赤血球膜異常症における膜蛋白の病態に関する研究 : 特に遺伝性楕円赤血球症について

遺伝性楕円赤血球症25例(HE),遺伝性球状赤血球症5例(HS)および遺伝性有口赤血球症5例(H.St.)における溶血の病因について,それらのspectrinの生化学的性状,膜機能および細胞形態の立場から検討した.HE症例では,その細胞形態によって2群に分類された.第1はrod shape type(rod型細胞が15%以下の群),第2はnon-rod type(rod型細胞が5%以下の群)で,前者は16例,後者は9例であった.溶血型の多くはnon-rod typeであった.さらに典型的な溶血型では,その楕円赤血球にstomatocytic changeが加わっていた.一方,膜機能Na-influxから溶血型をみると9例中8例に,Na-influxの亢進が認められた.rod型細胞を遠心法により集め,そのrod型細胞のcell ageとNa-influxについて検討した.結果はrod型細胞は,ovalocyteおよびdiscocyteよりさらにageingの進行した細胞と考えられた.また,Na-influxに関しては何ら正常赤血球と有意な差を示さなかった.しかし,このrod型細胞より作られたTriton shellでは,明らかにmechanical stabilityの低下が認められた.溶血型HE症例のうちで,膜蛋白band 4.2欠損例が発見され,この症例ではspectrin α-IV domainの等電点にも異常が検出された.その他のHE,HSおよびH.St.症例におけるspectrinの検討では,各domain,dimer-dimer associationおよび耐熱安定性には異常を認めなかった.The pathogenesis of increased hemolysis was studied on spectrin biochemistry, membrane functions and morphology in hereditary elliptocytosis (25), spherocytosis (5) and stomatocytosis. Based on morphological features, the HE patients were classified into two major groups; those with a rod shape type (>15%) of elliptocytosis (16), and those with a non-rod type (<5%) of elliptocytosis. Most of cases with overt hemolysis were detected among the non-rod type cases. Overt hemolysis typically tended to be accompanied with stomatocytic changes, which appear to be superimposed on elliptic changes. Sodium influx increased in 8 of 9 HE patients with overt hemolysis. Rod shaped elliptocytes were collected by the centrifugation method, and these cells were examined on the cell age and sodium influx. By this method, it was concluded that the cell age of rod shaped elliptocytes was older than ovalocytes and discocytes, and that no significant difference was detected between rod shaped elliptocytes and normal discocytes in sodium influx. On the other hand, instability of these rod shaped elliptocytes in triton shells was detected under the mechanical shaking. The membrane protein band 4.2 deficiency was detected in a case of hemolytic HE, in which abnormal isoelectric point of spectrin α-IV domain was observed. Spectrin abnormality in domain composition, dimer-dimer association, and thermal stability were not observed in other cases with HE, HS, H.St. patients studied

マツノザイセンチュウ，Bursaphelenchus xylophilusに随伴する松萎凋性細菌の単離とその毒性代謝物質

Based on the observation that ray parenchyma cell death took place prior to nematode population increase in pine wood,the authors suspected that any microorganisms carried by pathogenic nematodes would be involvedin the pathogenic process.The authors screened pathogenic nematode-accompanying microbes for their toxicity against cultured cells of Pinus thunbergiis and isolated and identified 3 toxic strains,Bacillus cereus HY-3,B.subtilis HY-16,and Bmegaterium HY-17 , whose toxic products were identified as phenylacertic acid.Inoculation of pine seedlings with the toxic bacterium alone did not cause the seedling to wilt , but inoculation of pine seedlings with the toxic bacterium carried by weakly pathogenic nematodes wilted the seedling as much as strongly pathogenic nematodes . These results suggested that phenyllacetic acid-producing bacteria could invade pine trees by accompanying pine wood nematodes , and produce phenylacetic acid , a toxic metabolite , in the wood.マツ材線虫病の初期症状である樹脂道エピセリウム細胞や周辺柔細胞の変性は、マツノザイセンチュウのその場への到着および増殖に先行して起こることから、マツノザイセンチュウに随伴する微生物が発病に関与しているのだはないかと推論し、本研究では、クロマツ培養細胞に対する毒性を指標にして強病原生マツノザイセンチュウから毒物質生産細菌を数株を単離したえ。さらに、この毒性代謝物質を単離し、フェニル酢酸と同定した。フェニル酢酸生産細菌は、普遍的に存在するが、フェニル酢酸生産性には、大きい差があることを確認した。このフェニル酢酸生産細菌のみを接種しても、アカマツ実生は萎凋しなかったが、弱病原性マツノザイセンチュウに保持されて接種すると、ザイセンチュウの病原性が強くなった。このかとから、フェニル酢酸生産細菌は、マツノザイセンチュウに運搬されて松樹体内を移動し病原毒素フェニル酢酸を生産するものと推論した

A Compound Which Can Be Used for Selecting Transfomed Plant Cells

Streptomyces sp,KBFP-2025株が生産するOxazolomycinは,Agrobacterium tumefaciensに対する特異的な抗菌活性により,ジャガイモのクラウンゴール形成を阻害する.さらに,本化合物はアルファルファの発芽を強く阻害し,ジャガイモ塊茎細胞を壊死させたが,ジャガイモのタラウンゴール細胞に対する生育阻害を示さなかった.すなわち,本化合物は非形質転換植物細胞に対する選択毒性を有しており,形質転換細胞の選抜に有用である

Excessive daytime napping independently associated with decreased insulin sensitivity in cross-sectional study – Hyogo Sleep Cardio-Autonomic Atherosclerosis cohort study

BackgroundAlthough excessive daytime napping has been shown to be involved in diabetes occurrence, its impact on insulin secretion and sensitivity has not been elucidated. It is speculated that excessive napping disrupts the sleep-wake rhythm and increases sympathetic nerve activity during the day, resulting in decreased insulin sensitivity, which may be a mechanism leading to development of diabetes. We previously conducted a cross-sectional study that showed an association of autonomic dysfunction with decreased insulin sensitivity, though involvement of autonomic function in the association between napping and insulin sensitivity remained unclear. Furthermore, the effects of napping used to supplement to short nighttime sleep on insulin secretion and sensitivity are also unknown. In the present cross-sectional study, we examined the relationships of daytime nap duration and autonomic function with insulin secretion and sensitivity in 436 subjects enrolled in the Hyogo Sleep Cardio-Autonomic Atherosclerosis (HSCAA) Cohort Study who underwent a 75-g oral glucose tolerance test (75-g OGTT), after excluding those already diagnosed with diabetes.MethodsDaytime nap duration was objectively measured using actigraphy, with the subjects divided into the short (≤1 hour) and long (&gt;1 hour) nap groups. Insulin secretion and sensitivity were determined using 75-g OGTT findings. Standard deviation of normal to normal R-R interval (SDNN), a measure of autonomic function, was also determined based on heart rate variability. Subgroup analysis was performed for the associations of napping with insulin secretion and sensitivity, with the results stratified by nighttime sleep duration of less or greater than six hours.ResultsSubjects in the long nap group exhibited lower insulin sensitivity parameters (QUICKI: β=-0.135, p&lt;0.01; Matsuda index: β=-0.119, p&lt;0.05) independent of other clinical factors. In contrast, no associations with insulin secretion were found in either group. Furthermore, the association of long nap duration with insulin sensitivity was not confounded by SDNN. Specific subgroup analyses revealed more prominent associations of long nap habit with lower insulin sensitivity in subjects with a short nighttime sleep time (β=-0.137, p&lt;0.05).ConclusionLong daytime nap duration may be a potential risk factor for decreased insulin sensitivity