Separation of lymphocytes by electrophoresis under terrestrial conditions and at zero gravity, phase 3

Electrophoretic mobilities (EPM) of peripheral lymphocytes were studied from normal subjects, chronic hemodialysis patients and kidney transplant recipients. A technique to separate B lymphocytes and null cells from non-T lymphocyte preparation was developed. The experiments were designed to determine which subpopulation of the non-T lymphocytes is primarily affected and shows a decreased EPM in chronic hemodialysis patients and kidney transplant recipients

Kidney transplant nephrotic syndrome: Relationship between allograft histopathology and natural course

Kidney transplant nephrotic syndrome: Relationship between allograft histopathology and natural course. We analyzed clinical and pathologic data from 36 recipients of 38 renal allografts who developed nephrotic syndrome following transplantation. Three groups were identified on the basis of histologic changes in the graft, and each group had a distinct clinical course. Nine grafts (23.7%) had recurrent glomerulonephritis (GN) (5 membrano-proliferative, 4 focal glomerulosclerosis) and developed nephrotic syndrome at 5.1 months (mean) posttransplant. Renal function deteriorated rapidly, with a 2-year graft survival of 29.7%. Four grafts (10.5%) with de novo GN (3 epimembranous, 1 minimal change) developed nephrotic syndrome at 32 months post-transplant, and all functioned for more than 3 years. Twenty-five grafts (65.8%) had allograft glomerulopathy with the onset of nephrotic syndrome at 9.1 months posttransplant and a 2-year graft survival of 66.6%. The differences in duration of graft function between grafts with allograft glomerulopathy and recurrent GN (P < 0.01) and in graft survival rates at 2 years among the three groups (P < 0.05) are statistically significant. This analysis indicates that allograft glomerulopathy is the most common cause of kidney transplant nephrotic syndrome. Membranopro-liferative GN and focal glomerulosclerosis may recur soon after transplantation and rapidly progress to renal failure in marked contrast to grafts with either de novo epimembranous nephropathy or minimal glomerular change, lesions that are compatible with prolonged graft function.Syndrome néphrotique du rein transplanté: Relations entre l'histopathologies de l'allogreffe et l'évolution. Nous avons analysé les dossiers cliniques et anatomo-pathologiques de 36 receveurs de 38 allogreffes qui ont développé un syndrome néphrotique après transplantation. Trois groupes ont été identifiés sur la base des modifications histologiques de la greffe et chaque groupe a eu une évolution distincte. Neuf greffes (23,7%) ont eu une récidive de glomérulonéphrite (GN) (5 membrano-prolifératives, 4 gloméruloscléroses focales) et ont développé un syndrome néphrotique 5,1 mois (moyenne) après la transplantation. La fonction rénale s'est détériorée rapidement, avec une survie de la greffe à 2 ans de 29,7%. Quatre greffes (10,5%) atteintes de GN nouvelle (3 extra-membraneuses, 1 à modifications minimes) ont développé un syndrome néphrotique 32 mois après la transplantation et ont toutes fonctionné plus de 3 ans. Vingt cinq greffes (65,8%) ont eu une glomérulopathie de greffe avec l'installation d'un syndrome néphrotique à 9,1 mois après la transplantation et une survie de la greffe à 2 ans de 66,6%. Les différences de durée du fonctionnement de la greffe selon l'atteinte par une récidive de GN ou une glomérulopathie de greffe (P < 0,01) et dans la survie des greffes à 2 ans dans les trois groupes (P < 0,05) sont statistiquement significatives. Cette analyse indique que la glomérulonéphrite de la greffe est la cause la plus répandue de syndrome néphrotique du rein transplanté. La GN membrano-proliférative et la glomérulosclérose focale peuvent récidiver précocement après la transplantation et progresser rapidement vers l'insuffisance rénale à la différence des greffes atteintes de néphropathie extramembraneuse ou de modifications minimes, lésions compatibles avec une fonction prolongée de la greffe

Fermentation by Lactobacillus enhances anti-inflammatory effect of Oyaksungisan on LPS-stimulated RAW 264.7 mouse macrophage cells

<p>Abstract</p> <p>Background</p> <p>Oyaksungisan (OY) has been used as a traditional drug in east-Asian countries. However, its effect on inflammation still remains unknown. In this study, to provide insight into the biological effects of OY and OY fermented by <it>Lactobacillus</it>, we investigated their effects on lipopolysaccharide (LPS)-mediated inflammation in the RAW 264.7 murine macrophage cells.</p> <p>Methods</p> <p>The investigation was focused on whether OY and fermented OYs could inhibit the production of pro-inflammatory mediators such as nitric oxide (NO) and prostaglandin (PG) E₂as well as the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, tumor necrosis factor (TNF)-α, interleukin (IL)-6, nuclear factor (NF)-κB and mitogen-activated protein kinases (MAPKs) in LPS-stimulated RAW 264.7 cells.</p> <p>Results</p> <p>We found that OY inhibits a little LPS-induced NO, PGE₂, TNF-α and IL-6 productions as well as the expressions of iNOS and COX-2. Interestingly, the fermentation significantly increased its inhibitory effect on the expression of all pro-inflammatory mediators. Furthermore, the fermented OYs exhibited elevated inhibition on the translocation of NF-κB p65 through reduced IκBα degradation as well as the phosphorylations of extracellular signal-regulated kinase (ERK), p38 and c-Jun NH₂-terminal kinase (JNK) MAPKs than untreated control or original OY.</p> <p>Conclusions</p> <p>Finally, the fermentation by <it>Lactobacillus </it>potentiates the anti-inflammatory effect of OY by inhibiting NF-κB and MAPK activity in the macrophage cells.</p

Complete Genome Sequence of Weissella koreensis KACC 15510, Isolated from Kimchi

Weissella koreensis KACC 15510 was isolated from kimchi, a representative traditional Korean fermented food. Here, we announce the complete genome sequence of W. koreensis KACC 15510, consisting of a 1,422,478-bp chromosome and one 18,992-bp plasmid, and provide a description of their annotation