Results 41 to 50 of about 17,473,500 (289)

Therapeutic Apheresis in Nigeria: A Multi‐Center Summary of Abstracts From the Inaugural Nigerian Society for Apheresis Scientific Meeting

open access: yesTherapeutic Apheresis and Dialysis, EarlyView.
ABSTRACT Background Therapeutic apheresis (TA) is an established treatment modality for hematologic, neurologic, and immunologic disorders, yet access remains severely limited in sub‐Saharan Africa. Donor apheresis, including platelet apheresis collection from healthy donors, represents an important complementary modality supporting blood product ...
Nosa Bazuaye   +33 more
wiley   +1 more source

Hegel and the Sciences of Spirit (Geisteswissenschaften) [PDF]

open access: yes, 2023
Brolly. Journal of Social Sciences | ISSN (print) 2516-869X; ISSN (online) 2516-8703 | eSupplement - November 2023 - Brolly+ | Hegel and the Sciences of Spirit (Geisteswissenschaften) | *This eSupplement reproduces: Hegel and the Sciences of Spirit ...
Onu, Mădălin
core   +1 more source

Peripheral lysosomes recruit PLEKHG3 to focal adhesions and restrain protrusion dynamics

open access: yesFEBS Letters, EarlyView.
Proximity‐dependent labeling at the LAMTOR complex revealed the Rho GEF PLEKHG3 as a lysosome‐proximal protein directing the study toward the influence of lysosome positioning on actin dynamics and cell motility. We show that PLEKHG3 colocalizes with lysosomes at focal adhesion sites and observe that forced peripheral dispersion of lysosomes hinders ...
Rainer Ettelt   +8 more
wiley   +1 more source

Golgi enzymes are retrieved from the plasma membrane to the trans‐Golgi network

open access: yesFEBS Letters, EarlyView.
Golgi enzymes are traditionally considered resident proteins retained within the Golgi apparatus. Here, we demonstrate that a subset transiently reaches the cell surface and is subsequently retrieved to the trans‐Golgi network via retrograde transport. Using a nanobody‐based toolkit, we uncover a dynamic trafficking cycle of several Golgi enzymes.
Dominik P. Buser, Tina Junne
wiley   +1 more source

Translophagy—A potential link between autophagy impairment and translational errors

open access: yesFEBS Letters, EarlyView.
Neurodegenerative diseases are characterised by the accumulation of abnormal proteins and protein aggregates, but their origin often remains unknown. We propose that selective autophagy removes damaged protein‐making machinery, preventing errors during protein synthesis.
Mykola V. Korolchuk   +11 more
wiley   +1 more source

Books for an Open Society - Experts' View

open access: yesKnygotyra, 2003
Evaluation of the academic literature publishing in Lithuania was twofold. Some of the experts estimated situation as critical, others stressed the obvious improvement in the field of academic publishing.
Arūnas Poviliūnas
doaj   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder   +10 more
wiley   +1 more source

Predators and hijackers in academic publishing

open access: yesEuropean Journal of General Practice, 2015
A theme that has recently received increasing attention in medical publishing is predatory journals.
Igor, Švab, Irena, Makivić
openaire   +2 more sources

Publishing 101: The Basics of Academic Publishing [PDF]

open access: yesThe Serials Librarian, 2008
ABSTRACT Rolnik's preconference went well beyond the “business of publishing from a very basic perspective” as described in the conference program. Rolnik's preconference described the publishing market, operations within publishing companies, and how publishers find content. Dr.
Zachary Rolnik   +2 more
openaire   +1 more source

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

open access: yesMolecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu   +13 more
wiley   +1 more source

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