Biomedical subjects

T Miwa

Publications and source records attributed to T Miwa.

At least 55 records · Page 3Linked to original sources

PubMed2000

Involvement of sigma 1 receptors in methamphetamine-induced behavioral sensitization in rats.

MS-377 is a novel selective sigma(1) ligand, currently being developed for the treatment of schizophrenia. In the present study, we examined the effects of MS-377 on behavioral sensitization induced by subchronic treatment with methamphetamine. MS-377 was administered at doses of 1.875-15 mg/kg (p.o.), to rats, and methamphetamine was administered at doses of 2 mg/kg (i.p.), 60 min later once daily for 10 days. Repeated administration of methamphetamine caused enhanced stereotypy, and behavioral sensitization was developed. MS-377 did not affect the acute effects of methamphetamine. However, co-administration of MS-377 attenuated the development of methamphetamine-induced behavioral sensitization in a dose-dependent manner. These results suggested that sigma(1) receptors play an important role in the developmental period of behavioral sensitization induced by methamphetamine in rats.

Administration, Oral↗

PubMed2000

Pro-carboxypeptidase R is an acute phase protein in the mouse, whereas carboxypeptidase N is not.

Carboxypeptidase R (EC 3.4.17.20; CPR) and carboxypeptidase N (EC 3. 4.17.3; CPN) cleave carboxyl-terminal arginine and lysine residues from biologically active peptides such as kinins and anaphylatoxins, resulting in regulation of their biological activity. Human proCPR, also known as thrombin-activatable fibrinolysis inhibitor, plasma pro-carboxypeptidase B, and pro-carboxypeptidase U, is a plasma zymogen activated during coagulation. CPN, however, previously termed kininase I and anaphylatoxin inactivator, is present in a stable active form in plasma. We report here the isolation of mouse proCPR and CPN cDNA clones that can induce their respective enzymatic activities in culture supernatants of transiently transfected cells. Potato carboxypeptidase inhibitor can inhibit carboxypeptidase activity in culture medium of mouse proCPR-transfected cells. The expression of proCPR mRNA in murine liver is greatly enhanced following LPS injection, whereas CPN mRNA expression remains unaffected. Furthermore, the CPR activity in plasma increased 2-fold at 24 h after LPS treatment. Therefore, proCPR can be considered a type of acute phase protein, whereas CPN is not. An increase in CPR activity may facilitate rapid inactivation of inflammatory mediators generated at the site of Gram-negative bacterial infection and may consequently prevent septic shock. In view of the ability of proCPR to also inhibit fibrinolysis, an excess of proCPR induced by LPS may contribute to hypofibrinolysis in patients suffering from disseminated intravascular coagulation caused by sepsis.

Acute-Phase Proteins↗

PubMed2000

Molecular cloning and genomic structure of the betaTRCP2 gene on chromosome 5q35.1.

Beta-catenin, IkappaBalpha, and HIV Vpu are recruited to the ubiquitin-proteasome degradation pathway by betaTRCP, one of the components of the ubiquitin ligase complex. betaTRCP2, a related gene of betaTRCP, was cloned and characterized. Three isoforms, betaTRCP2A, betaTRCP2B, and betaTRCP2C, were identified. All of these betaTRCP2 isoforms consist of an F-box and seven WD repeats. Human betaTRCP2A shows 86% total amino acid identity with human betaTRCP. betaTRCP2 mRNA of 4.5 kb in size was detected almost ubiquitously. Sequence analyses on betaTRCP2 genomic clones revealed that the betaTRCP2 gene consists of at least 14 exons. Exons 1 and 4-14 are shared among all betaTRCP2 isoforms. betaTRCP2A of 508 amino acids lacks exons 2 and 3, betaTRCP2B of 529 amino acids contains exon 3, and betaTRCP2C of 542 amino acids contains exon 2. These results indicate that three betaTRCP2 isoforms are transcribed due to alternative splicing. The betaTRCP2 gene has been mapped to human chromosome 5q35.1 by fluorescence in situ hybridization.

Amino Acid Sequence↗

PubMed2000

3,4-dihydro-2(1H)-quinolinone as a novel antidepressant drug: synthesis and pharmacology of 1-[3-[4-(3-chlorophenyl)-1-piperazinyl]propyl]-3,4- dihydro-5-methoxy-2(1H)-quinolinone and its derivatives.

To develop a novel antidepressant drug with central nervous system-stimulating activity, we prepared a series of 1-[omega-(4-substituted phenyl-1-piperazinyl)alkyl]-3, 4-dihydro-2(1H)-quinolinone derivatives and examined their activities by their effects at 30 and 100 mg/kg po on the sleeping time of mice anesthetized with halothane and on the time required for recovery from coma induced in mice by cerebral concussion. We examined their binding affinities for sigma receptors by evaluating their ability to inhibit [(3)H]-1,3-di(o-tolyl)guanidine ([(3)H]DTG) binding to the rat whole brain membrane in comparison with three putative sigma receptor agonists: 1,3-di(o-tolyl)guanidine (DTG, 66), (+)-1,2,3,4,5,6-hexahydro-6,11-dimethyl-3-(2-propenyl)-2, 6-methano-3-benzazecin-8-ol (SKF10,047, 67), and (+)-1,2,3,4,5, 6-hexahydro-6,11-dimethyl-3-(3-methyl-2-butenyl)-2, 6-methano-3-benzazecin-8-ol (pentazocine, 68). Among the series of derivatives, 1-[3-[4-(3-chlorophenyl)-1-piperazinyl]propyl]-3, 4-dihydro-5-methoxy-2(1H)-quinolinone hydrochloride (34b) and its mesylate (34c), at a dose of 30 mg/kg po, reduced the sleeping time and the time for recovery from coma and they inhibited [(3)H]DTG binding for sigma receptors. The putative sigma receptor agonists reduced the sleeping time and the time for recovery from coma whereas two sigma receptor antagonists, alpha-(4-fluorophenyl)-4-(5-fluoro-2-pyrimidinyl)-1-piperazinebutanol hydrochloride (BMY14802, 69) and cis-9-[3-(3, 5-dimethyl-1-piperazinyl)propyl]carbazole dihydrochloride (rimcazole, 70), were inactive in the two tests. Preadministration of the putative sigma receptor antagonists 69 (3 mg/kg po) and 70 (30 mg/kg po) completely antagonized the actions of 34b and the sigma receptor agonists in the test for recovery from coma. These results suggested that 34b and 34c are sigma receptor agonists. Furthermore, a single administration of 1 and 10 mg/kg po 34b and 34c showed antidepressant-like activity by reducing the immobility time in the forced-swimming test with mice, while a tricyclic antidepressant, 10, 11-dihydro-N,N-dimethyl-5H-dibenz[b,f]azepine-5-propanamine hydrochloride (imipramine, 1) (10 and 30 mg/kg po), did not reduce the time after a single administration. 1 reduced the time after repeated administration of 30 mg/kg po once a day for 4 days. The structure-activity relationship of the series of compounds is also discussed.

Animals↗

PubMed2000

GPR1 regulates filamentous growth through FLO11 in yeast Saccharomyces cerevisiae.

Cell growth and differentiation are regulated by nutrient availability in the yeast Saccharomyces cerevisiae. Under conditions of nitrogen limitation, diploid cells of S. cerevisiae differentiate to a filamentous growth known as a pseudohyphal growth, while haploid cells produce invasive filaments which penetrate the agar in nutrient-rich medium. We have found that GPR1, which encodes a putative G-protein-coupled receptor, is required for both pseudohyphal and invasive growth. Pseudohyphal growth was defective in Deltagpr1/Deltagpr1 mutant strain and this defect was reversed by addition of cAMP. Also, haploid Deltagpr1 mutant strain was defective in invasive growth. Northern blot analysis revealed that the transcriptional level of FLO11, which encodes a recently identified cell surface flocculin required for pseudohyphal growth, was reduced in Deltagpr1 mutant strain. These results indicate that GPR1 regulates both pseudohyphal and invasive growth by a cAMP-dependent mechanism.

Blotting, Northern↗

PubMed2000

Alternative exon usage in the 3' region of a single gene generates glycosylphosphatidylinositol-anchored and transmembrane forms of rat decay-accelerating factor.

Several cDNA clones encoding genetic homologues of human decay-accelerating factor (DAF) were isolated from rat testis cDNA libraries and reverse transcription-polymerase chain reaction products. Sequence analysis revealed that rat DAF exists as two membrane forms, a glycosylphosphatidylinositol (GPI)-anchored and a transmembrane (TM) form. Southern blotting analysis showed that GPI- and TM-form mRNAs of rat DAF are derived from a single gene, as is the case for guinea pig, though both forms of mouse DAF mRNA are derived from two genes. Gene analysis of the C-terminal region of rat DAF indicated that both forms of mRNA are presumably generated by alternative splicing of exons which encode a GPI/3'-untranslated (3'UT) region and a TM/3'UT region in the 3' end of the Ser/Thr-rich region. Northern blot analysis indicated that rat GPI-DAF mRNA was present in all tissues examined except for liver, while rat TM-DAF mRNA was preferentially expressed in testis. Infant rat testis barely expressed TM-DAF and membrane cofactor protein (MCP) but highly expressed 5I2 antigen (5I2Ag, rat Crry). However, adult rat testis showed increased expression of the 1.6-kb transcript of rat GPI-DAF, TM-DAF, MCP, and the 0.7-kb transcript of CD59, with a decreased level of 5I2Ag expression. These results suggest that rat 5I2Ag/Crry may play an important role in regulating complement activation during the early stages of testis development, and that DAF, MCP, and CD59 expressed in testis may enable sperm to survive complement attack in the mucus of the female genital organ, and/or to interact with an ovum.

3' Untranslated Regions↗

PubMed2000

Cervical cancer in young Japanese women.

This study was performed to determine whether the incidence of cervical cancer in women aged 35 or younger has changed over the last 10 years and to examine the clinical characteristics of the cases. The incidence of cervical cancer in women aged 35 or younger were significantly greater in 1987-1991 than 1992-1996 (p = 0.001). Most new cases were detected by routine cytological screening.

Adenocarcinoma↗

PubMed2000

Idiopathic portal hypertension associated with systemic lupus erythematosus.

A case of idiopathic portal hypertension (IPH) associated with systemic lupus erythematosus (SLE) is reported in a 38-year-old man who had been diagnosed with SLE and treated for 18 years. Esophageal varices. found in 1994 on endoscopic examination, had been followed up for 2 years. On July 16, 1996, he was admitted to Nagoya University Hospital because there was a high risk of bleeding from the esophageal varices due to severe thrombocytopenia. As partial splenic embolization had temporarily controlled the thrombocytopenia, splenectomy and devascularization of the stomach vessels were performed after endoscopic ligation of the esophageal varices. Histological specimens of wedge biopsied liver showed chronic inactive hepatitis without cirrhosis. The presence of anticardiolipin antibody, indicated by positivity for lupus anticoagulant, was suggestive of the presence of a common immunological mechanism in the etiology of SLE and IPH.

Adult↗

PubMed2000

Local neurohumoral regulation in the transition to isolated diastolic heart failure in hypertensive heart disease: absence of AT1 receptor downregulation and 'overdrive' of the endothelin system.

OBJECTIVE: Although isolated diastolic heart failure with preserved left ventricular (LV) systolic function frequently occurs, regulation of local neurohumoral factors in the transition from diastolic dysfunction without signs of heart failure to diastolic failure, a target for therapeutic strategy, remains to be clarified, partly because of a lack of animal models. Our laboratory recently demonstrated that Dahl-Iwai salt-sensitive (Dahl-S) rats fed on a high-salt diet since 7 weeks of age develop hypertension followed by compensated LV hypertrophy at 13 weeks and transition to isolated diastolic heart failure at 19 weeks. METHODS: Gene expression of the components of the renin-angiotensin system, endothelin (ET) system and natriuretic peptide system in the left ventricle was investigated in the transition to isolated diastolic heart failure in this model. RESULTS: The compensated ventricular hypertrophy was associated with slight increases in angiotensin-converting enzyme (ACE) and angiotensin II type-1a (AT1a) receptor mRNA levels. Although preproET-1 (ppET-1) and ET-converting enzyme-1 (ECE-1) mRNA levels were not increased, mRNA levels of ET type-A (ETA) and ET type-B (ETB) receptors were increased. Atrial natriuretic peptide (ANP) mRNA level increased, but not brain natriuretic peptide (BNP) mRNA level. At the decompensated failing stage (at 19 weeks), ACE mRNA level further increased without downregulation of ATla receptor mRNA level. The mRNA levels of ppET-1 and ECE-1 increased with persistent upregulation of mRNA levels of ETA and ETB receptors, and immunohistochemical staining for ET-1 was found at endothelial cells and myocytes. BNP mRNA level increased with a further increase in ANP mRNA level. CONCLUSIONS: The transition to isolated diastolic heart failure in hypertrophied hearts was associated with preserved gene expression of the renin-angiotensin system and 'overdrive' of gene expression of the ET system. BNP gene expression is likely to be activated by the progression of diastolic failure rather than by LV hypertrophy alone.

Analysis of Variance↗

PubMed2000

Roles of renin-angiotensin and endothelin systems in development of diastolic heart failure in hypertensive hearts.

OBJECTIVE: Although interest in diastolic heart failure is growing because of its clinical frequency, little is known about this type of heart failure. Our laboratory recently developed a diastolic heart failure model using Dahl salt-sensitive rat. In this model, gene expression of angiotensin-converting enzyme and endothelin (ET) system in the left ventricle was enhanced at heart failure stage without downregulation of angiotensin type 1a receptor mRNA level. However, the roles of these humoral systems in the transition to diastolic failure remain unclear. METHODS: Subdepressor doses of angiotensin II type 1 (AT1) receptor and ET type A (ETA) receptor antagonists were administered in this model just after onset of hypertension, and their effects were investigated. RESULTS: Neither AT1 nor ETA receptor blockade inhibited the early (13 weeks) compensatory left ventricular (LV) hypertrophy. This form of compensatory hypertrophy is associated with subnormal LV end-systolic stress, which was normalized by AT1 receptor blockade but not by ETA receptor blockade. Progression of LV hypertrophy and fibrosis and transition to heart failure (19 weeks) in the untreated rats were prevented by both antagonists, resulting in normalization of LV end-diastolic pressure and lung weight. AT1 receptor blockade, but not ETA receptor blockade, normalized time constant of LV relaxation. Enhanced gene expression for ET system in the left ventricle observed in the untreated rats was suppressed with AT1 receptor antagonist administration. ETA receptor blockade slightly but significantly elevated the AT1a receptor mRNA level as compared with the untreated rats. CONCLUSIONS: RAS and ET system contribute to the transition to diastolic heart failure through the development of excessive hypertrophy and ventricular fibrosis in hypertensive heart diseases, however, neither RAS nor ET system is mandatory for normal compensation for pressure overload. RAS apparently causes such diastolic effects at least partly through the ET system.

Angiotensin Receptor Antagonists↗

PubMed2000

A novel diiron complex as a functional model for hemerythrin.

Diiron(II) complexes with a novel dinucleating polypyridine ligand, N,N,N',N'-tetrakis(6-pivalamido-2-pyridylmethyl)-1,3-diaminopropan-2-ol (HTPPDO), were synthesized as functional models of hemerythrin. Structural characterization of the complexes, [Fe2II(Htppdo)(PhCOO)](ClO4)3 (1), [Fe2II(Htppdo)((p-Cl)PhCOO)](ClO4)3 (2), [Fe2II(Htppdo)((p-Cl)PhCOO)](BF4)3 (2') and [Fe2II(tppdo)((p-Cl)PhCOO)](ClO4)2 (3), were accomplished by electronic absorption, and IR spectroscopic, electrochemical, and X-ray diffraction methods. The crystal structures of 1 and 2' revealed that the two iron atoms are asymmetrically coordinated with HTPPDO and bridging benzoate. One of the iron centers (Fe(1)) has a seven-coordinate capped octahedral geometry comprised of an N3O4 donor set which includes the propanol oxygen of HTPPDO. The other iron center (Fe(2)) forms an octahedron with an N3O3 donor set and one vacant site. The two iron atoms are bridged by benzoate (1) or p-chlorobenzoate (2). On the other hand, both Fe atoms of complex 3 are both symmetrically coordinated with N3O4 donors and two bridging ligands; benzoate and the propanolate of TPPDO. Reactions of these complexes with dioxygen were followed by electronic absorption, resonance Raman and ESR spectroscopies. Reversible dioxygen-binding was demonstrated by observation of an intense LMCT band for O2(2-) to Fe(III) at 610 (1) and 606 nm (2) upon exposure of dioxygen to acetone solutions of 1 and 2 prepared under an anaerobic conditions at -50 degrees C. The resonance Raman spectra of the dioxygen adduct of 1 exhibited two peaks assignable to the nu(O-O) stretching mode at 873 and 887 cm(-1), which shifted to 825 and 839 cm(-1) upon binding of (18)O2. ESR spectra of all dioxygen adducts were silent. These findings suggest that dioxygen coordinates to the diiron atoms as a peroxo anion in a mu-1,2 mode. Complex 3 exhibited irreversible dioxygen binding. These results indicate that the reversible binding of dioxygen is governed by the hydrophobicity of the dioxygen-binding environment rather than the iron redox potentials.

Crystallography, X-Ray↗

PubMed2000

Zinc modulates the electro-olfactogram of the frog.

OBJECTIVE: Zinc is considered an important element in olfaction, however, its exact role is still unclear. A large amount of zinc is contained in the olfactory mucosa, so Zn(2+) may behave as a neuromodulator, as in the hippocampus. To reveal the acute effects of Zn(2+) on olfactory mucosa, electro-olfactograms (EOG) were recorded with or without Zn(2+). METHODS: The isolated olfactory mucosa of a bullfrog (Rana catesbiana) was set in an EOG recording chamber and bathed in Ringer's solution. Effects of ZnSO(4) (25 microM) on EOGs were examined. Four types of stimulants, n-amyl acetate (200 microM), menthone (10 microM), forskolin (2 microM), and 3-isobutil-methylxisanthine (IBMX, 100 microM) were tested. RESULTS: Zn(2+) (25 microM) charged with the ciliated surface of the olfactory mucosa attenuates EOGs which were produced not only by odorants but also by forskolin and IBMX. The attenuating ratios of EOGs for stimulants were as follows; n-amyl acetate (0.51+/-0.18, n=4), menthone (0.48+/-0.28, n=4), forskolin (0.61+/-0.16, n=4), and IBMX (0.68+/-0.19, n=4); (mean+/-S.D.). These attenuations were reversible. The results indicate that Zn(2+) may block the c-AMP dependent transduction channels of the olfactory cells. CONCLUSION: Micro molar Zn(2+) attenuates EOG of the frog. Zn(2+) may be thought to behave as one of the modulators in olfactory reception.

1-Methyl-3-isobutylxanthine↗

PubMed2000

Indirect amperometric detection of underivatized amino acids in microcolumn liquid chromatography with carbon film based ring-disk electrodes.

An indirect amperometric detection of underivatized amino acids has been developed using a carbon film based ring-disk electrode (CFBRDE) in microcolumn liquid chromatography (LC). Bromide present in the mobile phase could be efficiently oxidized to bromine at the upstream (disk) electrode, and was subsequently detected at the downstream (ring) electrode. Most of the underivatized amino acids that are electroinactive under conventional amperometric conditions react rapidly with the electrogenerated bromine, the concentration of amino acids can therefore be indirectly determined by continuously monitoring the reduction current of bromine. The signal monitored at the downstream electrode was largely dependent on the bromide concentration in the mobile phase. Under optimized conditions, the response linearly increased with the concentration for most of the amino acids over a concentration range of 1-100 microM, with a correlation coefficient of 0.990-0.993. The detection limits for most of the amino acids were below 1 microM (0.2 pmol). It was demonstrated that detection with a ring-disk electrode offers the advantages of achieving a much higher collection efficiency caused by a decrease in flow rate in the microcolumn LC.

Amino Acids↗

PubMed2000

The effect of Helicobacter pylori on cell proliferation and apoptosis in gastric epithelial cell lines.

BACKGROUND: Helicobacter pylori has been implicated in the pathogenesis of gastric cancer and malignant lymphoma. It is not known whether the bacterium stimulates cell proliferation directly or if apoptosis induced by H. pylori leads to a hyperproliferative response. AIM: To clarify the precise mechanism of H. pylori action on gastric epithelial cell growth, we compared the response of two cell lines, Kato III (p53 deletion) and MKN 45 (p53 wild type), to the organism. To determine the role of Helicobacter vacuolating cytotoxin in gastric mucosal injury, we examined the relation between vacuolating activity and apoptosis under several conditions. METHODS: Five cytotoxic and four noncytotoxic strains of H. pylori were used, each with an inoculum of 10(7) cfu/mL. The effect on the growth in MKN 45 and Kato III cells was studied by MTT assay. Vacuolating cytotoxin activity was determined using RK-13 cells. RESULTS: Neither cytotoxic nor noncytotoxic strains induced apoptosis, but death of MKN 45 cells was induced by pre-treatment with interferon-gamma and culture with TNF-alpha. In contrast, some strains of H. pylori increased proliferation of Kato III cells. Furthermore, cell death induced by cytotoxic strains, but not noncytotoxic strains, was significantly augmented by amoxycillin 5-50 g/mL (P=0.0016). On the other hand, acid-treated supernatant fluids from cultures of H. pylori showed enhanced vacuolating activity but did not induce cell death, suggesting that death is attributable to some factor other than the cytotoxin. CONCLUSION: These findings suggest that H. pylori induces apoptosis by a means independent of vacuolating cytotoxin.

Apoptosis↗

PubMed2000

Helicobacter pylori induces apoptosis in gastric epithelial cells through inducible nitric oxide.

BACKGROUND: Gastric mucosal injury by Helicobacter pylori has been suggested to be mediated by various cytokines induced by this organism. Nitric oxide (NO) is an important effector molecule involved in immune regulation and defence. To clarify the mechanisms by which H. pylori induces gastric mucosal cell injury, we examined whether H. pylori induces gastric epithelial death via NO production. METHODS: Cytotoxic and non-cytotoxic strains of H. pylori were used. The death of MKN45 cells caused by H. pylori was examined by the 3-(4,5-dimethyl-thiazole-2yl)-2,5-diphenyl tetrazolium bromide (MTT) assays. Aminoguanidine was used to inhibit inducible nitric oxide synthase (iNOS) activity. Expression of iNOS mRNA was determined by the reverse transcriptase-polymerase chain reaction and the DNA fragmentation analysis was performed by using agarose gel electrophoresis. RESULTS: The MTT assay revealed that neither viable H. pylori nor other components of the microorganism induced cell death. Both preincubation of MKN45 cells with interferon-gamma for 6 h and coculture with TNF-alpha significantly increased the cytotoxicity of H. pylori. Both cytotoxic and non-cytotoxic strains of H. pylori induced cell death. Expression of iNOS mRNA was observed in MKN45 cells at 6, 8 and 12 h after H. pylori inoculation. The cytotoxicity of H. pylori was inhibited by aminoguanidine and DNA fragmentation analysis showed that H. pylori induced apoptosis. CONCLUSIONS: These findings suggested that viable H. pylori induces apoptosis of gastric epithelial cells via nitric oxide. Our study indicated that iNOS expression plays an important role in gastric cell injury.

Apoptosis↗

PubMed2000

Plaunotol suppresses interleukin-8 secretion induced by Helicobacter pylori: therapeutic effect of plaunotol on H. pylori infection.

BACKGROUND: It has been suggested that gastric mucosal injury induced by Helicobacter pylori infection is mediated by interleukin-8 (IL-8). METHODS: We studied the effect of plaunotol, a drug extracted from the Plau-noi tree of Thailand, and reported it to be effective in the treatment of ulcers, of IL-8 secretion induced by H. pylori and of the inhibitory adhesion activity of the bacterium to gastric epithelial cells. Moreover, the therapeutic effect of plaunotol on H. pylori infection was assessed by using the gnotobiotic murine model. RESULTS: Plaunotol inhibited the growth of H. pylori (1.5 x 10(4) c.f.u./mL) at high doses (24-48 microg/mL), but not at low doses (3-6 microg/mL). Interleukin-8 secretion induced by H. pylori was inhibited by coculture with plaunotol in a dose-dependent manner. The adhesion of H. pylori to MKN45 cells was also suppressed by coculture with plaunotol in a dose-dependent manner. An in vivo study showed that plaunotol improved histological gastritis and decreased the H. pylori antibody titre. CONCLUSIONS: These findings suggest that plaunotol has a therapeutic effect on gastritis induced by H. pylori.

Administration, Oral↗

PubMed2000

Anaesthetic management of children with congenital insensitivity to pain with anhidrosis.

Congenital insensitivity to pain with anhidrosis (CIPA) is a rare sensory neuropathy, which affects patients' pain sensation and thermoregulation. There are several issues to consider when planning anaesthesia for those with this congenital disorder. Over a 20-year period, six patients with CIPA underwent 20 surgical procedures under general anaesthesia in our institution. We analysed our experience with these patients retrospectively. We conclude that patients with CIPA are able to undergo surgical procedures under general anaesthesia without major problems.

Adolescent↗

PubMed2000

Differences in the effects of 20 K- and 22 K-hGH on water retention in rats.

Antidiuretic actions induced by two growth hormone (GH) isoforms (20 K- and 22 K-hGH; 0.2 and 2.0 mg/kg) were evaluated in rats, as fluid retention may cause oedema, one of the adverse effects of GH. Both GH isoforms (2.0 mg/kg) suppressed urine excretion in hypophysectomized rats (P< 0.01), but only the 22 K-hGH isoform (2.0 mg/kg) suppressed urine excretion in intact rats (P< 0.01). In addition, prolactin (PRL) suppressed urine excretion in intact rats (P< 0.05). In conclusion, 20 K-hGH has less potency in causing urine retention than 22 K-hGH and since 20 K-hGH is missing 15 amino acids found in 22 K-hGH, these amino acids may be important for the antidiuretic action of GH. Since prolactin suppressed urine excretion, a part of the antidiuretic action of GH may be related to PRL-R activation.

Animals↗