[Gastric mucosal hexosamine content in outpatients free of gastric lesions and those with gastric ulcer].
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Biomedical subjects
Publications and source records attributed to F Sato.
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A 62-year-old man with small cell carcinoma (oat cell type) of the lung who had hyponatremia and renal sodium loss with inappropriate antidiuresis is reported. Plasma levels of arginine vasopressin (AVP) were not elevated inappropriately. Plasma levels of atrial natriuretic peptide (ANP), however, were high, and increased after water loading and hypertonic saline infusion. The renin-aldosterone axis was normal, as were adrenal, thyroid, and renal functions. Water restriction to 500 to 700 ml/d resulted in a rise in serum sodium. Analysis of the tumor tissue failed to demonstrate the presence of AVP or ANP. The findings (1) suggest that hyponatremia and renal sodium loss with inappropriate antidiuresis observed in the patient is due to an antidiuretic substance distinct from AVP, and (2) point to the possibility that hypersecretion of ANP may play a role in the pathophysiology.
An autopsy case of a 75-year-old female with lymphoid interstitial pneumonia with monoclonal gammopathy of IgA kappa type is reported. The patient was admitted to UOEH Hospital suffering from a cough, sputum and fever. After examining a specimen of transbronchial lung biopsy and chest X ray films, lymphoid interstitial pneumonia was suspected. Serum immunological examination showed monoclonal IgA kappa type hypergammaglobulinemia. Marked clinical and radiological improvement was attained after prednisolone administration. After 16 months, however, the patient deteriorated and expired on January 21, 1986. On postmortem examination, a number of plasma cells as well as lymphoid cells were seen to have infiltrated in the thickened interalveolar septa and the parenchyme of the lymph nodes throughout the whole body. The architecture of lymph nodes remained preserved, while the cortex as well as the medulla was almost completely replaced by plasma cells and lymphoplasmacytoid cells. Immunohistochemical examination demonstrated the presence of IgA kappa in the plasma cells and some of the lymphoplasmacytoid cells in both lymph nodes and lungs. These findings suggest that the proliferating plasma cells and lymphoplasmacytoid cells were in neoplastic or preneoplastic states and support the hypothesis that lymphoid interstitial pneumonia may be an expression of the systemic lymphoproliferative disorders in the lung.
A spin-trapping method combined with ESR spectroscopy was utilized to obtain evidence for the presence of precursor radicals leading to damage in X-irradiated DNA. Two technical improvements were introduced to the conventional spin-trapping method to make possible its application to large molecules such as DNA: prior to X irradiation, sonolysis of aqueous DNA solution by 19.5-kHz ultrasound was made to get a highly concentrated DNA solution and to lower the viscosity of the solution; after precursor radicals in X-irradiated DNA were trapped by a spin-trapping reagent, the DNA was digested to oligonucleotides by DNase I to get an ESR spectrum with a well-resolved hyperfine structure. Thus, it was recognized that the ESR spectrum obtained after X irradiation of the aqueous solution containing DNA and the nitroso spin-trapping reagent 2-methyl-2-nitrosopropane consisted of at least three sets of signals in the DNA. Identification of free radicals was made by comparing the spectrum with that of thymidine, which was precisely examined by a spin-trapping method combining two kinds of spin traps (nitroso and nitrone compounds) with liquid chromatography. As a result, all the signals were identified as the spin adducts of radicals produced at the thymine base moiety of DNA. The 5-hydroxy-5,6-dihydrothymin-6-yl radical was identified as a precursor of 5,6-dihydroxy-5,6-dihydrothymine (thymine glycol), the 6-hydroxy-5,6-dihydrothymin-5-yl radical as a precursor of 6-hydroxy-5,6-dihydrothymine, and the 5-methyleneuracil radical as a precursor of 5-(hydroxymethyl) uracil.
Sixty-three embryos produced after in vitro fertilization in 30 infertile couples were frozen and stored. Dimethylsulfoxide was used as a cryoprotectant and embryos were frozen from the two-cell stage to early blastocyst development. Replacement occurred during spontaneous ovulatory cycles 2 to 15 months after embryo freezing. Embryo replacement was performed 3 to 6 days following identification of the luteinizing hormone surge in the spontaneous cycle. Thirty-five embryos were replaced into 25 women and two viable pregnancies resulted.
The Lincoln strain of bovine rotavirus was found to replicate with cytopathic effects in cultures of GBK cells, a stable cell line derived from bovine kidney, when the cultures were maintained in the presence of trypsin. The virus was readily passaged and the infected cells were shown to contain specific viral antigen by indirect immunofluorescent staining. The virus formed plaques in GBK cell monolayers, when trypsin was incorporated in the agar overlay medium. The plaque count increased about twofold when diethylaminoethyl dextran was further included in the overlay medium. Plaque assay in GBK cells was more sensitive than that in MA-104 cells previously reported by Matsuno et al. The specificity of plaques was confirmed by specific inhibition with antiserum against the Lincoln strain.
An inhibitor of blood coagulation, a new protein with an apparent molecular weight of 34,000 and an isoelectric point of 4.9, was purified from human placental tissue by EDTA extraction. Five cDNA clones were isolated from the human placental lambda gt11 cDNA library using the mouse monoclonal antibody raised against the coagulation inhibitor as the probe. The longest insert consists of 1,566 nucleotides, and contains 960 nucleotides entirely encoding the 320 amino acids of the inhibitor, and a poly A tail. The deduced amino acid sequence was corroborated by chemical analyses of the protein. The entire amino acid sequence shows homology to those of lipocortin I, lipocortin II, and endonexin-related proteins. The cDNA for the inhibitor was expressed in Escherichia coli under the regulation of the trc promotor of the plasmid pKK233-2. The resulting recombinant protein manifested inhibitory activities against both blood coagulation and phospholipase A2 activity, as did the coagulation inhibitor isolated from human placenta.
1. The effects of peritubular ions and transport inhibitors were studied on methacholine (MCH)-induced sweat secretion by the isolated, cannulated monkey palm sweat glands in vitro and on the transepithelial and basolateral membrane potential (p.d.). 2. Sweat secretory rate was a curvilinear function of peritubular Na+ and Cl- concentration. Among the anion substitutes only Br- was able to totally substitute for Cl-. Presence of HCO3- or H2PO4- in the bath was not essential. 3. Both bumetanide and furosemide inhibited sweat secretion in a dose-dependent manner with the median effective concentration (EC50) of 3 X 10(-6) and 3 X 10(-5) M, respectively. 4. Bumetanide (10(-4) M) had no significant effect on basolateral membrane p.d. but nearly abolished the transepithelial p.d. 5. Hydrochlorothiazide (HCTZ, 3 X 10(-4) M) inhibited sweat secretion by only 35%. Inhibitors of ion exchangers amiloride (10(-4) M) and DIDS (4,4'-diisothiocyanostilbene-2,2'-disulphonic acid, 10(-4) M) lowered sweat secretion by less than 20%. 6. Removal of peritubular K+ as well as addition of 5 mM-Ba2+ also inhibited sweat rate. 5 mM-Ba2+ abolished the transepithelial p.d. and depolarized the basolateral p.d. by 26 mV, although the effects of Ba2+ on sweating and the transepithelial p.d. were only transient. 7. The data raise a possibility that either the NaCl or Na+-K+-2Cl- co-transport system or both may be involved in MCH-induced sweat secretion, whereas the role of parallel ion exchangers, if any, may be rather minor.
Evidence is presented that in adult human axillae there exists a third type of sweat gland tentatively designated as the apoeccrine sweat gland. This type of gland shows a segmental or diffuse apocrinelike dilatation of its secretory tubule but has a long and thin duct which does not open into a hair follicle. The electron microscopy of its dilated segment is often indistinguishable from that of the classical apocrine gland. The less remarkably dilated segment of the apoeccrine gland tends to retain intercellular canaliculi and/or dark cells. These apoeccrine glands are consistently present in adult human axillae regardless of sex or race. In the axillae of the two 6-yr-old subjects, both classical apocrine and eccrine glands were present but no apoeccrine glands were found. Between 8-14 yr of age, the number of large eccrine glands with or without partial segmental dilatation gradually increased. At 16-18 yr of age, the number of apoeccrine glands increased to as high as 45% of the total axillary glands. The data support the notion that apoeccrine glands develop during puberty in the axillae from eccrine or eccrinelike sweat glands.
Functional characteristics of isolated single human axillary apoeccrine sweat glands have been studied using in vitro sweat induction methods. Sustained copious clear fluid secretion was evoked by methacholine (MCh), epinephrine (EP), isoproterenol (ISO), and phenylephrine (PL) in decreasing order in a pharmacologically specific manner. Apoeccrine glands showed a higher cholinergic sensitivity than eccrine sweat glands, as shown by the apparent association constant for MCh of 2.7 X 10(-7) M compared with 2.1 X 10(-6) M for the axillary eccrine sweat gland. The average total sweat rate of the apoeccrine gland for a 30-min period was sevenfold higher than that of the eccrine sweat gland. In contrast, isolated apocrine glands showed intermittent pulsatile turbid sweat secretion in response to MCh or EP. The Na+ and K+ concentration of apoeccrine glands was nearly isotonic, whereas those of apocrine sweat was 120-140 mM for Na+ and 10-20 mM for K+. Apoeccrine ductal Na+ absorption was also observed in the apoeccrine glands and was no more efficient than that of the axillary eccrine sweat gland. Thus apoeccrine sweat glands are functionally and pharmacologically distinct from axillary apocrine glands and significantly contribute to overall axillary sweating in humans.
Na+, K+, Cl-, and HCO-3 concentrations were determined in both methacholine (MCh)-induced and isoproterenol (ISO)-induced primary sweat collected directly from isolated and cannulated rhesus monkey palm eccrine secretory coils in vitro. Na+ concentration [( Na+]) of MCh-induced sweat was higher than that of the bathing medium by 4.2 mM, i.e., 155.4 vs. 151.2 mM. Sweat [Cl-] was consistently higher than that of the medium by 13.7 and 11.2 mM in both MCh- and ISO-induced primary fluid, respectively. The sweat-to-bath Cl- gradient increased as [Cl-] in the bath was lowered by substituting with less-permeable anions. In contrast sweat [HCO-3] was much lower in both MCh- and ISO-induced sweat than that of the bathing medium, i.e., approximately 6 mM in sweat vs. 25 mM in the bath. [K+] in MCh-induced primary sweat (mean of 6.63 mM) was consistently higher than that of the bathing medium (5 mM). Furthermore, [K+] tended to be the highest in the first sweat sample after MCh stimulation, reaching as high as 9 mM. In sharp contrast ISO-induced primary sweat showed [K+] that was almost always less than 5 mM with the mean of 4.03 mM. These electrolyte profiles of the primary fluid have been discussed relative to the transport model generally applied for Cl- secretory epithelia.
Although vasoactive intestinal peptide (VIP)-immunoreactive nerves have been identified around the eccrine sweat glands, their functional significance is unknown. We found that VIP evokes eccrine sweat secretion in isolated monkey palm eccrine sweat glands in vitro as profusely as does isoproterenol (Iso), however, at concentrations two orders of magnitude lower than that of Iso. Like Iso sweating, the VIP sweating was relatively insensitive to removal of Ca2+ from the medium. The time course of adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in the secretory coil paralleled that of sweat secretion. However, unlike Iso stimulations, both VIP-induced cAMP level and VIP sweat rate markedly declined with time. The attenuation of VIP sweat rate was reversed by forskolin and by theophylline, suggesting that the attenuation is caused partially by desensitization of the receptor-cyclase complex and/or by cAMP breakdown by phosphodiesterase. Forskolin stimulated the VIP-induced cAMP level more than can be expected from a simple additive effect. The sudorific effects of a submaximal concentration of VIP (6 X 10(-9) M) and that of methacholine (MCh) (10(-8) M) were only additive. The VIP-induced cAMP level was markedly augmented by MCh and further enhanced by Iso with or without theophylline. Thus the most salient biochemical consequence of the VIP-ergic component of sweat gland innervation is to induce synergistic amplification of tissue cAMP accumulation. The functional significance of synergistically accumulated cAMP in physiological eccrine sweating remains to be studied.
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In an attempt to clarify the clinical significance of atrial natriuretic peptide (ANP) in man, plasma levels of immunoreactive ANP were studied in patients with heart diseases and in those with chronic renal failure. When ANP concentrations in pulmonary arterial plasma were compared with hemodynamic variables in patients with heart diseases who underwent cardiac catheterization, a significant positive correlation was found between plasma ANP levels and mean pulmonary capillary wedge pressure, while plasma ANP levels were not significantly correlated to mean right atrial pressure (MRAP). After the injection of contrast medium, both MRAP and plasma ANP levels increased and a significant positive correlation was observed between two variables. Plasma levels of ANP were elevated in patients with congestive heart failure according to the severity. In addition, patients associated with atrial fibrillation showed significantly higher plasma ANP levels than those on sinus rhythm. In patients with paroxysmal atrial arrhythmias, plasma ANP levels increased markedly during paroxysms. Patients with chronic renal failure had elevated plasma ANP levels, which fell after hemodialysis. These results suggest that both left and right atrial tissue can secrete ANP as a result of stretching of the cardiocytes in man and that plasma ANP levels are elevated in patients with congestive heart failure and in those with chronic renal failure by increased atrial pressure due to volume expansion. Abnormal atrial contraction per se, in addition, may stimulate ANP secretion.
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