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Tunisian children with hereditary vitamin D-resistant rickets showed improvement with calcium treatment, and new genetic mutations were identified.

CYP11A1 is crucial for skin health and disease by producing important steroids.

LY191704 is a compound that effectively blocks a specific enzyme involved in hormone conversion and could help treat enlarged prostate and hair loss.

LY320236 is a strong blocker of two enzymes that change testosterone into dihydrotestosterone and might help treat conditions related to male hormones.

5α-reductase-2 deficiency causes ambiguous genitalia at birth and affects male sexual development, but individuals often develop male characteristics at puberty.

The equine epididymis mainly uses type 1 5α-reductase, and both finasteride and dutasteride can inhibit its activity.

Two rare genetic diseases cause severe rickets in children due to defects in vitamin D metabolism.

A specific gene mutation causes vitamin D-resistant rickets and hair loss.

Androstanediol glucuronide is a reliable marker for hirsutism in women.

Certain genetic variants impair enzyme activity, contributing to non-classic congenital adrenal hyperplasia.

Congenital Adrenal Hyperplasia is mainly caused by enzyme deficiencies, leading to varying symptoms like hormone imbalances and physical changes.

A new gene mutation causes vitamin D resistance and hair loss in two unrelated girls.

Vitamin D receptor is crucial for bone health and mineral metabolism.

Different forms of the Vitamin D receptor can impact metabolic and hormone issues in Polycystic Ovary Syndrome.

Curcumin and its derivatives can block an enzyme important for making testosterone, with one derivative being particularly strong.

A Chinese family had a child with a specific gene mutation causing vitamin D-resistant rickets, but the child improved with calcium and low-dose calcitriol.

A unique gene mutation causes vitamin D-resistant rickets without causing hair loss.

Idiopathic hirsutism may be linked to increased enzyme activity.

Siblings with signs of virilization should be tested for non-classical congenital adrenal hyperplasia, which does not affect adult height but may impact fertility and well-being if untreated.

Certain genetic variants reduce enzyme activity, contributing to non-classic congenital adrenal hyperplasia.

Testing basal 17-HP levels is a good way to screen for nonclassic adrenal hyperplasia in women with high androgen levels.

The research helps understand how finasteride works and aids drug development.

The severity of symptoms in nonclassical congenital adrenal hyperplasia is not determined by CYP21A2 gene variations.

Routine genetic testing is crucial for early diagnosis and better management of Turner’s syndrome with 21-hydroxylase deficiency.

5α-reductase deficiency can cause ambiguous genitalia and gender dysphoria, treatable with testosterone.

Congenital Adrenal Hyperplasia is a rare inherited disease causing hormone imbalances, affecting growth, fertility, and heart health, diagnosed through blood tests and treated with medication and lifestyle changes.

The discovery of 5α-reductase deficiency in guevedoces led to the development of important urologic medications.

Testosterone and dihydrotestosterone treatments can help with penile growth in males with 5α-reductase type 2 deficiency, with dihydrotestosterone being more effective in infancy.

Two siblings with a genetic mutation had a form of rickets that doesn't respond to vitamin D.

A postmenopausal woman's masculine symptoms improved after surgery for a hormone-producing ovarian tumor.