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Biomedical subjects

H Fukumoto

Publications and source records attributed to H Fukumoto.

At least 73 records · Page 4Linked to original sources

[A successful repair of concomitant rupture of the interventricular septum and left ventricular free wall after acute myocardial infarction].

A 74-year-old woman had acute anteroseptal myocardial infarction. Tissue plasminogen activator (t-PA) was infused intravenously about five hours later from the onset of myocardial infarction. Six hours after the infusion of t-PA her blood pressure fell suddenly with the appearance of a grade 3/6 holosystolic murmur. There was a prominent step up of oxygen saturation in the right ventricle which indicated the presence of a left-to-right shunt. Intraaortic balloon pumping for the support of cardiac function was ineffective. At the emergent operation concomitant rupture of the left ventricular free wall and interventricular septum was seen and successfully repaired. She could be weaned from cardiopulmonary bypass easily with the aid of the intraaortic balloon pumping. Her postoperative course was uneventful. The postoperative angiography showed good left ventricular wall motion without any residual shunt.

Aged↗

[A case of hypertrophic pulmonary osteoarthropathy caused by adenocarcinoma of the lung].

A 58 year old housewife with tumor shadow in the right upper lung field on the chest X-ray was admitted. Marked swelling and severe arthralgia of both extremities and soft tissue clubbing of the fingers had been presented for two years prior to admission. The radiographs and bone scintigrams indicated proliferating periostitis along the long bones. Bronchofiberscope showed the obstruction of B2a of the right bronchus but the histological diagnosis was not established. Serum level of CEA and IAP were found to be high. Soon after the right upper lobectomy, arthralgia was significantly improved. The histological evaluation revealed a well differentiated adenocarcinoma of a primary lung cancer without mediastinal lymph node metastasis. Within 4 months the serum level of CEA and IAP normalized, the clubbing and the periosteal changes of the bones regressed.

Adenocarcinoma↗

Liver and muscle-fat type glucose transporter gene expression in obese and diabetic rats.

In order to investigate the regulation of glucose transporter gene expression in the altered metabolic conditions of obesity and diabetes, we have measured mRNA levels encoding GLUT2 in the liver and GLUT4 in the gastrocnemius muscle from various insulin resistant animal models, including Zucker fatty, Wistar fatty, and streptozocin(STZ)-treated diabetic rats. Northern blot analysis revealed that GLUT2 mRNA levels were significantly (P less than 0.001) elevated in 14 wk Zucker fatty and Wistar fatty rats relative to lean littermates but were similar in these two groups at 5 wk of age. Furthermore, there was significant increase (P less than 0.01) in GLUT2 mRNA levels in STZ diabetic rats at 3 wk after treatment. GLUT4 mRNA levels were not significantly different between control and insulin resistant rats in all animal models. These results indicate that neither hyperinsulinemia nor hyperglycemia affects GLUT4 mRNA levels in the muscle. However, GLUT2 mRNA levels in the liver were elevated in obesity and diabetes, although this regulatory event occurred independently from circulating insulin or glucose concentrations.

Animals↗

Recombinant human basic fibroblast growth factor (rhbFGF) induces secretion of nerve growth factor (NGF) in cultured rat astroglial cells.

Recombinant human basic fibroblast growth factor (rhbFGF) was found to induce secretion of nerve growth factor (NGF) in cultured astrocytes from rat brain. The induction was concentration dependent; a maximum increase of 2-fold was observed at concentrations of 3-10 ng/ml or rhbFGF. When rhbFGF was added to the astrocytes, the induction occurred within 8 h and leveled off after 12 h. Antiserum against rhbFGF completely blocked the induction. Maximum induction occurred under serum-free culture conditions and in cultures with a high cell density. These results suggest that rhbFGF may exert a neurotrophic effect on the central nervous system through the induction of NGF secretion by astrocytes.

Animals↗

[A case of delayed mediastinitis after coronary bypass grafting].

We experienced a case of delayed mediastinitis, who had coronary bypass surgery using saphenous vein graft fifteen months before. At that time, a Gore-Tex pericardial sheet had been used for protection from adhesion. Persistent discharge from unhealed small fistula, which appeared at ten months after surgery, gave notice of mediastinitis. It was supposed that complicated diabetes mellitus might be causative of this infection. A bacterial examination detected serratia marcescence and a fistulography proved a cavity between the sternum and the Gore-Tex pericardial sheet. At first, we took out the infected sternum and the Gore-Tex pericardial sheet, and mediastinal lavage was carried out for three days with 0.5% povidone iodine solution 80 ml/hour. After the wound was aseptic, the left major pectral muscle flap with vascular pedicle was transferred into the anterior mediastinal space. For twenty-two months after repair, he has been free from recurrence.

Angina Pectoris↗

[Main pulmonary artery injury caused by golf-swing].

A 87-year-old man suddenly complained of dyspnea and fell into shock just after tee-shot. UCG revealed a large amount of pericardial effusion and good wall motion of the heart. Enhanced CT scan didn't prove any intimal flaps in the aorta. With cardiopulmonary bypass stand-by, we opened the pericardium and found a small laceration in the main pulmonary artery. The site of the laceration corresponded to a hard and sharp pericardial reflection ridge. We speculated that the difference of deceleration power between body and the heart resulted in pendulous or torsional motion of his heart. Supposedly the mutual actions between sharp pericardial reflection ridge and strange motion of the heart injured his main pulmonary artery.

Aged↗

[Multiple coronary aneurysms due to Kawasaki disease in young man--successful triple coronary bypass grafting by utilizing the right gastroepiploic artery, internal thoracic artery and saphenous vein].

A 28-year-old man developed acute anteroseptal myocardial infarction. Emergency coronary angiography revealed multiple coronary aneurysms, associated with complete obstruction of left anterior descending artery (LAD) and 50 to 99% stenosis of the right and the circumflex coronary artery (CX). Coronary artery bypass graftings were performed seven weeks after successful emergency intracoronary thrombolysis. The saphenous vein graft was anastomosed to CX, the internal thoracic artery to LAD, the right gastroepiploic artery to RCA just above the bifurcation. Post-operative course was uneventful. On sixth post operative week cardiac catheterization was performed. The study showed all three bypass grafts and native coronary artery to be patent. The patient is now followed up under anticoagulant therapy.

Adult↗

Human facilitative glucose transporters. Isolation, functional characterization, and gene localization of cDNAs encoding an isoform (GLUT5) expressed in small intestine, kidney, muscle, and adipose tissue and an unusual glucose transporter pseudogene-like sequence (GLUT6).

Two novel facilitative glucose transporter-like cDNAs have been isolated from human small intestine and fetal skeletal muscle cDNA libraries by low stringency cross-hybridization with a fragment of the human erythrocyte/GLUT1 facilitative glucose transporter cDNA. One encodes a 501-amino acid facilitative glucose transporter, designated as the small intestine/GLUT5 isoform, having 41.7, 40.0, 38.7, and 41.6% identity with the previously described human erythrocyte/GLUT1, liver/GLUT2, brain/GLUT3, and muscle-fat/GLUT4 isoforms, respectively. GLUT5 mRNA is expressed at highest levels in small intestine and at much lower levels in kidney, skeletal muscle, and adipose tissue. Expression of in vitro synthesized human GLUT5 mRNA in Xenopus laevis oocytes indicates that the GLUT5 protein is a cytochalasin B-sensitive glucose carrier. The gene encoding the GLUT5 protein is located on the short arm of human chromosome 1. The second facilitative transporter-like cDNA sequence, designated GLUT6, is part of an 11-kilobase transcript that is expressed in all tissues examined. The sequence of a partial-length GLUT6 cDNA having an insert of 3.4 kilobase pairs revealed a region of 1.5 kilobase pairs that has 79.6% identity with the human brain/GLUT3 facilitative glucose transporter cDNA. However, because of the presence of multiple stop codons and frame shifts, this sequence cannot encode a functional glucose transporter protein. The region of facilitative glucose transporter nucleotide sequence homology in the GLUT6 transcript may have arisen by insertion of a reverse-transcribed GLUT3 transcript into the untranslated region of another gene. The GLUT6 gene is located on the long arm of human chromosome 5.

Adipose Tissue↗

Over-expression of facilitative glucose transporter genes in human cancer.

The expression of five facilitative glucose transporter genes, GLUT1 (erythrocyte type), GLUT2 (liver type), GLUT3 (brain type), GLUT4 (muscle/fat type), and GLUT5 (small intestine type), was examined in human cancer tissues of the digestive system by RNA blotting analysis. The amounts of the GLUT1, GLUT2, and GLUT3 transcripts were elevated in most cancer tissues studied, although the expression of the GLUT2 gene is primarily restricted to the liver. On the other hand, mRNA levels of GLUT4 and GLUT5 were below sensitivity in all cancer tissues examined. These results suggest that over-expression of GLUT1 and GLUT3 might be closely related with tissue development and that the acceleration of glucose uptake by transformed cells may result, at least in part, from the increase in the expression of these two glucose transporters.

Digestive System Neoplasms↗

Increase in liver glucose transporter mRNA levels during rat liver regeneration.

Gene expression of liver facilitated glucose transporter was rapidly induced during the liver regenerating process in rats. It reached maximum of 2.7 times at 8 hr of the regenerating course and returned to normal by 48 hr. The protein synthesis inhibitor, cycloheximide, did not interfere with the increased gene expression of liver facilitated glucose transporter. By contrast, erythrocyte/brain-type glucose transporter mRNA could not be detected in the livers of partially hepatectomized rats and sham-operated rats. The plasma glucose levels were transiently increased within 2 hr of the regenerative course and then decreased to a nadir at 4 hr. These results suggest that the increased gene expression of liver facilitated glucose transporter contributes to the decrease in plasma glucose levels.

Animals↗

Molecular biology of mammalian glucose transporters.

The oxidation of glucose represents a major source of metabolic energy for mammalian cells. However, because the plasma membrane is impermeable to polar molecules such as glucose, the cellular uptake of this important nutrient is accomplished by membrane-associated carrier proteins that bind and transfer it across the lipid bilayer. Two classes of glucose carriers have been described in mammalian cells: the Na(+)-glucose cotransporter and the facilitative glucose transporter. The Na(+)-glucose cotransporter transports glucose against its concentration gradient by coupling its uptake with the uptake of Na+ that is being transported down its concentration gradient. Facilitative glucose carriers accelerate the transport of glucose down its concentration gradient by facilitative diffusion, a form of passive transport. cDNAs have been isolated from human tissues encoding a Na(+)-glucose-cotransporter protein and five functional facilitative glucose-transporter isoforms. The Na(+)-glucose cotransporter is expressed by absorptive epithelial cells of the small intestine and is involved in the dietary uptake of glucose. The same or a related protein may be responsible for the reabsorption of glucose by the kidney. Facilitative glucose carriers are expressed by most if not all cells. The facilitative glucose-transporter isoforms have distinct tissue distributions and biochemical properties and contribute to the precise disposal of glucose under varying physiological conditions. The GLUT1 (erythrocyte) and GLUT3 (brain) facilitative glucose-transporter isoforms may be responsible for basal or constitutive glucose uptake. The GLUT2 (liver) isoform mediates the bidirectional transport of glucose by the hepatocyte and is responsible, at least in part, for the movement of glucose out of absorptive epithelial cells into the circulation in the small intestine and kidney. This isoform may also comprise part of the glucose-sensing mechanism of the insulin-producing beta-cell. The subcellular localization of the GLUT4 (muscle/fat) isoform changes in response to insulin, and this isoform is responsible for most of the insulin-stimulated uptake of glucose that occurs in muscle and adipose tissue. The GLUT5 (small intestine) facilitative glucose-transporter isoform is expressed at highest levels in the small intestine and may be involved in the transcellular transport of glucose by absorptive epithelial cells. The exon-intron organizations of the human GLUT1, GLUT2, and GLUT4 genes have been determined. In addition, the chromosomal locations of the genes encoding the Na(+)-dependent and facilitative glucose carriers have been determined. Restriction-fragment-length polymorphisms have also been identified at several of these loci.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗

Cloning and characterization of the major insulin-responsive glucose transporter expressed in human skeletal muscle and other insulin-responsive tissues.

Complementary DNA clones encoding a facilitative glucose transporter-like protein have been isolated from human small intestine and muscle cDNA libraries. This 509-amino acid protein has 65.3, 54.3, and 57.5% identity with the previously described human erythrocyte/HepG2, liver, and fetal muscle glucose transporter/transporter-like proteins, respectively. RNA blotting studies indicate that transcripts encoding this protein are very abundant in adult human skeletal muscle and subcutaneous fat. The adult skeletal muscle glucose transporter-like protein was expressed in vitro by cDNA-directed transcription and cell-free translation of the synthetic mRNA. The in vitro-synthesized protein reacted with a monoclonal antibody, 1F8, which recognizes the insulin-regulatable glucose transporter expressed in rat skeletal muscle, heart, and adipocytes. In contrast, in vitro-synthesized erythrocyte/HepG2 and fetal muscle glucose transporters did not react with 1F8. The high levels in adult skeletal muscle and subcutaneous fat of mRNA encoding the adult skeletal muscle glucose transporter and its specific reactivity with monoclonal antibody 1F8 suggest that this protein is the major insulin-regulatable glucose transporter expressed in skeletal muscle and other insulin-responsive tissues.

Adipose Tissue↗