Effects of Mannosen on Hydroponically Grown Barley

To examin the effects of mannose on iron absorption of barley roots,barley was hydroponically grown for 36 days in a greenhouse. Potassium and phosphate of barley plants grown in a diluted mannose solution were obserbed at similar as the controls. On the otherhand, some morphological changes were observed in mannose-treated barley plants.薄いマンノース溶液がオオムギの養分吸収に及ぼす影響を調べるために、水耕栽培実験を行った。マンノース添加の有無は植物体のカリウム及びリン酸含量にはほとんど影響しなかったが、植物体の形態に若干の影響を与えた

マウス接種法および螢光抗体法による屠殺豚からのToxoplasma gondiiの検出について

Ninety five pigs suspicious of Toxoplasma-infection were selected from 18,867 ones killed at Isahaya City Slaughterhouse and used for the isolation of T. gondii with mouse inoculations of their hilar or hepatic lymph nodes and also for the microscopic detection of the parasite in the lymph nodes with direct fluorescent antibody technic. In the mouse inoculation method, Toxoplasma hemagglutination test was carried out with sera of mice killed 6 weeks after the inoculation of the lymph nodes into the mice. Further, T. gondii strains newly isolated were subinoculated into mice and hamsters to investigate their virulence. The isolation rate of T. gondii was 8/95 or 8.4%, while 33 of 95 (34.7%) were positive in hemagglutination test. Fluorescent antibody technic indicated a positive response in 19 of 95 pig lymph nodes (20.0%). Eight T. gondii strains were isolated and demonstrated a high virulence for mice and hamsters. In this paper, the methods used and the above mentioned results are stated in detail and discussed.長崎県諫早市立屠場に1966年12月より1967年3月までに搬入された豚18,867頭より,屠場獣医師の協力により選抜されたトキソプラズマ症の疑いある病変豚(肺水腫,肝壊死斑,腸充血など)95頭の肝または肺門リンパ腺の螢光抗体法(直接法)により原虫検出,マウス接種法による原虫分離,および接種マウスのHA抗体価を測定し,それらの成績を比較検討した.また分離された株の毒性についてもRH株と比較し検討した.1.マウス接種法によるトキソプラズマ原虫分離は95例中8例(原虫分離率8.4%)で,いずれも栄養型が検出された.分離8株中5株は継代初期においては,シスト型も検出された.2.マウス接種法によるHA抗体価陽性(256倍以上陽性)は95例中33(陽性率34.7%)であった.原虫分離8株はいずれもHA陽性であった.3.豚の肝または肺リンパ腺の割面スタンプ標本の,螢光抗体法(直接法)によるトキソプラズマ原虫の検出率は95例中19例(検出率20.0%)であった.この19例中4例からマウス接種法により原虫が分離できた.4.分離株のマウスおよびハムスターに対する毒性はRH株と同じ程度かやや弱毒であった

屠場の低温室内におけるToxoplasma gondiiの生存期間に関する研究

Examination was made of the survival period of Toxoplasma gondii in the low temperature rooms of a slaughterhouse. Materials for the examination were the mouse bodies themselves and the organs, such as the liver and brain, of mice infected with the RH or Beverley strain. These materials were stored in both of the refrigerating and the cold-storage rooms, then taken out of the rooms one after another at a short interval and examined on the existence of live Toxoplasma in them with the intraperitoneal inoculation into healthy mice. In the first experiment, it was revealed that the survival of the proliferative form of Toxoplasma in an infected mouse body was 8 days in the refrigerating room and 4 days in the cold-storage room, but a putrefactive sign was manifesting slowly in the mice stored more than 13 days in the refrigerating room and 6 days in the other. In the following experiment, the livers excised from RH-infected mice and the brains from Beverley-infected ones were stored only in the refrigerating room. It was recognized as the result that cysts were capable of survival for as long as 67 days and proliferative forms could survive for 11 days in the room. A control experiment was attempted on the resistance of T. gondii to -14℃ in a freezer and it was shown that both forms of this protozoa in the infected mouse organs could remain alive more than an hour but did not for 3 hours in a freezer of -14℃. Temperatures in both rooms were continuously measured by auto-recording thermometers. In the refrigerating room, it was 0.47℃ in average and the cold-storage room always had 3 to 4℃ higher temperature than the refrigerating room.Toxoplasma gondiiの低温に対する抵抗性についての報告は少なくない。しかし、これらの研究では、実験室内の冷蔵庫またはフリーザーなどの精確に調節された温度条件下に実施されたものである。屠畜肉やその内臓中に潜在する本原虫が、もっとも重要な感染源と見なされている現在では、屠場の低温室中で畜肉中の本原虫が、どれ程の期間生存しつづけるかが疫学上重要な意味を持つことはいうまでもない。事実、屠場の冷却室あるいは冷蔵室の温度は、頻回の扉の開閉や大量の温かい大動物肉塊の搬入などのため、相当な変動を受けることが予測され、実験室の冷蔵庫内温度条件とはかなり異なるものであると考えられた。　本研究は、以上の趣旨に沿って長崎市営屠場内の低温室を利用し、T. gondiiの増殖型および？子の生存期間を検討した。被検材料は、大動物肉塊や内臓を用いることができなかったので、RHおよびBeverley株感染マウスおよびその臓器を使用した。　第1実験では、PH株感染マウス自体を冷却室および冷蔵室に保存した。以後、毎日または隔日に保存マウス体を取り出し、その肝および脾乳剤を健常マウス腹膣内接種し、そのマウスからの原虫検出を試みた。接種ご30日以内に死亡したマウスは即時に、それ以上生存したものは屠殺して、その腹膣液および脳中の原虫の有無を顕微鏡下に検討した。その成績では、マウス体内のRH株増殖型は冷却室中で8日間、冷蔵室中で4日間生存することを認めた。しかし、保存マウスの腹膣内臓器の腐敗が冷却室では13日め以降から、また冷蔵室では6日めから認められたことから、その成績にはマウスの腐敗が影響を及ぼしていることが想像された。実験中の室温は、冷却室では平均0.9℃、最高2.5℃、最低-1.1℃、冷蔵室では平均4.2℃、最高低巾は5.1～3.2℃であった。　第2実験では、RH株感染マウス肝とBeverley株感染マウス脳を冷却室中に保存し、一定期間毎に取り出し、乳剤として健常マウスに接種した。本実験によりマウス肝中のRH株増殖型は11日間、マウスの脳中のBeverley株囊子は実に67日間冷却室で生存することが判明した。実験期間中の冷却室温度は平均0.47℃、最高低巾は3.2～-3.5℃におよんだ。対照実験として、-14℃のフリーザーの中で第2実験と同一材料を用いて検査したが、その結果、囊子、増殖型とも、1時間保存材料中に生存することを認めたが、3時間材料からは証明できなかった。　以上の実験で、屠場冷却室中で囊子は67日間、増殖型は11日間生存し、かつ、感染力を保有していることが判明したが、大動物肉塊や臓器中では、より長時間生存することが想定された

Population density, call-response interval, and survival of out-of-hospital cardiac arrest

<p>Abstract</p> <p>Background</p> <p>Little is known about the effects of geographic variation on outcomes of out-of-hospital cardiac arrest (OHCA). The present study investigated the relationship between population density, time between emergency call and ambulance arrival, and survival of OHCA, using the All-Japan Utstein-style registry database, coupled with geographic information system (GIS) data.</p> <p>Methods</p> <p>We examined data from 101,287 bystander-witnessed OHCA patients who received emergency medical services (EMS) through 4,729 ambulatory centers in Japan between 2005 and 2007. Latitudes and longitudes of each center were determined with address-match geocoding, and linked with the Population Census data using GIS. The endpoints were 1-month survival and neurologically favorable 1-month survival defined as Glasgow-Pittsburgh cerebral performance categories 1 or 2.</p> <p>Results</p> <p>Overall 1-month survival was 7.8%. Neurologically favorable 1-month survival was 3.6%. In very low-density (<250/km²) and very high-density (≥10,000/km²) areas, the mean call-response intervals were 9.3 and 6.2 minutes, 1-month survival rates were 5.4% and 9.1%, and neurologically favorable 1-month survival rates were 2.7% and 4.3%, respectively. After adjustment for age, sex, cause of arrest, first aid by bystander and the proportion of neighborhood elderly people ≥65 yrs, patients in very high-density areas had a significantly higher survival rate (odds ratio (OR), 1.64; 95% confidence interval (CI), 1.44 - 1.87; p < 0.001) and neurologically favorable 1-month survival rate (OR, 1.47; 95%CI, 1.22 - 1.77; p < 0.001) compared with those in very low-density areas.</p> <p>Conclusion</p> <p>Living in a low-density area was associated with an independent risk of delay in ambulance response, and a low survival rate in cases of OHCA. Distribution of EMS centers according to population size may lead to inequality in health outcomes between urban and rural areas.</p

Body Weight Control by a High-Carbohydrate/Low-Fat Diet Slows the Progression of Diabetic Kidney Damage in an Obese, Hypertensive, Type 2 Diabetic Rat Model

Obesity is one of several factors implicated in the genesis of diabetic nephropathy (DN). Obese, hypertensive, type 2 diabetic rats SHR/NDmcr-cp were given, for 12 weeks, either a normal, middle-carbohydrate/middle-fat diet (MC/MF group) or a high-carbohydrate/low-fat diet (HC/LF group). Daily caloric intake was the same in both groups. Nevertheless, the HC/LF group gained less weight. Despite equivalent degrees of hypertension, hyperglycemia, hyperlipidemia, hyperinsulinemia, and even a poorer glycemic control, the HC/LF group had less severe renal histological abnormalities and a reduced intrarenal advanced glycation and oxidative stress. Mediators of the renoprotection, specifically linked to obesity and body weight control, include a reduced renal inflammation and TGF-beta expression, together with an enhanced level of adiponectin. Altogether, these data identify a specific role of body weight control by a high-carbohydrate/low-fat diet in the progression of DN. Body weight control thus impacts on local intrarenal advanced glycation and oxidative stress through inflammation and adiponectin levels

Monocyte/macrophage response to β2-microglobulin modified with advanced glycation end products

Monocyte/macrophage response to β2-microglobulin modified with advanced glycation end products. We recently found that acidic β2-microglobulin (β2m), a major isoform of β2m in amyloid fibrils of patients with dialysis-related amyloidosis (DRA), contained early Amadori products and advanced glycation end products (AGEs) formed nonenzymatically between sugar and protein. Further analysis revealed that acidic β2m induces monocyte chemotaxis and macrophage secretion of bone-resorbing cytokines, suggesting the involvement of acidic β2m in the pathogenesis of DRA. Acidic β2m, however, is a mixture of heterogeneous molecular adducts due to various types of modification. In the present study, we investigated the modification responsible for the biological activity of acidic β2m toward monocytes/macrophages. The presence of a fair amount of β2m species with deamidation was detected in acidic β2m isolated from urine of non-diabetic long-term hemodialysis patients, but deamidated β2m had no biological activity. In contrast, normal β2m acquired the activity upon incubation with glucose in vitro. Among the glycated β2m, the pigmented and fluorescent β2m that formed after a long incubation period, that is, AGE-modified β2m, exhibited biological activity, whereas β2m modified with Amadori products, major Maillard products in acidic β2m, had no such activity. These findings suggest that AGEs, although only a minor constituent of acidic β2m, are responsible for monocyte chemotaxis and macrophage secretion of cytokines, implicating the contribution of AGEs to bone and joint destruction in DRA

ETB receptor protects the tubulointerstitium in experimental thrombotic microangiopathy

ETB receptor protects the tubulointerstitium in experimental thrombotic microangiopathy.BackgroundThe characteristic features of thrombotic microangiopathy (TMA) include glomerular and peritubular capillary endothelial cell injury with thrombus formation and subsequent ischemic tubulointerstitial damage. The endothelin ETB receptor has been shown to mediate both endothelial cell proliferation and vasodilation, and we therefore hypothesized that blockade of this receptor might promote more severe injury in this model.MethodsTMA was induced in recently established transgenic rats that lack expression of ETB receptor in the kidney; these animals were compared to control rats with TMA both in the short-term (days 1 and 3) when acute glomerular injury was most manifest, and the long-term (day 17) when glomeruli have recovered but tubulointerstitial injury is still present. Renal damage was assessed by histological analysis and blood urea nitrogen (BUN) measurements.ResultsNo difference in the TMA model was observed between rats with and without ETB receptor on days 1 or 3. At day 17, however, rats without the ETB receptor showed more severe tubulointerstitial injury compared with those with ETB receptor, which was associated with higher BUN levels. The tubulointerstitial damage was associated with a more severe loss of peritubular capillaries.ConclusionsThese findings suggest that the ETB receptor may protect peritubular capillaries under the ischemic insult, and serve a defensive role in the tubulointerstitium induced by renal microvascular injury

Crry, a complement regulatory protein, modulates renal interstitial disease induced by proteinuria11See Editorial by Quigg, p. 2315

Crry, a complement regulatory protein, modulates renal interstitial disease induced by proteinuria.BackgroundRecent studies have suggested a role for urinary complement components in mediating tubulointerstitial damage, which is known to have a good correlation with progression of chronic renal diseases. Although accumulating evidence suggests that complement regulatory proteins play an important protective role in glomeruli, their role in renal tubules remains unclear. In order to establish the role of a complement regulatory protein, Crry, in renal tubular injury, we employed a molecular biological approach to block the expression of Crry in tubules of animals with proteinuria induced with puromycin aminonucleoside nephritis (PAN).Methods and ResultsTwo different antisense oligodeoxynucleotides (ODNs) against Crry were designed and applied to cultured rat mesangial cells in vitro in order to establish their efficacy. Antisense ODN treatment resulted in decreased expression of Crry protein associated with increased sensitivity to complement attack in cell lysis assays compared with control ODN treatment or no treatment (44.7, 1.50, and 1.34%, respectively). Antisense ODNs did not affect the expression of Thy1 as a control, confirming the specificity of our ODNs. In vivo, we performed selective right renal artery perfusion to administer antisense ODNs to the kidney and showed prominent uptake of ODNs by proximal tubular cells. Reduced expression of Crry protein was demonstrated in proximal tubular cells in antisense ODNs-treated kidneys. Normal rats treated with the antisense ODNs did not show any pathological changes. However, in PAN, rats with massive proteinuria showed increased deposition of C3 and C5b-9 in tubules in antisense-treated kidneys, and histological assessment revealed more severe tubulointerstitial injury in antisense-treated animals compared with controls.ConclusionThese results establish a pathogenic role for complement in leading to tubulointerstitial injury during proteinuria and, to our knowledge for the first time, show a protective role of a complement regulatory protein, Crry, in renal interstitial disease