מנהיג חמאס בעזה: “נסיים את המצור בכל האמצעים”

They, Azza citizens.  they are living  already in the Holy Land of the Bible –  what they want more from the Globe?
Only kill   the neighbours??
They  want “to finish the siege  by any means”-
WHEN  they  begin  to  take care about every corner of   the Holy Land they  now keep and own?
THE Ancient Azza  was the area of Juda and Simeon tribes, the Sons of  Jacob and Lea.
The  border of  Juda  was  even  a bit more southward, to the BROOK  of Egypt,  in the midst of Sinai. 
THERE REALLY  ARE MUCH PLACE FOR  MANY PEOPLE WHO WANTS PEACE AND TO TAKE CARE OF THE NATURE AND OLD  BIBLICAL AREA and prosper.

https://www.kidney-international.org/article/S0085-2538(18)30281-3/fulltext

https://www.ncbi.nlm.nih.gov/pubmed/?term=Karpman%2C+Bekassy.+Aliskire

Aliskiren inhibits renin-mediated complement activation.

Abstract

Certain kidney diseases are associated with complement activation although a renal triggering factor has not been identified.

Here we demonstrated that renin, a kidney-specific enzyme, cleaves C3 into C3b and C3a, in a manner identical to the C3 convertase. Cleavage was specifically blocked by the renin inhibitor aliskiren. Renin-mediated C3 cleavage and its inhibition by aliskiren also occurred in serum. Generation of C3 cleavage products was demonstrated by immunoblotting, detecting the cleavage product C3b, by N-terminal sequencing of the cleavage product, and by ELISA for C3a release. Functional assays showed mast cell chemotaxis towards the cleavage product C3a and release of factor Ba when the cleavage product C3b was combined with factor B and factor D. The renin-mediated C3 cleavage product bound to factor B. In the presence of aliskiren this did not occur, and less C3 deposited on renin-producing cells. The effect of aliskiren was studied in three patients with dense deposit disease and this demonstrated decreased systemic and renal complement activation (increased C3, decreased C3a and C5a, decreased renal C3 and C5b-9 deposition and/or decreased glomerular basement membrane thickness) over a follow-up period of four to seven years. Thus, renin can trigger complement activation, an effect inhibited by aliskiren. Since renin concentrations are higher in renal tissue than systemically, this may explain the renal propensity of complement-mediated disease in the presence of complement mutations or auto-antibodies.

Video: Näin rakettimoottori jumittui kantorakettiin – Sojuz-onnettomuuden syy selvisi nopeasti: miehitetyt lennot jatkuvat jo joulukuussa

TEKNIIKKA &TALOUS: Kolme viikkoa sitten yhdysvaltalaisen astronautin ja venäläisen kosmonautin matka kansainväliselle avaruusasemalle keskeytyi Sojuz-raketin vian vuoksi. Miehet selvisivät onnettomuudesta Sojuzin hätäjärjestelmien avulla.

Venäläisviranomaiset ovat selvittäneet, mikä aiheutti kantoraketin vian 118 sekuntia lähdön jälkeen. Tutkimusten mukaan yksi Sojuzin neljästä rakettimoottorista oli vioittunut kokoamisvaiheessa, minkä vuoksi moottori ei irtaantunut raketin rungosta suunnitellusti, vaan jäi hetkeksi kiinni raketin runkoon. Tämä aiheutti raketin pyörimisen ja laukaisun keskeyttämisen.

Sojuzin kyljessä olevat neljä rakettimoottoria irtoavat nousun aikana. Tällä kertaa kokoamisvaiheessa yhden moottorin kosketusanturi oli vääntynyt kuusi astetta, mikä jumitti moottorin hetkeksi raketin runkoon.

Venäjän avaruusjärjestö Roscosmos on ohjeistanut raketin kokoamiskäytännöt ja tarkistusrutiinit uudestaan. Myös jo kootut kantoraketit kootaan uudelleen.

Onnettomuuden syyn varmistuttua miehitettyjen lentojen on määrä jatkua joulukuun 3. päivä.

Sojuz on tällä hetkellä ainoa alus, joka kykenee kuljettamaan miehistöä kansainväliselle avaruusasemalle. Yhdysvalloissa SpaceX ja Boeing kehittävät miehitettyihin lentoihin kykeneviä aluksia Nasalle. Yhtiöiden on määrä aloittaa testilennot ensi vuonna. Alusten kehitystyö on viivästynyt useita kertoja.

Roscosmos on laukaissut onnettomuuden jälkeen kaksi miehittämätöntä Sojuz-lentoa.

Nasa puolestaan on kiitellyt Venäjän Roscosmosia avoimuudesta onnettomuuden syyn selvittämisessä.

Roscosmos julkaisi aiemmin uutta videomateriaalia onnettomuudesta, jossa näkyy, miten rakettimoottori jumittuu silmänräpäykseksi runkoon.

https://www.lu.se/article/koden-knackt-for-det-sista-blodgruppssystemet

2018 Jul 19;132(3):334-338. doi: 10.1182/blood-2018-03-842542. Epub 2018 May 10.

Disruption of a GATA1-binding motif upstream of XG/PBDX abolishes Xga expression and resolves the Xg blood group system.

Abstract

The Xga blood group is differentially expressed on erythrocytes from men and women. The underlying gene, PBDX, was identified in 1994, but the molecular background for Xga expression remains undefined. This gene, now designated XG, partly resides in pseudoautosomal region 1 and encodes a protein of unknown function from the X chromosome. By comparing calculated Xga allele frequencies in different populations with 2612 genetic variants in the XG region, rs311103 showed the strongest correlation to the expected distribution. The same single-nucleotide polymorphism (SNP) had the most significant impact on XG transcript levels in whole blood (P = 2.0 × 10-22). The minor allele, rs311103C, disrupts a GATA-binding motif 3.7 kb upstream of the transcription start point. This silences erythroid XG messenger RNA expression and causes the Xg(a-) phenotype, a finding corroborated by SNP genotyping in 158 blood donors. Binding of GATA1 to biotinylated oligonucleotide probes with rs311103G but not rs311103C was observed by electrophoretic mobility shift assay and proven by mass spectrometry. Finally, a luciferase reporter assay indicated this GATA motif to be active for rs311103G but not rs311103C in HEL cells. By using an integrated bioinformatic and molecular biological approach, we elucidated the underlying genetic basis for the last unresolved blood group system and made Xga genotyping possible.

PMID:
29748255
DOI:
10.1182/blood-2018-03-842542

http://lemaanzion.se/understanding-our-time/

Isaiah 60: 17 (Your Redeemer , the Mighty One of Jacob says) …

“I will make your overseers PEACE

and your taskmasters RIGHTEOUSNESS.

Violence shall no more be heard in YOUR LAND,

devastation  or destruction within YOUR BORDERS;

you shall call YOUR   WALLS SALVATION,

and YOUR GATES PRAISE.”

 

WHO Weekly rapport

November 7, 2018

http://apps.who.int/iris/bitstream/handle/10665/275719/WER9344.pdf

CHI3L1 , synonym YKL-40

November 7, 2018

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5575189/

http://ar.iiarjournals.org/content/38/6/3357

Background/Aim: An increased level of chitinase 3 like 1 protein (CHI3L1) expression is observed in patients with cancer and may have potential prognostic value.

https://jeccr.biomedcentral.com/articles/10.1186/s13046-018-0876-2

The roles of CHI3L1/CD44 axis in GC metastasis were investigated in GC cell lines and experimental animal model by gain and loss of function.

CHI3L1 binding to CD44v3 activates Erk, Akt, and β-catenin signaling, therefore enhances GC metastasis. CHI3L1 expression is a novel biomarker for the prognosis of GC, and these findings have thus identified CHI3L1/CD44 axis as a vital pathway and potential therapeutic target in GC.

Gastric cancer (GC) remains the second leading cause of cancer-related mortality worldwide, with the invasion and metastasis of GC constituting the major reason underlying its poor prognosis. Lymph node metastasis presents in over 50% of patients with GC when initially diagnosed, whereas peritoneum metastasis might be already present in 5% to 20% of patients undergoing gastric resection with curative intent [1]. GC develops and metastasizes as a result of the accumulation of multiple genetic and epigenetic changes. Thus, a greater understanding of how key molecular and cellular regulators drive GC invasion and metastasis is required.

WHO Bulletin

November 6, 2018

http://www.who.int/bulletin/volumes/96/11/17-206227.pdf?ua=1

Bull World Health Organ
2018;96:738–749
|
doi: http://dx.doi.org/10.2471/BLT.17.206227
Research 738
Introduction
Tuberculosis is a major global public health concern.
In 2016, the World Health Organization (WHO) estimated that there were 10.4 million new tuberculosis patients worldwide and 1.8 million tuberculosis-related deaths.
Diabetes mellitus affects the host immune response to tuberculosis, and people with diabetes have a threefold increased risk of developing active tuberculosis.
In 2015, the International Diabetes Federa tion estimated that there were 415 million adults living with diabetes mellitus worldwide, many undiagnosed, and mostly living in low- and middle-income countries where there is often a high burden of tuberculosis.
Diabetes patients with concurrent tuberculosis also have poorer tuberculosis treatment outcomes, so it is important to identify these patients promptly to optimize treatment
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