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Biomedical subjects

M Yoshimura

Publications and source records attributed to M Yoshimura.

At least 433 records · Page 24Linked to original sources
PubMed1994

[Experimental study of an intratracheal stent made of shape memory alloy].

To develop a new prosthesis for treating tracheal stenosis and tracheobronchomalacia, we examined the usefulness of an intratracheal stent made of shape memory alloy (SMA), a titanium-nickel alloy composed of 50% of each metal. At its recovery temperature (37 degrees C), the SMA stent was designed to recall the memorized shape of a coil with a diameter of 5 or 6 mm and a length of 10 mm. For the present experiment, it was transformed to a smaller coil 3 mm in diameter at a low temperature (-50 degrees C) and then loaded into the prosthesis introducer tube. An experimental model of potentially fatal tracheomalacia was made surgically by cutting and fracturing the tracheal cartilages of rabbits and tracheal collapse was confirmed by rigid bronchoscope. The introducer tube with the SMA stent was inserted and then the prosthesis was advanced into the collapsed segment of the trachea using the stent pusher. The SMA stent warmed bo body temperature and recovered its memorized shape after 1-2 min. In 3 out of 8 rabbits, follow-up bronchoscopy performed at 6, 8, and 10 months after implantation revealed satisfactory patency of the SMA stent and the trachea. After follow-up, 3 animals were sacrificed for histological observation, which showed little proliferation of granulation tissue and no dislocation of the SMA stent from the malacic portion. The remaining 5 rabbits have been followed for 18-24 months and are doing well. We conclude that the SMA stent maintains good tracheal patency, causes little reaction in the tracheal wall, and is easy to handle. Thus, it shows the potential for clinical application.

Alloys↗
PubMed1994

[A case of the localized fibrous mesothelioma which size decreased temporarily].

A 46-year-old woman complained of a back pain and was pointed the abnormal shadow on chest X-ray by the physician, so she consulted our hospital in January 1987. After a few weeks, the size of the shadow decreased with no treatment, then we followed up her with roentgenograms. Since '91, its size had increased again. Needle biopsy did not give us the diagnosis, but we performed the operation because we suspected some malignant disease. We resected the tumor with the enough surgical margin. Its size was 4 x 3 x 3 cm, its surface was white and smooth. Its was elastic hard and had the pedicle which jointed the visceral pleura. Histological diagnosis was the localized fibrous mesothelioma.

Female↗
PubMed1994

TNF-alpha-induced antiproliferation is not dependent on the autocrine action of TGF-beta 1 in a thyroid cancer cell line.

The autocrine inhibitory action of transforming growth factor-beta 1 (TGF-beta 1) may play an important role in maintaining the normal state of thyroid follicular epithelial cells. Deficiency of this regulatory mechanism has been implicated in the pathogenesis of nontoxic nodular goiter and thyroid epithelial cell cancer. Tumor necrosis factor-alpha (TNF-alpha) has an antiproliferative action in a human papillary thyroid carcinoma cell line, NP-PTC cells, through a receptor-mediated mechanism. In the present work, we studied the antiproliferative action of TNF-alpha and TGF-beta 1 in NP-PTC cells. TNF-alpha induced TGF-beta 1 mRNA and secretion of the latent form of TGF-beta 1. Both TNF-alpha and TGF-beta 1 inhibited the proliferation of NP-PTC cells. A neutralizing antibody specific to human TGF-beta 1 blocked the antiproliferative action of TGF-beta 1 on NP-PTC cells, but it failed to block TNF-alpha-induced antiproliferation. Further, TNF-alpha and TGF-beta 1 acted synergistically to inhibit NP-PTC cell proliferation. The results show that both TNF-alpha and TGF-beta 1 inhibit the proliferation of NP-PTC cells. However, the actions of TGF-beta 1 and TNF-alpha differ in NP-PTC cells; TNF-alpha activates nuclear factor kappa B (NF-kappa B) and TGF-beta 1 does not. Although TNF-alpha induced TGF-beta 1 mRNA and secretion of the latent form of TGF-beta 1, the antiproliferative action of TNF-alpha is not dependent on the autocrine action of TGF-beta 1 in NP-PTC cells.

Antibodies↗
PubMed1994

[A case of intrathoracic meningocele associated with neurofibromatosis].

A rare case of intrathoracic meningocele associated with neurofibromatosis was reported. A 47-year-old female was admitted to our institute because of an abnormal shadow on chest X-ray. The chest X-ray film showed homogenous opacity with a well defined margin in the right apex. Chest CT showed an enlarged intervertebral foramen and defect of the vertebral arch around the tumor. There was no scoliosis. Though preoperative diagnosis was dumbbell type neurinoma, the tumor was found to be a protrusion of dura mater with spinal fluid out of the spinal canal, covered by thickening tumorous tissue. Part of the wall was excised and the residual opening was carefully repaired and wrapped by the pedicled parietal pleura. Retrospectively, MRI showed characteristic findings of intrathoracic meningocele. The tumorous part of it was diagnosed as neurofibroma on histological examination.

Female↗
PubMed1993

Suppression of hyperventilation-induced attacks with infusion of atrial natriuretic peptide in patients with variant angina pectoris.

Atrial natriuretic peptide (ANP) is reported to dilate a major coronary artery in both experimental animals and humans. Spasm of a major coronary artery is the cause of variant angina pectoris and can be induced by hyperventilation. The effect of the ANP infusion on anginal attack induced by hyperventilation was studied in patients with variant angina pectoris. The study was performed in the early morning on 3 consecutive days in 11 patients with variant angina pectoris in whom the attacks were reproducibly induced by hyperventilation. On days 1 and 3 (saline solution infusion), and day 2 (ANP infusion), hyperventilation was started 14 minutes after beginning infusion of ANP (0.1 microgram/kg/min) or saline solution for 6 minutes. The attacks were induced in all 11 patients by hyperventilation on days 1 and 3. However, the attacks were not induced in any patient on day 2 of the ANP infusion. The plasma ANP level increased from 33 +/- 7 pg/ml to the peak level of 2,973 +/- 479 pg/ml (p < 0.01) at the end of the ANP infusion, and the plasma level of cyclic guanosine monophosphate (cGMP) increased from 5 +/- 1 pmol/ml to the peak level of 58 +/- 6 pmol/ml (p < 0.01) 5 minutes after the ANP infusion. The plasma levels of ANP and cGMP did not change after hyperventilation on days 1 and 3. It is concluded that the ANP infusion suppresses the attacks induced by hyperventilation in patients with variant angina pectoris, and cGMP is related to the mechanisms of suppression of the attacks.

Adult↗
PubMed1993

Predominant expression of type-VI adenylate cyclase in C6-2B rat glioma cells may account for inhibition of cyclic AMP accumulation by calcium.

In C6-2B cells, agonist-stimulated cyclic AMP accumulation is inhibited when the cytosolic Ca2+ concentration is increased. We now demonstrate that in C6-2B cells: (i) the early kinetics of the cyclic AMP inhibition by substance K (t1/2 = 35 s) and thapsigargin (t1/2 = 1.6 min) closely mimic the kinetics of the cytosolic Ca2+ increase evoked by either agent (t1/2 = 25 s and 1.5 min respectively); (ii) the Ca2+ rise and cyclic AMP inhibition by substance K or thapsigargin are similarly affected in EGTA-containing medium; (iii) PCR detects type-III and type-VI adenylate cyclase cDNAs, and RNAase protection assays show that the mRNA for type-VI adenylate cyclase, an isoform inhibitable by submicromolar Ca2+ concentrations, is the predominant species, strongly suggesting that type-VI adenylate cyclase is probably the target molecule for Ca(2+)-mediated inhibition of cyclic AMP accumulation.

Adenylyl Cyclases↗
PubMed1993

DNA-binding proteins and their cis-acting sites controlling hormonal induction of a mouse beta-casein::CAT fusion protein in mammary epithelial cells.

Transcription of the mouse beta-casein (beta CAS)-encoding gene (casB) is regulated by the synergistic actions of insulin, glucocorticoid and prolactin in the mammary gland (MG). To delineate its regulatory sequence(s), we examined the hormonal inducibility of various chimeric constructs containing the promoter sequence of casB and the cat reporter gene in primary MG epithelial cells. A DNA fragment from bp -258 to +7 of casB was sufficient for the hormonal induction. Using a series of 5'- and internal deletions of the casB promoter region, at least three DNA elements were found to be necessary for full induction. These were located at bp positions -258 to -180, -154 to -136, and -98 to -62. DNase I footprinting analysis with a partially purified extract from lactating MG cells detected at least seven protected sequences, I(-242 to -219), II(-213 to -202), III(-151 to -139), IV(-125 to -110), V(-98 to -90), VI(-79 to -70) and VII(-59 to -45). Regions I/II, III and V/VI were included in the three DNA elements required for the hormonal induction, and the IV region corresponded to the MG consensus sequences of several milk protein-encoding genes. Competition gel retardation assays using nuclear extracts of lactating mouse MG revealed the presence of specific binding proteins for regions I, II, IV and VI, as well as specific protein(s) binding to both regions III and V. The binding activities of these proteins, except that associated with region IV, were increased from the virgin to lactating periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Involvement of cholinergic neurons in intestinal contraction caused by vasoactive intestinal contractor.

The mechanism of the contractile response to vasoactive intestinal contractor (VIC) was examined in the isolated guinea-pig small intestine. VIC at 10(-9) to 10(-7) M produced a transient relaxation followed by a contraction, and this contraction was partially inhibited, to the same degree, by either atropine or tetrodotoxin. VIC (10(-8) M) induced an increase in the release of [3H]acetylcholine from the ileum preloaded with [3H]choline. The VIC-induced acetylcholine release was dependent on external Ca2+. Thus, the VIC-induced contractions may relate to stimulation of cholinergic neurons and smooth muscle cells.

Acetylcholine↗
PubMed1993

A novel adenylyl cyclase sequence cloned from the human erythroleukemia cell line.

The polymerase chain reaction (PCR) was used to detect several forms of adenylyl cyclase (AC's) expressed in human erythroleukemia (HEL) cells. Degenerate oligonucleotide primers were synthesized based on the conserved sequences in the C2a area of the AC's. HEL cells were found to contain mRNA for type III and type VI AC. In addition, a novel AC message was identified. The cloned sequence, excluding primer areas, represented 69 amino acids with most similarity to rat AC's II and IV. Northern analysis of RNA from HEL cells demonstrated a 6.7 kilobase message. RNase protection assays revealed that in HEL cells the novel AC mRNA was dominant compared to types III and VI. Human embryonic kidney cells (HEK293) were also used a source of mRNA to synthesize cDNA for PCR reactions. The HEK293 cells were found to contain message corresponding to type II, III, VI AC as well as the novel AC message. The novel AC message was also detected in human brain tissue and was most abundant in the caudate, cerebellum and hippocampus. The smallest amount of novel AC mRNA in the tested brain tissue was found in the cortex. The mRNA for the novel AC was relatively abundant in human liver.

Adenylyl Cyclases↗
PubMed1993

Type-specific stimulation of adenylylcyclase by protein kinase C.

Ca(2+)-stimulable (type I), Ca(2+)-insensitive (type II), and Ca(2+)-inhibitable adenylylcyclase (type VI) were transiently expressed in the human embryonic kidney 293 cell line. Phorbol 12,13-dibutyrate (PDBu) increased cAMP synthesis by the Ca(2+)-insensitive type II adenylylcyclase more than 9-fold within 10 min, while the treatment had no effect on the other two types of adenylylcyclases. This stimulatory effect of PDBu on type II activity was dose-dependent and synergistic with the effect of forskolin. Another phorbol ester, phorbol 12-myristate 13-acetate (PMA), had a similar stimulatory effect on type II activity, while its inactive isomer, 4 alpha-phorbol 12-myristate 13-acetate (4 alpha-PMA), had no effect. Staurosporine, a potent protein kinase C (PKC) inhibitor, markedly attenuated the action of PDBu on cAMP synthesis by type II adenylylcyclase. These results are particularly significant in that they indicate that a species of adenylylcyclase that is insensitive to regulation by one arm of the phosphatidylinositide pathway, i.e. Ca2+, nevertheless can be regulated by the other arm, i.e. PKC.

Adenylyl Cyclases↗