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Under these conditions, autophagy may become essential for viability.
These findings suggest that autophagy activation via CREG1 may be a viable therapeutic strategy autophagy for improving cardiac performance under pathologic conditions.
There appears to be scientific merit to the claim that creatine is ergogenic when taken in large amounts.

Related Questions

Does creatine work?5 answersCreatine supplementation has been shown to have positive effects on exercise and sports performance, including increases in maximal strength, power production, sprint performance, and fat-free mass. It can also speed up recovery time between bouts of intense exercise by mitigating muscle damage and promoting faster recovery. However, there are contradictory findings regarding the potential ergogenic benefits of creatine during endurance-type exercise and in activities where an increase in body mass may hinder performance. Creatine supplementation can enhance glycogen resynthesis and content, lower inflammation and oxidative stress, and potentially increase mitochondrial biogenesis, which may contribute to improved endurance performance. Additionally, creatine has been found to play key roles in the brain, including buffering energy supply, improving mitochondrial efficiency, acting as an anti-oxidant, and acting as a neuroprotectant. Studies have consistently shown that creatine supplementation is safe and well tolerated in healthy individuals and in various patient populations. Early clinical trials also indicate that creatine may have efficacy as an antidepressant agent.
What are the effects of creatine on health?5 answersFoi demonstrado que a suplementação de creatina tem vários efeitos na saúde. Pode aumentar a capacidade de energia anaeróbica, a síntese protéica e a massa muscular, levando a um melhor desempenho físico. A creatina também pode ter benefícios terapêuticos potenciais para condições como diabetes, sarcopenia, osteoporose, câncer, reabilitação e saúde pulmonar e cardiovascular. Além disso, a creatina tem se mostrado promissora na atenuação dos sintomas de concussão, lesão cerebral traumática leve e depressão. Também foi descoberto que desempenha um papel crítico no metabolismo celular e pode melhorar a recuperação de lesões e controlar doenças crônicas. Além disso, a creatina exibe efeitos antioxidantes e antiinflamatórios e pode ter potencial como terapia adjuvante para a saúde cardiovascular. No geral, descobriu-se que a suplementação de creatina tem vários benefícios terapêuticos e de saúde ao longo da vida.
Does creatine affect HRT?5 answersCreatine is not mentioned in any of the provided abstracts, therefore there is no information available to suggest whether or not creatine affects hormone replacement therapy (HRT).
What is the effect of creatine?4 answersCreatine has various effects on the body. It has been found to positively influence the growth and elongation of plants in vitro. In terms of human health, creatine supplementation has been shown to have several benefits, including promoting general health as we age and aiding in recovery from injury and management of chronic disease. Additionally, creatine has been studied for its potential neuroprotective effects and its ability to diminish the harmful effects of peripheral nerve injury. In the context of exercise, creatine supplementation has been shown to transiently increase arterial stiffness after high-intensity resistance exercise. Overall, creatine has a wide range of effects on plants, human health, and exercise performance.
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How have previous studies explored the role of astrocytes in Aβ clearance through autophagy and phagocytosis?
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Previous studies have extensively investigated the role of astrocytes in Aβ clearance through autophagy and phagocytosis in Alzheimer's disease (AD). Astrocytes have been found to contribute significantly to Aβ clearance and degradation. Specifically, astrocytes play a crucial role in engulfing and degrading Aβ aggregates, preventing their accumulation and subsequent neurotoxic effects. Additionally, astrocytes have been shown to aid in the clearance of amyloid plaques and support synaptic plasticity, highlighting their protective role in AD pathology. Furthermore, studies have identified specific mechanisms, such as the involvement of LRP4 in promoting Aβ uptake by astrocytes, emphasizing the importance of astrocytic function in Aβ pathology and cognitive function. These findings underscore the potential therapeutic implications of targeting astrocytes to enhance Aβ clearance mechanisms in AD.
AMPK is activated
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AMPK (5' adenosine monophosphate-activated protein kinase) can be activated through various mechanisms, including an increase in cellular AMP levels or phosphorylation of specific sites. Activation of AMPK plays a crucial role in regulating energy homeostasis, glucose uptake, fatty acid oxidation, and autophagy processes. Studies have shown that AMPK activation is associated with the inhibition of fatty acid, glycogen, and cholesterol synthesis, while promoting processes like fatty acid oxidation, glucose uptake independent of insulin, and autophagy. Furthermore, AMPK activation has been linked to the treatment of various diseases such as prediabetes, diabetes, obesity, and cancer, making it a potential therapeutic target. Understanding the mechanisms and compounds that activate AMPK is essential for developing treatments targeting AMPK dysregulation in different diseases.
What are the mechanisms by which gold compounds exhibit antitumor activity?
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Gold compounds exhibit antitumor activity through various mechanisms. They primarily target thioredoxin reductase (TrxR), triggering cell death via reactive oxygen species (ROS). Additionally, gold complexes induce DNA damage, autophagy, and apoptosis in cancer cells. Some gold compounds have been shown to inhibit cancer and endothelial cell migration, as well as angiogenesis. Moreover, gold compounds have been reported to reverse tumor immune escape and enhance immune cell functions, contributing to enhanced anticancer effects. Overall, the multifaceted mechanisms of action of gold compounds make them promising candidates for cancer therapy, with potential for further development and clinical application.
What is the level of TFEB in psoriasis?
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The level of Transcription Factor EB (TFEB) in psoriasis is not directly addressed in the provided contexts. However, TFEB is a master regulator of autophagy and lysosomal biogenesis, with potential implications in various biological processes. In psoriasis, studies have focused on factors like Vascular Endothelial Growth Factor (VEGF), Transforming Growth Factor β1 (TGF-β1), and Pentraxin 3 (PTX 3) to understand disease severity and pathogenesis. These studies suggest that TFEB, although not directly measured, could play a role in the complex pathophysiology of psoriasis. Further research specifically investigating TFEB levels in psoriasis patients could provide valuable insights into its involvement in the disease process.
How does Autotoxicity Work for seagrasses in marine organisms?
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Autotoxicity in seagrasses involves the negative impact of high ammonium concentrations on these marine organisms. Seagrasses like Zostera species face toxic effects due to ammonium enrichment, which can lead to internal accumulation of ammonium, affecting processes like energy metabolism, carbon fixation, and photosynthesis. The interaction between ammonium and other environmental stressors intensifies the toxic effects, with factors like light reduction and hyposaline stress exacerbating the detrimental outcomes of high ammonium levels on seagrasses. This highlights the importance of understanding how multiple stressors interact to predict and manage the impact of pollutants like ammonium on seagrass ecosystems in the face of increasing coastal pollution.
What is the current understanding of the physiological effects of piretrine and pyrethroid exposure on humans?
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Current research indicates that exposure to pyrethroids like allethrin and prallethrin can induce various physiological effects in humans. Pyrethroids, synthetic derivatives of natural pyrethrins, primarily target the sodium channels in insect neurons, potentially leading to toxicity in vertebrates, including humans. Acute exposure to pyrethroids can enhance the late sodium current in the heart, causing cardiac arrhythmias, while long-term exposure may result in oxidative stress and tissue remodeling. Furthermore, studies have shown that exposure to pyrethroids equivalent to human consumption levels can lead to systemic and reproductive toxicity, impacting organ function, antioxidant status, and anatomical structures. These findings emphasize the importance of understanding the potential health risks associated with pyrethroid exposure in humans.
Interaction between energy and protein in the nutrient utilization ruminants?
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The interaction between energy and protein in nutrient utilization in ruminants is crucial for optimizing animal productivity and health. Balancing the supply of nitrogen and energy to rumen microbes is essential for efficient nutrient utilization. Synchronization of rumen-available protein and energy enhances nutrient efficiency in ruminants. Ruminants are anatomically adapted to utilize non-proteinaceous nitrogen compounds, emphasizing the importance of considering both protein and energy sources for effective utilization. New feeding systems focus on digestive interactions to improve predictions of diet responses by integrating energy and protein digestion mechanisms. Understanding the dynamics between energy and protein is key to formulating diets that maximize microbial synthesis efficiency and reduce environmental nitrogen excretion.
How does the disruption of circadian rhythms affect coronary heart disease?
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Disruption of circadian rhythms can significantly impact coronary heart disease. Studies have shown that circadian misalignment, whether due to genetic mutations like ClockΔ19/Δ19 or Bmal1 deletion, shift work-induced disturbances, or conditional deletion of core circadian gene Bmal1, can exacerbate cardiovascular conditions. This disruption leads to increased risk of ischemic heart disease, worsened outcomes post-myocardial infarction, and impaired cardiac function. The dysregulation of microRNAs involved in circadian rhythm modulation, under the influence of core clock genes, has been associated with inflammatory conditions of the endothelium and atherosclerosis, contributing to coronary heart disease. Therapeutic interventions targeting the circadian clock, such as exercise to restore autophagy gene expression, have shown promise in mitigating the adverse effects of circadian disruption on cardiovascular health.
What are the haemotoxicity of Carbon Dots in vitro?
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The haemotoxicity of Carbon Dots (CDs) and Carbon Quantum Dots (CQDs) in vitro, as derived from the provided contexts, reveals a nuanced understanding of their interaction with biological systems, particularly concerning their impact on blood components. The studies collectively indicate that while CDs and CQDs exhibit promising biocompatibility and potential therapeutic applications, their haemotoxic effects, when present, are minimal and highly dependent on specific conditions such as concentration, cell type, and exposure duration. From the provided contexts, only one directly addresses haemotoxicity, indicating that the antibacterial functional CDs prepared from chitosan derivatives exhibit low haemolytic effects, suggesting minimal haemotoxicity to human normal hepatocytes. This finding is crucial as it highlights the potential of CDs for biomedical applications, including antibacterial treatments, without significant adverse effects on blood cells. The low haemolytic effect implies that these CDs do not significantly disrupt the integrity of red blood cells, a critical factor in evaluating the safety of nanomaterials for medical applications. Other contexts, while not directly addressing haemotoxicity, contribute to the overall understanding of CDs' biocompatibility and safety profile. For instance, studies have shown that CDs possess high biocompatibility, with no significant cytotoxic effects observed in various cell types, including liver cells, macrophages, and breast cancer cell lines, under certain conditions. Additionally, the therapeutic application of CQDs in immunomodulation without cytotoxicity or in vivo damage further supports their safety. Moreover, the absence of significant toxic effects in acute and subacute toxicity experiments with mice underscores the potential non-toxic nature of CDs. In summary, the haemotoxicity of CDs and CQDs appears to be minimal, with specific studies indicating low haemolytic effects under certain conditions. This, combined with their high biocompatibility and safety profile in various biological systems, suggests that CDs and CQDs could be safe for biomedical applications, although the specific conditions under which they are used must be carefully considered to ensure safety.
What evidence is there of the efficacy of PBT in treating cancer tumors?
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Proton boron capture therapy (pBCT) has been investigated for its efficacy in treating cancer tumors. Studies have explored the physical and biological aspects of pBCT, including alternative alpha-particle production channels and cell viability during proton irradiation, but the biological efficacy of pBCT remains inconclusive. Additionally, combining traditional Chinese medicine molecules like Tetramethylpyrazine (TMP) with chemotherapeutic drugs has shown enhanced antitumor effects, reduced angiogenesis, and increased apoptosis in ovarian cancer cells and xenograft models. Furthermore, a polyacetal-based nanocarrier conjugated with paclitaxel (PTX) demonstrated sustained release, reduced systemic toxicities, and inhibited tumor growth and metastasis in prostate cancer models. Another study highlighted the potential of a casein nanoparticle for oral administration of Caesalpinia spinosa extract, showing delayed tumor growth and reduced metastasis in a mouse model of breast cancer. Overall, these findings provide insights into various approaches that show promise in treating cancer tumors.
Best medical treatment for CACNA1A mutation?
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The best medical treatment for CACNA1A mutations varies depending on the specific neurological phenotype. For CACNA1A-related encephalopathies, a personalized emergency treatment protocol involving combined corticosteroid pulses and hypertonic solution has shown efficacy in reducing the severity and duration of acute attacks. In cases of Episodic Ataxia Type 2 (EA2), pharmacological treatments like acetazolamide and 4-aminopyridine exist but may not be effective for all patients, suggesting a need for novel therapeutic approaches such as modulating splicing of CACNA1A to develop improved therapies. Additionally, for individuals with both EA2 and sporadic hemiplegic migraine, administration of flunarizine has been reported to effectively reduce attacks and alleviate symptoms. Understanding the pathogenesis of CACNA1A mutations and exploring pharmacological interventions targeting lysosomal function and calcium homeostasis may offer promising directions for future treatments.