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Maternal cell-free DNA in early pregnancy for preeclampsia screening: a systematic review.

Arch Gynecol Obstet

January 2025

Faculty of Medicine and Health Sciences, Tel Aviv University, Tel Aviv, Israel.

Purpose: To quantify the separation between maternal blood cell-free (cf)DNA markers in preeclampsia and unaffected pregnancies and compare with existing markers. This approach has not been used in previous studies.

Methods: Comprehensive systematic literature search of PubMed to identify studies measuring total cfDNA, fetal cf(f)DNA or the fetal fraction (FF) in pregnant women.

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Milk-derived bioactive peptides in insulin resistance and type 2 diabetes.

J Nutr Biochem

January 2025

Neurobiology of Nutrition Laboratory, Department of Nutritional Sciences, College of Human Sciences, Texas Tech University, Lubbock, TX 79409, USA. Electronic address:

Diabetes is a global health issue affecting over 6% of the world and 11 % of the US population. It is closely linked to insulin resistance, a pivotal factor in Type 2 diabetes development. This review explores a promising avenue for addressing insulin resistance through the lens of Milk-Derived Bioactive Peptides (MBAPs).

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Red blood cells (RBCs) serve as natural transporters and can be modified to enhance the pharmacokinetics and pharmacodynamics of a protein cargo. Affinity targeting of Factor IX (FIX) to the RBC membrane is a promising approach to improve the (pro)enzyme's pharmacokinetics. For RBC targeting, purified human FIX was conjugated to the anti-mouse glycophorin A monoclonal antibody Ter119.

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Synapse dysfunction is an early event in Alzheimer's disease (AD) caused by various factors such as Amyloid beta, p-tau, inflammation, and aging. However, the exact molecular mechanism of synapse dysfunction in AD is largely unknown. To understand this, we comprehensively analyzed the synaptosome fraction in postmortem brain samples from AD patients and cognitively normal individuals.

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The folded auto-inhibited state of kinesin-1 is stabilized by multiple weak interactions and binds weakly to microtubules. Here we investigate the extent to which homodimeric kinesin-1 lacking light chains is activated by the dynein activating adaptor BicD. We show that one or two kinesins can bind to the central region of BicD (CC2), a region distinct from that which binds dynein-dynactin (CC1) and cargo-adaptor proteins (CC3).

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