Publications by authors named "Ganz T"

Objectives: The primary objective was to determine iron deficiency (ID) anemia (IDA) monitoring practices in children during PICU stay. A secondary objective was to determine the current follow-up practices for IDA after PICU discharge.

Design: Retrospective observational study of 2 years (2021-2022).

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Extensive neovascularization is a hallmark of glioblastoma (GBM). In addition to supplying oxygen and nutrients, vascular endothelial cells provide trophic support to GBM cells via paracrine signaling. Here we report that Endocan (ESM1), an endothelial-secreted proteoglycan, confers enhanced proliferative, migratory, and angiogenic properties to GBM cells and regulates their spatial identity.

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Anemia is a common and disabling complication of chronic kidney disease (CKD). Current therapies can be burdensome, and full correction of anemia is limited by cardiovascular side effects. New approaches that may offer additional therapeutic options are needed.

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Objectives: Psychological stress has been suggested as a contributory factor in the onset and progression of multiple sclerosis (MS). The 7 October 2023 terrorist attacks in Israel caused significant psychological stress, providing a unique context to study its impact on MS activity. This study aims to assess the impact of war-related psychological stress on MS activity using magnetic resonance imaging (MRI) scans and clinical follow-up.

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  • The study examines how predator hunting strategies (stalking by cougars and coursing by wolves) affect the movement behaviors of both predators and their ungulate prey in eastern Washington.
  • Using hidden Markov models on data from over 400 GPS-collared animals, researchers found that while predators adjusted their movements based on prey type, ungulates reduced their movement in areas with large predators, regardless of the predator's strategy.
  • The results indicate that predator and prey movements are influenced more by long-term patterns of risk and resource distribution than by specific hunting behaviors, highlighting the complexity of interactions in multi-predator, multi-prey systems.
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Demyelination and axonal injury in chronic-progressive Multiple Sclerosis (MS) are presumed to be driven by a neurotoxic bystander effect of meningeal-based myeloid infiltrates. There is an unmet clinical need to attenuate disease progression in such forms of CNS-compartmentalized MS. The failure of systemic immune suppressive treatments has highlighted the need for neuroprotective and repair-inducing strategies.

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Iron is an essential nutrient and a constituent of ferroproteins and enzymes crucial for human life. Generally, nonmenstruating individuals preserve iron very efficiently, losing less than 0.1% of their body iron content each day, an amount that is replaced through dietary iron absorption.

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  • Multiple sclerosis (MS) treatment strategies have typically focused on either immune modulation or promoting regeneration through oligodendrocyte progenitor cells (OPCs), which are essential for myelin generation in the central nervous system.
  • Recent findings reveal that OPCs also play critical roles in the immune response, suggesting that inflammation can actually enhance their ability to promote myelination in a chronically inflamed CNS.
  • The review proposes a balanced therapeutic approach that integrates both pro-myelinating and immune-modulating functions of OPCs, indicating that indiscriminate immune suppression may hinder their effectiveness.
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  • Vadadustat is an oral medication being researched for treating anemia in patients with chronic kidney disease (CKD) by inhibiting a specific enzyme involved in oxygen regulation.
  • The studies involved healthy volunteers receiving varying doses of vadadustat to assess how the drug is processed in the body (pharmacokinetics), its effects (pharmacodynamics), and safety.
  • Results showed that vadadustat increased levels of erythropoietin (EPO), a hormone that stimulates red blood cell production, and had mild side effects, supporting its potential for treating CKD-related anemia.
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Large terrestrial mammals increasingly rely on human-modified landscapes as anthropogenic footprints expand. Land management activities such as timber harvest, agriculture, and roads can influence prey population dynamics by altering forage resources and predation risk via changes in habitat, but these effects are not well understood in regions with diverse and changing predator guilds. In northeastern Washington state, USA, white-tailed deer (Odocoileus virginianus) are vulnerable to multiple carnivores, including recently returned gray wolves (Canis lupus), within a highly human-modified landscape.

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Key Points: Serum ferritin was the strongest independent correlate of greater marrow iron stores in children with kidney failure supported by dialysis. Compared with current clinical guideline-based cutoffs for iron deficiency, ferritin outperforms these cut points for stainable marrow iron stores.

Background: Iron deficiency is common in children with kidney failure, but current guidelines are based on biomarkers of iron stores that may be influenced by inflammation.

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Alzheimer's disease (AD) is a devastating neurodegenerative disorder affecting millions worldwide. Emerging research has challenged the conventional notion of a direct correlation between amyloid deposition and neurodegeneration in AD. Recent studies have suggested that amyloid and Tau deposition act as a central nervous system (CNS) innate immune driver event, inducing chronic microglial activation that increases the susceptibility of the AD brain to the neurotoxicity of infectious insults.

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Aims: Among persons with prevalent heart failure (HF), iron deficiency has been linked to HF admissions, and intravenous iron replacement improves HF outcomes. Recent studies in persons with chronic kidney disease (CKD) demonstrate that iron deficiency is associated with incident HF. This study aimed to determine the relationship of iron status with incident HF in community-dwelling older adults irrespective of their kidney function.

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Primum non nocere! Can iron deficiency, an abnormality that causes anemia, benefit people with sickle cell disease (SCD) who already have an anemia? The published literature we review appears to answer this question in the affirmative: basic science considerations, animal model experiments, and noncontrolled clinical observations all suggest a therapeutic potential of iron restriction in SCD. This is because SCD's clinical manifestations are ultimately attributable to the polymerization of hemoglobin S (HbS), a process strongly influenced by intracellular HbS concentration. Even small decrements in HbS concentration greatly reduce polymerization, and iron deficiency lowers erythrocyte hemoglobin concentration.

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To manage predation risk, prey navigate a dynamic landscape of fear, or spatiotemporal variation in risk perception, reflecting predator distributions, traits, and activity cycles. Prey may seek to reduce risk across this landscape using habitat at times and in places when predators are less active. In multipredator landscapes, avoiding one predator could increase vulnerability to another, making the landscape of fear difficult to predict and navigate.

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As a functional component of erythrocyte hemoglobin, iron is essential for oxygen delivery to all tissues in the body. The liver-derived peptide hepcidin is the master regulator of iron homeostasis. During anemia, the erythroid hormone erythroferrone regulates hepcidin synthesis to ensure the adequate supply of iron to the bone marrow for red blood cell production.

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Current iron overload therapeutics have inherent drawbacks including perpetuated low hepcidin. Here, we unveiled that lactate, a potent hepcidin agonist, effectively reduced serum and hepatic iron levels in mouse models of iron overload with an improved erythropoiesis in β-thalassemic mice.

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Hyperlactatemia and anemia commonly coexist and their crosstalk is a longstanding mystery with elusive mechanisms involved in physical activities, infections, cancers, and genetic disorders. For instance, hyperlactatemia leads to iron restriction by upregulating hepatic hepcidin expression. Increasing evidence also points to lactate as a crucial signaling molecule rather than merely a metabolic byproduct.

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Background: Murine data suggest that the placenta downregulates ferroportin (FPN) when iron is limited to prioritize iron for its own needs. Human data on the impact of maternal and neonatal iron status on placental FPN expression are conflicting.

Objectives: This study aimed to identify determinants of placental FPN protein abundance and to assess the utility of the placental iron deficiency index (PIDI) as a measure of maternal/fetal iron status in newborns at high risk for anemia.

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Iron delivery to the plasma is closely coupled to erythropoiesis, the production of red blood cells, as this process consumes most of the circulating plasma iron. In response to hemorrhage and other erythropoietic stresses, increased erythropoietin stimulates the production of the hormone erythroferrone (ERFE) by erythrocyte precursors (erythroblasts) developing in erythropoietic tissues. ERFE acts on the liver to inhibit bone morphogenetic protein (BMP) signaling and thereby decrease hepcidin production.

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Remyelination failure is considered a major obstacle in treating chronic-progressive multiple sclerosis (MS). Studies have shown blockage in the differentiation of resident oligodendrocyte progenitor cells (OPC) into myelin-forming cells, suggesting that pushing OPC into a differentiation program might be sufficient to overcome remyelination failure. Others stressed the need for a permissive environment to allow proper activation, migration, and differentiation of OPC.

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Overproduction of lactate (LA) can occur during exercise and in many diseases such as cancers. Individuals with hyperlactatemia often display anemia, decreased serum iron, and elevated hepcidin, a key regulator of iron metabolism. However, it is unknown whether and how LA regulates hepcidin expression.

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