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A detailed study of Mössbauer spectra for K 2 Fe(SO 4 ) 2 ·nH 2 O(n=2,4,6) has been performed. Isomer shift and quadrupole splitting of 57 Fe were measured as functions of temperature between 90 K and 370 K. Single crystals of dipotassium iron sulfate, K 2 Fe(SO 4 ) 2 ·nH 2 O were grown by slow evaporation of aqueous solutions of K 2 SO 4 and FeSO 4 in equimolar ratio. Since it was necessary to keep the solution above 360 K to obtain dihydrate crystals, K 2 Fe(SO 4 ) 2 ·2H 2 O was grown at 369 K. The crystal is known to undergo a phase transition which is associated with the water molecular orientation. The Mössbauer study was also performed on the crystals K 2 Fe(SO 4 ) 2 ·4H 2 O and K 2 Fe(SO 4 ) 2 ·6H 2 O for the search of the possible phase transitions similar to that of K 2 Fe(SO 4 ) 2 ·2H 2 O. The part of the X-ray structure analysis for these crystals is also given.

SATB1 is expressed primarily in thymocytes and can act as a transcriptional repressor. SATB1 binds in vivo to the matrix attachment regions (MARs) of DNA, which are implicated in the loop domain organization of chromatin. The role of MAR-binding proteins in specific cell lineages is unknown. We generated SATB1-null mice to determine how SATB1 functions in the T-cell lineage. SATB1-null mice are small in size, have disproportionately small thymi and spleens, and die at 3 weeks of age. At the cellular level, multiple defects in T-cell development were observed. Immature CD3(-)CD4(-)CD8(-) triple negative (TN) thymocytes were greatly reduced in number, and thymocyte development was blocked mainly at the DP stage. The few peripheral CD4(+) single positive (SP) cells underwent apoptosis and failed to proliferate in response to activating stimuli. At the molecular level, among 589 genes examined, at least 2% of genes including a proto-oncogene, cytokine receptor genes, and apoptosis-related genes were derepressed at inappropriate stages of T-cell development in SATB1-null mice. For example, IL-2Ralpha and IL-7Ralpha genes were ectopically transcribed in CD4(+)CD8(+) double positive (DP) thymocytes. SATB1 appears to orchestrate the temporal and spatial expression of genes during T-cell development, thereby ensuring the proper development of this lineage. Our data provide the first evidence that MAR-binding proteins can act as global regulators of cell function in specific cell lineages.

The relationship between gastric mucosal glutathione (GSH) levels, vascular permeability, gastric motility and mucosal injury caused by ethanol was investigated in rats. Oral administration of 50% ethanol (1 ml) produced elongated reddish bands of lesions in the mucosa with a significant reduction of GSH levels and increase of microvascular permeability. These lesions were significantly inhibited by pretreatment with s.c. administered diethylmaleate (DEM: 1 ml/kg), cysteamine (100 mg/kg) and 16, 16-dimethyl prostaglandin E2 (dmPGE2, 10 micrograms/kg) but worsened markedly by N-ethylmaleimide (NEM: 10 mg/kg). Irrespective of whether the animals were treated with 50% ethanol or not, the mucosal GSH levels were significantly decreased or increased, respectively, by DEM or cysteamine, and were not affected by both NEM and dmPGE2. NEM significantly enhanced the vascular permeability in the absence or presence of ethanol (greater than 10%), whereas other agents significantly inhibited only the increased vascular permeability caused by ethanol. On the other hand, gastric motility was potently and persistently inhibited by either DEM, cysteamine or dmPGE2 at the doses which prevented ethanol-induced mucosal injury, whereas NEM had no effect on the motility. These results suggest that 1) the mucosal GSH levels do not relate directly to either development or prevention of ethanol-induced gastric injury, 2) potentiation by NEM of the mucosal injury may be accounted for by its enhancement of the vascular permeability and 3) inhibition of gastric motility may be associated with prevention of mucosal lesions.

Repeated administration of diethyldithiocarbamate (DDC : 750 mg/kg, s. c), a superoxide dismutase (SOD) inhibitor, to fed rats induced ulcers in the duodenum with less lesion in the stomach. DDC not only reduced basal acid output but also impaired duodenal alkaline secretion under both basal and acid-stimulated conditions. The duodenal ulcers induced by DDC were significantly prevented by either allopurinol, SOD or dmPGE2 at the doses which significantly reversed the inhibited alkaline responses caused by DDC. The pathogenesis of DDC-induced duodenal ulcers may involve impairment of duodenal alkaline secretion, probably caused by insufficiency of antioxidant machinery in the mucosa.

Iron environment was investigated by 57Fe Mossbauer spectroscopy on the crystals [N(CH3)4]2FeCl4 and K2Fe(SO4)2•2O. The former crystal undergoes successive phase transitions including an incommensurate phase. Single doublet was observed in the orthorhombic phase (Phase I). The spectrum is almost the same in the incommensurate phase (Phase II) and in the Phase II'where the structure is modulated in the z-direction with the wavenumber 3/7. These modulation seems to raise no large EFG modulation to cause noticeable change in the spectrum. A new doublet appears in the Phase III where the structure is commensurate with the cell tripling along the c axis. This doublet persists even to the Phase IV where the structure is monoclinic with Z = 4. If we consider the crystal symmetry, the extra doublet is prohibited in this phase. The extra EFG is interpreted as the peculiarity to the powder sample. The spectrum of K2Fe(SO4)2•2H2O shows only one EFG and its temperature dependence is quite similar to the order parameter.

Duodenal pH, potential difference and acid-neutralizing capacity (HCO3- output) were measured in anesthetized rats, in an attempt to characterize these responses induced by cholinergic agents. When the proximal duodenum (1.7 cm) was perfused at a flow rate of 1 ml/min with saline adjusted to pH 4.5, the pH, potential difference and HCO3- output were 5.2 to 5.5, -3 to -5 mV (mucosa negative) and 1.5 to 1.8 muEq/10 min, respectively. Both carbachol (4 micrograms/kg, i.v.) and bethanechol (100 micrograms/kg, i.v.) significantly elevated all these parameters at the doses that stimulated gastric acid secretion; the net HCO3- output caused by these agents was about 35% of that produced by prostaglandin E2 (300 micrograms/kg, i.v.). These responses induced by carbachol were significantly inhibited by pretreatment with verapamil (0.2 mg/kg, i.v.), a Ca channel blocker, and atropine (0.1 mg/kg, i.v.), a nonselective M1 and M2 antagonist, while they remained unaltered in the presence of pirenzepine (1 mg/kg, i.v.), a selective M1 antagonist, or indomethacin (5 mg/kg, s.c.). However, the effects of prostaglandin E2 on duodenal pH, potential difference and HCO3- output were not significantly affected by any of these agents. These results suggest that the cholinergic agents stimulate HCO3- output in the duodenum, probably mediated by M2 receptors and through the Ca-dependent and electrogenic processes. Endogenous prostaglandins may not be involved in this mechanism.

Influences of restraint plus water-immersion stress on gastric alkaline response and mucosal blood flow were investigated in the rat. Under normal conditions, the stomach secreted alkali at the rate of approximately 1 microEq/15 min in the presence of omeprazole (60 mg/kg i.p.) and responded to mucosal acidification (1000 mM HCI for 10 min) by a significant rise of output (approximately 2.5 microEq/15 min), and the latter process was significantly blocked by indomethacin (5 mg/kg s.c.), quinacrine (100 mg/kg s.c.) and vasopressin (10 unit/kg/hr i.v.). Restraint alone decreased basal rates of HCO3- secretion but had no effect on acid-induced HCO3- output. Additional water-immersion stress further reduced alkaline secretion, totally abolished the increased HCO3- response to acid and significantly suppressed the increase of HCO3- output caused by 16,16-dimethyl prostaglandin E2 (3-30 micrograms/kg s.c.). During restraint stress mucosal blood flow was reduced only by 30% but after exposure to additional water-immersion, it further decreased to about 25% of normal values. Both indomethacin and quinacrine had no effect on mucosal blood flow, whereas vasopressin markedly reduced mucosal blood flow by about 80%. These results suggest that stress not only reduced basal rates of alkaline secretion in the stomach but also impaired the mucosal ability to increase HCO3- output in response to acid. These secretory disorders caused by stress may be attributed to both a decrease of mucosal blood flow and prostaglandin deficiency in the mucosa.

γ-Mn alloys containing Ga undergo a distortion from the face-centered-cubic structure to the face-centered-tetragonal structure with c/a < 1 or c/a > 1, depending on composition. The face-centered-orthorhombic structure also exists in a composition range between the two tetragonal phases. The antiferromagnetic structures of these phases have been determined by neutron-diffraction experiments. The tetragonal and orthorhombic phases exhibit collinear and noncollinear moments, respectively. The results are consistent with the theoretical prediction by Jo et al.