Search

Saltpetre constitutes one of the major ingredients of gunpowder, which was a driving force during the political changes in late medieval to early modern times in Japan. Two types of model saltpetre mineralization are studied. One represents efflorescent saltpetre formed as the byproduct of indigo dye manufacture, whereas the second is anthropogenic, derived from relict nitre‐beds. Here, oxygen and nitrogen isotopic analysis, as expressed by δ18O and δ15N notations, is applied. The calculated δ18O values for ambient water, responsible for the microbial‐mediated oxidation of ammonium into oxygen in nitrates, tended to have higher ranges than average local meteoric waters of the relevant regions. An overall trend could be seen, showing the apparent positive nitrogen isotopic fractionation during the microbial transformation from initial organic nitrogen into nitrate product. Dual isotopic analysis for industrial nitrates provides a useful tool for investigation of the provenance of historic gunpowder. Present anthropogenic saltpetre involves positive control over temperature–moisture regimes and oxygen fugacity during formation, the process being distinctive from those prevailed in British India and other European countries. [ABSTRACT FROM AUTHOR]

Fe K-XANES spectra of a series of pottery sherds excavated from the archaeological site of Kaman-Kalehöyük, Turkey, were measured to reveal the firing technique of the pottery. The analysis disclosed relationships among the chemical form of the iron, the firing conditions and the colour of the pottery. The pottery referred to as ‘Grey Ware’ found at this site was classified into two groups according to the chemical form of the iron. Also, it was revealed that the Iron Age pottery referred to as ‘Cream Ware’ was produced first under reducing conditions, and then fired under oxidizing conditions. [ABSTRACT FROM AUTHOR]

In order to determine whether l-DOPA-derived extracellular dopamine (DA) in the striatum with dopaminergic denervation is affected by activation of serotonin autoreceptors (5-HT[sub 1A] and 5-HT[sub 1B] receptors), we applied in vivo brain microdialysis technique to 6-hydroxydopamine-lesioned rats and examined the effects of the selective 5-HT[sub 1A] receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and the selective 5-HT[sub 1B] receptor agonist CGS-12066 A on l-DOPA-derived extracellular DA levels. Single l-DOPA injection (50 mg/kg i.p.) caused a rapid increase and a following decrease of extracellular DA, with a peak value at 100 min after l-DOPA injection. Pretreatment with both 0.3 mg/kg and 1 mg/kg 8-OH-DPAT (i.p.) significantly attenuated an increase in l-DOPA-derived extracellular DA and the times of peak DA levels were prolonged to 150 min and 225 min after l-DOPA injection, respectively. These 8-OH-DPAT-induced changes in l-DOPA-derived extracellular DA were antagonized by further pretreatment with WAY-100635, a selective 5-HT[sub 1A] antagonist. In contrast, intrastriatal perfusion with the 5-HT[sub 1B] agonist CGS-12066 A (10 nm and 100 nm) did not induce any changes in l-DOPA-derived extracellular DA. Thus, stimulation of 5-HT[sub 1A] but not 5-HT[sub 1B] receptors attenuated an increase in extracellular DA derived from exogenous l-DOPA. These results support the hypothesis that serotonergic neurons are primarily responsible for the storage and release of DA derived from exogenous l-DOPA in the absence of dopaminergic neurons. [ABSTRACT FROM AUTHOR]

Two Graves' patients were found to have no OT4+cells in their peripheral blood lymphocytes (PBL), However, the reactivity of their lymphocytes with T4(T4A) and anti Leu-3a was normal and no autoantibodies to the OKT4 determinant were found in their sera. Cytofluorographic analysis of PBL from their family members showed three types of immunofluorescence profiles with OKT4, The first type was the complete OKT4+ cell deficiency, the second was the normal percentage of OKT4+ cells with half immunofluorescence intensity and the third was the normal staining pattern with OKT4. Phytohaemagglutinin (PHA) and pokeweed mitogen (PWM) induced blastogenesis; PWM induced IgG synthesis, autologous and allogeneic mixed lymphocyte reaction, and Interleukin-2 (IL-2) production of their PBL were also normal. These results suggest that (i) the expression of determinant to OKT4 is transmitted as autosomal incomplete dominant trait and (ii) OKT4+ cell deficiency is not accompanied by a lack of the inducer/helper subset of T cells. [ABSTRACT FROM AUTHOR]

In this study the existence of mixed isotype AβbEαd molecules in Eαd gene-introduced C57BL/6 (B6Eαd) transgenic mice is demonstrated. Biosynthetically labelled B6Eαd transgenic spleen cells were immunoprecipitated with anti-Aβb or anti-Eαdmonoclonal antibody (mAb) and analysed by twodimensional gel electrophoresis (NEPHGE/SDS-PAGE). Anti-Aβb mAb precipitated Eαd molecules in addition to Aβb and Aαa molecules. Anti-Eα d mAb precipitated Aβbolecules in addition to Eβb and Eαd molecules. No Eαd molecule was precipitated by anti-Aβb mAb from B10.A(3R) spleen cells, which have a very similar organization of class II molecules to B6Eαd transgenic mice. Since this B6Eαdtransgenic mouse was shown to have 20-40 copies per cell of the Eαd transgene (Kashiwamura et al., 1988), it is speculated that large amounts of Eαd transgene are made but, according to the data presented here, only a small amount actually associates with Aβb as opposed to Eβb. [ABSTRACT FROM AUTHOR]

A unique mixed lymphocyte-stimulating determinant(s) was detected in Eαd gene-introduced C57BL/6 transgenic mice using, alloreactive T-cell clones. Such unique determinant(s) was not detected by primary mixed lymphocyte culture reactions. The possibility that such unique determinant(s) was created by the combinatorial association of Eαd transgene products with endogenous Aβb gene products is discussed. [ABSTRACT FROM AUTHOR]

Reports on a case of multiple sclerosis manifesting as a Brown-Sequard Syndrome. Characteristics of multiple scleroris; Method of treatment; Symptoms.

Recent studies have indicated that brain and gut activities are interrelated and exposure to several stressors, such as water-avoidance stress, stimulates the motor function of the gut through corticotropin-releasing factor (CRF)-signalling pathways in the brain. Central oxytocin is known to attenuate stress responses, including CRF expression in the brain. Here, we examined whether central oxytocin attenuated the acceleration of colonic motility induced by water-avoidance stress. A force transducer was attached to the distal colon of male rat, and the colonic motility and faecal pellet output were recorded while the rats were exposed to water-avoidance stress. Intracerebroventricular (i.c.v.) injections of oxytocin (5, 50 and 500 pmol) and the oxytocin receptor antagonist tocinoic acid (25 μg) were administered before exposure to water-avoidance stress, and the effect of oxytocin on colonic motor function was determined. Centrally administered oxytocin inhibited the accelerated colonic motility induced by water-avoidance stress. The effective dose ranged between 5 and 50 pmol on i.c.v. injection. Oxytocin also decreased the number of CRF-positive cells in the paraventricular nucleus and corticosterone release. The inhibitory effect of oxytocin on accelerated colonic motility was blocked by pretreatment with oxytocin receptor antagonist. Furthermore, centrally administered tocinoic acid enhanced the acceleration of colonic motility. These results suggested that endogenous central oxytocin may contribute to the regulation of colonic function and inhibit the brain CRF-signalling pathways targeting the gut, resulting in the inhibition of stress-induced colonic contractions. [ABSTRACT FROM AUTHOR]

Objectives/hypothesis: In 2013, we introduced a modified technique for mucosal/muscle layer defect coverage with fibrin glue and polyglycolic acid (PGA) sheets (mMCFP technique) in patients undergoing endoscopic transoral surgeries for laryngopharyngeal cancers. This technique allows easy and convenient coverage of the wound surface, even when it involves the laryngopharyngeal lumen. To our knowledge, use of the MCFP technique for coverage of postoperative mucosal and/or muscle layer defects involving the laryngopharyngeal lumen has not been reported. The aim of the present study was to retrospectively evaluate the safety of our mMCFP technique used simultaneously with endoscopic transoral resection of Tis, T1, T2, and select T3 pharyngeal and supraglottic cancers., Study Design: A single centre retrospective study., Methods: Between June 2013 and February 2019, 102 patients underwent simultaneous end-flexible-rigidscopic transoral surgery and wound coverage using our mMCFP technique. All patients required mucosal and/or muscle layer resection. For all patients, we recorded the incidence of postoperative complications and the time period for which the PGA sheets could be observed after surgery., Results: In 41%, 35%, and 8% patients, the PGA sheets could be observed on the wound surface for 2, 3, and 4 weeks, respectively. Other than postoperative bleeding in two patients (2%), no postoperative complications were recorded., Conclusions: The findings of this study suggest that our mMCFP technique is a safe and simple method for the repair of mucosal and/or muscle layer defects after endoscopic transoral surgery for laryngopharyngeal cancers., Level of Evidence: 4 Laryngoscope, 130:1740-1745, 2020., (© 2019 The American Laryngological, Rhinological and Otological Society, Inc.)

Changes in plasma active and inactive renin concentration (ARC and IRC) after captopril administration and angiotensin II (AII) infusion were studied in six patients with Bartter's syndrome. A single oral dose of captopril (8-25 mg) lowered the blood pressure and increased both ARC and IRC. AII infusion elevated blood pressure, suppressed ARC and increased IRC. In this syndrome of high renin levels, infused AII appeared to increase inactive renin secretion by reducing its conversion to active renin. On the other hand, an acute fall in AII levels and/or renal perfusion pressure by captopril increased both active and inactive renin. This indicates that the increase in the secretion of inactive renin, stimulated by captopril, might exceed any increase in its conversion to active renin in patients with Bartter's syndrome, in whom the production of renin is accelerated, and conversion of inactive renin to active renin probably already operates near its maximum.