147 research outputs found
Assessment of hemostatic profile in neonates with necrotizing enterocolitis using Rotational Thromboelastometry (ROTEM)
Background: This study aimed to explore the hemostatic profile of neonates with necrotizing enterocolitis (NEC) using Rotational Thromboelastometry (ROTEM) and to investigate if ROTEM parameters have the capacity to play a role in the differentiation of NEC from sepsis at the disease onset. Methods: This observational study included 62 neonates (mean gestational age 31.6 weeks and mean birth weight 1620g) hospitalized in a neonatal intensive care unit. The neonates were categorized in three groups: neonates with NEC (Bell stage II and above), neonates with sepsis and healthy neonates and they were matched 1:1:1 with regards to gestational age, delivery mode, and sex. Clinical, laboratory data as well as measurements of ROTEM parameters at disease onset were recorded. Results: ROTEM parameters differed between neonates with NEC and neonates with sepsis, indicating that NEC results in accelerated clot formation and higher clot strength compared to sepsis. The EXTEM CFT and A10 parameters demonstrated the highest diagnostic performance for NEC in terms of discrimination between NEC and sepsis (AUC, 0.997; 95% CI: 0.991–1.000 and 0.973; 95% CI: 0.932–1.000, respectively). Conclusions: Neonates with NEC manifested accelerated clot formation and higher clot strength compared to septic and healthy neonates, as these were expressed by ROTEM parameters. Impact: This work reports data on the hemostatic profile of neonates with necrotizing enterocolitis (NEC) using Rotational Thromboelastometry (ROTEM) and the capacity of ROTEM parameters in differentiating of NEC from sepsis at the disease onset. Neonates with NEC present acceleration of coagulation and exhibit a hypercoagulable profile, as this is expressed by ROTEM parameters, in comparison to septic and healthy neonates. ROTEM parameters demonstrated a good diagnostic capacity in differentiating NEC from sepsis at the disease onset. © The Author(s), under exclusive licence to the International Pediatric Research Foundation, Inc 2023
"Simha Rotem (1924-2018): Ad memoriam. The broom and the resilience"
Simha Rotem was born in Warsaw in 1924. He was one of the most important member of the Warsaw
Ghetto uprising in April 1943. Under the cover name of Kazik. He was a leader of the young Jews who were one of the
first in Europe to rebel against the Nazi occupation. His original name is Symon Rathajzer, who upon his arrival in
Israel he changed in Simha Rotem to symbolize a new beginning. His heroic and history is full of anecdotes that
encroach of the unbelievable. Rotem came in and out of the ghetto, through the city’s sewers, besieged and burned, to
bringing news and organizing the escape of the few survivors. Thanks to him the last fighters of the ghetto succeeded in
acriding the “Aryan” area of the city, finding refuge from not Jewish people connected with the Polish resistance. In
1944 Rotem fighted in the Warsaw uprising against the Nazi occupation. He was one of the leader of the Jewish exodus
from Poland to Israel. He contributed to save thousands of people. The author died in Jerusalem in 2018
Measuring message gossiping in P2P networks and providing incentives in cryptocurrencies
Thesis: M. Eng., Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science, 2018.This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.Cataloged from student-submitted PDF version of thesis.Includes bibliographical references (pages 47-48).In this thesis, we present Plutus, an efficient and game-theoretically proven incentive mechanism for Algorand, a proof-of-stake cryptocurrency. In order to operate, Algorand requires users to constantly propagate messages but has no mechanism to incentivize users to do so. Plutus solves this problem by keeping track of each message propagation path and rewarding the users who propagated messages using a lottery. We implemented a prototype of Plutus on top of Algorand to measure the performance and overhead of Plutus. Experimental results show that with Plutus, Algorand's block confirmation time increases by only 7% and that there is no penalty on Algorand's scalability.by Rotem Hemo.M. Eng
GILA, a Replacement for the Soft‐Agar Assay that Permits High‐Throughput Drug and Genetic Screens for Cellular Transformation
Astrocyte immunometabolic regulation of the tumour microenvironment drives glioblastoma pathogenicity
Abstract
Malignant brain tumours are the cause of a disproportionate level of morbidity and mortality among cancer patients, an unfortunate statistic that has remained constant for decades. Despite considerable advances in the molecular characterization of these tumours, targeting the cancer cells has yet to produce significant advances in treatment. An alternative strategy is to target cells in the glioblastoma microenvironment, such as tumour-associated astrocytes. Astrocytes control multiple processes in health and disease, ranging from maintaining the brain’s metabolic homeostasis, to modulating neuroinflammation. However, their role in glioblastoma pathogenicity is not well understood. Here we report that depletion of reactive astrocytes regresses glioblastoma and prolongs mouse survival. Analysis of the tumour-associated astrocyte translatome revealed astrocytes initiate transcriptional programmes that shape the immune and metabolic compartments in the glioma microenvironment. Specifically, their expression of CCL2 and CSF1 governs the recruitment of tumour-associated macrophages and promotes a pro-tumourigenic macrophage phenotype. Concomitantly, we demonstrate that astrocyte-derived cholesterol is key to glioma cell survival, and that targeting astrocytic cholesterol efflux, via ABCA1, halts tumour progression. In summary, astrocytes control glioblastoma pathogenicity by reprogramming the immunological properties of the tumour microenvironment and supporting the non-oncogenic metabolic dependency of glioblastoma on cholesterol. These findings suggest that targeting astrocyte immunometabolic signalling may be useful in treating this uniformly lethal brain tumour.</jats:p
A Transitional Gundi (Rodentia: Ctenodactylidae) from the Miocene of Israel
abstract: We describe a new species of gundi (Rodentia: Ctenodactylidae: Ctenodactylinae), Sayimys negevensis, on the basis of cheek teeth from the Early Miocene of the Rotem Basin, southern Israel. The Rotem ctenodactylid differs from all known ctenodactylid species, including Sayimys intermedius, which was first described from the Middle Miocene of Saudi Arabia. Instead, it most resembles Sayimys baskini from the Early Miocene of Pakistan in characters of the m1-2 (e.g., the mesoflexid shorter than the metaflexid, the obliquely orientated hypolophid, and the presence of a strong posterolabial ledge) and the upper molars (e.g., the paraflexus that is longer than the metaflexus). However, morphological (e.g., presence of a well-developed paraflexus on unworn upper molars) and dimensional (regarding, in particular, the DP4 and M1 or M2) differences between the Rotem gundi and Sayimys baskini distinguish them and testify to the novelty and endemicity of the former. In its dental morphology, Sayimys negevensis sp. nov. shows a combination of both the ultimate apparition of key-characters and incipient features that would be maintained and strengthened in latter ctenodactylines. Thus, it is a pivotal species that bridges the gap between an array of primitive ctenodactylines and the most derived, Early Miocene and later, gundis.The article is published at http://journals.plos.org/plosone/article?id=10.1371/journal.pone.015180
The Angiostrongylus vasorum excretory/secretory and surface proteome contains putative modulators of the host coagulation
Angiostrongylus vasorum is a cardiopulmonary nematode of canids and is, among others, associated with bleeding disorders in dogs. The pathogenesis of such coagulopathies remains unclear. A deep proteomic characterization of sex specific A. vasorum excretory/secretory proteins (ESP) and of cuticular surface proteins was performed, and the effect of ESP on host coagulation and fibrinolysis was evaluated in vitro. Proteins were quantified by liquid chromatography coupled to mass spectrometry and functionally characterized through gene ontology and pathway enrichment analysis. In total, 1069 ESP (944 from female and 959 from male specimens) and 1195 surface proteins (705 and 1135, respectively) were identified. Among these were putative modulators of host coagulation, e.g., von Willebrand factor type D domain protein orthologues as well as several proteases, including serine type proteases, protease inhibitors and proteasome subunits. The effect of ESP on dog coagulation and fibrinolysis was evaluated on canine endothelial cells and by rotational thromboelastometry (ROTEM). After stimulation with ESP, tissue factor and serpin E1 transcript expression increased. ROTEM revealed minimal interaction of ESP with dog blood and ESP did not influence the onset of fibrinolysis, leading to the conclusion that Angiostrongylus vasorum ESP and surface proteins are not solely responsible for bleeding in dogs and that the interaction with the host’s vascular hemostasis is limited. It is likely that coagulopathies in A. vasorum infected dogs are the result of a multifactorial response of the host to this parasitic infection.University of Zurich, SwitzerlandBusiness Unit Animal Health, German
Abstract 600: Melanoma and ovarian cancer cells tested for drug sensitivity using anchorage-independent growth
Inhibition of miR-193a Expression by Max and RXRα Activates K-Ras and PLAU to Mediate Distinct Aspects of Cellular Transformation
Abstract
MicroRNA profiling in isogenic models of cellular transformation involving either breast epithelial cells or fibroblasts reveals that expression of miR-193a is lower in transformed cells than in nontransformed cells. The transcription factors Max and RXRα bind directly to the miR-193a promoter and inhibit miR-193a expression during transformation. miR-193a inhibits cellular transformation by directly targeting the 3′ untranslated regions of PLAU and K-Ras. Interestingly, miR-193a controls anchorage-independent growth in soft agar through K-Ras, whereas it affects invasive growth through PLAU. miR-193a overexpression inhibits the tumorigenicity of developmentally diverse but not all cancer cell types, and it inhibits tumor growth in colon- and breast-derived xenografts. Finally, expression of miR-193a is inversely correlated with PLAU and K-Ras in human colon adenocarcinomas. Thus, a pathway in which Max and RXRα inhibit miR-193a expression, thereby activating the PLAU and K-Ras oncogenes is important for distinct aspects of cellular transformation, as well as tumor growth and colon (and perhaps other types of) cancer. Cancer Res; 71(15); 5144–53. ©2011 AACR.</jats:p
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