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Biomedical subjects

M Hirano

Publications and source records attributed to M Hirano.

At least 55 records · Page 3Linked to original sources

[Inferior vena cava cannulation using Forgaty catheter for partial cardiopulmonary bypass].

Partial cardiopulmonary bypass is adopted in operation for aneurysm of descending aorta or DeBakey IIIb dissection. Cannulation from left common femoral vein to inferior vena cava (IVC) is often difficult because of operative position and anatomical relation of iliac veins to IVC. In this paper, IVC cannulation using Forgaty catheter is reported to be easy and safe for prevention of IVC perforation.

Aortic Aneurysm↗

Transcriptional up-regulation of p27(Kip1) during contact-induced growth arrest in vascular endothelial cells.

By plating porcine aortic endothelial cells at two different densities and thereby inducing two different time courses of contact-induced growth arrest, the temporal correlation between p27(Kip1) expression and cell cycle progression was investigated. When the quiescent cells were replated, they synchronously entered S phase with a peak at 20 h in both cases, while the cells plated at 25 and 80% of confluent densities exited the cell cycle by 96 and 48 h, respectively. Nuclear p27(Kip1) disappeared when the cells reentered the cell cycle and then recovered when the cells exited the cell cycle. The change in p27(Kip1) was associated with a concomitant change in Kip1 mRNA. The p27(Kip1) degradation activity did not increase in the cells reentering the cell cycle, nor did it decrease in the cells exiting the cell cycle. The Kip1 mRNA stability decreased in the growing cells and increased in the cells exiting the cell cycle and at confluence. A nuclear run-on assay revealed a close correlation between the Kip1 transcriptional activity and the level of Kip1 mRNA. We conclude that the cell-cell contact up-regulated the Kip1 gene transcription and increased the Kip1 mRNA stability, which was related to the recovery of p27(Kip1) protein during contact-induced growth arrest in endothelial cells.

Animals↗

Laparoscopic lumbar sympathectomy for lower-limb disease.

BACKGROUND: The standard procedure for sympathectomy is open surgery. The oblique retroperitoneal approach is popular because it provides good visibility, albeit at the expense of requiring a long skin incision. Chemical sympathectomy has been introduced as a less invasive means of achieving sympatholysis; however, this method is also associated with a significant incidence of incomplete block and transient denervation. Laparoscopic surgery is a new approach that simplifies various surgical procedures. The aim of our report was to evaluate the benefits of endoscopic retroperitoneal surgery for lumbar sympathectomies. METHODS: Between March 1997 and April 2000, seven patients underwent laparoscopic lumbar sympathectomy in our department (all men, with an average age or 45.1 years). The predominant presenting symptoms were unilateral pain at rest and lower-extremity coldness. Symphaectomy was performed using a retroperitoneal approach on six patients and an anterior transperitoneal approach on one patient. After laparoscopic lumbar sympathectomy, skin thermometry was carried out on all patients. RESULTS: The postoperative skin temperature of the affected leg rose to 36.6 +/- 0.5 degrees C, as compared to 33.8 +/- 0.8 degrees C preoperatively. After laparoscopic lumbar sympathectomy, none of the patients complained of neuralgia. All patients achieved sustained symptomatic relief, and no major postoperative complications were noted. CONCLUSIONS: Lumbar sympathectomy can be performed laparoscopically. Currently, our standard technique is the retroperitoneal approach. More clinical experience and long-term follow-up will ultimately determine if this will become the procedure of choice. However, we believe that a learning period is necessary for this technique to be fully mastered.

Adult↗

Endoscopic thyroid resection using cutaneous elevation in lieu of insufflation.

BACKGROUND: Laparoscopic surgery to resect cervical masses has gained increasing acceptance during the past decade. This report describes the authors' technique and experience using total video endoscopic surgery to resect thyroid masses. METHODS: The video camera is introduced through a 12-mm trocar inserted via a 10-mm infraclavicular incision in the sternal line. This incision will be hidden by the patient's undergarments postoperatively. An incision for a 12-mm trocar is made in each axilla, with additional incisions in the anterior chest made as necessary for the endoscope and instruments. Excellent exposure is produced by elevating the skin with hooks rather than by using carbon dioxide insufflation. This method reduces the incidence of subcutaneous emphysema and pneumomediastinum. RESULTS: Twenty-two thyroid lesions were resected using total video endoscopic surgery (adenoma, 13; cancer, 5; benign cyst, 3; and Graves' disease, 1). Procedures included thyroidectomy (12), thyroidectomy and isthmusectomy (4), and subtotal thyroidectomy (2). Subtotal cervical adenectomy was performed in 3 patients with papillary carcinoma. Cosmetic results were excellent. CONCLUSION: Endoscopic surgery of the neck is safe, minimally invasive, and produces excellent cosmetic results. However, it is in an early stage of development. Techniques have yet to be standardized, and specialized instruments are not available. The field is likely to mature as surgeons gain more experience.

Adenoma↗

Physical disorder and optical properties in the vacuum ultraviolet region of amorphous SiO(2).

The optical absorption of point-defect-free SiO(2) glass in the vacuum ultraviolet region is primarily controlled by the concentrations of three- and four-membered ring structures composed of heavily strained Si-O-Si bonds. The main channel of color center formation by F(2) excimer laser (7.9 eV) irradiation is not Frenkel-defect generation of oxygen via two-photon absorption processes but a pair generation of E' and nonbridging oxygen hole centers by the one-photon excitation of these strained bonds with 7.9 eV photons.

Journal Article↗

Infantile autophagic vacuolar myopathy is distinct from Danon disease.

Lysosomal glycogen storage disease with normal acid maltase (Danon) is caused by primary lysosome-associated membrane protein-2 (LAMP-2) deficiency. Typically, the disease begins after the first decade; however, two infantile patients had similar histologic features. The infantile disorder is distinct from Danon disease, because, in both infants, LAMP-2 protein is present in skeletal muscle. Deposition of C5b-9 and multilayered basal lamina in one patient suggest that the infantile disease is pathogenically similar to X-linked myopathy with excessive autophagy.

Antigens, CD↗

Crystallization and preliminary X-ray diffraction analysis of the light-harvesting protein phycocyanin from the thermophilic cyanobacterium Synechococcus elongatus.

The crystallization and preliminary crystallographic study of phycocyanin from the thermophilic cyanobacterium Synechococcus elongatus is reported. Phycocyanin is composed of alpha- and beta-subunits consisting of 162 and 172 amino-acid residues, respectively. These associate to form an alphabeta heterodimer, which further associates to give a ring-shaped trimer (alphabeta)(3). Two trimers bind head-to-head to form a hexamer (alphabeta)(6). Phycocyanin crystals have been obtained by the sitting-drop vapour-diffusion method with a precipitant solution containing 30%(w/v) PEG 4000 and 100 mM MES pH 7.5-8.0. Using synchrotron radiation, the crystals diffract to 2.0 A resolution. They belong to the trigonal space group R32, with unit-cell parameters a = b = 186.75 (3), c = 59.75 (4) A, alpha = beta = 90, gamma = 120 degrees. Assuming that the crystallographic triad is identical to the threefold axis of the hexamer and with three (alphabeta)(6) molecules in a unit cell, the calculated molar volume (V(M)) is 2.64 A(3) Da(-1). This value corresponds to a solvent content of approximately 53%, with one alphabeta heterodimer occupying the asymmetric unit.

Crystallization↗

Acute and chronic haloperidol treatments increase parkin mRNA levels in the rat brain.

Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism. We examined the effects of acute and chronic treatment with haloperidol on parkin mRNA expression in the rat brain by reverse transcription-polymerase chain reaction. Acute haloperidol treatment (2 mg/kg) increased parkin mRNA levels in the striatum and nucleus accumbens but not in the medial prefrontal cortex and substantia nigra. Four-week-treatment with haloperidol decanoate (25 mg eq/kg) produced a significant increase in parkin mRNA levels in the striatum without affecting to those in the medial prefrontal cortex, nucleus accumbens and substantia nigra. These results suggest that Parkin may be involved in the haloperidol-induced synaptic plasticity, since Parkin regulates the turnover of the synaptic protein, CDCrel-1.

Animals↗

Bimodal activation of SMC ATPase by intra- and inter-molecular interactions.

Structural maintenance of chromosomes (SMC) proteins play fundamental roles in higher-order chromosome dynamics from bacteria to humans. It has been proposed that the Bacillus subtilis SMC (BsSMC) homodimer is composed of two anti-parallel coiled-coil arms, each having an ATP-binding domain at its distal end. It remains totally unknown, however, how the two-armed structure supports ATP-dependent actions of BsSMC. By constructing a number of mutant derivatives including 'single-armed' BsSMC, we show here that the central hinge domain provides a structural flexibility that allows opening and closing of the two arms. This unique structure brings about bimodal regulation of the SMC ATPase cycle. Closing the arm can trigger ATP hydrolysis by allowing an end-end interaction within a dimer (intramolecular mode). When bound to DNA, ATP promotes a dimer-dimer interaction, which in turn activates their DNA-dependent ATPase activity (intermolecular mode). Our results reveal a novel mechanism of ATPase regulation and provide mechanistic insights into how eukaryotic SMC protein complexes could mediate diverse chromosomal functions, such as chromosome condensation and sister chromatid cohesion.

Adenosine Triphosphatases↗

Protein determination by high-performance gel-permeation chromatography: applications to human pancreatic juice, human bile and tissue homogenate.

A high-performance gel-permeation chromatography (HPGPC) method to determine the proteins of human pancreatic juice, bile, and tissue homogenate has been developed. A diol-type silica gel column (35 x 8 mm I.D., 5 nm average pore diameter) was used under a column temperature of 8 degrees C. The eluent was acidic phosphate buffer with a high concentration of sodium chloride, nonionic detergent of polyoxyethylene (20) cetyl ether (Brij 58), glycerol and 2-propanol. The UV wavelength used for the protein detection was 210 nm. Analytical time was within 3.5 min. Good correlation coefficients were obtained with this HPLC method at a column temperature of 8 degrees C and a spectrophotometric bicinchoninic acid (BCA) method. A photometric pyrogallol-red molybdate complex method was found to correlate well with this HPLC method and with the BCA method only for tissue homogenate. Since this HPGPC protein assay method is simple, convenient, rapid, reproducible, and reliable, it is expected to be generally applicable to clinical and also to biochemical research.

Animals↗

Familial cerebellar ataxia with muscle coenzyme Q10 deficiency.

OBJECTIVE: To describe a clinical syndrome of cerebellar ataxia associated with muscle coenzyme Q10 (CoQ10) deficiency. BACKGROUND: Muscle CoQ10 deficiency has been reported only in a few patients with a mitochondrial encephalomyopathy characterized by 1) recurrent myoglobinuria; 2) brain involvement (seizures, ataxia, mental retardation), and 3) ragged-red fibers and lipid storage in the muscle biopsy. METHODS: Having found decreased CoQ10 levels in muscle from a patient with unclassified familial cerebellar ataxia, the authors measured CoQ10 in muscle biopsies from other patients in whom cerebellar ataxia could not be attributed to known genetic causes. RESULTS: The authors found muscle CoQ10 deficiency (26 to 35% of normal) in six patients with cerebellar ataxia, pyramidal signs, and seizures. All six patients responded to CoQ10 supplementation; strength increased, ataxia improved, and seizures became less frequent. CONCLUSIONS: Primary CoQ10 deficiency is a potentially important cause of familial ataxia and should be considered in the differential diagnosis of this condition because CoQ10 administration seems to improve the clinical picture.

Adolescent↗

Serum nm23-H1 protein as a prognostic factor in aggressive non-Hodgkin lymphoma.

Advances in chemotherapy have led to a favorable long-term prognosis in approximately 50% of patients with aggressive non-Hodgkin lymphoma (NHL). However, the remaining patients do not enjoy such prolonged survival after standard treatment. New prognostic factors are needed to define this poor-prognosis group and to plan an appropriate treatment strategy. It has been reported that serum nm23-H1 protein may be a new prognostic factor for aggressive NHL. In the present study involving multiple institutions and a large number of patients, the level of nm23-H1 protein was compared among different types of lymphoma; it was lowest for indolent lymphoma, followed by aggressive lymphoma and then highly aggressive lymphoma. In addition, patients with aggressive NHL and higher nm23-H1 levels had worse overall and progression-free survival rates than those with lower nm23-H1 levels. The nm23-H1 level was also compared between patients with diffuse large B-cell lymphoma and patients with peripheral T-cell lymphoma. The results suggest that the level of nm23-H1 could serve as a prognostic factor in both groups. Moreover, the prognosis of lymphoma patients could be ascertained even more precisely by combining soluble interleukin-2 receptor or soluble CD44 and nm23-H1 levels. A multivariate analysis confirmed that the nm23-H1 level is an independent and important prognostic factor in aggressive NHL. Therefore, it may provide useful information for clinicians to determine the appropriate therapy for each type of lymphoma.

Actuarial Analysis↗

Autosomal dominant limb-girdle muscular dystrophy: a large kindred with evidence for anticipation.

BACKGROUND: Fourteen genetically distinct forms of limb-girdle muscular dystrophy (LGMD) have been identified, including five types of autosomal dominant LGMD (AD-LGMD). OBJECTIVE: To describe clinical, histologic, and genetic features of a large Spanish kindred with LGMD and apparent autosomal dominant inheritance spanning five generations. METHOD: The authors examined 61 members of the family; muscle biopsies were performed on five patients. Linkage analysis assessed chromosomal loci associated with other forms of AD-LGMD. RESULTS: A total of 32 individuals had weakness of the pelvic and shoulder girdles. Severity appeared to worsen in successive generations. Muscle biopsy findings were nonspecific and compatible with MD. Linkage analysis to chromosomes 5q31, 1q11-q21, 3p25, 6q23, and 7q demonstrated that this disease is not allelic to LGMD forms 1A, 1B, 1C, 1D, and 1E. CONCLUSIONS: This family has a genetically distinct form of AD-LGMD. The authors are currently performing a genome-wide scan to identify the disease locus.

Adolescent↗

Effects of fluvoxamine on morphine-induced inhibition of gastrointestinal transit, antinociception and hyperlocomotion in mice.

In the present study, the effects of fluvoxamine on the inhibition of gastrointestinal transit, antinociception and hyperlocomotion induced by morphine were investigated in mice. Treatment with morphine (10 mg/kg, subcutaneously (s.c.)) inhibited gastrointestinal transit and hyperlocomotion. These effects were attenuated by fluvoxamine in a dose-dependent manner. On the other hand, morphine (1 mg/kg, s.c.)-induced antinociception was significantly potentiated by fluvoxamine. These results suggest that fluvoxamine combined with morphine may be useful for the treatment of not only depression but also pain in cancer patients without constipation or activation of the mesolimbic dopaminergic system. However, further understanding and clinical studies will be required to confirm this possibility.

Analgesics, Opioid↗

Cloning and functional expression of a degradation-resistant novel isoform of p27Kip1.

p27(Kip1) is an inhibitor of cyclin-dependent kinases. It has been implicated as having a role in the induction of growth arrest at the G(1) phase of the cell cycle in response to anti-mitogenic signals such as cell contact and serum starvation. Proteasome-mediated degradation plays an important role in the rapid inactivation of p27(Kip1), causing quiescent cells to re-enter the cell cycle. Although the existence of a second isoform has been suggested, no such isoform was isolated. Through screening of a cDNA library derived from growth-arrested confluent porcine endothelial cells, we obtained clones for a novel isoform of p27(Kip1) in addition to the original isoform. The novel isoform differed from the original isoform at the C-terminus. The tissue-specific expression of the original and novel isoforms was demonstrated at the mRNA and protein levels. An in vitro degradation assay demonstrated this novel isoform to be resistant to proteasome-mediated destruction. The expression as a fusion protein with green fluorescent protein revealed this isoform to be targeted to the nucleus by a bipartite nuclear-localization signal with a C-terminal part different from that of the original isoform. The expression of the novel isoform caused the growth arrest of HeLa cells and an accumulation of cells in the G(0)/G(1) phase, and this effect was similar to that seen with the original isoform. The present study suggests that the novel isoform functions as a negative regulator of the cell cycle, and may play a distinct role. The novel isoform was named p27(Kip1R) because of its resistance to degradation.

Alternative Splicing↗

Defects of intergenomic communication: autosomal disorders that cause multiple deletions and depletion of mitochondrial DNA.

Depletion and multiple deletions of mitochondrial DNA (mtDNA) have been associated with a growing number of autosomal diseases that have been classified as defects of intergenomic communication. MNGIE, an autosomal recessive disorder associated with mtDNA alterations is due to mutations in thymidine phosphorylase that may cause imbalance of the mitochondrial nucleotide pool. Subsequently, mutations in the mitochondrial proteins adenine nucleotide translocator 1, Twinkle, and polymerase gamma have been found to cause autosomal dominant progressive external ophthalmoplegia with multiple deletions of mtDNA. Uncovering the molecular bases of intergenomic communication defects will enhance our understanding of the mechanisms responsible for maintaining mtDNA integrity.

Chromosome Disorders↗