bluuebunny/crossref_metadata_2025_split huggingface dataset:
SAT-442 The Impact of Chronic Excess Iodine Intake in Adult Mice Behavior
Authors: Amano Izuki , Takatsuru Yusuke , Haijima Asahi , Haraguchi Shogo , Koibuchi Noriyuki 
Published: May 2020

Abstract
Iodine is one of the essential micronutrient which is required for the synthesis of thyroid hormones. Thus, iodine deficiency may result in the hypothyroidism. Iodine deficiency is one of the most common causes of preventable mental retardation and brain damage in the world. On the other hand, Japanese iodine intake exceeds that of most other countries, due to the significant seaweed consumption such as kelp. The Japanese Ministry of Health, Labour and Welfare estimates average iodine consumption at 1.2mg/day in Japan. In contrast, the recommended tolerable upper intake levels for adult is 1.1 mg / day in the United States. Generally, Japanese takes twenty times higher amount of iodine than Americans. Iodine tolerance among individual humans varies greatly, and the excess iodine can cause both hyper- and hypo- thyroidism. Furthermore, the effect of thyroid dysfunction due to iodine excess on brain function has not been clarified. In this study, we generated a mouse models for chronic iodine excess and evaluated its effect on brain development. C57BL/6 dams and their pups mice were treated with KIO3 37.4mg/l through drinking water. Behavioral experiments (novel object recognition test, novel object in location test, visual discrimination test, and three-room social behavior test) were conducted at 10-weeks-old. After the behavioral analysis, mice were sacrificed to collect trunk blood and tissues. Excess iodine intake caused hypertrophy of thyroid follicles regardless of the administered dose. However, there were no differences in thyroid hormone status among groups. Thyroid hormone responsive genes in the hippocampus were also not affected in experiment group. In the behavioral analysis, female mice showed an increase in learning ability. In summary, although the chronic overdose of iodine does not affect thyroid hormone levels, it may affect cognitive learning function. The gender difference in the consequence was also observed. These results indicate that the chronic iodine excess may cause various changes, although the body is tolerable with excess iodine.
MON-506 Assessment of Quality of Life in Persons with Thyroid Cancer and Thyroid Nodules: A Single Center Experience
Authors: Raghunathan Sapna , Ouellette Caroline , Fingeret Abbey , Goldner Whitney 
Published: May 2020

Abstract
INTRODUCTION: Despite an excellent prognosis and survival rate, quality of life (QOL) in thyroid cancer is lower than expected. QOL in thyroid cancer survivors is similar to persons with colon and gynecologic cancers, but worse than breast cancer.1 The SF-36 QOL questionnaire has shown to be a valid tool for assessing QOL in thyroid cancer subjects.2 We evaluated QOL in both thyroid nodule and thyroid cancer patients in an institutional cancer registry.
METHODS: The Short Form-36 data version 2 (SF-36) QOL data was obtained from single institution prospective bioinformatics thyroid cancer and benign nodule registry. Physical and mental health scores from the SF-36 questionnaire were obtained from both thyroid cancer and nodule patients. Physical and mental QOL responses were scored on a scale from 20-80 and categorized as either “the same or better than the average population,”; “below average,”; or “well below average.” A two sample Wilcoxon rank sum test and a chi-squared test were used to compare QOL between thyroid cancer and nodule subjects, using QOL as a continuous or categorical variable. Univariate descriptive statistics and bivariate analyses were performed using a Wilcoxon Rank Sum and Chi-squared test for categorical QOL data and Kruskal-Wallis for continuous QOL data.
RESULTS: We analyzed 321 thyroid cancer and 32 nodule subjects who completed the SF-36 at a single point in time after diagnosis. There was no difference between the groups with regard to sex, age or QOL scores overall. Average age was 43 and 48 years in cancer and nodule groups respectively. Average Physical QOL score was 50.8 (standard deviation SD + 8.8) and 29.6 (SD+ 12.1), respectively (p=0.42). Average Mental QOL score was 48.9 (SD + 9.9) and 48.3 (SD + 8.1) respectively, p=0.16. Physical QOL score was significantly decreased as cancer stage increased when evaluating results as a continuous variable: Stage 1: 51.8 + 8.7; Stage 2: 50.6 +9.5; Stage 3: 48.7 + 7.2; Stage 4: 47.4 + 9.2. Results for mental QOL as a continuous variable by cancer stage showed improvement in reported QOL with increasing cancer stage: Stage 1: 48 (SD+ 9.9); Stage 2: 50.6 (SD + 11.1); Stage 3: 51.1 (SD + 9.13); Stage 4: 53 (SD+ 6.4), p=0.03.
CONCLUSIONS: We found no overall difference in physical nor mental QOL between patients with thyroid cancer or benign thyroid nodules. Overall, QOL was in the “same or better than average” for all respondents, but low cancer stage was associated with higher physical and lower mental QOL scores.
REFERENCES:
1. Barbus, Elena & Peştean, Claudiu & Iulia Larg, Maria & Piciu, Doina. (2016). Quality of life in thyroid cancer patients: A literature review. Clujul Medical. 90. 10.15386/cjmed-703
2. Lubitz CC, De Gregorio L, Fingeret AL, et al. Measurement and Variation in Estimation of Quality of Life Effects of Patients Undergoing Treatment for Papillary Thyroid Carcinoma. Thyroid. 2017;27(2):197-206. doi:10.1089/thy.2016.0260
MON-683 Assessment of Features Associated with Diabetic Foot Risk in General Hospital in Lima-Peru
Authors: Yovera-Aldana Marlon Augusto , Perez-Cavero Sonia Helen , Sipiran Candy Ivoone , Barrios Haydee , Callacna Eduardo , Cruz-Estacio Delia , Flores Diana Consuelo , Roncal Lorena , Huayta Julio , Damas-Casani Lucy Nelly , Zubiate Carlos 
Published: May 2020

Abstract
Objectives: To determine the frequency of diabetic foot risk of ulceration and associated factors in patients with type 2 diabetes mellitus.
Methods and materials: We used a cross-sectional descriptive design. Data collection was performed in the foot at risk office at Maria Auxiliadora hospital over a period of 3 years, dating from the october 2016 to september 2019.
Foot risk assessment was based on the International Working Group of Diabetic Foot (IWGDF) system, which evaluates peripheral neuropathy (with monofilament or tuning fork), biomechanical deformity, peripheral arterial disease (altered pulse or ankle branchial index) or a history of foot ulcer1,2. Foot risk frequency was found according to epidemiological characteristics, and the prevalence ratios with 95% confidence interval were calculated to association analysis, we perform bivariate and multivariate analysis using a generalized linear model. This study has the approval of the María Auxiliadora HospitaĹs Ethics Committee.
Results: a total of 402 subjects were included in this study, 63.3% were women, average age 62 yo and diabetes duration &lt;10 years in 56%. 76.6% presented risk to develop ulcer, of which 54.7% presented biomechanical deformation, 37.3% Peripheral Neuropathy (NP), 35.4% Peripheral Arterial Disease (PAD), and 12.7% history of foot ulcer. Patients with foot at risk were associated with older age (RP 1,006, 95% CI 1,001-1.01), and with a score&gt; 5 with respect to &lt;5 in the Total Symptom Score (RP 1.26, 95% CI 1.05-1.51).
Conclusions: 3 of 4 patients have a foot at risk of ulceration, predominantly due to biomechanical deformation and peripheral neuropathy, and this risk was associated with older age and greater pain symptomatology.
References
1. Bakker K, Apelqvist J, Schaper NC. Practical Guidelines on the management and prevention of the diabetic foot 2011. International Working Group on the Diabetic Foot Guidelines. Diabetes Metab Res Rev. 2012; 28(1):225-231
2. Peters E, Lavery L. Effectiveness of the Diabetic Foot Risk Classification System of the International Working Group on the Diabetic Foot. Diabetes Care. 2001 24:1442–7.
SAT-062 Twins with a Homozygous Variant of ARNT2, This Is a Known Saudi Mutation (KSM) of Webb- Dattani Syndrome
Authors: Aljasser Abdullah Abdulruhman 
Published: May 2020

Abstract
Webb-Dattani syndrome (WEDAS) is an autosomal recessive disorder caused by mutation in the ARNT2 gene characterized by frontotemporal hypoplasia, globally delayed development, and pituitary and hypothalamic insufficiency. The condition is reported to be associated with consanguinity and with Saudi Arabian ancestry. We presented twin baby girls with developmental delayment seizures, and microcephaly. They have also hypopituitarism in the form of diabetes insipidus and hypocortlisim. also they have cortical blindness. Their brain MRI shows brain atrophic changes and delayed myelination thin corpus callosum,and small pituitary gland ad absence posterior high signal spot and pituitary stalk. Genetic testing by Exome sequencing was done and it shows A homozygous variant of ARNT2 (ARNT2:NM_014862:exon3:c.147-1G&gt;A). One of this twin her condition deteriorated with uncontrolled seizures and spasticity and died at age 22 months. Conclusion: we report another cases of the ARNT2 mutation in a Saudi family illustrating the disease of webb-dattani Syndrome with seizures and hypopituitarism and severe visual impairment and global developmental delayment.
MON-594 The Peculiarity of the Gut Microbiota in Patients with Different Phenotypes of Obesity (Pilot Study)
Authors: Volkova Natalia , Naboka Julia , Ganenko Lilia , Oksenuk Oksana , Davidenko Ilia , Dzherieva Irina , Zibarev Alexander , Reshetnikov Igor , Sorokina Julia , Degtyareva Julia 
Published: May 2020

Abstract
Recent studies have shown that obesity is not a homogeneous condition and that there is a subgroup of people with obesity, but without metabolic disturbance. This phenotype of obesity is called “metabolically healthy obesity” (MHO) [1]. More and more data are appearing in the scientific literature, indicating that quantitative and qualitative changes in the gut microbiota (GM) can be a trigger in the development of obesity and metabolic disorders [2]. In order to study the role of GM in the development of various types of obesity, 37 patients were examined, divided into 3 groups: group 1 (n = 11) - healthy people without obesity and overweight (control), group 2 (n = 13) - patients with MHO, group 3 (n = 13) - patients with metabolically unhealthy obesity (MUHO). The basic metabolic parameters were determined for all of them and a quantitative assessment of the condition of the GM was performed using the Real-time PCR method. Results: 1. In people from the control group (group 1) in the GM, compared with formal normative indicators, the number of Lactobacillus spp., Bifidobacterium spp., B. thetaiotaomicron was reduced (p&lt;0.05) and indicators of the total bacterial mass and Enterobacter spp./Citrobacter spp. were increased (p&lt;0.05). 2. In subjects with MHO (group 2), GM changes similar to group 1 were observed. However, in comparison to group 1, Klebsiella spp. and Proteus spp. were recorded in feces in quantities exceeding the formal regulatory. In patients with MUHO (group 3), in addition to changes detected in group 2, C. difficile was found in feces, as well as a significant (p &lt;0.05) decrease in F. prausnitzii and an increase (p &lt;0.05) in the detection frequency of banal E.coli, as well as the more diverse composition of the microbiota. Thus, the data obtained as a result of a pilot study certainly indicate changes in the GM in people with different phenotypes of obesity and in healthy ones. Further study of the GM in patients with various types of obesity, but in a larger groups, is required. Reference: 1) Phillips C.M. Metabolically healthy obesity across the life course: epidemiology, determinants and implications. Ann N.Y. Acad Sci 2017 Mar;139(1):85-100.doi:10.1111/nyas.13230. 2). Giovanna Muscogiuri, Elena Cantone, Sara Cassarano, Dario Tuccinardi, Luigi Barrea, Silvia Savastano, Annamaria Colao & on behalf of the Obesity Programs of nutrition, Education, Research and Assessment (OPERA) group. Gut microbiota: a new path to treat obesity. International Journal of Obesity Supplements 2019 Apr;9(1):10-19. doi: 10.1038/s41367-019-0011-7
MON-244 Adenocarcinoma Pituitary Metastasis with Suprasellar Extension
Authors: Reddy Nithin Modhugu , Sethi Bipin Kumar , Kandula Srinivas G N S V , Modi Kirtikumar D , Praveen Kumar 
Published: May 2020

Abstract
Background
Metastasis to the pituitary gland (MP) is an infrequent clinical problem, however, during the last few decades, MPs is increasing in frequency, due both to the improved cancer survival rates and availability of better imaging techniques. Breast cancer, lung cancer and lymphoma are the most common primary sites. MP mimics pituitary adenoma making the diagnosis difficult, especially when clinical evidence of the primary malignancy is absent. We report a case of histologically confirmed pituitary metastasis (adenocarcinoma) from carcinoma of unknown primary, leading to and presenting as panhypopituitarism.
Case details
54 year male HBV carrier, asthmatic, non smoker, non alcoholic was seen elsewhere with complaints of increased frequency of micturition associated with nocturia, increased thirst, asthenia and weight loss of 05 kg since 06 months. He also had loss of libido and erectile dysfunction. Patient never experienced headache, vomiting or visual disturbances. There was no personal or family history of malignancy. On physical examination skin was pale, atrophic with fine wrinkles around the eyes. He had BP of 96/60mmHg and PR 100/min but system examination was otherwise unremarkable. Biochemical evaluation confirmed diabetes insipidus, secondary hypothyroidism, adrenal insufficiency and hypogonadism. MRI Brain showed a mass like thickening (11.6 x 11 x 16mm) of the infundibulum and posterior portion of the pituitary gland with upward displacement of optic chiasm. Workup for granulomatous conditions (sarcoidosis/ disseminated Koch’s) was negative. He was initiated on desmopressin, thyroxine, hydrocortisone, testosterone and managed elsewhere as hypophysitis.
At presentation to us after 3 months of treatment, visual field examination showed decrease in peripheral vision involving right superior temporal quadrant and an attempt was made to delineate the size and etiology of the lesion. Repeat imaging revealed increase in size of the lesion to 12 x 15 x 18mm. He underwent TSS and the lesion was biopsied. Histopathology showed infiltrative adenocarcinoma with CK20 +, CK7 -, and GATA3 + on IHC. Post procedure WB-PET CT, showed metabolically active residual tumor in suprasellar region and negative for metabolically active disease in other areas. Upper GI Endoscopy, Colonoscopy and Bronchoscopy were also normal. Currently he is on adjuvant radiation therapy for residual suprasellar lesion.
Conclusion
Pituitary metastasis may be difficult to differentiate from other lesions in the sellar/parasellar region, presentation as DI and thickened stalk confounded the diagnosis, given that it is a feature of the commoner lesion- hypophysitis. This case reports the rare occurrence of CK20 positive, CK7 negative adenocarcinoma metastasis to pituitary and no evidence of primary.
MON-713 Nuclear Corepressor; SMRT Acts as an Important Regulator for Both Beta-Oxidation and the Maturation of Myogenesis in Mouse C2C12 Cell
Authors: Shimizu Hiroaki , Horibata Yasuhiro , Aoyama Chieko , Amano Izuki , Ritter Megan , Ando Hiromi , Sugimoto Hiroyuki , Hollenberg Anthony Neil 
Published: May 2020

Abstract
Background: Silencing Mediator of Retinoid and Thyroid hormone receptors (SMRT; NCoR2) is a transcriptional corepressor which has been recognized as an important player in the regulation of hepatic lipogenesis and the somatic development in mouse embryo. SMRT protein is also widely expressed in the mouse connective tissues, for example adipocyte and skeletal muscle, and we recently reported that the mouse of global deletion of SMRT causes significant obesity which is independent from thyroid hormone signaling and thermogenesis. However, the tissue specific role of SMRT in skeletal muscle is still unelucidated. Methods: To clarify this, we took the gene targeting strategy for SMRT using CRISPR Cas9, and made the myogenic C2C12 clone which lacks SMRT protein (C2C12-SMRTKO; SKO). For this study, wild type C2C12 cell (WT) and SKO cell were cultured in differentiation medium (DMEM+2% horse serum) for 5-6 days, and analyses for gene expression compared two cell types were performed. Results: We found the significant up-regulations of muscle specific beta-oxidation related genes (ex. Ppar delta, Ampk2), and higher protein level of PGC-1A in the SKO cell, suggesting that SKO cell had similar gene profile to that of rodent skeletal muscle in the exercise test. On the other hand, confocal microscopic analysis showed SKO cell had decreased cell-fusion and loss of myotube, indicating that the morphology was similar to immature mouse myoblasts. Further gene analyses compared between WT and SKO cell demonstrated that SKO cell had higher expressions of myogenic markers; MyoD and Myogenin. However, interestingly, the lower expressions of muscle constitutive genes; MHC, Actin, and Alpha-dystrobrevin were found in the SKO cell. These data indicate that the SKO cell has incomplete muscle fiber formation. Conclusion: Taken together, we demonstrate that SMRT works as a pivotal transcriptional mediator for both beta-oxidation and the process of myotube formation in C2C12 cell. Further inquiry for the cause of sarcopenia-like phenotype manifested in the SKO cell will be needed.
MON-486 Polygenic Susceptibility to Papillary Thyroid Cancer in Italian Subjects
Authors: Brigante Giulia , Lazzaretti Clara , Paradiso Elia , Foersti Asta , Hemminki Kari , Elisei Rossella , Romei Cristina , Rochira Vincenzo , Simoni Manuela , Landi Stefano , Casarini Livio 
Published: May 2020

Abstract
INTRODUCTION AND AIM. Thyroid cancer is the most common endocrine neoplasia, with an estimated age-standardized incidence rate of 6.7 per 100000 worldwide in 2018 [1]. This rate is rapidly increasing and papillary thyroid carcinoma (PTC) is the main histotype. PTC susceptibility is the result of genetic predisposition, environmental factors and lifestyle. We studied the genetic combination that characterizes PTC affected subjects, differentiating them from healthy controls.
METHODS AND RESULTS. We considered the genetic variants (SNPs) significantly associated with PTC on the PubMed database. 184 informative SNPs were selected, considering linkage disequilibrium. Then, SNPs data were extracted from the online 1000 Genomes database, comprising genome of 2504 unselected individuals collected worldwide. The combination of 184 SNPs associated with PTC was used to group individuals in different risk-clusters according to their genetic structure, calculated by Bayesian statistics, as previously performed for polycystic ovary syndrome [2]. Individuals were distributed among 7 groups worldwide, indicating different degree of genetic predisposition to PTC. We then considered genetic data from about 1200 individuals (697 PTC versus 497 healthy controls) of Central/South Italian origin registered in a GWAS, specific for PTC [3]. This first analysis was refined using the 33 SNPs reasonably most causative of genetic clustering (26 with p&lt;0.05 at trend test in GWAS and 7 with p&lt;0.05 in the model of recessive inheritance). At multivariate logistic regression analysis, PTC and healthy controls resulted genetically different (ODDS RATIO 188.6, 95%CI 64.35-552.8), revealing diverse predisposition to develop cancer. Afterwards, these results have been confirmed in an independent cohort of Italian subjects (234 PTC and 100 controls). Then, the genetic structure of each subject was indicated as a percentage of affinity to each risk-cluster and re-analyzed together with other risk factors: sex, body-mass index, area of origin and familiarity (quantified in a growing score as the degree of kinship increases). These data were analyzed together by principal component analysis and clustering of the two groups was even more pronounced. The most contributive factors to the diversity between PTC and healthy controls were genetics and familiarity.
CONCLUSION. We demonstrated that PTC affected subjects are genetically different from healthy controls, and that the difference is identifiable in a peculiar combination of genetic variants.
REFERENCES
1. Bray F et al. CA: a cancer journal for clinicians. 2018; 68 (6):394-424
2. Casarini and Brigante. JCEM. 2014; 99:E2412-20
3. Köhler et al. Genome-wide association study on differentiated thyroid cancer. J Clin Endocrinol Metab. 2013;98:E1674-81.
SAT-265 An Asynchronous Double Growth Hormone Secreting Pituitary Adenoma as a Cause of Rapid Tumor Regrowth After Initially Successful Surgery
Authors: Trofimiuk-Muldner Malgorzata , Lukasz Kluczynski , Zielinski Grzegorz , Sokolowski Grzegorz , Maksymowicz Maria , Pekul Monika , Hubalewska-Dydejczyk Alicja 
Published: May 2020

Abstract
Background. Double pituitary adenomas are a rare entity, which requires clinical attention and a careful follow-up. Case report. A 37-year-old man presented with left-sided painful gynecomastia. He denied typical symptoms of excessive growth hormone (GH) secretion and did not show any acromegalic features. Due to low testosterone and LH levels with mild hyperprolactinaemia, the patient was referred to pituitary MR, which revealed an 11x13 mm right-sided sellar tumor. An increased IGF-1 was noted subsequently (1482 ng/mL; N 109-284 ng/mL), together with the lack of GH suppression in OGTT. Transphenoidal resection of pituitary tumor performed in 2012 led to biochemical (IGF-1 260 ng/mL, GH 0.08 ng/mL) and radiological remission of the disease. A histopathology report revealed a densely granulated somatotropic pituitary adenoma with mild nuclear atypia, expressing somatostatin receptors [sstr2A (+), sstr5 (+/-)]. Due to gradually increasing IGF-1 levels (with low, although rising, GH values ranging from 0.07 to 0.92 ng/mL) in subsequent years, OGTT was repeated in 2015, showing appropriate GH suppression. In 2016, however, acromegaly recurrence was confirmed both biochemically (increasingly high IGF-1 - 664 ng/mL - and unsuppressed post-OGTT growth hormone) and in MR imaging. The patient was reoperated in June 2017. The second histopathology reported an oncocytic somatotropic acidophil stem cell pituitary adenoma with Ki-67 &gt;3% and mitotic figures. Subsequent anterior pituitary lobe insufficiency (adrenal, thyroid and gonadal axis) was found and adequately treated. Complete tumor removal was confirmed by MR performed three months after repeated surgery, as well as a low GH level (0.97 ng/mL), although accompanied by borderline IGF-1 values (277 ng/mL). Eighteen months after surgery, the recurrence of acromegaly was again confirmed, with adenoma regrowth and increased GH (2.31 ng/mL) and IGF-1 (474 ng/mL) levels. Octreotide LAR was started (despite retina wrinkling which was observed when lanreotide was administered before the first surgery), which led to a normalization of GH (0.96 ng/mL) and IGF-1 levels (152 ng/mL), as well as partial pituitary tumor regression after six months therapy. Conclusion. In a case of GH-secreting pituitary adenoma recurrence after apparent successful surgery, a double pituitary tumor with more aggressive histology should be considered.