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Atypical chronic central serous chorioretinopathy with cystoid macular edema: Therapeutic response to medical and laser therapy.

Journal of current ophthalmology

Do JL, Olmos de Koo LC, Ameri H.
PMID: 28626824
J Curr Ophthalmol. 2017 Feb 17;29(2):133-135. doi: 10.1016/j.joco.2017.01.004. eCollection 2017 Jun.

PURPOSE: To describe an atypical case of chronic central serous chorioretinopathy (CSCR).METHODS: A 58-year-old man with longstanding, bilateral visual impairment was self-referred for a second opinion.RESULTS: Findings by direct ophthalmoscopy, optical coherence tomography, fluorescein angiography, and fundus autofluorescence (FAF)...

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Do JL, Olmos de Koo LC, Ameri H. Atypical chronic central serous chorioretinopathy with cystoid macular edema: Therapeutic response to medical and laser therapy. J Curr Ophthalmol. 2017;29(2):133-135doi: 10.1016/j.joco.2017.01.004.
Do, J. L., Olmos de Koo, L. C., & Ameri, H. (2017). Atypical chronic central serous chorioretinopathy with cystoid macular edema: Therapeutic response to medical and laser therapy. Journal of current ophthalmology, 29(2), 133-135. https://doi.org/10.1016/j.joco.2017.01.004
Do, Jiun L, et al. "Atypical chronic central serous chorioretinopathy with cystoid macular edema: Therapeutic response to medical and laser therapy." Journal of current ophthalmology vol. 29,2 (2017): 133-135. doi: https://doi.org/10.1016/j.joco.2017.01.004
Do JL, Olmos de Koo LC, Ameri H. Atypical chronic central serous chorioretinopathy with cystoid macular edema: Therapeutic response to medical and laser therapy. J Curr Ophthalmol. 2017 Feb 17;29(2):133-135. doi: 10.1016/j.joco.2017.01.004. eCollection 2017 Jun. PMID: 28626824; PMCID: PMC5463008.
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A case of 17 alpha-hydroxylase deficiency.

Clinical and experimental reproductive medicine

Kim SM, Rhee JH.
PMID: 26161337
Clin Exp Reprod Med. 2015 Jun;42(2):72-6. doi: 10.5653/cerm.2015.42.2.72. Epub 2015 Jun 30.

17α-hydroxylase and 17,20-lyase are enzymes encoded by the CYP17A1 gene and are required for the synthesis of sex steroids and cortisol. In 17α-hydroxylase deficiency, there are low blood levels of estrogens, androgens, and cortisol, and resultant compensatory increases in...

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Kim SM, Rhee JH. A case of 17 alpha-hydroxylase deficiency. Clin Exp Reprod Med. 2015;42(2):72-6doi: 10.5653/cerm.2015.42.2.72.
Kim, S. M., & Rhee, J. H. (2015). A case of 17 alpha-hydroxylase deficiency. Clinical and experimental reproductive medicine, 42(2), 72-6. https://doi.org/10.5653/cerm.2015.42.2.72
Kim, Sung Mee, and Rhee, Jeong Ho. "A case of 17 alpha-hydroxylase deficiency." Clinical and experimental reproductive medicine vol. 42,2 (2015): 72-6. doi: https://doi.org/10.5653/cerm.2015.42.2.72
Kim SM, Rhee JH. A case of 17 alpha-hydroxylase deficiency. Clin Exp Reprod Med. 2015 Jun;42(2):72-6. doi: 10.5653/cerm.2015.42.2.72. Epub 2015 Jun 30. PMID: 26161337; PMCID: PMC4496435.
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Effect of Chronic Blockade of the Kallikrein-Kinin System on the Development of Hypertension in Rats.

Hypertension (Dallas, Tex. : 1979)

Rhaleb NE, Yang XP, Nanba M, Shesely EG, Carretero OA.
PMID: 11208766
Hypertension. 2001 Jan;37(1):121-128. doi: 10.1161/01.hyp.37.1.121.

-The kallikrein-kininogen-kinin system is an important vasodilator and vasodepressor component of the cardiovascular system. Acting mainly through B(2) receptors, kinins may counterbalance the pressor effect of angiotensin II, salt, and mineralocorticoids plus salt. Using rats lacking the bradykinin precursors...

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Rhaleb NE, Yang XP, Nanba M, et al. Effect of Chronic Blockade of the Kallikrein-Kinin System on the Development of Hypertension in Rats. Hypertension. 2001;37(1):121-128doi: 10.1161/01.hyp.37.1.121.
Rhaleb, N. E., Yang, X. P., Nanba, M., Shesely, E. G., & Carretero, O. A. (2001). Effect of Chronic Blockade of the Kallikrein-Kinin System on the Development of Hypertension in Rats. Hypertension (Dallas, Tex. : 1979), 37(1), 121-128. https://doi.org/10.1161/01.hyp.37.1.121
Rhaleb, Nour-Eddine, et al. "Effect of Chronic Blockade of the Kallikrein-Kinin System on the Development of Hypertension in Rats." Hypertension (Dallas, Tex. : 1979) vol. 37,1 (2001): 121-128. doi: https://doi.org/10.1161/01.hyp.37.1.121
Rhaleb NE, Yang XP, Nanba M, Shesely EG, Carretero OA. Effect of Chronic Blockade of the Kallikrein-Kinin System on the Development of Hypertension in Rats. Hypertension. 2001 Jan;37(1):121-128. doi: 10.1161/01.hyp.37.1.121. PMID: 11208766.
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Mineralocorticoid Receptor Blocker Protects against Podocyte-Dependent Glomerulosclerosis.

Nephron extra

Takagi N, Tanizawa T, Kon V, Fogo AB, Ichikawa I, Ma J.
PMID: 22479265
Nephron Extra. 2012 Jan;2(1):17-26. doi: 10.1159/000334961. Epub 2012 Jan 31.

BACKGROUND: We previously showed that angiotensin type 1 receptor (AT1) blocker (ARB) attenuates glomerular injury in Nphs1-hCD25 (NEP25) transgenic mice, a model of selective podocyte injury. However, subsequent studies in NEP25 mice with podocyte-specific deficiency of AT1 revealed that...

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Takagi N, Tanizawa T, Kon V, et al. Mineralocorticoid Receptor Blocker Protects against Podocyte-Dependent Glomerulosclerosis. Nephron Extra. 2012;2(1):17-26doi: 10.1159/000334961.
Takagi, N., Tanizawa, T., Kon, V., Fogo, A. B., Ichikawa, I., & Ma, J. (2012). Mineralocorticoid Receptor Blocker Protects against Podocyte-Dependent Glomerulosclerosis. Nephron extra, 2(1), 17-26. https://doi.org/10.1159/000334961
Takagi, Nobuaki, et al. "Mineralocorticoid Receptor Blocker Protects against Podocyte-Dependent Glomerulosclerosis." Nephron extra vol. 2,1 (2012): 17-26. doi: https://doi.org/10.1159/000334961
Takagi N, Tanizawa T, Kon V, Fogo AB, Ichikawa I, Ma J. Mineralocorticoid Receptor Blocker Protects against Podocyte-Dependent Glomerulosclerosis. Nephron Extra. 2012 Jan;2(1):17-26. doi: 10.1159/000334961. Epub 2012 Jan 31. PMID: 22479265; PMCID: PMC3318935.
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Congenital Adrenal Hyperplasia due to 17-alpha-hydoxylase/17,20-lyase Deficiency Presenting with Hypertension and Pseudohermaphroditism: First Case Report from Oman.

Oman medical journal

Mula-Abed WA, Pambinezhuth FB, Al-Kindi MK, Al-Busaidi NB, Al-Muslahi HN, Al-Lamki MA.
PMID: 24498484
Oman Med J. 2014 Jan;29(1):55-9. doi: 10.5001/omj.2014.12.

This is the first report of congenital adrenal hyperplasia (CAH) due to combined 17α-hydroxylase/17,20 lyase deficiency in an Omani patient who was initially treated for many years as a case of hypertension. CAH is an uncommon disorder that results...

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Mula-Abed WA, Pambinezhuth FB, Al-Kindi MK, et al. Congenital Adrenal Hyperplasia due to 17-alpha-hydoxylase/17,20-lyase Deficiency Presenting with Hypertension and Pseudohermaphroditism: First Case Report from Oman. Oman Med J. 2014;29(1):55-9doi: 10.5001/omj.2014.12.
Mula-Abed, W. A., Pambinezhuth, F. B., Al-Kindi, M. K., Al-Busaidi, N. B., Al-Muslahi, H. N., & Al-Lamki, M. A. (2014). Congenital Adrenal Hyperplasia due to 17-alpha-hydoxylase/17,20-lyase Deficiency Presenting with Hypertension and Pseudohermaphroditism: First Case Report from Oman. Oman medical journal, 29(1), 55-9. https://doi.org/10.5001/omj.2014.12
Mula-Abed, Waad-Allah S, et al. "Congenital Adrenal Hyperplasia due to 17-alpha-hydoxylase/17,20-lyase Deficiency Presenting with Hypertension and Pseudohermaphroditism: First Case Report from Oman." Oman medical journal vol. 29,1 (2014): 55-9. doi: https://doi.org/10.5001/omj.2014.12
Mula-Abed WA, Pambinezhuth FB, Al-Kindi MK, Al-Busaidi NB, Al-Muslahi HN, Al-Lamki MA. Congenital Adrenal Hyperplasia due to 17-alpha-hydoxylase/17,20-lyase Deficiency Presenting with Hypertension and Pseudohermaphroditism: First Case Report from Oman. Oman Med J. 2014 Jan;29(1):55-9. doi: 10.5001/omj.2014.12. PMID: 24498484; PMCID: PMC3910417.
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Autosomal dominant pseudohypoaldosteronism type 1 in an infant with salt wasting crisis associated with urinary tract infection and obstructive uropathy.

Case reports in endocrinology

Bowden SA, Cozzi C, Hickey SE, Thrush DL, Astbury C, Nuthakki S.
PMID: 24455331
Case Rep Endocrinol. 2013;2013:524647. doi: 10.1155/2013/524647. Epub 2013 Dec 19.

Type 1 pseudohypoaldosteronism (PHA1) is a salt wasting syndrome caused by renal resistance to aldosterone. Primary renal PHA1 or autosomal dominant PHA1 is caused by mutations in mineralocorticoids receptor gene (NR3C2), while secondary PHA1 is frequently associated with urinary...

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Bowden SA, Cozzi C, Hickey SE, et al. Autosomal dominant pseudohypoaldosteronism type 1 in an infant with salt wasting crisis associated with urinary tract infection and obstructive uropathy. Case Rep Endocrinol. 2013;2013:524647doi: 10.1155/2013/524647.
Bowden, S. A., Cozzi, C., Hickey, S. E., Thrush, D. L., Astbury, C., & Nuthakki, S. (2013). Autosomal dominant pseudohypoaldosteronism type 1 in an infant with salt wasting crisis associated with urinary tract infection and obstructive uropathy. Case reports in endocrinology, 2013524647. https://doi.org/10.1155/2013/524647
Bowden, Sasigarn A, et al. "Autosomal dominant pseudohypoaldosteronism type 1 in an infant with salt wasting crisis associated with urinary tract infection and obstructive uropathy." Case reports in endocrinology vol. 2013 (2013): 524647. doi: https://doi.org/10.1155/2013/524647
Bowden SA, Cozzi C, Hickey SE, Thrush DL, Astbury C, Nuthakki S. Autosomal dominant pseudohypoaldosteronism type 1 in an infant with salt wasting crisis associated with urinary tract infection and obstructive uropathy. Case Rep Endocrinol. 2013;2013:524647. doi: 10.1155/2013/524647. Epub 2013 Dec 19. PMID: 24455331; PMCID: PMC3880733.
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Benign adrenal adenomas secreting excess mineralocorticoids and glucocorticoids.

Endocrinology, diabetes & metabolism case reports

Yoon V, Heyliger A, Maekawa T, Sasano H, Carrick K, Woodruff S, Rabaglia J, Auchus RJ, Ghayee HK.
PMID: 24616772
Endocrinol Diabetes Metab Case Rep. 2013;2013:130042. doi: 10.1530/EDM-13-0042. Epub 2013 Sep 23.

OBJECTIVE: To recognize that benign adrenal adenomas can co-secrete excess aldosterone and cortisol, which can change clinical management.METHODS: We reviewed the clinical and histological features of an adrenal tumor co-secreting aldosterone and cortisol in a patient. Biochemical testing as...

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Yoon V, Heyliger A, Maekawa T, et al. Benign adrenal adenomas secreting excess mineralocorticoids and glucocorticoids. Endocrinol Diabetes Metab Case Rep. 2013;2013:130042doi: 10.1530/EDM-13-0042.
Yoon, V., Heyliger, A., Maekawa, T., Sasano, H., Carrick, K., Woodruff, S., Rabaglia, J., Auchus, R. J., & Ghayee, H. K. (2013). Benign adrenal adenomas secreting excess mineralocorticoids and glucocorticoids. Endocrinology, diabetes & metabolism case reports, 2013130042. https://doi.org/10.1530/EDM-13-0042
Yoon, Vivienne, et al. "Benign adrenal adenomas secreting excess mineralocorticoids and glucocorticoids." Endocrinology, diabetes & metabolism case reports vol. 2013 (2013): 130042. doi: https://doi.org/10.1530/EDM-13-0042
Yoon V, Heyliger A, Maekawa T, Sasano H, Carrick K, Woodruff S, Rabaglia J, Auchus RJ, Ghayee HK. Benign adrenal adenomas secreting excess mineralocorticoids and glucocorticoids. Endocrinol Diabetes Metab Case Rep. 2013;2013:130042. doi: 10.1530/EDM-13-0042. Epub 2013 Sep 23. PMID: 24616772; PMCID: PMC3922398.
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Editorial: Updates and New Concepts in Regulation of Proinflammatory Gene Expression by Steroid Hormones.

Frontiers in endocrinology

Glezer I, Scavone C, Avellar MCW.
PMID: 29755408
Front Endocrinol (Lausanne). 2018 Apr 27;9:191. doi: 10.3389/fendo.2018.00191. eCollection 2018.

No abstract available.

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Glezer I, Scavone C, Avellar MCW. Editorial: Updates and New Concepts in Regulation of Proinflammatory Gene Expression by Steroid Hormones. Front Endocrinol (Lausanne). 2018;9:191doi: 10.3389/fendo.2018.00191.
Glezer, I., Scavone, C., & Avellar, M. C. W. (2018). Editorial: Updates and New Concepts in Regulation of Proinflammatory Gene Expression by Steroid Hormones. Frontiers in endocrinology, 9191. https://doi.org/10.3389/fendo.2018.00191
Glezer, Isaias, et al. "Editorial: Updates and New Concepts in Regulation of Proinflammatory Gene Expression by Steroid Hormones." Frontiers in endocrinology vol. 9 (2018): 191. doi: https://doi.org/10.3389/fendo.2018.00191
Glezer I, Scavone C, Avellar MCW. Editorial: Updates and New Concepts in Regulation of Proinflammatory Gene Expression by Steroid Hormones. Front Endocrinol (Lausanne). 2018 Apr 27;9:191. doi: 10.3389/fendo.2018.00191. eCollection 2018. PMID: 29755408; PMCID: PMC5934434.
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Thyroid carcinoma with atypical metastasis to the pituitary gland and unexpected postmortal diagnosis.

Endocrinology, diabetes & metabolism case reports

Popławska-Kita A, Wielogórska M, Poplawski Ł, Siewko K, Adamska A, Szumowski P, Myśliwiec P, Myśliwiec J, Reszeć J, Kamiński G, Dzięcioł J, Tobiaszewska D, Szelachowska M, Krętowski AJ.
PMID: 32168468
Endocrinol Diabetes Metab Case Rep. 2020 Mar 13;2020. doi: 10.1530/EDM-19-0148. Epub 2020 Mar 13.

SUMMARY: Papillary thyroid gland carcinoma is the most common type of malignancy of the endocrine system. Metastases to the pituitary gland have been described as a complication of papillary thyroid cancer in few reported cases since 1965. We report...

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Popławska-Kita A, Wielogórska M, Poplawski Ł, et al. Thyroid carcinoma with atypical metastasis to the pituitary gland and unexpected postmortal diagnosis. Endocrinol Diabetes Metab Case Rep. 2020;2020doi: 10.1530/EDM-19-0148.
Popławska-Kita, A., Wielogórska, M., Poplawski, �. �., Siewko, K., Adamska, A., Szumowski, P., Myśliwiec, P., Myśliwiec, J., Reszeć, J., Kamiński, G., Dzięcioł, J., Tobiaszewska, D., Szelachowska, M., & Krętowski, A. J. (2020). Thyroid carcinoma with atypical metastasis to the pituitary gland and unexpected postmortal diagnosis. Endocrinology, diabetes & metabolism case reports, 2020. https://doi.org/10.1530/EDM-19-0148
Popławska-Kita, Anna, et al. "Thyroid carcinoma with atypical metastasis to the pituitary gland and unexpected postmortal diagnosis." Endocrinology, diabetes & metabolism case reports vol. 2020 (2020). doi: https://doi.org/10.1530/EDM-19-0148
Popławska-Kita A, Wielogórska M, Poplawski Ł, Siewko K, Adamska A, Szumowski P, Myśliwiec P, Myśliwiec J, Reszeć J, Kamiński G, Dzięcioł J, Tobiaszewska D, Szelachowska M, Krętowski AJ. Thyroid carcinoma with atypical metastasis to the pituitary gland and unexpected postmortal diagnosis. Endocrinol Diabetes Metab Case Rep. 2020 Mar 13;2020. doi: 10.1530/EDM-19-0148. Epub 2020 Mar 13. PMID: 32168468; PMCID: PMC7077587.
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[The specific features of adrenal steroidogenesis in patients with congenital adrenal cortical dysfunction due to 21-hydroxylase deficiency].

Problemy endokrinologii

Serebryakova IP, Velikanova LI, Vorokhobina NV, Silnitskiy PA, Strelnikova EG.
PMID: 31627545
Probl Endokrinol (Mosk). 2005 Aug 15;51(4):22-26. doi: 10.14341/probl200551422-26.

Forty-two patients with classical forms of congenital adrenal cortical dysfunction (CACD) (22 patients with salt-loosing form and 20 patients with simple virile form) caused by 21-hydroxylase deficiency and 29 female with an obscure form of the disease were examined....

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Serebryakova IP, Velikanova LI, Vorokhobina NV, et al. [The specific features of adrenal steroidogenesis in patients with congenital adrenal cortical dysfunction due to 21-hydroxylase deficiency]. Probl Endokrinol (Mosk). 2005;51(4):22-26doi: 10.14341/probl200551422-26.
Serebryakova, I. P., Velikanova, L. I., Vorokhobina, N. V., Silnitskiy, P. A., & Strelnikova, E. G. (2005). [The specific features of adrenal steroidogenesis in patients with congenital adrenal cortical dysfunction due to 21-hydroxylase deficiency]. Problemy endokrinologii, 51(4), 22-26. https://doi.org/10.14341/probl200551422-26
Serebryakova, I P, et al. "[The specific features of adrenal steroidogenesis in patients with congenital adrenal cortical dysfunction due to 21-hydroxylase deficiency]." Problemy endokrinologii vol. 51,4 (2005): 22-26. doi: https://doi.org/10.14341/probl200551422-26
Serebryakova IP, Velikanova LI, Vorokhobina NV, Silnitskiy PA, Strelnikova EG. [The specific features of adrenal steroidogenesis in patients with congenital adrenal cortical dysfunction due to 21-hydroxylase deficiency]. Probl Endokrinol (Mosk). 2005 Aug 15;51(4):22-26. doi: 10.14341/probl200551422-26. Russian. PMID: 31627545.
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Dysfunction of the hypothalamic‑pituitary‑adrenal axis in male rat offspring with prenatal food restriction: Fetal programming of hypothalamic hyperexcitability and poor hippocampal feedback.

Molecular medicine reports

Wen Y, Cheng S, Lu J, He X, Jiao Z, Xu D, Wang H.
PMID: 34796908
Mol Med Rep. 2022 Jan;25(1). doi: 10.3892/mmr.2021.12537. Epub 2021 Nov 19.

Prenatal food restriction (PFR) induces dysfunction of the hypothalamic‑pituitary‑adrenal (HPA) axis in the adult offspring. The aim of the present study was to identify the underlying mechanism of this process. Pregnant rats were placed on a restricted diet between...

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Wen Y, Cheng S, Lu J, et al. Dysfunction of the hypothalamic‑pituitary‑adrenal axis in male rat offspring with prenatal food restriction: Fetal programming of hypothalamic hyperexcitability and poor hippocampal feedback. Mol Med Rep. 2021;25(1)doi: 10.3892/mmr.2021.12537.
Wen, Y., Cheng, S., Lu, J., He, X., Jiao, Z., Xu, D., & Wang, H. (2022). Dysfunction of the hypothalamic‑pituitary‑adrenal axis in male rat offspring with prenatal food restriction: Fetal programming of hypothalamic hyperexcitability and poor hippocampal feedback. Molecular medicine reports, 25(1), . https://doi.org/10.3892/mmr.2021.12537
Wen, Yinxian, et al. "Dysfunction of the hypothalamic‑pituitary‑adrenal axis in male rat offspring with prenatal food restriction: Fetal programming of hypothalamic hyperexcitability and poor hippocampal feedback." Molecular medicine reports vol. 25,1 (2022). doi: https://doi.org/10.3892/mmr.2021.12537
Wen Y, Cheng S, Lu J, He X, Jiao Z, Xu D, Wang H. Dysfunction of the hypothalamic‑pituitary‑adrenal axis in male rat offspring with prenatal food restriction: Fetal programming of hypothalamic hyperexcitability and poor hippocampal feedback. Mol Med Rep. 2022 Jan;25(1). doi: 10.3892/mmr.2021.12537. Epub 2021 Nov 19. PMID: 34796908; PMCID: PMC8619836.
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Acute coronary syndrome with ST segment elevation in a patient with Addison disease: Case report and brief review of physiopathological mechanisms: A case study.

Experimental and therapeutic medicine

Maranduca MA, Statescu C, Sascau RA, Dima N, Hurjui LL, Serban DN, Serban IL.
PMID: 32742359
Exp Ther Med. 2020 Aug;20(2):1230-1236. doi: 10.3892/etm.2020.8855. Epub 2020 Jun 10.

The adrenal gland serve important roles in the modulation of the immune response, the adjustment of blood pressure, the stress reaction via glucocorticoids and the hydroelectrolytic balance via mineralocorticoids. Primary adrenal insufficiency, known as Addison disease, is characterized by...

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Maranduca MA, Statescu C, Sascau RA, et al. Acute coronary syndrome with ST segment elevation in a patient with Addison disease: Case report and brief review of physiopathological mechanisms: A case study. Exp Ther Med. 2020;20(2):1230-1236doi: 10.3892/etm.2020.8855.
Maranduca, M. A., Statescu, C., Sascau, R. A., Dima, N., Hurjui, L. L., Serban, D. N., & Serban, I. L. (2020). Acute coronary syndrome with ST segment elevation in a patient with Addison disease: Case report and brief review of physiopathological mechanisms: A case study. Experimental and therapeutic medicine, 20(2), 1230-1236. https://doi.org/10.3892/etm.2020.8855
Maranduca, Minela Aida, et al. "Acute coronary syndrome with ST segment elevation in a patient with Addison disease: Case report and brief review of physiopathological mechanisms: A case study." Experimental and therapeutic medicine vol. 20,2 (2020): 1230-1236. doi: https://doi.org/10.3892/etm.2020.8855
Maranduca MA, Statescu C, Sascau RA, Dima N, Hurjui LL, Serban DN, Serban IL. Acute coronary syndrome with ST segment elevation in a patient with Addison disease: Case report and brief review of physiopathological mechanisms: A case study. Exp Ther Med. 2020 Aug;20(2):1230-1236. doi: 10.3892/etm.2020.8855. Epub 2020 Jun 10. PMID: 32742359; PMCID: PMC7388315.
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