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cachexia/hypoxia

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Cancer cachexia impairs neural respiratory drive in hypoxia but not hypercapnia.

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BACKGROUND Cancer cachexia is an insidious process characterized by muscle atrophy with associated motor deficits, including diaphragm weakness and respiratory insufficiency. Although neuropathology contributes to muscle wasting and motor deficits in many clinical disorders, neural involvement in
The transcription factor hypoxia-inducible factor-1 (HIF-1) consists of oxygen-sensitive HIF-1α and constitutive HIF-1β. HIF-1α is undetectable in normal cells, but cancer cells frequently express HIF-1α to support their growth, angiogenesis, and high glycolysis (also known as the Warburg effect).

β-Pentagalloyl-Glucose Sabotages Pancreatic Cancer Cells and Ameliorates Cachexia in Tumor-Bearing Mice.

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Pancreatic cancer cells overexpress the insulin receptor (IR) and the insulin-like growth factor-1 receptor (IGF1R). Activating these receptors, insulin and insulin-like growth factor-1 increase the growth and glycolysis of pancreatic cancer cells. The high glycolysis in pancreatic cancer cells

Alterations in Skeletal Muscle Oxidative Phenotype in Mice Exposed to 3 Weeks of Normobaric Hypoxia.

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Skeletal muscle of patients with chronic respiratory failure is prone to loss of muscle mass and oxidative phenotype. Tissue hypoxia has been associated with cachexia and emphysema in humans. Experimental research on the role of hypoxia in loss of muscle oxidative phenotype, however, has yielded

Increased hypoxia-inducible factor-1α in striated muscle of tumor-bearing mice.

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Cancer cachexia is a progressive wasting disease resulting in significant effects on the quality of life and high mortality. Most studies on cancer cachexia have focused on skeletal muscle; however, the heart is now recognized as a major site of cachexia-related effects. To elucidate possible

[Systemic and local mechanisms leading to cachexia in cancer].

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Cachexia is a multifactorial syndrome of atrophy of skeletal muscle and adipose tissue, resulting in progressive loss of body weight associated with low quality of life and poor prognosis in cancer. Studies on experimental animal models and observations on patients have shown that the soluble

Chronic metabolic acidosis may be the cause of cachexia: body fluid pH correction may be an effective therapy.

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Cachexia is a pathological state characterized by weight loss and protein mobilization during various diseases. Nutritional supplementation or appetite stimulants are unable to restore the loss of lean body mass. Agents interfering with TNF-alpha have not been very successful to date. Only

A tumor-in-host DEB-based approach for modeling cachexia and bevacizumab resistance.

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Adequate energy intake and homoeostasis are fundamental for the appropriate growth and maintenance of an organism; the presence of a tumor can break this equilibrium. Tumor energy requests can lead to extreme weight loss in animals and cachexia in cancer patients. Angiogenesis inhibitors, acting on

The effects of cachexia and related components on pulmonary functions in patients with COPD.

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Malnutrition is an important problem in patients with chronic obstructive pulmonary disease (COPD). It still remains unclear whether malnutrition contributes to poor pulmonary function through a loss of respiratory muscle mass, or if advanced disease and hypoxemia are the causes of weight loss and

Possible mechanisms underlying the development of cachexia in COPD.

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About 25% of patients with chronic obstructive pulmonary disease (COPD) will develop cachexia (fat-free body mass index <17 kg.m(-2) (males) or <14 kg.m(-2) (females)). This is associated with approximately 50% reduction in median survival. The pathogenetic mechanism has been variously suggested to

Cachexia Anorexia Syndrome and Associated Metabolic Dysfunction in Peritoneal Metastasis.

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: Patients with peritoneal metastasis (PM) of gastrointestinal and gynecological origin present with a nutritional deficit characterized by increased resting energy expenditure (REE), loss of muscle mass, and protein catabolism. Progression of peritoneal metastasis, as with other advanced

Nutritional status in chronic obstructive pulmonary disease: role of hypoxia.

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In patients with chronic obstructive pulmonary disease (COPD), malnutrition and limited physical activity are very common and contribute to disease prognosis, whereas a balance between caloric intake and exercise allows body weight stability and muscle mass preservation. The goal of this review is

Pathophysiology of anorexia in the cancer cachexia syndrome.

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Anorexia is commonly present in persons with cancer and a major component of cancer cachexia. There are multiple causes of anorexia in cancer. Peripherally, these can be due to (i) substances released from or by the tumour, e.g. pro-inflammatory cytokines, lactate, and parathormone-related peptide;

Hypoxia induced tumor metabolic switch contributes to pancreatic cancer aggressiveness.

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Pancreatic ductal adenocarcinoma remains one of the most lethal of all solid tumors with an overall five-year survival rate of only 3-5%. Its aggressive biology and resistance to conventional and targeted therapeutic agents lead to a typical clinical presentation of incurable disease once diagnosed.

Tumour-derived transforming growth factor-β signalling contributes to fibrosis in patients with cancer cachexia.

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Cachexia is a paraneoplastic syndrome related with poor prognosis. The tumour micro-environment contributes to systemic inflammation and increased oxidative stress as well as to fibrosis. The aim of the present study was to characterise the inflammatory circulating factors and tumour
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