Neoplasms

Urinary Tract, Sexual Organs, and Pregnancy Conditions

All Conditions

Urinary Bladder Neoplasms

Non-Muscle Invasive Bladder Neoplasms

Urologic Neoplasms

Urogenital Neoplasms

Urogenital Diseases

Female Urogenital Diseases

Pregnancy Complications

Female Urogenital Diseases and Pregnancy Complications

Urinary Bladder Diseases

Urologic Diseases

Male Urogenital Diseases

Carcinoma

Neoplasms, Glandular and Epithelial

Neoplasms by Histologic Type

Antineoplastic Agents

All Drugs and Chemicals

Natriuretic Agents

Mitomycins

Mitomycin

Ethacrynic Acid

Diuretics

Enzyme Inhibitors

Administration of a single, 50 mg oral dose of ethacrynic acid prior to bladder tumor removal surgery (Transurethral Resection of Bladder Tumor \[TURBT\])

One oral dose at 50 mg prior to bladder tumor removal surgery

Eugene K Lee, MD

Phase 1 study to provide quantitative characterization of the renal elimination of ethacrynic acid and metabolites in patients with non-muscle invasive bladder cancer (NMIBC) at the time of transurethral resection of bladder tumor

Bladder cancer continues to be a significant healthcare and financial liability in the United States. Patients with Non-Muscle Invasive Bladder Cancer (NMIBC) are in desperate need for both effective and easily tolerated treatment options. Current standard of care includes immediate post-operative Mitomycin C (MMC), which decreases the rate of recurrence but does not alter progression. Furthermore, in patients with high-grade NMIBC, standard of care dictates that patients undergo intravesical Bacillus Calmette-Guerin (BCG) therapy. This treatment has a high degree of morbidity with both local and systemic side effects along with significant discomfort from treatment (intra-urethral catheterization and bladder instillation). Our goal is to develop a bladder cancer treatment strategy designed to decrease recurrence/progression rates in addition to decreasing the morbidity of treatment.

Twelve evaluable NMIBC patients will participate in this Phase 1 trial.

Treatment - patients will receive a single, 50 mg oral dose of ethacrynic acid administered as two 25 mg strength EDECRIN® tablets immediately prior to transurethral resection of bladder tumor.

Concentrations and excretion rates of ethacrynic acid in the urine, as well as of cysteine, glutathione, and mercapturate metabolites, will be measured for each of 4 urine specimens collected on the day of surgery (before, during, and at 2 timepoints after surgery).

Adverse events, serious adverse events, laboratory values, and vital sign measurements will be collected.

Efficacy of ethacrynic acid treatment will be estimated by recording recurrence/non-recurrence of disease at 3 months post-treatment

Ethacrynic Acid Elimination in Non-Muscle Invasive Bladder Cancer Patients Undergoing Transurethral Resection

Concentration of Ethacrynic acid and its conjugates in urine for baseline at 30 minutes before surgery. A: Ethacrynic acid concentration (ng/mL) B: Glutathione (ng/mL) C: Cysteine (ng/mL) D: Mercapturic acid (ng/mL) will be measured.

Concentration of Ethacrynic acid and its conjugates in urine during surgery. A: Ethacrynic acid concentration (ng/mL) B: Glutathione (ng/mL) C: Cysteine (ng/mL) D: Mercapturic acid (ng/mL) will be measured.

Concentration of Ethacrynic acid and its conjugates in urine at 2 hours after surgery. A: Ethacrynic acid concentration (ng/mL) B: Glutathione (ng/mL) C: Cysteine (ng/mL) D: Mercapturic acid (ng/mL) will be measured.

Concentration of Ethacrynic acid and its conjugates in urine at 4 hours after surgery. A: Ethacrynic acid concentration (ng/mL) B: Glutathione (ng/mL) C: Cysteine (ng/mL) D: Mercapturic acid (ng/mL) will be measured.

Urinary excretion rates of ethacrynic acid and its conjugates for baseline at 30 minutes before surgery. A: Ethacrynic acid concentration (ng) B: Glutathione (ng) C: Cysteine (ng) D: Mercapturic acid (ng) will be measured.

Urinary excretion rates of ethacrynic acid and its conjugates during surgery. A: Ethacrynic acid concentration (ng) B: Glutathione (ng) C: Cysteine (ng) D: Mercapturic acid (ng) will be measured.

Urinary excretion rates of ethacrynic acid and its conjugates 2 hours after surgery.

A: Ethacrynic acid concentration (ng) B: Glutathione (ng) C: Cysteine (ng) D: Mercapturic acid (ng) will be measured.

Urinary excretion rates of ethacrynic acid and its conjugates 4 hours after surgery.

A: Ethacrynic acid concentration (ng) B: Glutathione (ng) C: Cysteine (ng) D: Mercapturic acid (ng) will be measured.

Adverse events / toxicity related to Ethacrynic Acid as reported by participants will be recorded. Toxicity will be measured via analysis of patient adverse events (physiological parameter). Adverse events will be scored using NCI Common Toxicity Criteria for Adverse Events v 4.0.3 (June 14,2010).

Tumor Recurrence / Non-Recurrence will be measured using RECIST version 1.1 to assess efficacy of ethacrynic acid

University of Kansas Medical Center

Eugene Lee, MD

Medical Doctor

Nutritional and Metabolic Diseases

Symptoms and General Pathology

Vitamin D Deficiency

Wasting Syndrome

Cachexia

Syndrome

Avitaminosis

Deficiency Diseases

Malnutrition

Nutrition Disorders

Body Weight

Weight Loss

Body Weight Changes

Thinness

Metabolic Diseases

Micronutrients

Bone Density Conservation Agents

Vitamins

Vitamin D

Cholecalciferol

Trace Elements

Vitamin D3

Calciferol

Standard of Care resistance exercise and timed protein supplementation with placebo capsule daily for 12 weeks

Standard of Care resistance exercise and timed protein supplementation with 5,000IU vitamin D supplementation daily for 12 weeks

5,000IU vitamin D given daily for 12 weeks

Placebo capsules given daily for 12 weeks

Placebo

The proposed study is aimed at examining mitochondrial function as a potential target of action of vitamin D on muscle metabolism, size, and strength in preventing the progression of cachexia. This is the first clinical trial designed to understand the effects of vitamin D on muscle metabolic dynamics driving dysfunction in cachectic muscle. Our preliminary data suggest that vitamin D promotes lipid partitioning and muscle metabolic function, which the investigators hypothesize, will mitigate cachexia via improved muscle health and quality that translates into reduced fatigue, and improved patient resilience to multimodal cancer therapy.

Vitamin D repletion is linked to improved muscle mitochondrial function, lipid deposition and preservation; however, while vitamin D insufficiency is common in cancer, the mechanistic effects of vitamin D on muscle metabolic health in cancer patients have not been studied. This is important to address because cancer cachexia is characterized by marked muscle wasting, anabolic resistance, ectopic fat infiltration, mitochondrial dysfunction and contributes to decreased survival. With novel strategies to address this knowledge gap, the investigators will use a combination of advanced metabolic analytical approaches with complementary model systems in cell culture and human subjects to understand the biochemical and physiological mechanisms underlying cancer cachexia in relation to the role of vitamin D in conjunction with resistance exercise (RE). By combining analyses of muscle size and local tissue hemodynamics in vivo, metabolomics analyses of muscle tissue and isolated mitochondria, and changes in anabolic cell signaling, lipid metabolism and oxidative capacity of primary muscle cells in vitro, the investigators will identify mechanisms underlying muscle response to vitamin D repletion. Our previous findings, together with data that exercise improves muscle vitamin D storage and retrieval, suggest that vitamin D repletion synergizes with RE to improve muscle metabolic function and protein synthesis. Our overall objective is to examine mitochondrial function and anabolic resistance as potential targets of action of vitamin D on muscle metabolism, size and strength in preventing the progression of cachexia. The aims of this study are to: 1) non-invasively quantify lipid redistribution, local muscle tissue metabolism and muscle mass and strength of cancer patients before and after 12 weeks of double blinded vitamin D repletion with exercise and protein supplementation (VitD) compared to exercise and protein supplementation only (Ctl); 2) determine differences in muscle mitochondrial function in live tissue biopsied from human gastrocnemius from VitD compared to Ctl; and 3) identify mechanisms whereby vitamin D and exercise regulate muscle anabolic signaling and mitochondrial activity in primary human myotube cultures. Our central hypothesis is that vitamin D promotes muscle lipid availability for β-oxidation in response to exercise, thereby preventing lipotoxicity in the muscle and potentially improving anabolic sensitivity in muscle during cancer cachexia. The impact of this project, the first nutrition and exercise study designed as an inexpensive intervention, is to understand the effect of vitamin D on the metabolic and anabolic dynamics which underpin dysfunction in cachectic muscle. If vitamin D promotes lipid partitioning, muscle metabolic function and/or anabolic sensitivity, these adaptations will ultimately improve cancer therapy by combating cancer cachexia. Further, diffuse optical spectroscopy techniques have the potential to identify the minimum effective intervention dose for optimizing metabolic health leading to more practical and individualized lifestyle prescriptions to reduce health care costs.

Prospective, double-blinded randomized controlled clinical trial

All subjects receive exercise and protein supplementation. Participants, Investigators, Care Providers, and outcome assessors will be blinded to vitamin D vs. placebo capsule allocation

Vitamin D for Muscle Metabolic Function in Cancer Cachexia

The Contribution of Vitamin D to Muscle Metabolic Function in Cancer Cachexia

Near Infrared Spectroscopy + Diffuse Correlation Spectroscopy measures will be combined to assess changes in local muscle tissue oxygen consumption (VO2 measure)

Maximal voluntary contractions and 1-Repetition Maximum will be aggregated to to provide a comprehensive assessment of muscle strength

Determine the differences in muscle mitochondrial function in live tissue biopsied from human gastrocnemius from VitD compared to Ctl by measure live tissue oxygen consumption rate. Respiration measures will be combined to assess mitochondrial function

Mitochondrial respiration will be measured by the XF96 Seahorse extracellular flux analyzer

Determine the differences in muscle mitochondrial function in live tissue biopsied from human gastrocnemius from VitD compared to Ctl by measure live tissue oxygen consumption rate. Fatty acid oxidation measures will be combined to assess mitochondrial function

Fatty acid oxidation will be estimated by monitoring the OCR of cells with no exogenous glucose or glutamine (Gln) ± a specific fatty acid oxidation (FAO) inhibitor, etomoxir (40 µM)

Determine the relative importance of vitamin D on lipid, amino acid and energy metabolism involving glucose, glutamine, and β-oxidation in intact muscle fibers. We will culture with 13C8-octanoate, 13C6-glucose, or 13C5-Gln and measure metabolite isotopomer distributions to accomplish this goal.

Identify mechanisms whereby vitamin D and RE regulate anabolic signaling in primary human myotube cultures. Changes in signaling pathways associated with hypertrophy, including Akt, mTOR, MAPK, and AMPK, will be measured by phospho-western blot to determine response to calcitriol, palmitate, and stretch treatment in myotubes.

To understand how vitamin D and RE regulate mitochondrial activity in primary human myotube cultures, the investigators will measure extracellular acidification rate (ECAR) in response to calcitriol supplementation. This will be assessed through the addition of CPT-1 inhibitor etomoxir (40 µM) and the ATP-synthase inhibitor oligomycin

Identify mechanisms whereby vitamin D and RE regulate mitochondrial activity in primary human myotube cultures.

The investigators will measure the concentration of ATP in myotubes in response to calcitriol supplementation.

David Travis Thomas

Principal Investigator

Nervous System Diseases

Respiratory Tract (Lung and Bronchial) Diseases

Muscular Atrophy

Lung Neoplasms

Atrophy

Pathological Conditions, Anatomical

Neuromuscular Manifestations

Neurologic Manifestations

No intervention

Julien ANIORT

Muscle wasting is present in almost 50% of patients treated with chronic hemodialysis. It is associated with an increased risk of death (particularly from cardiovascular causes) and compromises quality of life (loss of autonomy and fatigue). The mechanisms leading to muscle wasting in chronic kidney disease have been the subject of several studies in animals. These have highlighted the role of the ubiquitin-proteasome system (UPS). Activation of UPS during chronic kidney disease is multifactorial. It is the result of resistance to the action of insulin/IGF1, metabolic acidosis, low grade prolonged inflammation and increased production of myostatin. To date few studies have been conducted in humans.

The investigators want to identify blood markers related to muscle protein breakdown in patients undergoing hemodialysis. In parallel, the investigators want to adress the mechanisms involved in muscle proteolysis. In addition, the investigators want to identify the proteins degraded and the ubiquitination enzymes (E2/E3 couples) specifically involved in muscle loss during hemodialysis.

Muscle biopsies and blood sample will beperformed during scheduled surgeries in healthy volunteers (negative control), cancer patients (positive control) or undergoing chronic hemodialysis. RNA seq analysis will be performed in blood samples and proteomic mass spectrometry analysis for establishing a specific profile between muscle and blood markers. A limited subset of blood markers common to cancer and hemodialysis atrophying muscles will be used for elaborating a chip dedicated to early detect an atrophying process.

Thus, the investigators will first design a diagnostic tool for detecting non-invasively muscle protein breakdown before the onset of muscle atrophy. This will enable early and efficient nutritional counter-measures.

Hypothesis Measuring urinary 3-methylhistidine is a simple tool to assess proteolysis in clinical practice. However it is not totally specific of muscle proteolysis because it may reflect an intestinal catabolism. Moreover, its dosage cannot be used in patients with renal impairment especially in case of anuria. Apart from achieving muscle biopsy or measuring the overall kinetics of proteins it does not yet exist simple and reproducible diagnostic tool for measuring muscle proteolysis. With the present study, the investigators expect to identify in the blood of patients a particular transcriptomic profile related to the activation of muscle proteolysis, including increased proinflammatory cytokine transcripts.

Rodent models of CKD were used to identify major proteolytic system and signal pathway implicated in muscle wasting caused by uremia. These finding needs to be confirmed in humans studies. Also, other actors of muscle atrophy could be identified in humans. Notably, so far, few studies have been performed in order to determine which E2 are involved in muscle atrophy, and to knowledge of the investigators no one in CKD. Finally, data on muscle proteasome substrates are limited since only actin was clearly identified in humans by the team. The investigators expect an activation of the proteasome system with an increase in the expression of enzymes E2s, E3s including MURF1 and MAFbx and proteasome subunit in patients treated with hemodialysis. The investigators could also observe an activation of caspase system which is thought to work in concert with the UPS.

Materials and methods 2.1. Population The experiments will be performed using blood sample and human muscle biopsies obtained during programmed orthopedic surgery (negative control), cancer (positive control) and hemodialysis patients. This translational research program has already been accepted (DGS 2008-A00479-46) and inclusion of patients already started. A maximum of 15 patients per group will be included. Inclusion and exclusion criteria were set-up according to the objectives (absence of any pathology for controls, etc.) and the legislation (written consent, etc.). Thirty-two patients have already been included so far, and biopsies are stored in liquid nitrogen. Blood samples are collected just before surgery using Paxgene RNA tubes and stored following the manufacturer's instructions until analysis.

2.2. Blood sample Total RNA will be extracted from blood using Paxgene RNA Extraction kit and analysed by RNAseq 2.3. Muscle biopsies 2.3.1. Transcriptomic analysis Total RNA will be extracted from human muscle biopsies using commercial kits. The investigators will first verify that known muscles markers are up-regulated in cancer patient biopsies (positive controls) and address their levels in muscle biopsies from hemodialysis patients. We will thus perform qRT-PCR UBE2B, UBE2D2, MaFbx, MuRF1, Ozz, ASB2, E4B, Nedd4, Mdm2 and 26S proteasome subunits.

2.3.2. Proteomic analysis Proteomic analysis will be performed usin shot gun spectrometry analysis

Muscle Wasting in Hemodialysis Patient

Study of Muscle Wasting Mechanisms and Biomarkers in Hemodialysis Patient

Total RNA will be extracted from blood using Paxgene RNA Extraction kit and analysed by RNAseq and a comparison made between patients and control.

1. To confirm the implication of UPS in muscular proteolysis of IRCH patients by the detection of an increasing of ARNm, except ubiquitin, implicated in the quantitative RT-PCR system and by the identification of substrates.
2. To locate on the proteins that have to be deteriorated, the sites used by the UPS to fix polyubiquitin chains.

Total RNA will be extracted from human muscle biopsies using commercial kits. We will first verify that known muscles markers are up-regulated in cancer patient biopsies (positive controls) and address their levels in muscle biopsies from hemodialysis patients. We will thus perform qRT-PCR UBE2B, UBE2D2, MaFbx, MuRF1, Ozz, ASB2, E4B, Nedd4, Mdm2 and 26S proteasome subunits.

Proteomic analysis will be performed usin shot gun spectrometry analysis

University Hospital, Clermont-Ferrand

Digestive System Diseases

Gland and Hormone Related Diseases

Rare Diseases

Fatigue

Cholangiocarcinoma

Pancreatic Neoplasms

Gastrointestinal Neoplasms

Digestive System Neoplasms

Endocrine Gland Neoplasms

Gastrointestinal Diseases

Pancreatic Diseases

Endocrine System Diseases

Adenocarcinoma

Pancreatic Cancer

Bile Duct Cancer

Vasodilator Agents

Urological Agents

Gastrointestinal Agents

Anticoagulants

Other Dietary Supplements

Sildenafil Citrate

Pancrelipase

Pancreatin

Citric Acid

Sodium Citrate

Phosphodiesterase 5 Inhibitors

Phosphodiesterase Inhibitors

Citrate

Sildenafil

Melinda Sheffield-Moore, PhD

Investigation of the effects of daily sildenafil on patients with pancreatic or cholangiocarcinoma cancer undergoing treatment.

This is a double-blinded, placebo-controlled trial in men and women, 40-75 years old, diagnosed with pancreatic or cholangiocarcinoma cancer. Patients will receive placebo or sildenafil daily for 4 weeks during their initial chemotherapy cycle.

Study of Sildenafil as a Therapy for Fatigue in Pancreatic Cancer

Phase I Assessment of NO Mediated Signaling in Cancer Cachexia

Lean body mass will be measured by DEXA scan

Skeletal muscle fatigue will be measured by leg dynamometer.

The University of Texas Medical Branch, Galveston

Diseases and Abnormalities at or Before Birth

Polycystic Ovary Syndrome

Hyperandrogenism

Amenorrhea

Gonadal Disorders

Cysts

Ovarian Cysts

Ovarian Diseases

Adnexal Diseases

Genital Diseases, Female

Genital Diseases

Menstruation Disturbances

Hypoglycemic Agents

Vasoconstrictor Agents

Respiratory System Agents

Insulin

Insulin, Globin Zinc

Hormones

Epinephrine

Racepinephrine

Epinephryl borate

10 women with exercise-associated hypothalamic amenorrhea

5 lean women with hyperandrogenic polycystic ovary syndrome. 5 women with weight excess and hyperandrogenic polycystic ovary syndrome.

5 lean women with non-hyperandrogenic polycystic ovary syndrome 5 women with weight excess and non-hyperandrogenic polycystic ovary syndrome

10 women who exercise as intensively as women with exercise-associated hypothalamic amenorrhea but with normal ovulatory cycles.

10 women matched by age and body mass index with women with polycystic ovary syndrome who do not perform physical activity on a regular basis

* Weight and height.
* Waist-to-hip ratio.
* Body composition: Bioelectrical impedance and \[Dual energy X-ray absorptiometry (DEXA)\].

Anthropometric and physical examination

Indirect calorimetry, accelerometer and seven-day dietary recall

* Lipid profile.
* Oral glucose tolerance test: plasma glucose and insulin, insulin sensitivity indices, gastrointestinal hormones, adipokines, oxidative stress markers.
* Sex steroid profile.
* Hypothalamic-pituitary-adrenal axis study.
* Ferrokinetic study.
* Subclinical chronic inflammatory markers.

Biochemical, hormonal and metabolic phenotyping

* Polycystic ovarian morphology.
* Carotid intima-media thickness.
* Eco-FAT: Ultrasound measurements of adipose tissue depots including sc, preperitoneal, intraperitoneal (ip), mesenteric, and perirenal fat thickness.

Sonographic studies

A\&D TM2430EX oscillometric devices (A\&D Company Limited, Tokyo, Japan).

24-hour Ambulatory blood pressure monitoring

Subcutaneous fat tissue and muscle tissue for proteomics an gene expression studies.

Percutaneous biopsy

Parasympathetic and sympathetic responses to deep breathing, Valsalva's maneuver and orthostatism.

Cardiovascular autonomic function studies

Oral smear and feces specimen

Elena Fernández Durán

Héctor F Escobar-Morreale, PhD, MD

Manuel Luque-Ramírez, PhD, MD

Reproduction requires from women enough energy depots to warrant an adequate nutritional supply to the fetus. Hence, adipose tissue is able to communicate with female hypothalamic-pituitary-ovary axis. The hypothesis of the project is that abnormalities in the quantity (absolute and relative to lean body mass), distribution and/or function of adipose tissue are associated with functional forms of female gonadal dysfunction in predisposed women, in a spectrum of anomalies that go from hypothalamic amenorrhea to the polycystic ovary syndrome (PCOS). To challenge this hypothesis, the investigators will study 5 groups of 10 women each: women with exercise-associated hypothalamic amenorrhea, women without ovulatory dysfunction that exercise equally, non-hyperandrogenic patients with PCOS, hyperandrogenic patients with PCOS, and healthy control women comparable to those with PCOS. The aims of the study will be:

Primary objective: To identify novel signalling factors originating from adipose tissue and muscle using targeted and nontargeted evaluation of the proteome and of gene expression of superficial subcutaneous fat, deep subcutaneous fat (which mimics visceral adipose tissue) and skeletal muscle.

Secondary objectives:

1. To study the serum adipokine profile - including those identified by the primary objective - and circulating gut hormones during fasting and after a glucose load in the 5 groups of women, and their associations with sexual hormones and body fat distribution.
2. To study body composition and body fat distribution in these women and their relationships with:

2.1, Sex steroid profiles.

2.2. Classic cardiovascular risk factors: carbohydrate metabolism, lipid profiles and blood pressure.

2.3 Markers of low-grade chronic inflammation.

2.4. Oxidative stress markers.

2.5. Cardiovascular autonomic function.

2.6. Surrogate markers of subclinical atherosclerosis.

2.7. Circulating concentrations of endocrine disruptors.

2.8. Oral and gut microbiome.

The results will provide a better understanding of the mechanisms linking body energy depots with the female reproductive axis and, hopefully, the identification of potential biomarkers for the diagnosis and treatment of the disorders studied here.

Serum Plasma Whole blood samples Subcutaneous adipose tissue by percutaneous biopsy Muscle tissue by percutaneous biopsy Feces Oral smear

Body Fat as Determinant of Female Gonadal Dysfunction

Amount, Distribution and Dysfunction of Body Fat as Determinants of Female Gonadal Dysfunction: From Functional Hypothalamic Amenorrhea to the Polycystic Ovary Syndrome

The investigators will deposit any datasets and supplemental materials to a generalist repository. The investigators will refer to the deposited material as an item in the bibliography of any manuscript and number the reference appropriately within the text.

At fasting and after an oral glucose challenge: Circulating concentrations of Leptin, Adiponectin, Chemerin, Lipocalin-2, Adipsin, Plasminogen Activator Inhibitor (PAI)-1, Monocyte Chemoattractant Protein (MCP)-1, and Soluble Leptin Receptor by multianalyte profiling on the Luminex Magpix system (Luminex Technologies, Austin, USA.).

At fasting and after an oral glucose challenge: Circulating concentrations of Amylin, C-Peptide, Ghrelin, Gastric Inhibitory Peptide (GIP), Glucagon-Like Peptide (GLP)-1, Glucagon, IL-6, Insulin, Pancreatic Polypeptide (PP), Peptide YY, Tumor Necrosis Factor (TNF)-α by multianalyte profiling on the Luminex Magpix system (Luminex Technologies, Austin, USA.).

Body mass index in in kg/m\^2. Sex steroids (including circulating total testosterone, estradiol, androstenedione, dehydroepiandrosterone-sulphate and estrone) measured by liquid chromatography tandem mass spectrometry (LC-MS/MS). Free testosterone will be calculated from total testosterone and sex hormone binding globulin levels.

Fat mass% by bioelectric impedanciometry and DEXA. Sex steroids (including circulating total testosterone, estradiol, androstenedione, dehydroepiandrosterone-sulphate and estrone) measured by liquid chromatography tandem mass spectrometry (LC-MS/MS). Free testosterone will be calculated from total testosterone and sex hormone binding globulin levels.

Lean mass% by bioelectric impedanciometry and DEXA. Sex steroids (including circulating total testosterone, estradiol, androstenedione, dehydroepiandrosterone-sulphate and estrone) measured by liquid chromatography tandem mass spectrometry (LC-MS/MS). Free testosterone will be calculated from total testosterone and sex hormone binding globulin levels.

Adipose tissue depots will be estimated using a Toshiba Nemio XG SSA-580A Diagnostic Ultrasound System. Minimum sc and preperitoneal fat thicknesses will be measured at the level of the xyphoid process. Maximum sc fat thickness will be measured at the level of the umbilicus. Intraperitoneal fat thickness will be measured placing a probe transversally in the midline of abdomen, 2 cm above the umbilicus. Three measures of ip fat thickness will be obtained: the distance from the fascia of rectus abdominis muscle to the vertebral column, the distance from the peritoneum to the vertebral column, and the distance from the linea alba to the vertebral column. Perirenal fat thickness will be estimated as the distance from the perirenal fascia to the renal surface. Sex steroids will be measured as previously described.

Fat mass, lean mass and body fat depots will be measured as previously described. Fasting glucose and insulin levels will be used for calculating the homeostasis model assessment of insulin resistance (HOMA-IR), and the composite insulin sensitivity index will be estimated from the glucose and insulin concentrations measured during the oral glucose tolerance test. Sex steroids will be measured as previously described.

Fat mass, lean mass and body fat depots will be measured as previously described. Circulating HDL-cholesterol and phospholipid levels will be measured by enzymatic methods after precipitation of plasma with phosphotungstic acid and Mg2+. Total cholesterol and triglyceride levels will be determined by enzymatic methods. LDL-cholesterol concentrations will be estimated by Friedewald's equation. Circulating apolipoprotein (Apo) AI, Apo B100, and lipoprotein (a) levels will be determined by kinetic immunonephelometry. Sex steroids will be measured as previously described.

Fat mass, lean mass and body fat depots will be measured as previously described. Office blood pressure will be determined as the mean of three manual sphygmomanometer readings in the sitting position. Sex steroids will be measured as previously described.

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
Ethacrynic Acid Elimination in Non-Muscle Invasive Bladder Cancer Patients Undergoing Transurethral Resection	NCT02852564	Bladder Cancer	Ethacrynic Acid	18 Years -	University of Kansas Medical Center
Vitamin D for Muscle Metabolic Function in Cancer Cachexia	NCT03144128	Cancer Cachexia Vitamin D Defic...	Vitamin D Placebo	45 Years - 75 Years	University of Kentucky
Muscle Wasting in Hemodialysis Patient	NCT03583177	Muscle Atrophy ...	No intervention	18 Years - 75 Years	University Hospital, Clermont-Ferrand
Study of Sildenafil as a Therapy for Fatigue in Pancreatic Cancer	NCT02106871	Pancreatic Canc... Cholangiocarcin...	Sildenafil	40 Years - 75 Years	The University of Texas Medical Branch, Galveston
Body Fat as Determinant of Female Gonadal Dysfunction	NCT03841981	Polycystic Ovar... Hypothalamic Am...	Anthropometric ... Indirect calori... Biochemical, ho... Sonographic stu... 24-hour Ambulat... Percutaneous bi... Cardiovascular ... Oral smear and ...	18 Years - 40 Years	Fundacion para la Investigacion Biomedica del Hospital Universitario Ramon y Cajal
Vitamin D for Muscle Metabolic Function in Cancer Cachexia	NCT03144128	Cancer Cachexia Vitamin D Defic...	Vitamin D Placebo	45 Years - 75 Years	University of Kentucky
EDICT - Exercise inDuced Changes In Colorectal Cancer Tissues	NCT02056691	Colorectal Canc...	Exercise progra... Muscle biopsy	18 Years -	The Royal Bournemouth Hospital
Gene Electrotransfer to Muscle With Plasmid AMEP in Patients With Disseminated Cancer	NCT01664273	Metastatic Mali...	Plasmid AMEP	18 Years -	Copenhagen University Hospital at Herlev
Correlation Between Ultrasound-assessed Quadriceps Muscle Mass and Baseline Whole-body Densitometry Muscle Index in the Post-cancer Population (JUMP Research II)	NCT06007794	Cancer Post-cancer Hematology	JUMP group	18 Years - 74 Years	Hospices Civils de Lyon
Optical Detection of Peripheral Nerve Bundles During Surgery	NCT01731379	Malignant Lymph... Malignant Lymph... Malignant Lymph... Carcinoma of Pa... Colon Rectal Ca... Tumor of Soft T...	Surgical resect...	18 Years -	Philips Healthcare
Ethacrynic Acid Elimination in Non-Muscle Invasive Bladder Cancer Patients Undergoing Transurethral Resection	NCT02852564	Bladder Cancer	Ethacrynic Acid	18 Years -	University of Kansas Medical Center

Spots Global Cancer Trial Database for muscle

Every month we try and update this database with for muscle cancer trials from around the world to help patients and their families find trials that might be right for them.
We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.

Spots Global Cancer Trial Database for muscle

Every month we try and update this database with for muscle cancer trials from around the world to help patients and their families find trials that might be right for them. We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.

Every month we try and update this database with for muscle cancer trials from around the world to help patients and their families find trials that might be right for them.
We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.