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[PMID]: 29502244
[Au] Autor:Simonetti I; Trovato P; Verde F; Tarotto L; Della Casa R; Lonardo MC; Vallone G; Caprio MG
[Ad] Address:Department of Advanced Biomedical Sciences, University of Naples Federico II, Naples, Italy. igino.simonetti@gmail.com.
[Ti] Title:A rare case of hydrometrocolpos from persistent urogenital sinus in patient affected by adrenogenital syndrome.
[So] Source:J Ultrasound;, 2018 Mar 03.
[Is] ISSN:1876-7931
[Cp] Country of publication:Italy
[La] Language:eng
[Ab] Abstract:Persistent urogenital sinus (PUGS) is a congenital pathological condition characterized by an abnormal communication between the urethra and vagina, which has an estimated incidence of 0.6/10,000 female births. It could be the only known malformation or part of a syndrome. PUGS is commonly shown by a pelvic mass, related to a distended bladder, hydrometrocolpos which is due to an obstruction leading to the dilation of the vagina and uterus (i.e., imperforate hymen, transverse vaginal septum or atresia, and PUGS) or both. We present a case of female patient with classical congenital adrenal hyperplasia, diagnosed on the 7th day of life, with ambiguous genitalia, untreated surgically only with hormone therapy by parental decision. The patient, at the age of 5 years and 5 months, came to our observation for a pelvic ultrasound, which revealed retrovesical neoformation with anechoic content and regular walls. We performed the ultrasound examination that showed the dilation of the cervix and the vaginal canal with anechoic finely corpuscolated content in the declining portion, compatible with hydrometrocolpos from probable persistence of the urogenital sinus. The voiding cystourethrography (VCUG) confirmed the ultrasound diagnosis, with evidence of urogenital sinus. In conclusion, ultrasound is the first diagnostic tool, but need to be completed by other technical procedures, which VCUG or magnetic resonance imaging to observe the site of fusion of the urinary and genital tract.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:Publisher
[do] DOI:10.1007/s40477-018-0290-9

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[PMID]: 28471529
[Au] Autor:Trivisano M; Lucchi C; Rustichelli C; Terracciano A; Cusmai R; Ubertini GM; Giannone G; Bertini ES; Vigevano F; Gecz J; Biagini G; Specchio N
[Ad] Address:Neurology Unit, Department of Neuroscience, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
[Ti] Title:Reduced steroidogenesis in patients with PCDH19-female limited epilepsy.
[So] Source:Epilepsia;58(6):e91-e95, 2017 06.
[Is] ISSN:1528-1167
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Patients affected by protocadherin 19 (PCDH19)-female limited epilepsy (PCDH19-FE) present a remarkable reduction in allopregnanolone blood levels. However, no information is available on other neuroactive steroids and the steroidogenic response to hormonal stimulation. For this reason, we evaluated allopregnanolone, pregnanolone, and pregnenolone sulfate by liquid chromatographic procedures coupled with electrospray tandem mass spectrometry in 12 unrelated patients and 15 age-matched controls. We also tested cortisol, estradiol, progesterone, and 17OH-progesterone using standard immunoassays. Apart from estradiol and progesterone, all the considered hormones were evaluated in basal condition and after stimulation with adrenocorticotropic hormone (ACTH). A generalized decrease in blood levels of almost all measured neuroactive steroids was found. When considering sexual development, cortisol and pregnenolone sulfate basal levels were significantly reduced in postpubertal girls affected by PCDH19-FE. Of interest, ACTH administration did not recover pregnenolone sulfate serum levels but restored cortisol to control levels. In prepubertal girls with PCDH19-FE, by challenging adrenal function with ACTH we disclosed defects in the production of cortisol, pregnenolone sulfate, and 17OH-progesterone, which were not apparent in basal condition. These findings point to multiple defects in peripheral steroidogenesis associated with and potentially relevant to PCDH19-FE. Some of these defects could be addressed by stimulating adrenocortical activity.
[Mh] MeSH terms primary: Cadherins/genetics
Epilepsy/blood
Epilepsy/genetics
Genetic Diseases, X-Linked/blood
Genetic Diseases, X-Linked/genetics
Gonadal Steroid Hormones/blood
Intellectual Disability/blood
Intellectual Disability/genetics
Pregnanolone/blood
Pregnanolone/deficiency
Pregnenolone/blood
[Mh] MeSH terms secundary: 17-alpha-Hydroxyprogesterone/blood
Adolescent
Adrenocorticotropic Hormone/pharmacology
Adrenogenital Syndrome/blood
Case-Control Studies
Child
Child, Preschool
DNA Mutational Analysis
Estradiol/blood
Female
Humans
Hydrocortisone/blood
Progesterone/blood
Prospective Studies
Puberty, Precocious/blood
Puberty, Precocious/genetics
Reference Values
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Cadherins); 0 (Gonadal Steroid Hormones); 0 (PCDH19 protein, human); 04Y4D91RG0 (pregnenolone sulfate); 4G7DS2Q64Y (Progesterone); 4TI98Z838E (Estradiol); 68-96-2 (17-alpha-Hydroxyprogesterone); 73R90F7MQ8 (Pregnenolone); 9002-60-2 (Adrenocorticotropic Hormone); BXO86P3XXW (Pregnanolone); WI4X0X7BPJ (Hydrocortisone)
[Em] Entry month:1707
[Cu] Class update date: 180107
[Lr] Last revision date:180107
[Js] Journal subset:IM
[Da] Date of entry for processing:170505
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13772

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[PMID]: 29279502
[Au] Autor:Hashimoto A; Yoshino H; Yoshikawa F; Kumashiro N; Ando Y; Yamabe F; Akishima-Fukasawa Y; Honma N; Uchino H; Hirose T
[Ad] Address:Department of Internal Medicine. Division of Diabetes, Metabolism and Endocrinology, Japan.
[Ti] Title:Giant Cavernous Hemangioma of the Adrenal Gland in an Elderly Patient.
[So] Source:Intern Med;, 2017 Dec 27.
[Is] ISSN:1349-7235
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:Cavernous hemangioma is a rare, non-functional, benign adrenal tumor. Adrenal cavernous hemangioma is often diagnosed after surgery with a histologic examination. A 70-year-old man complaining of appetite loss was admitted to our hospital. An incidental large left adrenal mass was found by computed tomography (CT). There were no clinical signs of adrenogenital syndrome, Cushing's syndrome or primary aldosteronism. Total resection was carried out. The pathological diagnosis was cavernous hemangioma. The differentiation of adrenal tumor is necessary in cases of large tumors, and resection is desirable given the risks of hemorrhaging and rupture.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 171227
[Lr] Last revision date:171227
[St] Status:Publisher
[do] DOI:10.2169/internalmedicine.9711-17

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[PMID]: 28549629
[Au] Autor:Naouar S; Braiek S; El Kamel R
[Ad] Address:Ibn El Jazzar teaching hospital, Les Aghlabides surgical division, urology department, 3100 Kairouan, Tunisia. Electronic address: snaouar@laposte.net.
[Ti] Title:Testicular tumors of adrenogenital syndrome: From physiopathology to therapy.
[So] Source:Presse Med;46(6 Pt 1):572-578, 2017 Jun.
[Is] ISSN:2213-0276
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Testicular tumor of adrenogenital syndrome is a rare and benign anomaly usually presenting as bilateral testicular masses. It is the most important cause of infertility in adult male congenital adrenal hyperplasia. Distinction between testicular tumors of adrenogenital syndrome and Leydig cell tumors can be problematic; it is based on clinical, histopathologic, immunohistochemical and endocrine features. Biopsy is advised in cases of longstanding tumors in infertile patients and when surgery is indicated. Fertility preservation is a key management goal in testicular tumor of adrenogenital syndrome. In stages 2 and 3, intensified glucocorticoid treatment is recommended as a first step treatment. Sparing surgical approach is preferred for tumors of stage 4 and steroid unresponsive masses. Magnetic resonance imaging is recommended before surgery. The only indication of surgery in stage 5 is testicular pain.
[Mh] MeSH terms primary: Adrenogenital Syndrome/physiopathology
Adrenogenital Syndrome/therapy
Testicular Neoplasms/physiopathology
Testicular Neoplasms/therapy
[Mh] MeSH terms secundary: Adrenal Rest Tumor/diagnosis
Adrenal Rest Tumor/pathology
Adrenal Rest Tumor/physiopathology
Adrenal Rest Tumor/therapy
Adrenocorticotropic Hormone/blood
Adrenogenital Syndrome/diagnosis
Adrenogenital Syndrome/pathology
Adult
Diagnosis, Differential
Glucocorticoids/therapeutic use
Humans
Leydig Cell Tumor/diagnosis
Leydig Cell Tumor/pathology
Leydig Cell Tumor/physiopathology
Leydig Cell Tumor/therapy
Magnetic Resonance Imaging
Male
Testicular Neoplasms/diagnosis
Testicular Neoplasms/pathology
Testis/pathology
Testis/physiopathology
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Glucocorticoids); 9002-60-2 (Adrenocorticotropic Hormone)
[Em] Entry month:1708
[Cu] Class update date: 170817
[Lr] Last revision date:170817
[Js] Journal subset:IM
[Da] Date of entry for processing:170528
[St] Status:MEDLINE

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[PMID]: 27696245
[Au] Autor:Mesa H; Gilles S; Datta MW; Murugan P; Larson W; Dachel S; Manivel C
[Ad] Address:Department of Pathology and Laboratory Medicine, Veterans Administration Health Care System, One Veterans Drive, Minneapolis, MN, 55417, USA. Hector.Mesa@va.gov.
[Ti] Title:Immunophenotypic differences between neoplastic and non-neoplastic androgen-producing cells containing and lacking Reinke crystals.
[So] Source:Virchows Arch;469(6):679-686, 2016 Dec.
[Is] ISSN:1432-2307
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:We performed a detailed morphologic, immunophenotypic, and endocrine characterization of neoplastic and non-neoplastic lesions of androgen-producing cells known to harbor or lack Reinke crystals (RCs) with an aim to provide further insight into the nature of these cells and crystals. Study cases were selected from the files of participating hospitals and subclassified according to current classifications: 20 with Leydig cell tumors (LCTs), 2 with testicular adrenal rest tumors (TARTs), 2 with testicular tumors of adrenogenital syndrome (TTAGS), and 2 with androgen insensitivity syndrome (AIS). An extensive immunophenotypic panel including markers used in sex cord-stromal cell tumors, androgen hormones, enzymes, and receptors was applied to the cases and 10 non-tumoral adrenal glands. Non-tumoral tissues were scored separately. RCs were present in 90 % of LCT cases and all cases with normal Leydig cells; RCs stained specifically with calretinin and 3ß-hydroxysteroid dehydrogenase (3BHSD) and were present only in cells with high concomitant expression of both proteins, a phenotype unique to Leydig cells and LCTs. Leydig cells from AIS cases lack RCs due to decreased expression of 3BHSD. Calretinin is decreased in testicular adrenal-like tumors and absent in normal adrenocortical cells, which explain why they lack RCs. Calretinin expression in androgen-producing cells is independent from androgen receptors and androgen synthesis. RCs represent for the most part, if not exclusively, crystallized forms of a 3BHSD/calretinin complex. Androgen-producing cells containing and lacking RCs differ mainly in the level of expression of these proteins and androgen receptors.
[Mh] MeSH terms primary: Calbindin 2/metabolism
Leydig Cells/cytology
Ovarian Neoplasms/metabolism
Sex Cord-Gonadal Stromal Tumors/metabolism
Testicular Neoplasms/metabolism
[Mh] MeSH terms secundary: Adolescent
Adult
Aged
Androgens/biosynthesis
Biomarkers, Tumor/metabolism
Child
Female
Humans
Immunophenotyping/methods
Male
Middle Aged
Ovarian Neoplasms/pathology
Receptors, Androgen/metabolism
Sex Cord-Gonadal Stromal Tumors/diagnosis
Sex Cord-Gonadal Stromal Tumors/pathology
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Androgens); 0 (Biomarkers, Tumor); 0 (Calbindin 2); 0 (Receptors, Androgen)
[Em] Entry month:1702
[Cu] Class update date: 171006
[Lr] Last revision date:171006
[Js] Journal subset:IM
[Da] Date of entry for processing:161004
[St] Status:MEDLINE

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[PMID]: 27242977
[Au] Autor:González R; Ludwikowski BM
[Ad] Address:Pediatric Surgery and Urology, Auf der Bult Kinder- und Jugendkrankenhaus , Hannover , Germany.
[Ti] Title:Should CAH in Females Be Classified as DSD?
[So] Source:Front Pediatr;4:48, 2016.
[Is] ISSN:2296-2360
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Great controversies and misunderstandings have developed around the relatively recently coined term disorders of sex development (DSD). In this article, we question the wisdom of including XX individuals with congenital adrenal hyperplasia (CAH) in the DSD category and develop arguments against it based on the published literature on the subject. It is clear that females with CAH assigned the female gender before 24 months of age and properly managed retain the female gender identity regardless of the Prader grade. Females with CAH and low Prader grades have the potential for a normal sexual and reproductive life. Those with greater degrees of prenatal androgen exposure (Prader grades IV and V) raised as females also identify themselves as females but experience more male-like behavior in childhood, have a greater rate of homosexuality, and have greater difficulty with vaginal penetration and maintaining pregnancies. Improvement in surgical techniques, better endocrinological, psychological, and surgical follow-up may lessen these problems in the future. Given the fact that the term DSD includes many conditions with problematic gender identity and conflicts with the gender assigned at birth, it may be appropriate to exclude females with CAH from the DSD classification.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1605
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Da] Date of entry for processing:160601
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.3389/fped.2016.00048

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[PMID]: 26965407
[Au] Autor:D'Cunha AR; Kurian JJ; Jacob TJ
[Ad] Address:Department of Paediatric Surgery, Christian Medical College and Hospital, Vellore, Tamil Nadu, India.
[Ti] Title:Idiopathic female pseudohermaphroditism with urethral duplication and female hypospadias.
[So] Source:BMJ Case Rep;2016, 2016 Mar 10.
[Is] ISSN:1757-790X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Female hypospadias is a rare anomaly of the female urethra where it opens on the anterior vaginal wall anywhere between the introitus and the fornix. It is often associated with other genitourinary anomalies such as Cloacal malformation, female pseudohermaphroditism, nonneurogenic neurogenic bladder and urethral duplication. Idiopathic female pseudohermaphroditism is extremely rare, and most cases occur secondary to adrenogenital syndrome or maternal androgen exposure. We report a unique case of a 1-year and 4-month-old girl who presented with ambiguous genitalia and renal failure secondary to a non-neurogenic neurogenic bladder. On further evaluation, she was found to have urethral duplication with a hypospadiac female urethra. She initially underwent a vesicostomy and was further planned to undergo an appendicular Mitrofanoff at an older age. The mainstay of treatment in these cases includes relief of bladder outlet obstruction and recovery of renal function by adequate urinary drainage. Clitoral reduction, if cosmetically warranted, may be planned at puberty.
[Mh] MeSH terms primary: 46, XX Disorders of Sex Development
Abnormalities, Multiple/surgery
Hypospadias
Urethra/abnormalities
[Mh] MeSH terms secundary: 46, XX Disorders of Sex Development/diagnostic imaging
46, XX Disorders of Sex Development/surgery
Cystostomy
Disorders of Sex Development
Female
Humans
Male
Ultrasonography
Urinary Bladder Neck Obstruction/surgery
Urinary Diversion/methods
Vagina/abnormalities
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Em] Entry month:1612
[Cu] Class update date: 161230
[Lr] Last revision date:161230
[Js] Journal subset:IM
[Da] Date of entry for processing:160312
[St] Status:MEDLINE

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[PMID]: 26660266
[Au] Autor:Altieri VM; Altieri B; Castellucci R; Alba S; Bottone F; Fragalà E; Mirone V; Greco F
[Ad] Address:Department of Urology, Romolo Hospital, Rocca di Neto (Crotone) - Italy.
[Ti] Title:Leydig cell tumour and giant adrenal myelolipoma associated with adrenogenital syndrome: a case report with a review of the literature.
[So] Source:Urologia;83(1):43-8, 2016 Jan-Mar.
[Is] ISSN:0391-5603
[Cp] Country of publication:Italy
[La] Language:eng
[Ab] Abstract:CONTEXT: Male patients with congenital adrenal hyperplasia (CAH) may develop bilateral testicular adrenal rest tumours (TARTs). These tumours, in most cases, regress with glucocorticoid therapy and their histological differentiation from Leydig-cell tumors is quite difficult. OBJECTIVE: The aim of this study was to differentiate the histological and clinical features of the TARTs from those of the Leydig-cell tumours. METHODS: The authors report a case of bilateral Leydig-cell tumour associated with giant bilateral adrenal myelolipoma in a male with adrenogenital syndrome who was submitted to a bilateral orchiectomy. RESULTS: Testicular neoplasia continue to grow despite adequate hormonal treatment and a bilateral orchiectomy was performed. The histopathological examination of the specimen ultimately confirmed the diagnosis of bilateral Leydig-cell tumour. CONCLUSIONS: This case shows the importance of all the relevant examinations, blood chemistry analysis, and instrumental tests in the differential diagnosis of TARTs and other testicular tumours.
[Mh] MeSH terms primary: Adrenal Gland Neoplasms/complications
Adrenogenital Syndrome/complications
Leydig Cell Tumor/complications
Myelolipoma/complications
Neoplasms, Multiple Primary/complications
Testicular Neoplasms/pathology
[Mh] MeSH terms secundary: Adrenal Gland Neoplasms/pathology
Adrenal Gland Neoplasms/surgery
Adrenogenital Syndrome/pathology
Adrenogenital Syndrome/surgery
Adult
Humans
Leydig Cell Tumor/pathology
Leydig Cell Tumor/surgery
Male
Myelolipoma/pathology
Myelolipoma/surgery
Neoplasms, Multiple Primary/pathology
Neoplasms, Multiple Primary/surgery
Testicular Neoplasms/surgery
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Em] Entry month:1704
[Cu] Class update date: 170428
[Lr] Last revision date:170428
[Js] Journal subset:IM
[Da] Date of entry for processing:151215
[St] Status:MEDLINE
[do] DOI:10.5301/uro.5000162

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[PMID]: 26610199
[Au] Autor:Zennaro MC; Fernandes-Rosa F; Boulkroun S; Jeunemaitre X
[Ad] Address:INSERM, UMRS 970, Paris Cardiovascular Research Center, Paris, France.
[Ti] Title:Bilateral Idiopathic Adrenal Hyperplasia: Genetics and Beyond.
[So] Source:Horm Metab Res;47(13):947-52, 2015 Dec.
[Is] ISSN:1439-4286
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Bilateral adrenal hyperplasia currently accounts for up to 2 thirds of cases of primary aldosteronism. As such, it represents a major opportunity for targeted medical management as opposed to unilateral surgically correctable forms of the disease. Although the majority of cases of primary aldosteronism are sporadic, bilateral adrenal hyperplasia may occur in the context of familial hyperaldosteronism where it is associated with specific germline mutations. Over the past 5 years, impressive progress has been made in our understanding of the genetic basis underlying primary aldosteronism, allowing us to identify and characterize new familial forms of the disease and to understand the mechanisms involved in the formation of aldosterone producing adenoma. In contrast, our knowledge of the genetic contribution to the development of bilateral adrenal hyperplasia, and in a larger context, to renin and aldosterone levels in the general population, is still poor. This review summarizes our current knowledge on the genetics of bilateral adrenal hyperplasia and addresses some open questions to be addressed by future research. In particular, genome-wide association studies in large populations may provide clues to understanding the genetic susceptibility underlying the development of primary aldosteronism.
[Mh] MeSH terms primary: Adrenal Glands/pathology
Adrenogenital Syndrome/genetics
Genetic Predisposition to Disease
[Mh] MeSH terms secundary: Germ-Line Mutation
Humans
Hyperaldosteronism/genetics
Hyperplasia
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Entry month:1609
[Cu] Class update date: 151215
[Lr] Last revision date:151215
[Js] Journal subset:IM
[Da] Date of entry for processing:151127
[St] Status:MEDLINE
[do] DOI:10.1055/s-0035-1565198

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[PMID]: 26351608
[Au] Autor:Vukina J; Chism DD; Sharpless JL; Raynor MC; Milowsky MI; Funkhouser WK
[Ad] Address:Department of Urology, University of North Carolina, Chapel Hill, NC 27599, USA.
[Ti] Title:Metachronous Bilateral Testicular Leydig-Like Tumors Leading to the Diagnosis of Congenital Adrenal Hyperplasia (Adrenogenital Syndrome).
[So] Source:Case Rep Pathol;2015:459318, 2015.
[Is] ISSN:2090-6781
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:A 33-year-old male with a history of left testis Leydig cell tumor (LCT), 3-month status after left radical orchiectomy, presented with a rapidly enlarging (0.6 cm to 3.7 cm) right testicular mass. He underwent a right radical orchiectomy, sections interpreted as showing a similar Leydig cell-like oncocytic proliferation, with a differential diagnosis including metachronous bilateral LCT and metachronous bilateral testicular tumors associated with congenital adrenal hyperplasia (a.k.a. "testicular adrenal rest tumors" (TARTs) and "testicular tumors of the adrenogenital syndrome" (TTAGS)). Additional workup demonstrated a markedly elevated serum adrenocorticotropic hormone (ACTH) and elevated adrenal precursor steroid levels. He was diagnosed with congenital adrenal hyperplasia, 3ß-hydroxysteroid dehydrogenase deficiency (3BHSD) type, and started on treatment. Metachronous bilateral testicular masses in adults should prompt consideration of adult presentation of CAH. Since all untreated CAH patients are expected to have elevated serum ACTH, formal exclusion of CAH prior to surgical resection of a testicular Leydig-like proliferation could be accomplished by screening for elevated serum ACTH.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1509
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Da] Date of entry for processing:150910
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1155/2015/459318


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