Yasutami Kinoshita

Identification of β-aminoisobutyric acid in uremic serum

Abstract An unidentified ninhydrin-positive substance found in uremic sera but not found in normal sera was isolated by gel-filtration through Sephadex G-75 followed by high voltage paper electrophoresis (pH 3.5), and identified as β-aminoisobutyric acid using paper chromatography and automated amino acid analyzer. The quantitative determination of β-aminoisobutyric acid in serum revealed that the level of β-aminoisobutyric acid in uremic sera was much higher than that of normal sera. Gas chromatographic determination of the enantiomorphs of β-aminoisobutyric acid showed that uremic sera contain R- and S-isomers of the amino acid, but with the R-isomer as the dominating form.

A Lack of Burst-Forming Unit (BFU-e) and Lymphocyte-Mediated Suppression of Erythropoiesis in Patients with Aplastic Anemia

The pathogenesis of idiopathic aplastic anemia remains obscure.1 Since all cellular components of the blood are depressed in aplastic anemia, it is reasonable to suggest that the defect resides at the level of the pluripotential hematopoietic stem cells, as a result of a defect in the matrix of the hematopoietic system or of humoral regulation. However, several recent reports2,3 suggest that immune processes may be involved in the pathogenesis of aplastic anemia in some patients. In work reported in this chapter, using a plasma clot assay for the growth of burst-forming unit (BFU-e) including more mature (CFU-e) erythroid precursors in vitro, we examined changes in CFU-e and BFU-e in the marrow and blood of patients with aplastic anemia. Both marrow and circulating CFU-e and BFU-e were found to be markedly reduced in aplastic anemia. In addition, whether or not such a reduction of colony forming capacity in vitro may be related to cell-mediated suppression of erythropoiesis3 was investigated in co-cultures with peripheral blood lymphocytes and normal human bone marrow cells.

Identification of β-Aspartylglycine in Uremic Serum and Its Toxicity1

: An unidentified ninhydrin-positive substance of acidic nature was found in the serum of uremic patients. This substance was isolated from hemodialysate by the methods of ion-exchange chromatography, gel-filtration and paper electrophoresis, and identified as beta-aspartylglycine by amino acid analysis, N-terminal amino acid determination and comparison with authentic sample synthesized in this laboratory. The quantitative determination of beta-aspartylglycine in serum revealed that the serum concentrations of beta-aspartyl-glycine in uremic patients increased much higher than those in normal subjects. The toxicity of beta-aspartylglycine in mice with acute renal failure induced by uranyl acetate was investigated. The mice given more than 1,0 g/kg body weight of beta-aspartylglycine showed behavioral alterations: low response to the stimuli and low activity, and some mice died by the injection of 4.0 g/kg body weight of the peptide. These results suggested that beta-aspartyl-glycine might be a possible factor which influences the development of uremic toxaemia.

Classification of chronic glomerulonephritis based on prognostic considerations.

Based on the correlation of LM, EM and IF findings of kidney biopsy tissues with the clinical and laboratory findings as well as renal function, classification of primary GN is proposed with special reference to the smouldering and progressive forms of chronic GN. The two forms of chronic GN should be differentiated because their prognoses are different.

Primary nonspecific chronic ulceration of small intestine report of two cases in sisters

1. In first infected rabbi ts showed foreign body reaction in t issue around the worm body. 2. In second infected rabbi ts demonstra ted the severe allergic reaction in tissue. 3. Degenerat ion process of worm body were more rapidly in reinfected rabbi ts than first infected. 4, Allergic reaction in immunized same rabbi t were more rapidly in intes t ine than stomach, 5. The resul t of exper imenta l studies showed a lmost the same reaction in human Anisakiasis,

METABOLIC STUDIES ON NEPHROTIC SYNDROME

ラットのaminonucleoside nephrosisについて蛋白,脂質,糖質およびenergy代謝の面から病態生理学的研究を行なつた. nephrosisラットでは血清蛋白やalbumin濃度の著減,遊離脂肪酸を除く諸脂質の血清濃度の著増,高度の蛋白尿と腹水を認めた.肝重量は増加し,肝核酸濃度と核酸へのP32取込み率の上昇がみられ,細胞数の増加を伴なつた肝肥大と蛋白合成能亢進が示唆された.血清および肝蛋白へのC14-amino酸の取込みは亢進していたが筋蛋白へのそれは減少し,血清蛋白補充の目的で肝中心の蛋白代謝亢進があると理解された. G14-glucoseあるいはacetateの肝脂質および脂肪組織脂酸へのC14-incorporationや肝燐脂質へのP32取込みは上昇し,他方肝脂質濃度や貯蔵脂肪量の増加を認めず,高脂血発展に肝および脂肪組織が重要な関係をもつことを示した.血糖値および,肝,筋glycogen濃度は減少し,糖利用度の増大を暗示したが組織の解糖系酵素の活性測定からこれを裏づける成績は得られなかつた.肝の糖や種々有機酸の酸化能は亢進し,また高energy燐酸体のP32-incorporationも増加し,蛋白や脂質合成亢進の基盤たるenergy代謝の増大を示した.

A CASE OF SYSTEMIC LUPUS ERYTHEMATODES ASSOCIATED WITH CRYPTOCOCCOSIS

近年抗生剤とsteroidhormoneの使用がその一つの誘因となつて真菌症が増加してきたが,私共も全身性エリテマトーデス(SLE)にクリプトコッカス症を合併した1例を経験した.患者は20才の女性.最初手掌,手背,両頬に紅斑が出現,次いで発熱,蛋白尿,顔面浮腫を来たし,某病院でSLEとしてsteroidhormoneを投与され,間もなく当科に転院した、続いてテトラナイクリンと共にsteroidhormone療法を行なつたが,約1年後に高熱と共にLE細胞が証明され, prednisolone 1日70mgの大量を与えても効果なく,やがて頭痛,嘔気,嘔吐,霧視,複視,外転筋麻痺及び欝血乳頭を認め,髄液にcryptococcus neoformansを証明した.次いで嗜眠状となり,腱反射消失,項部強直と病的反射が出現, nystatinで効なく, amphotericin Bを点滴静注中死亡した.剖検により脳脊髄膜,脳実質,腎,肺にcryptococcus性肉芽腫と菌を,又腎にwireloop lesion,脾にonionskin様変化を認めた.

INHIBITION OF AMINONUCLEOSIDE RENAL LESIONS IN RATS BY ADENINE, ADENOSINE TRIPHOSPHATE (ATP) AND FLAVINE ADENINE DINUCLEOTIDE (FAD)

抗生物質puromycinの誘導体であるaminonucleoside (AN)はラッテにおいてヒトのネフローゼに極めて類似した腎傷害を若起するため, ANによる腎傷害は最近ネフローゼ症候群の実験的モデルとして注目されている. ANの作用機序についてその構造がadenine,またはadenosine等の核酸前駆物質と似ているために, ANがこれらの物質と競り合うためであるとか,あるいはadenineおよびpyridine nucleotide産生がANにより抑制されるため等と推定されている.そこでわれわれはANによるラッテの実験的腎傷害の発生にたいしてadenine, ATPおよびFADを併用してその抑制効果を検討した.ANにたいし, FADの併用は特に効果を認めず, adenineの併用では初期変化の軽度抑制を認めた。ATPの併用は適量によっては尿蛋白,血清残余窒素およびコレステロールの増量が軽度で,かつ組識像でも特に尿細管の変化がAN群にくらべて軽度であつた.われわれはANによる実験的腎傷害の発生にたいしてATPが抑制作用を有する事実を初めて明らかにした。