Receptors, Cytoplasmic and Nuclear
Receptors, Steroid
Phenobarbital
Aryl Hydrocarbon Hydroxylases
Xenobiotics
Hepatocytes
Cytochrome P-450 CYP2B1
7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide
Propanediol Dehydratase
Cytochrome P-450 CYP3A
Zoxazolamine
Hep G2 Cells
Meclizine
Dihydroxydihydrobenzopyrenes
Steroid Hydroxylases
Transcription Factors
Pregnenolone Carbonitrile
Enzyme Induction
Cytochrome P-450 Enzyme System
Glycols
Liver
Metabolic Detoxication, Drug
Clotrimazole
Retinoid X Receptor alpha
Epoxy Compounds
Glucuronosyltransferase
Benzopyrenes
Androstenols
Oximes
PPAR alpha
Hepatocyte Nuclear Factor 4
Pyridines
Hinge Exons
Cynanchum
Stereoisomerism
Gene Expression Regulation, Enzymologic
RNA, Messenger
Lithocholic Acid
Metabolic Detoxication, Phase II
Ligands
Bay-Region, Polycyclic Aromatic Hydrocarbon
DNA Adducts
Organic Anion Transport Polypeptide C
Sulfotransferases
Ginkgolides
Genes, Reporter
Benzo(a)pyrene
Alcohols
Transcriptional Activation
Multidrug Resistance-Associated Proteins
Bile Acids and Salts
Nuclear Receptor Coactivator 2
Mice, Knockout
Active Transport, Cell Nucleus
Microsomes, Liver
Gene Expression Regulation
Steroid 16-alpha-Hydroxylase
Receptor Cross-Talk
Response Elements
Nuclear Receptor Coactivator 1
Retinoid X Receptors
Androstane-3,17-diol
Receptors, Aryl Hydrocarbon
Cells, Cultured
Steroids
Base Sequence
Reverse Transcriptase Polymerase Chain Reaction
Receptors, Glucocorticoid
Epoxide Hydrolases
Propylene Glycols
Carcinogens
Klebsiella oxytoca
Rifampin
Pharmaceutical Preparations
Molecular Sequence Data
P-Glycoproteins
Biotransformation
Luciferases
Glutathione Transferase
Molecular Structure
Mutagens
Benz(a)Anthracenes
DNA Primers
Promoter Regions, Genetic
Protein Binding
Species Specificity
Androstenediols
P-Glycoprotein
Transfection
Acetaminophen
Blotting, Western
Transcription, Genetic
DNA
Cell Nucleus
Receptors, Retinoic Acid
Binding Sites
COS Cells
Ethylene Glycols
Polycyclic Hydrocarbons, Aromatic
Hydro-Lyases
Chromatography, High Pressure Liquid
Tropolone
Real-Time Polymerase Chain Reaction
Dimerization
Gene Expression
Amino Acid Sequence
Dose-Response Relationship, Drug
Enzyme Reactivators
Protein Isoforms
Creosote
Pentanes
Cercopithecus aethiops
Lipid Metabolism
Signal Transduction
Butylene Glycols
Mice, Transgenic
Gas Chromatography-Mass Spectrometry
Plasmids
Catalysis
Cyclohexenes
Rats, Sprague-Dawley
Camphor
Ethanolamine Ammonia-Lyase
Cyclization
Isomerism
Oligonucleotide Array Sequence Analysis
RNA
Magnetic Resonance Spectroscopy
Gene Expression Profiling
Mutagenicity Tests
Cholestenes
Protein Structure, Tertiary
Chromatography, Thin Layer
Down-Regulation
Oxygenases
Chromatography, Paper
Polyacetylenes
Up-Regulation
DNA-Binding Proteins
Chromatography, Gas
Chemistry
Chemical Phenomena
1-Propanol
Structure-Activity Relationship
Atractylodes
Glycerol
Chlorohydrins
Deoxyadenosines
Citrobacter
Waxes
Trimethylsilyl Compounds
Spectrophotometry, Ultraviolet
Mass Spectrometry
Astatine
Bromine
Spectrophotometry, Infrared
Juvenile Hormones
Benzoflavones
Spectrum Analysis
Cytochrome P-450 CYP1A1
Substrate Specificity
Spectrometry, Mass, Electrospray Ionization
Furans
Acetoxyacetylaminofluorene
Hydrogenation
Examples of experimental liver neoplasms include:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and can be induced experimentally by injecting carcinogens such as diethylnitrosamine (DEN) or dimethylbenz(a)anthracene (DMBA) into the liver tissue of animals.
2. Cholangiocarcinoma: This type of cancer originates in the bile ducts within the liver and can be induced experimentally by injecting chemical carcinogens such as DEN or DMBA into the bile ducts of animals.
3. Hepatoblastoma: This is a rare type of liver cancer that primarily affects children and can be induced experimentally by administering chemotherapy drugs to newborn mice or rats.
4. Metastatic tumors: These are tumors that originate in other parts of the body and spread to the liver through the bloodstream or lymphatic system. Experimental models of metastatic tumors can be studied by injecting cancer cells into the liver tissue of animals.
The study of experimental liver neoplasms is important for understanding the underlying mechanisms of liver cancer development and progression, as well as identifying potential therapeutic targets for the treatment of this disease. Animal models can be used to test the efficacy of new drugs or therapies before they are tested in humans, which can help to accelerate the development of new treatments for liver cancer.
Liver neoplasms, also known as liver tumors or hepatic tumors, are abnormal growths of tissue in the liver. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant liver tumors can be primary, meaning they originate in the liver, or metastatic, meaning they spread to the liver from another part of the body.
There are several types of liver neoplasms, including:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and arises from the main cells of the liver (hepatocytes). HCC is often associated with cirrhosis and can be caused by viral hepatitis or alcohol abuse.
2. Cholangiocarcinoma: This type of cancer arises from the cells lining the bile ducts within the liver (cholangiocytes). Cholangiocarcinoma is rare and often diagnosed at an advanced stage.
3. Hemangiosarcoma: This is a rare type of cancer that originates in the blood vessels of the liver. It is most commonly seen in dogs but can also occur in humans.
4. Fibromas: These are benign tumors that arise from the connective tissue of the liver (fibrocytes). Fibromas are usually small and do not spread to other parts of the body.
5. Adenomas: These are benign tumors that arise from the glandular cells of the liver (hepatocytes). Adenomas are usually small and do not spread to other parts of the body.
The symptoms of liver neoplasms vary depending on their size, location, and whether they are benign or malignant. Common symptoms include abdominal pain, fatigue, weight loss, and jaundice (yellowing of the skin and eyes). Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and ultrasound, and a biopsy to confirm the presence of cancer cells.
Treatment options for liver neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery may be an option for some patients with small, localized tumors, while others may require chemotherapy or radiation therapy to shrink the tumor before surgery can be performed. In some cases, liver transplantation may be necessary.
Prognosis for liver neoplasms varies depending on the type and stage of the cancer. In general, early detection and treatment improve the prognosis, while advanced-stage disease is associated with a poorer prognosis.
The most common types of biliary fistulas are:
1. Bile duct-enteric fistula: This type of fistula connects the bile ducts to the small intestine.
2. Bile duct-skin fistula: This type of fistula connects the bile ducts to the skin, which can lead to a bile leak and infection.
3. Bile duct-liver fistula: This type of fistula connects the bile ducts to the liver, which can cause bleeding and infection.
Symptoms of biliary fistula may include:
* Jaundice (yellowing of the skin and whites of the eyes)
* Pale or clay-colored stools
* Dark urine
* Fatigue
* Loss of appetite
* Weight loss
Diagnosis of biliary fistula is typically made through a combination of imaging tests such as endoscopy, CT scan, and MRI. Treatment options for biliary fistula include:
1. Endoscopic therapy: This may involve the use of an endoscope to repair or close off the fistula.
2. Surgery: In some cases, surgery may be necessary to repair or remove the damaged bile ducts.
3. Stent placement: A stent may be placed in the bile ducts to help keep them open and allow for proper drainage.
It is important to seek medical attention if you experience any symptoms of biliary fistula, as it can lead to serious complications such as infection or bleeding.
There are several types of skin neoplasms, including:
1. Basal cell carcinoma (BCC): This is the most common type of skin cancer, and it usually appears as a small, fleshy bump or a flat, scaly patch. BCC is highly treatable, but if left untreated, it can grow and invade surrounding tissue.
2. Squamous cell carcinoma (SCC): This type of skin cancer is less common than BCC but more aggressive. It typically appears as a firm, flat, or raised bump on sun-exposed areas. SCC can spread to other parts of the body if left untreated.
3. Melanoma: This is the most serious type of skin cancer, accounting for only 1% of all skin neoplasms but responsible for the majority of skin cancer deaths. Melanoma can appear as a new or changing mole, and it's essential to recognize the ABCDE signs (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving size, shape, or color) to detect it early.
4. Sebaceous gland carcinoma: This rare type of skin cancer originates in the oil-producing glands of the skin and can appear as a firm, painless nodule on the forehead, nose, or other oily areas.
5. Merkel cell carcinoma: This is a rare and aggressive skin cancer that typically appears as a firm, shiny bump on the skin. It's more common in older adults and those with a history of sun exposure.
6. Cutaneous lymphoma: This type of cancer affects the immune system and can appear as a rash, nodules, or tumors on the skin.
7. Kaposi sarcoma: This is a rare type of skin cancer that affects people with weakened immune systems, such as those with HIV/AIDS. It typically appears as a flat, red or purple lesion on the skin.
While skin cancers are generally curable when detected early, it's important to be aware of your skin and notice any changes or unusual spots, especially if you have a history of sun exposure or other risk factors. If you suspect anything suspicious, see a dermatologist for an evaluation and potential biopsy. Remember, prevention is key to avoiding the harmful effects of UV radiation and reducing your risk of developing skin cancer.
There are two main types of vitamin K deficiency:
1. Hypovitaminosis A (mild deficiency): This type of deficiency is characterized by low levels of vitamin K in the blood, but not low enough to cause bleeding or other serious symptoms. It can be caused by a diet that is low in vitamin K, or by conditions that interfere with vitamin K absorption, such as inflammatory bowel disease or liver disease.
2. Vitamin K deficiency bleeding (VKDB): This type of deficiency is characterized by bleeding that is caused by a lack of vitamin K. It can be caused by a diet that is very low in vitamin K, or by conditions that interfere with vitamin K absorption or clotting factor production.
Symptoms of vitamin K deficiency may include:
* Prolonged bleeding after injuries or surgery
* Nosebleeds
* Bruising easily
* Bleeding gums
* Bloody stools
* Heavy menstrual periods
Causes of vitamin K deficiency may include:
* A diet that is low in vitamin K
* Conditions that interfere with vitamin K absorption, such as inflammatory bowel disease or liver disease
* Certain medications, such as anticoagulants (blood thinners)
* Malabsorption, such as in cases of celiac disease or Crohn's disease
* Vitamin K-dependent diseases, such as osteoporosis or cancer
Diagnosis of vitamin K deficiency is typically made based on a combination of symptoms, medical history, and laboratory tests. Treatment may involve supplementation with vitamin K, changes to the diet to increase vitamin K intake, and addressing any underlying conditions that may be contributing to the deficiency.
It is important to note that vitamin K deficiency can be difficult to diagnose, as symptoms can be subtle and may not always be immediately apparent. If you suspect you or someone you know may have a vitamin K deficiency, it is important to consult with a healthcare professional for proper evaluation and treatment.
17α-Ethynyl-3α-androstanediol
Androstenediol
Etiocholanediol
Androgen backdoor pathway
5α-Dihydroethisterone
Anordiol
Anordrin
Ethandrostate
17α-Ethynyl-3β-androstanediol
Hypothalamic-pituitary-adrenal axis
3β-Androstanediol
5α-Pregnan-17α-ol-3,20-dione
5α-Pregnane-3α,17α-diol-20-one
Androstenedione
List of androstanes
Prasterone
3α-Androstanediol
3α-Etiocholanediol
List of MeSH codes (D06)
Cetadiol
Chitchanok Pulsabsakul
Fluoxymesterone
3β-Etiocholanediol
Epiandrosterone
Methandriol
Androstanediol
HSD17B2
List of neurosteroids
List of MeSH codes (D04)
3α-Hydroxysteroid dehydrogenase
19-Nordehydroepiandrosterone
Dihydrotestosterone
Ethinylestradiol
Allopregnanolone
Ethinylandrostenediol
Bicalutamide
Sukanya Srisurat
List of EC numbers (EC 1)
Configurational analysis and relative binding affinities of 16-methyl-5alpha-androstane derivatives - PubMed
Publication Detail
MeSH Browser
Betaxolol Hydrochloride|N0000004400
Pancuronium Bromide Injection
Biomarkers Search
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MeSH Browser
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DeCS
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Research Festival | Intramural Research Program | National Institutes of Health
Taxifolin suppresses rat and human testicular androgen biosynthetic enzymes. | Fitoterapia;125: 258-265, 2018 Mar. |...
Pharos : Target Details - UGT2B28
Take Advantage Of https://canadian-pharmacyca.com/section/sports-nutrition/ - Read These 10 Tips - Wood Frame Pilar
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EurekaMag PDF full texts Chapter 6233
Volume8,Issue5 - IJPCR
Selected Publications - Structure Function Group
format-version: 1.2
Beta-diol2
5alpha-Androstane-3beta1
- The relative binding affinities of the 16-methyl-5alpha-androstane-3beta,17-diols 5, 6, 7, 8 and 17-hydroxy-16-methyl-5alpha-androstan-3-ones 13, 14, 15, 16 were studied. (nih.gov)
17beta2
Estradiol4
- High N-Acetyltransferase 1 Expression Is Associated with Estrogen Receptor Expression in Breast Tumors, but Is not Under Direct Regulation by Estradiol, 5α-androstane-3β,17β-Diol, or Dihydrotestosterone in Breast Cancer Cells. (nih.gov)
- 40. 17β-estradiol effect on testicular β-endorphin expression in Psammomys obesus. (nih.gov)
- Esteroide C19 delta-4 que no solo se produce en el TESTÍCULO, sino también en el OVARIO y la CORTEZA SUPRARRENAL Dependiendo del tipo de tejido, la androstenodiona puede ser precursora de la TESTOSTERONA, de la ESTRONA o del ESTRADIOL. (bvsalud.org)
- A semisynthetic alkylated ESTRADIOL with a 17-alpha-ethinyl substitution. (lookformedical.com)
Metabolite4
- As much as 25% of an injected dose may be recovered as 3-hydroxy metabolite, which is half as potent a blocking agent as pancuronium. (nih.gov)
- Less than 5% of the injected dose is recovered as 17-hydroxy metabolite and 3,17-dihydroxy metabolite, which have been judged to be approximately 50 times less potent than pancuronium. (nih.gov)
- Human prostate basal cell distributed UDP- glucuronosyltransferase (UGT) 2B17 and its 97%-identical UGT-2B15 homolog metabolize di-hydrotestosterone (DHT) and its 5α-androstane- 3α,17β- diol metabolite. (nih.gov)
- For equine, GC-MS/MS analysis identified the diagnostic 3α-chloro-17α-methyl-5α-androstane-16α,17ß-diol metabolite. (bvsalud.org)
Testosterone2
Isomers1
- In this way, comparison was possible with the C-16 epimers 5, 6 and 13, 14 prepared earlier by a different route, and the series of isomers could be completed with the steric structures of 16beta-methyl-17alpha-hydroxy-5alpha-androstan-3beta-ol 7 and 16alpha-methyl-17alpha-hydroxy-5alpha 8 and with their 3-keto derivatives 15 and 16. (nih.gov)
20222
- 87(3): 217-223, 2022. (bvsalud.org)
- 2022. Emerging chemical and biochemical tools for studying 3-O-sulfated heparan sulfate. (nih.gov)
Steroid1
- Due to the potential toxicity of the halogenated steroid, in vitro metabolic investigations of 3α-chloro-17α-methyl-5α-androstan-17ß-ol using equine and human S9 liver fractions were performed. (bvsalud.org)
20211
- 2021. Structural and substrate specificity analysis of 3-O-sulfotransferase isoform 5 to synthesize heparan sulfate. (nih.gov)
Levels2
- Likewise, NAT1 transcript levels were not increased by dihydrotestosterone (DHT) or 5α-androstane-3β, (3β-adiol) 17β-diol. (nih.gov)
- Following exchange of IYG in wt-2B15 for TYS in wt-2B17 at positions 98-100 and transfections into COS-1 cells, 2B17(IYG) generated 10-fold greater in-cellulo caspases 8/3 activations over wt-2B15, while 2B15(TYS) suppressed activation of caspases 8/3 over 50% of wt-2B15 levels. (nih.gov)
Effect1
- Trenbolone (17β-hydroxyestr-4,9,11-trien-3- one) and other substances with a similar chemical structure or similar biological effect(s). (wada-ama.org)
Women1
- These volunteers were 15 young men and 17 postmenopausal women. (nih.gov)
Structural1
- c) Many problems will be amenable to treatment by computer programs which exist or which will be leveloped, for example, structural isomer problems or HRMS interpretation on compounds in 3 well-understood class. (nih.gov)
Analysis1
- 2) A ztoordinated system of hardware and software for signal Tur 3) Pata reduction techniques based on a compntei (not theoretical) noiel of the MS, including peak shapes, mass/time function, and resolving power as a function of mass. 4) Poak profile analysis for nultiplet detection and resolution. (nih.gov)
Postmenopausal women2
- These volunteers were 15 young men and 17 postmenopausal women. (nih.gov)
- Modest benefit has been demonstrated in randomized controlled trials (RCTs) of supplemental transdermal testosterone to estrogen-replete [ 3-7 ] and estrogen-deficient [ 8 ] postmenopausal women reporting low sexual desire and inconsistent ability to be sexually satisfied. (medscape.com)
Hormones2
- Significantly lower levels of two precursor hormones, dehydroepiandrosterone sulfate and androstene-3β,17β-diol, were found in women with sexual dysfunction ( P = 0.006 and P = 0.020, respectively). (medscape.com)
- [ 17 ] Intracrinology is the production of hormones within a cell to exert their activity in that same cell with minimal release of active hormones into the circulation. (medscape.com)
Cells6
- High N-Acetyltransferase 1 Expression Is Associated with Estrogen Receptor Expression in Breast Tumors, but Is not Under Direct Regulation by Estradiol, 5α-androstane-3β,17β-Diol, or Dihydrotestosterone in Breast Cancer Cells. (nih.gov)
- 2. 2beta-(N-substituted piperazino)-5alpha-androstane-3alpha,17beta-diols: parallel solid-phase synthesis and antiproliferative activity on human leukemia HL-60 cells. (nih.gov)
- 3. Libraries of 2β-(N-substituted piperazino)-5α-androstane-3α, 17β-diols: chemical synthesis and cytotoxic effects on human leukemia HL-60 cells and on normal lymphocytes. (nih.gov)
- 4. Chemical synthesis of 2beta-amino-5alpha-androstane-3alpha,17beta-diol N-derivatives and their antiproliferative effect on HL-60 human leukemia cells. (nih.gov)
- 20. Synthesis of pregnane derivatives, their cytotoxicity on LNCap and PC-3 cells, and screening on 5alpha-reductase inhibitory activity. (nih.gov)
- Following exchange of IYG in wt-2B15 for TYS in wt-2B17 at positions 98-100 and transfections into COS-1 cells, 2B17(IYG) generated 10-fold greater in-cellulo caspases 8/3 activations over wt-2B15, while 2B15(TYS) suppressed activation of caspases 8/3 over 50% of wt-2B15 levels. (nih.gov)
Alpha1
- This isozyme has glucuronidating capacity with steroid substrates such as 5-beta-androstane 3-alpha,17-beta-diol, estradiol, ADT, eugenol and bile acids. (nih.gov)
Time1
- 2) A ztoordinated system of hardware and software for signal Tur 3) Pata reduction techniques based on a compntei (not theoretical) noiel of the MS, including peak shapes, mass/time function, and resolving power as a function of mass. 4) Poak profile analysis for nultiplet detection and resolution. (nih.gov)