serine/threonine kinases isolated by DNA transfection assay. In this study, we isolated cDNA for the human cot protooncogene (proto-cot gene) and examined the structure and function of its gene products. The proto-cot gene has an open reading frame encoding 467 amino acids of which the first 397 amino acids are identical to those in the corresponding part of the cot gene. The protein products of the proto-cot gene were identified as 58- and 52-kDa proteins with intrinsic protein serine/threonine kinase activity. These two protein species were suggested to be generated by alternative initiation from two AUGs. The 58- and 52-kDa proteins are both localized predominantly in the cytosol, but the 58-kDa protein has a shorter half-life than the 52-kDa protein, suggesting the importance of the amino-terminal domain in regulating the stability of the proto-Cot protein. More interestingly, the 58-kDa protein showed stronger transforming activity than the 52-kDa protein, although this activity was much weaker than that of the Cot oncoprotein. Thus, the amino-terminal domain of the Cot protein may be necessary for cellular transformation, whereas the carboxyl-terminal domain may negatively regulate the transforming activity.

Amino Acid Sequence↗

Distinct cytotoxicity against neuroblastoma cells of peripheral blood and tumor-infiltrating lymphocytes from patients with neuroblastoma.

The cytotoxicity against neuroblastoma cells of IL-2-activated peripheral blood (PBL) and tumor-infiltrating lymphocytes (TIL) was evaluated in seventeen patients with neuroblastoma. Regional lymph node lymphocytes (LNL) were similarly studied in some patients. Three allogeneic neuroblastoma cell lines, LA2D2, LA2B4 and SIFA, established from the different metastases of the same patient were used as targets. Of the three neuroblastoma lines, LA2D2, with low CD56 expression, was the most susceptible to IL-2-activated lymphocytes, while SIFA, with high CD56 expression, was resistant in the greatest degree. LA2B4 showed moderate susceptibility. Although TIL (73.9 +/- 2.1%), LNL (81.0%) and PBL (76.2 +/- 3.1%) revealed similar cytotoxic activity to K562, they demonstrated distinct cytotoxic activities to each neuroblastoma cell line, as follows: against LA2D2: TIL 56.3 +/- 4.2%, LNL 52.1%, PBL 33.6 +/- 4.9% (P < 0.01); against LA2B4: TIL 47.3 +/- 3.3%, LNL 37.8%, PBL 33.7 +/- 4.8% (P < 0.05); against SIFA: TIL 27.0 +/- 6.2%, LNL 20.7%, PBL 13.9 +/- 2.4% (P = 0.056). TIL always showed higher cytotoxic activity against neuroblastoma cells than those of LNL and PBL, whereas LNL were more cytotoxic than PBL. This data showed that TIL from neuroblastoma patients preferentially killed neuroblastoma cells. It was suggested that lymphocytes in the tumor site and regional lymph node could have been sensitized with neuroblastoma-related antigens and exert preferential killing activity against neuroblastoma cells. Phenotypical analysis revealed that TIL had a larger population of CD56+ cells than PBL. Conversely, PBL had a higher population of CD16+ cells than TIL. The cytotoxic activity of TIL significantly decreased by the depletion of CD56+ cells (10.9 +/- 6.2 from 49.9 +/- 5.9% against LA2D2, P < 0.001). These results indicated that CD56+ cells were most responsible for the killing of neuroblastoma cells, and that TIL, with a high proportion of CD56+ cells with strong activity, would be the best source for the immunotherapy of neuroblastoma. Additionally, since neuroblastoma cell lines used in the present study were derived from the different metastases of the same patient, heterogeneity in the susceptibility to lymphocytes might result from the differential expression of tumor-related antigens on these cell lines.

Antigens, Neoplasm↗

c-Fos expression by dorsal horn neurons chronically deafferented by peripheral nerve section in response to spared, somatotopically inappropriate nociceptive primary input.

Subcutaneous formalin injection into the hindpaw of rats induces c-Fos expression in neurons in the ipsilateral spinal cord dorsal horn. In laminae I and II of the dorsal horn at the junction of 4th and 5th segments of the lumbar spinal cord, neurons exhibiting c-Fos protein-like immunoreactivity (Fos-LI) are concentrated in the medial 3/4 that correspond to the terminal field of primary neurons innervating the sciatic nerve. Subacute tibial nerve section 24 h before formalin stimulation caused almost complete elimination of neurons with the formalin-induced Fos-LI in the medial 1/2 (tibial territory) of the above sciatic territory of the dorsal horn. Following a longer survival period (chronic tibial nerve section of 21 days standing), neurons with the formalin-induced Fos-LI re-appeared in the tibial territory. In addition, the number of neurons with the formalin-induced Fos-LI increased in the medial part of the peroneal territory (the lateral 1/2 of the sciatic territory). The results indicate that the activation of c-Fos expression in that part of dorsal horn that has been chronically deafferented by the tibial nerve section is taken over by the spared, but somatotopically inappropriate primary nociceptors. Furthermore, dorsal horn neurons outside but near the deafferented tibial nerve's territory exhibit hypersensitivity to c-Fos expression evoked by intact, somatotopically appropriate primary nociceptive input.

Animals↗

Atrial natriuretic peptide inhibits endothelin-1-induced activation of mitogen-activated protein kinase in cultured rat mesangial cells.

In cultured rat glomerular mesangial cells, endothelin-1 (ET-1) activated both pp 44 and pp 42 mitogen-activated protein (MAP) kinases. Atrial natriuretic peptide (ANP) inhibited ET-1-induced activation of both pp 44 and pp 42 MAP kinases. ANP also inhibited ET-1-induced translocation of protein kinase C (PKC) and TPA-induced activation of MAP kinase. These results indicate that ANP modulates the functions of mesangial cells, including proliferation and contraction through the inhibition of ET-1-induced activation of MAP kinase in various steps proximal to MAP kinase.

Animals↗

Structure determination and evolution of the chicken cDNA and gene encoding prepropancreatic polypeptide.

We have previously demonstrated that the C-terminal regions of the rat and human pancreatic polypeptide (PPP) precursors exhibit a high degree of divergence, whereas the N-terminal regions are highly conserved. This blend of structural conservation and divergence in the precursors appears to be caused by splice junction sliding and translational frameshift in the 3'-region of the PPP gene [Yonekura et al., J. Biol. Chem. 263 (1988) 2990-2997]. In the present study, we determined the nucleotide (nt) sequences of the chicken PPP (cPPP) cDNA and gene, and compared them with those of the mammals. In cPPP, the C-terminal region of the precursor is quite heterologous with respect to the rat (rPPP) and human (hPPP) precursors, and this heterogeneity is accentuated by the large deletion in exon 3 of cPPP. Furthermore, mutational accumulation during evolution caused the structural organization of the 3'-region of cPPP to change; cPPP is terminated in exon 3, whereas rPPP and hPPP are terminated in exon 4. Thus, our previous observation regarding the possibility of 'mosaic evolution' [Yamamoto et al., J. Biol. Chem. 261 (1986) 6156-6159] of PPP has been extended and confirmed by this study. Available evidence suggests that 'mosaic evolution' is a phenomenon unique to PPP, and not to the genes encoding the other members of the PPP family, neuropeptide-Y and peptide-YY.

Amino Acid Sequence↗