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SUMMARY 1. The release of adenyl purines such as ATP, ADP, AMP and adenosine, from the pulmonary artery trunk (PAT), extra-pulmonary artery (EPA) and intrapulmonary artery (IPA) were compared. 2. The amount of basal overflow of adenyl purines from the PAT was significantly smaller than those from EPA and IPA. There was no significant difference between the amount of the overflow from EPA and PAT. 3. Methoxamine, an α1-adrenoceptor agonist, significantly increased the overflow of adenine nucleotides from the PAT, EPA and IPA, but did not increase those of adenosine. Methoxamine-induced release of adenyl purines from IPA was significantly larger than those from EPA and PAT. 4. These results suggest that an α,-adrenoceptor-mediated mechanism for ATP-release is not homogeneously distributed in the pulmonary artery and a larger amount of ATP may be released in the peripheral part of the artery.

We studied metabolic changes in relation to chorea in two patients with diabetic haemichorea-haemiballism using positron emission tomography with (18)F-fluorodeoxyglucose. Metabolism of the striatum and globus pallidus did not change in the acute choreic stage, but it decreased in the later stage after the amelioration of chorea. Striatal and pallildal hypometabolism in the late stage in diabetic haemichorea-haemiballism may reflect tissue ischaemia with gliosis. Previous studies have demonstrated striatal hypometabolism in neurodegenerative choreic disorders and striatal hypermetabolism in acute inflammatory choreic disorders. Previous findings as well as our results suggest that striatal and pallidal metabolic changes may be correlated with histological changes more than with functional changes relevant to chorea.

We report a case with multiple sclerosis which showed bilateral hypogeusia due to a small lesion in the lower midbrain tegmentum. Sweet taste was diminished only on the contralateral side in the territory of the chorda tympani, and salty, sour and bitter tastes were diminished bilaterally. All taste modalities were preserved in the territory of the greater petrosal nerve. The findings in our patient and in the literature suggest that the second gustatory fibres ipsilaterally ascend from the nucleus of the solitary tract to the midbrain and partially cross at the inferior border of the midbrain. The features of hypogeusia in our case suggest segregated channels in the gustatory pathway conveying taste perception of distinct taste modalities and from distinct innervation territories.

Si thin film coated on a flexible polyimide (PI) substrate was successfully crystallized by blue multi-laser diode annealing (BLDA) in the CW mode. The precursor Si film of 50 nm thickness was stably deposited at room temperature using a radio-frequency (RF) sputtering machine. Subsequently, a blue (445 nm) laser beam of 1.1 W was irradiated onto the Si film at a scan speed of 500 mm/s. After irradiation, neither damage to the substrate nor degradation of the Si film surface was observed, and the Si surface was kept smooth within 4.2 nm (RMS). By Raman peak shift at 520 cm-1 and transmission electron microscope (TEM) observation, the crystalline fraction of 100% was estimated in spite of the presence of micro-grains of ∼50 nm in diameter. The BLDA allows the realization of ultra-low temperature polycrystalline silicon (poly-Si) and is suitable for the next-generation system on panel (SoP).

Remitting seronegative symmetrical synovitis with pitting edema (RS3PE), first described by McCarty (1), is characterized by symmetrical pitting edema of the hands and feet; tenderness, swelling, and/or limited motion of the joints; fatigue; and fever (1,2). It commonly occurs in elderly people (1,2). We have recently encountered two cases of RS3PE that developed shortly after the initiation of a dipeptidyl peptidase-4 (DPP4) inhibitor and resolved markedly upon cessation of it. Case 1 was a 74-year-old woman with a 30-year history of type 2 diabetes who presented with edema of the hands, low grade fever, and malaise, which developed 5 weeks after switching from 20 mg gliclazide to 50 mg sitagliptin. Physical examination revealed severe pitting edema …

To gain new insights into the pathogenesis of diabetic angiopathy, the influence of high glucose concentration on cation transport of vascular smooth muscle cell (VSMC) membrane was investigated by measuring Na, K and Ca transport in serially passaged cultured VSMC. (1) NaK pump activity, described as ouabain sensitive 86 Rb uptake, and NaK cotransport, described as bumetanide sensitive 86 Rb washout of VSMC, grown in high glucose concentration medium (460 mg/dl), was lower than that grown in normal glucose concentration medium (100 mg/dl). A smaller 5- N,N -hexamethylene amiloride (HMA) sensitive 22 Na uptake (NaH antiport) in high glucose concentration medium accounted for this difference. (2) 45 Ca uptake was also smaller in VSMC cultured in high glucose concentration medium. However, the washout rate constant for 45 Ca was comparable between high and normal glucose cultured VSMC. (3) Both intracellular concentration of Na and cytosolic free Ca concentration ([Ca] i ) of high glucose cultured VSMC were greater than normal glucose cultured VSMC. (4) Intracellular water volume based on the equilibrium distribution of 3- O -methyl-[ 14 C]glucose was not different between normal and high glucose cultured VSMC. It is concluded that VSMC grown in high glucose concentration milieu manifests a decreased NaK, and Ca transport in conjunction with an increase in intracellular concentration of Na and [Ca] i . These results suggest that high glucose, per se, may alter membrane permeability to cations, possibly leading to changes in VSMC contractility and/or proliferation. This abnormality seen in the diabetic state may closely link to the pathogenesis of diabetic angiopathy, thus as a result risking hypertenion and vascular disease.

In order to clarify the function of P210 bcr/abl oncogene in leukemogenesis, IL-3 dependent murine hematopoietic cell line, FDC-P2, was transfected with the plasmid containing cDNA of P210 bcr/abl oncogene (pGD'210) or murine IL-3 (pcDmIL3) by electroporation. Four out of five pGD'210 transfected clones as well as FDC-P2 transfected with pcDmIL3, acquired autonomous proliferation (i.e. lost the requirement for IL-3 supplementation). The expression of bcr/abl oncogene was weak in one clone, which remained dependent on IL-3. Unlike pcDmIL3 transfectants, which secrete IL-3 into the supernatant, IL-3 was not demonstrated in the culture supernatant of pGD'210 transfected FDC-P2. These findings suggest that P210 bcr/abl oncogene is directly associated with autonomous proliferation, which is the first process of leukemogenesis.

Semiconductor blue-multi-laser-diode annealing (BLDA) for amorphous silicon film prepared by radio frequency (RF) sputtering was performed to investigate the controllability of the crystallization behavior by changing the scanning velocity of BLDA ranging from 300 to 500 mm/s at a constant power of 3.4 W. From the evaluation results of polycrystallized Si films, crystallization occurred in solid phase under high temperature heating, and rather small grains of dendrite-like structure with distinctly preferred crystal orientation of (111) face was observed at the higher scanning velocity of 500 mm/s. On the other hand, crystallization occurred in liquid phase and randomly oriented rather larger grains with the size of 100–200 nm were observed for the scanning velocity at 300 mm/s. It was verified successfully that high crystallinity poly-Si films of arbitrary grain structure could be obtained by controlling the scanning velocity of BLDA.

The effect of methoxamine, an alpha 1-adrenoceptor agonist, on the electrically-evoked release of endogenous noradrenaline was examined in the isolated rabbit ear artery. Noradrenaline was quantified by high performance liquid chromatography-electrochemical detection. The release of adenine nucleotides and nucleosides by methoxamine was examined using high performance liquid chromatography-fluorescence detection. The release of noradrenaline evoked by electrical field stimulation (EFS) at 4 Hz was reduced by tetrodotoxin 0.3 mumol/l and clonidine 1 mumol/l by approximately 80% and 50%, respectively. On the other hand, methoxamine at 10 but not 1 mumol/l enhanced the release of noradrenaline to approximately twice the control, and the enhancement was prevented by prazosin 1 mumol/l. The facilitatory action of methoxamine was also abolished after desensitization of P2-purinoceptors by alpha,beta-methylene ATP 30 mumol/l as well as by the presumed P2-purinoceptor antagonist suramin given at 10 mumol/l. Exogenous ATP 10 mumol/l significantly enhanced the EFS-evoked release of noradrenaline, and the enhancement was abolished by alpha,beta-methylene ATP and suramin. None of the drugs changed the spontaneous outflow of noradrenaline. These results indicate that endogenous ATP, acting at prejunctional purinoceptors, may participate in the facilitatory effect of methoxamine. Indeed, methoxamine 10 mumol/l significantly enhanced the spontaneous outflow of ATP and, less so, ADP. The methoxamine evoked release of ATP and ADP was antagonized by prazosin 1 mumol/l. It is concluded that methoxamine releases endogenous ATP from postjunctional sites which then, via prejunctional purinoceptors, facilitates action potential-evoked release of noradrenaline in rabbit ear artery.

1. Isolated single smooth muscle cells from the fundus of the guinea-pig stomach were permeabilized by use of Staphylococcus aureus alpha-toxin. Receptor-coupled shortening of individual cells was monitored under phase contrast microscopy. 2. Most of the isolated cells responded to 0.6 microM Ca2+, but not to 0.3 microM Ca2+, with a resulting maximal shortening to approximately 65% of the resting cell length. The contractile activity of these permeabilized cells lasted for several hours and repeated shortening was readily achieved after washing out. 3. Addition of acetylcholine (ACh) at a maximal concentration (10 microM) resulted in a marked decrease in the concentration of Ca2+ required to trigger a threshold response from 0.6 microM to 0.2 microM, and 1 mM guanosine 5'-diphosphate (GDP) blocked this decrease. Moreover, treatment with 100 microM guanosine 5'-triphosphate (GTP) mimicked the action of ACh. 4. Addition of 100 microM inositol 1,4,5-trisphosphate (InsP3) with 0.2 microM Ca2+ did not cause cell shortening, whereas 10 microM ACh with 0.2 microM Ca2+ did, suggesting that InsP3-induced Ca2+ release is not involved in ACh-operated cell shortening. 5. The present study demonstrates an alpha-toxin-permeabilized single smooth muscle cell preparation which retains its receptor function and also provides an insight into mechanisms leading to augmentation of Ca2+ sensitivity by stimulation of muscarinic receptors or GTP-binding proteins.

To investigate the differences in the Na-K transport of the mesangial cell (MC) membrane in hypertension versus normotension, the activity of the Na-K pump and the passive cation permeability were measured in serially passaged cultured MC obtained from both spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. When Na-K pump was active, Na-K pump activity, described as ouabain-sensitive 86Rb uptake, was significantly greater in the cultured MC from SHR than WKY rats. The outward Na-K cotransport, described as the washout rate constant of bumetanide-sensitive 86Rb washout, was also greater in SHR MC than in WKY rat MC. When Na-K pump was inhibited by 1 mM ouabain, overall intracellular Na uptake was significantly greater in SHR MC. A greater 5-(N, N-hexamethylene)amiloride-sensitive Na uptake in SHR MC accounted for this difference. There was no difference in the intracellular concentration of Na and K in the cultured MC from the 2 strains when Na-K pump was active. It is concluded that there is an increased activity of Na-K pump in the cultured MC from SHR, and that this abnormality may be innate to SHR cells. It is also suggested that an increase in Na-K cotransport and Na-H antiport may explain this difference, and that these abnormalities observed in the SHR kidney may be involved in the pathogenesis of hypertension in this model.

We investigated the influence of serum from spontaneously hypertensive rats (SHR) on the Na-H antiport and Na-K pump activity of cultured vascular smooth muscle cells (VSMC). Subjecting the VSMC to rat serum stimulated the ouabain-sensitive 86Rb uptake. This activation of the Na-K pump was significantly greater with the SHR serum than the Wistar-Kyoto rat (WKY) serum. Furthermore, the serum from SHR exhibited a larger Na uptake in the presence of ouabain than that from WKY. A greater 5-(N,N-hexamethylene) amiloride-sensitive Na uptake accounted for this difference. When the Na-K pump was active, serum from either of the two strains did not cause an increase in intracellular Na concentrations. We concluded that serum from SHR produced a more pronounced activation of both the Na-H antiport and the Na-K pump. The study suggests that there are humoral factors in SHR serum which elicit the stimulation of the Na-H antiport, leading to the activation of the Na-K pump of VSMC.

Publisher Summary This chapter discusses a study to determine how iron ores mixed with sulfur are active for the direct coal liquefaction as a disposable catalyst and how they can become more active. Taiheiyo coal (Japan), Minamiohyubari coal (Japan), and Bukit Asam coal (Indonesia) were used. The liquefaction was carried out with a 300 ml shaking autoclave under the liquefaction condition of 20.3 MPa at 420°C and nominal liquefaction times (NRT) from 0–60 min. To elucidate the catalytic role of ores during coal liquefaction, coal hydrogenation in the presence of ores was analyzed with high pressure differential thermography (HPDT) and then ores after the reaction were characterized with X-ray diffraction spectrometry (XDP). To find a simple method for enhancing the catalytic activity of the ores, some pretreatments of ores were carried out. Most of the iron ores mixed with sulfur were as active as red mud mixed with sulfur, which has been regarded as a typical disposable catalyst for the liquefaction, and they gave the liquefaction products rich in oils.

Summary We studied the effects of ceruletide, a cholecystokinin analogue, on choreic involuntary movement in several neurological diseases by clinical scoring and electromyography in 11 patients. Ceruletide brought about a brief reduction of choreic movement reaching its maximum within 60 min and another long-lasting improvement over several weeks by single administration. The levels of homovanillic acid in cerebrospinal fluid before treatment were significantly higher in cases with long-lasting improvement than those in cases without improvement. We suggest that ceruletide may reduce choreic movement for a long period through effects on the central dopamine system and speculate that such a long-term effect may be accounted for by the change in transmission after the second messengers in neurons.

This is a report on the clinical courses and pathological findings in two gay male patients with acquired immunodeficiency syndrome (AIDS) infected in Japan. Case 1. A 39 year-old Japanese homosexual male was diagnosed as amebic dysentery complicated with liver abscess on admission. He was placed on Metronidazole with complete relief. Serological tests was positive for AIDS. On second admission, he was found to have pneumocystis carinii pneumonia (PCP) and cytomegalo-viral uveitis. Administration of Pentamidine was partially effective, however the therapy with Azidothimidine was discontinued by bone marrow suppression. On his third admission, he suffered from cryptococcal meningitis and therapy-resistant fungusemia. Finally he died of recurrent pneumonia regardless of appropriate therapies. Autopsy proved extended cryptococcal infection in the brain, meninx, lungs, liver and kidney, and cytomegalo-infection in the lungs, liver and kidney. Furthermore, atypical mycobacteriosis was found in the lymph nodes. There was no active findings compatible with PCP. Case 2. A 44 year-old Japanese homosexual male was admitted with oral candidiasis and diagnosed as AIDS related complex. He suffered from pneumonia with marked improvement on sulfamethoxazole-Trimethoprim. On his second admission, he developed diarrhea and was found to be infected with Giardia lambia. In addition, cytomegalo-viral infection damaged his eye sight. He died of pneumonia and meningitis shortly there after. Autopsy proved a cytomegalo-viral infection in the lung and colon, old lesions possibly caused by PCP in the lungs, and suppurative meningitis in the meninx. These experiences confirm that AIDS patients can be exposed to several opportunistic infections at the same time in the multiple organs. Furthermore, it is suggested that homosexual patients with AIDS may have unique opportunistic infections such as amebic dysentery or Giardia lamblia unlike other AIDS patients related to hemophilia.

SUMMARY 1. The release of endogenous noradrenaline (NA) and adenyl purine (ATP, ADP, AMP and adenosine) from the rabbit ear artery, evoked by electrical stimulation (ES; 16Hz), was examined. 2. ES evoked a significant release of NA and adenyl purine; the ratio of the amount of total purine released to NA released was approximately 180 on a molar base. 3. ES-evoked purine release was significantly reduced by the denudation of the endothelium and abolished by the α1-adrenoceptor antagonist, prazosin (1 μmol/L). 4. ES-evoked NA release was significantly reduced by a P1-purinoceptor antagonist, 8-sulfophenyl theophylline (8SPT). Purine release was slightly reduced by 8SPT. 5. These results suggest that endogenous NA released by ES results in the release of a large amount of purine, which may, in turn, increase the release of NA by acting on prejunctional purinoceptors on sympathetic nerve terminals.

Involvement of protein kinase C in receptor-operated Ca2+ sensitization of cell shortening was investigated by use of alpha-toxin-permeabilized smooth muscle cells from the fundus of the guinea-pig. Most of the isolated cells responded to 0.6 microM Ca2+ with a maximal shortening to approximately 65% of the resting cell length. Addition of acetylcholine (ACh) at a maximal concentration (10 microM) resulted in a marked decrease in the concentration of Ca2+ required to trigger a threshold response from 0.6 microM to 0.2 microM. The augmentation of Ca2+ sensitivity by ACh was not inhibited by specific protein kinase C inhibitors, calphostin C and K-252b at a concentration of 1 microM. These findings suggest that protein kinase C is not involved in the muscarinic receptor-operated augmentation of Ca2+ sensitivity.

1. Isolated single smooth muscle cells from the guinea pig stomach were permeabilized with Staphylococcus aureus alpha-toxin. 2. The permeabilized single cells showed a shortening in response to Ca2+ in an all-or-none manner. Moreover, the addition of acetylcholine (ACh) or guanosine 5'-triphosphate (GTP) resulted in a decrease in concentration of Ca2+ required to trigger a threshold response, suggesting that Ca2+ sensitization is induced by the stimulation of muscarinic acetylcholine receptors (mAChRs) or GTP-binding protein(s). 3. Short-term desensitization was induced by incubating the permeabilized cells with 100 microM ACh for 10 min. 4. In desensitized cells, the concentration of Ca2+ required to trigger a threshold response in the presence of ACh was increased, however, the cell shortening in response to Ca2+ in the absence of ACh and GTP-induced Ca2+ sensitization was not affected by short-term desensitization. 5. These results suggest that the receptor-operated augmentation of Ca2+ sensitivity is inhibited by short-term desensitization and that the development of short-term desensitization is due to an uncoupling of mAChR/GTP-binding protein(s).