Insulin-sensitive and insulin-resistant variants in nonobese Japanese type 2 diabetic patients. The role of triglycerides in insulin resistance.
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Body Mass Index↗
Biomedical subjects
A Taniguchi
Publications and source records attributed to A Taniguchi.
[A new bite block also serving as an endotracheal tube holder for infants].
We developed a new type of bite block with a combined function as an endotracheal tube (ETT) holder for infants and small children to prevent airway troubles caused by tube kinking, dislodging, extubation and oral membrane trauma. One mm thick plastic plate sized 3.5 x 2 cm was curved to make an open roll. The outer surface of the roll was covered and glued with soft plastic tube (5.0 mm ID endotracheal tube), cut in 3.5 cm length to give an elastic outer surface for the patient's comfort. The rolled ends were diagonally cut to make an oblique slit of 3 mm width. A t-shaped flange made of soft vinyl plate was fixed at a third of the length of the roll to maintain the block's position relative to the lips and to make the fixation of the tube easier. In practical use, after endotracheal intubation is performed as usual, this bite block is put into the mouth and positioned at the oral angle with the flange on the patient's skin. The ETT is fit into the slit of the roll. The skin-facing surface of the flange is pasted to the skin with the double stick material usually used for colostomy stoma. The ETT and the bite block are fixed en bloc with fixing tapes around the mouth. Our bite block has following advantages over other types of bite blocks and tube holders especially for children; 1) the volume of foreign bodies (ETT and bite block) occupying the oral cavity can be reduced and this attenuates the patient's discomfort, 2) good holding of the ETT can prevent its dislodging and decrease the incidence of accidental extubation and 3) suctioning is easier because of wide oral space. The four sizes of the bite block suitable for 4.0, 4.5, 5.0, 5.5 and 6.0 mm ID ETTs are manufactured. We applied this device to several ICU patients and found its use practical and safe.
Child, Preschool↗
Are some palliative care delivery systems more effective and efficient than others? A systematic review of comparative studies.
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Home Care Services↗
Differentiation elicits negative regulation of human beta-galactoside alpha2,6-sialyltransferase at the mRNA level in the HL-60 cell line.
We studied the regulation of the beta-galactoside alpha2,6-sialyltransferase (hST6Gal I) gene during HL-60 cell differentiation induced with dimethyl sulfoxide (DMSO), all transretinoic acid (ATRA), and phorbol myristate acetate (PMA). During HL-60 cell line differentiation, cell surface levels of alpha2,6-sialic acids expression decreased, as measured by flow cytometric analysis using Sambucus nigra agglutinin (SNA). Activities of hST6Gal I and levels of hST6Gal I mRNA dramatically decreased after 1 day of stimulation. Using reverse transcription polymerase chain reaction (PT-PCR), we found the major hST6Gal I mRNA isoform in HL-60 cells contains 5'-untranslated exons Y and Z. These results suggest that the expression of cell surface alpha2,6-sialic acids is controlled at the mRNA level, which is regulated by a promoter located 5'-upstream of exon Y.
Base Sequence↗
Down-regulation of human sialyltransferase gene expression during in vitro human keratinocyte cell line differentiation.
Sialic acids play important roles in biological processes, such as cell-cell communication and cell-matrix interaction. Histochemical analysis using PNA and LFA lectin has shown that the expression of alpha 2,3-sialic acid linked to Gal beta 1,3GalNAc is high in basal cells and decreases following further keratinocyte differentiation. In the present study, we used an in vitro keratinocyte cell line differentiation model to study expression of alpha 2,3-sialic acid linked to Gal beta 1,3 GalNAc. Treatment of the human papillomavirus type 16-immortalized human keratinocyte (PHK16) cell line with high concentrations (1.0 mM) of Ca2+ resulted in PHK16 cell differentiation and redistribution of PNA binding glycoproteins. The synthesis of alpha 2,3-sialic acid linked to Gal beta 1,3GalNAc is mediated by three beta-galactoside alpha 2,3-sialytransferases, which are the gene products of hST30, hST30/N and hST3 Gal II. Ca2+ treatment of PHK16 cells decreased the mRNA expression of hST30/N, whereas the mRNA of hST30 and hST3Gal II was not detected by Northern blot analysis, suggesting that the hST30/N gene is responsible for sialic acid down regulation during keratinocyte differentiation. In order to examine transcriptional regulation of the hST30/N gene, we first determined the transcriptional starting sites of the hST30/N gene in PHK 16 using 5'-RACE analysis. Two kinds of type B isoforms, types B3 and BX, were identified. Type BX is a novel isoform related to the type B form, but which differs upstream of the B3 exon. The results of Northern blot analysis using a type BX-specific probe suggest that the B3 promoter may be regulated by Ca2+. Using a luciferase assay, we identified a functional DNA portion within hST30/N genomic DNA that confers negative transcriptional regulation on the hST30/N B3 promoter during Ca2+ stimulated human keratinocyte differentiation. This element contains some putative transcriptional factor binding sequence motifs such as AP2.
Antigens, Tumor-Associated, Carbohydrate↗
A germline mutation abolishing the original stop codon of the human adenine phosphoribosyltransferase (APRT) gene leads to complete loss of the enzyme protein.
Adenine phosphoribosyltransferase (APRT) is a purine metabolic enzyme and a homozygous deficiency in this enzyme causes 2,8-dihydroxyadenine urolithiasis. Various germline abnormalities have been described, but we report here a unique type of germline mutation in a homozygous individual (SY) who had excreted 2,8-dihydroxyadenine crystals. In SY, TCA was substituted for the physiological stop codon TGA. This base substitution generates a new HinfI restriction site, and, using the polymerase chain reaction and subsequent digestion by this enzyme, it was confirmed that SY is homozygous for the base substitution. This base change is unique in that it generates an open reading frame that extends to the poly(A) addition site. The amount of mRNA in transformed B cells from SY was approximately a quarter of that in control subjects and no APRT proteins were detected. In eukaryotes, unlike in prokaryotes, no rescue systems for defective polypeptide termination caused by a missing stop codon have been found. Therefore, the outcome of the defect of SY is unclear from present knowledge about termination of polypeptide synthesis. Investigations into the mechanisms of the absence of protein in the cells of SY may lead to a better understanding of the physiological and nonphysiological termination of polypeptide synthesis in eukaryotic cells.
Adenine Phosphoribosyltransferase↗
Ligand-dependent and -independent interactions with the transforming growth factor type II and I receptor subunits reside in the aminoterminal portion of the ectodomain of the type III subunit.
The type III receptor for transforming growth factor beta (TGFbeta), which exhibits no kinase activity, binds TGFbeta1 and TGFbeta2 and is involved in assembly and activity of the multi-subunit TGFbeta signal transduction complex. Recently we showed that TGFbeta receptor type III (TbetaRIII) can participate in a complex composed of the dimeric TGFbeta ligand and a type III, II, and I receptor subunit. The interaction of the TbetaRIII subunit with TbetaRII is TGFbeta-dependent, whereas interaction with TbetaRI is TGFbeta-independent. Here we use coexpression of the three types of TGFbeta receptors in baculoviral-infected insect cells to determine which parts of the unglycosylated TbetaRIII receptor participate in the binding of TGFbeta, the TGFbeta-dependent interaction with TbetaRII and the TGFbeta-independent interaction with TbetaRI. The results suggest that the first 500 amino acid residues in the aminoterminal portion of TbetaRIII exhibit all three properties.
Activin Receptors, Type I↗
Serpin=serine protease-like complexes within neurofilament conglomerates of motoneurons in amyotrophic lateral sclerosis.
Neurofilamentous conglomerates (NfCg), as axonal spheroids or conglomerates in motoneurons, are the histopathologic hallmarks for early stages of amyotrophic lateral sclerosis (ALS). We hypothesize that NfCg may be formed by post-translational modifications of altered Nf proteins that include: (1) hyperphosphorylation, (2) glycosylation (or glycoxidation), (3) nitration, (4) ubiquitination and/or (5) crosslinking by the Ca++-dependent transglutaminase (TGase). These, as well as other changes, are predicted to be initiated or accentuated by oxidative damage. The damaged Nf proteins then activate cascades of intracellular protein degradation which include ATP-dependent ubiquitin/proteasome proteolysis. Other proteolytic systems, either Ca++-dependent or independent, may also be activated, such as serine and cysteine protease systems. These enzymes, either lysosomal or non-lysosomal may also participate in the degradation of damaged Nf proteins being balanced by their cognate inhibitors. Protein complexes formed by these protease=inhibitor systems, along with damaged Nf proteins, may accumulate within the cell bodies as neuronal inclusions, since a number of intracellular inclusions are found in motor neurons in ALS. In the current study, we investigated the involvement of serine proteases and their serpins in NfCg formation. Pairs of three serine proteases (trypsin, chymotrypsin and thrombin) and their cognate serpins (alpha1-anti-trypsin, alpha1-anti-chymotrypsin, and protease nexin I) were probed in motoneurons with their antibodies for both NfCg and inclusions. Positive immunoreactivities for all serine proteases and their cognate serpins support the contention that the imbalance of serine proteases and internalized serpins may have a role in formation of NfCg and inclusions, and hence, the pathogenesis of ALS.
Amyloid beta-Protein Precursor↗
Intravenous glucose tolerance test-derived glucose effectiveness in strength-trained humans.
The effect of long-term strenuous resistance training on glucose effectiveness (SG) was examined by comparing 11 strength-trained and 20 sedentary males by a minimal model approach. Lean body mass (LBM) was measured by hydrostatic weighing. The LBM in strength-trained subjects (65.7 +/- 3.1 kg) was significantly larger than in sedentary subjects (56.6 +/- 1.2 kg, P < .01). The glucose disappearance constant ([KG] 3.07% +/- 0.45% min(-1)) and insulin sensitivity ([SI] 17.5 +/- 2.0 x 10(-5) x min(-1) x pmol/L(-1)) in strength-trained subjects were significantly higher than in sedentary subjects (2.06% +/- 0.14% x min(-1) and 10.3 +/- 1.2 x 10(-5) x min(-1) x pmol/L(-1), P < .05). SG in strength-trained subjects (0.024 +/- 0.003 min(-1)) was significantly higher than in sedentary subjects (0.018 +/- 0.001 min(-1), P < .05). These results thus suggest that the improved glucose tolerance in strength-trained subjects was due to increased SG and SI.
Adult↗
Effect of ZTTA, a prolyl endopeptidase inhibitor, on memory impairment in a passive avoidance test of rats with basal forebrain lesions.
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Animals↗
Establishment of ameloblastoma cell line, AM-1.
Ameloblastomas are slowly growing, locally invasive neoplasms with a potentially destructive behaviour. The molecular mechanisms that regulate the cell growth and invasion of ameloblastoma cells are unknown. Because ameloblastoma cells placed in culture have a very limited lifespan, the establishment of immortalized clones of ameloblastoma cells would aid its study. We produced an immortalized ameloblastoma cell line (AM-1) using human papillomavirus type-16. This cell line maintains epithelial cell morphology and expresses cytokeratins K8, K14, K18, K19. Furthermore, bcl-2 protein, which prevents apoptosis, is expressed. We investigated the behaviour of these cells on a collagen matrix in vitro. These cells grew in a monolayer over foci of collagen degradation and could invade the collagen gel at such sites. Since the behavior of cell line AM-1 mimics the behavior of ameloblastoma in vivo, it may be a valuable model for the study of these neoplasms.
Ameloblastoma↗
Middle cerebral artery blood flow velocity during laparoscopic surgery in head-down position.
Laparoscopic surgery using intraperitoneal CO2 insufflation has become popular in many fields of surgical procedures. In this study, the authors examined the effects of intraperitoneal CO2 insufflation on the middle cerebral artery blood flow velocity (MCABFV) of patients in the head-down position. Fourteen patients undergoing laparoscopic surgery in the head-down position were studied. The MCABFV was measured at the following times: before CO2 insufflation and 15, 30, and 45 min after insufflation. The MCABFV increased significantly (61.4 +/- 14.5, 71.1 +/- 25.5, and 67.2 +/- 18.9 cm/s at 15, 30, and 45 min after insufflation, respectively) as compared with control (49.8 +/- 13.5 cm/s) following the CO2 insufflation. A positive correlation was observed between blood flow velocity and PaCO2 (y = 1.718 + 2.102x; r = 0.669). Our results suggest that the cerebral BFV is increased by intraperitoneal CO2 insufflation during laparoscopic surgery.
Adult↗
[A patient with acute sarcoidosis associated with fever, polyarthritis, and erythema nodosum: a typical of Löfgren's syndrome].
A 26-year-old female was admitted to Aoyama Hospital in February 1996, for evaluation of abnormal chest shadows and polyarthritis. She visited our clinic in December 1995 with complaints of fever, fatigue, and polyarthralgia which lasted for 3 weeks. Two weeks later she developed erythema nodosum on her lower legs with the exacerbation of polyarthritis. Erythrocyte sedimentation rate was 108 mm/hr and CRP 4.9 mg/dl. A chest radiograph showed hilar lymphadenopathy and multiple nodular shadows in both lung fields. On admission, she had arthritis of the shoulders and knees, erythema nodosum on her lower extremities, and keloid-like skin lesion on her left knee. Thoracoscopic lung biopsy of nodular lesion and skin biopsy of keloid-like lesion revealed noncaseating granuloma of epithelioid cells with lymphocytes, macrophages, and giant cells, confirming the diagnosis of sarcoidosis. She was cured in three months, and was well and free of the symptoms thereafter. Löfgren's syndrome is acute sarcoidosis, characterized by arthritis, erythema nodosum, and bilateral hilar lymphadenopathy. This syndrome is common in Europe and is closely related to HLA-B8 and DR-3. The frequency of HLA-B8 and DR-3 in Japanese is almost 0%, explaining the rare onset of this syndrome in Japan. Our case is the second report of typical Löfgren's syndrome in Japan, although the patient did not have these HLA loci.
Acute Disease↗
[Adenine phosphoribosyltransferase (APRT) deficiency].
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Adenine↗
Advanced glycation endproducts in neurofilament conglomeration of motoneurons in familial and sporadic amyotrophic lateral sclerosis.
BACKGROUND: Massive neurofilament conglomeration in motor neurons has been described to occur in the early stages of both familial and sporadic amyotrophic lateral sclerosis (ALS). Previously, neurofilament conglomerates were immunolabeled for both superoxide dismutase (SOD1) and nitrotyrosine, suggesting the potential for oxidative nitration damage to neurofilament protein by peroxynitrite. Long-lived neurofilaments may also undergo modification by advanced glycation endproducts (AGEs) with concomitant generation of free radicals, including superoxide. This radical species may then react with nitric oxide to form the potent oxidant, peroxynitrite, which in turn can nitrate neurofilament protein. Such a glycated and nitrated neurofilament protein may become resistant to proteolytic systems, forming high-molecular-weight protein complexes and cytotoxic, neuronal inclusions. MATERIALS AND METHODS: Paraffin sections containing both neurofilament conglomerates and neuronal inclusions were obtained from patients with sporadic (n = 5) and familial (n = 2) ALS and were probed with specific antibodies directed against the AGEs cypentodine/piperidine-enolone, arginine-lysine imidazole, pentosidine, and pyrraline. RESULTS: Neurofilament conglomerates, but not neuronal inclusions, were intensely immunolabeled with each of the anti-AGE antibodies tested. The immunoreactivity was selective for neurofilament conglomerates and suggested that AGEs may form inter- or intramolecular cross-links in neurofilament proteins. CONCLUSIONS: These data support the hypothesis that AGE formation affects neurofilament proteins in vivo and is associated with the concomitant induction of SODI and protein nitration in neurofilament conglomerates. AGE formation in neurofilament protein may not only cause covalent cross-linking but also generate superoxide and block nitric oxide-mediated responses, thereby perpetuating neuronal toxicity in patients with ALS.
Amyotrophic Lateral Sclerosis↗
Acute sympathetic hyperfunction in overlapping syndromes of systemic lupus erythematosus and polymyositis.
A 20-year-old woman with arthralgia, serositis, thrombocytopenia, proteinuria, muscle weakness, elevated creatinine kinase, and positive anti-Sm antibody was diagnosed as having polymyositis and systemic lupus erythematosus (SLE). She had persistent high temperature, sinus tachycardia, hyperhidrosis, mydriasis, visual disturbance, hallucination, and loss of consciousness. Levels of plasma adrenaline, noradrenaline, and dopamine and cerebrospinal fluid interleukin (IL)-6 and IL-8 were all high. A diagnosis of sympathetic hyperfunction accompanied by central nervous system (CNS) involvement in SLE was made parenteral. Pulse administration of high dose corticosteroid therapy was effective. This is the first reported case of a connective tissue disease with CNS involvement manifesting as sympathetic hyperfunction with high plasma catecholamine levels.
Acute-Phase Reaction↗
[Lupus cystitis and peritonitis successfully treated with intravenous cyclophosphamide pulse therapy: a case report].
The patient, a 35-year-old woman, had been diagnosed as SLE since she developed butterfly rash, arthritis and hair loss with positive antinuclear antibody, anti-DNA antibody, and LE cells in 1989, and treated with daily 20 mg prednisolone (PSL). She had been suffering from nausea, vomiting and waterly diarrhea since 1992. In June 1995, she noted pollakisuria and sense of residual urine, followed by dysuria and nocturia in October. She was admitted to our hospital in January 1996 with progressive gastrointestinal and urinary symptoms. Computerized tomography (CT) depicted thickening of the wall of intestine and bladder, diminished volume of bladder, and bilateral hydronephrosis and hydroureter. Biopsy of the bladder revealed erosion of mucosa and moderate infiltration with inflammatory cells. The diagnosis of lupus cystitis and peritonitis was made and she was initially given intravenous methylprednisolon pulse therapy (500 mg/day) for 3 days, and then switched to 100 mg of daily intravenous PSL. She responded partially to this regimen, but gradually developed gastrointestinal and urinary symptoms again when PSL was tapered down to 70 mg/day. Therefore, monthly intravenous cyclophosuphamide pulse therapy was started. With this therapy, her bladder and bowel symptoms improved, and then the thickness of her bladder and intestinal wall, and the bladder volume normalized. Five months after institution of therapy, PSL was successfully tapered down to 30 mg/day and she was discharged. Intravenous cyclophosphamidepulse therapy is a choice of treatment for steroid-resistant lupus cystitis and peritonitis.
Adult↗
[Perinatal and perianesthetic management of the sacrococcygeal teratoma in a neonate].
We report perinatal and perianesthetic management of a female infant with sacrococcygeal teratoma who underwent fetal bladder puncture and postnatal tumor resection. At 33 weeks' gestation, fetal ultrasonography revealed an intrapelvic mass, oligohydramnios and the dilatation of the bladder. At 34 weeks' gestation, bladder puncture was performed in utero to relieve urinary obstruction by the mass. And it served to reserve the renal function but caused remarkable ascites at birth due to urine leakage to the peritoneum through the puncture site. After the delivery by cesarean section, the patient underwent the tumor extirpation at 2 days of life. The operation and anesthesia proceeded uneventfully. In previous reports, several mortalities due to exsanguinating hemorrhage during surgery have been reported. In addition, sacrococcygeal teratoma is occasionally accompanied by coagulopathy and high output cardiac failure caused by arteriovenous fistulae. Therefore it is important for good patient outcomes to evaluate preoperatively the risks mentioned above.
Anesthesia, General↗