bluuebunny/crossref_metadata_2025_split huggingface dataset:
Adaptation of the Suicide Attempt Resilience Scale (SRSA-18, Spanish version) for adolescents
Authors: Sánchez-Teruel David , Robles-Bello María Auxiliadora , Sarhani-Robles Aziz , Sarhani-Robles Mariam 
Published: November 2022

Background
The assessment of resilience as an outcome in adolescents remains a challenge, with few instruments available. Some studies have focused on risk factors, but few have focused on protective factors as a formula for measuring resilient outcomes.

Aims
To adapt a new Suicide Attempt Resilience Scale (SRSA-18) for use with adolescents, analysing its structural validity, the gender and age invariance of the measure, and divergent and convergent validity, together with its reliability.

Method
The psychometric properties of the scale were assessed in 628 participants aged between 13 and 18 years, of whom 342 (54.5%) were girls.

Results
After a process of adaptation for adolescents, exploratory and confirmatory factor analysis yielded a three-dimensional structure with adequate goodness-of-fit indices, invariance of the measure according to gender and age, adequate levels of reliability (ω = 0.91), high convergent validity with the 14-Item Resilience Scale and high divergent validity with the suicidal act/planning subdimension of the Adolescent Suicidal Behavior Assessment Scale.

Conclusions
There is a need to create and adapt instruments to measure resilience in some populations with high psychosocial vulnerability as a key aspect for measuring the impact of prevention and mental health promotion programmes in adolescents.
Nonlinear speed-ups in ultracold quantum gases
Authors: Deffner Sebastian 
Published: November 2022

Abstract
Quantum mechanics is an inherently linear theory. However, collective effects in many body quantum systems can give rise to effectively nonlinear dynamics. In the present work, we analyze whether and to what extent such nonlinear effects can be exploited to enhance the rate of quantum evolution. To this end, we compute a suitable version of the quantum speed limit for numerical and analytical examples. We find that the quantum speed limit grows with the strength of the nonlinearity, yet it does not trivially scale with the “degree” of nonlinearity. This is numerically demonstrated for the parametric harmonic oscillator obeying Gross-Pitaevskii and Kolomeisky dynamics, and analytically for expanding boxes under Gross-Pitaevskii dynamics.
LBSUN87 Human Cidec Transgene Improves Lipid Metabolism And Protects Against High Fat-diet Induced Glucose Intolerance In Mice
Authors: Gupta Abhishek , Balakrishnan Bijinu , Karki Shakun , Slayton Mark , Gokce Noyan , Sharma Vishva M , Puri Vishwajeet 
Published: November 2022

Abstract
CIDEC expression in adipose tissue positively correlates with insulin sensitivity in obese humans. Further, a single-nucleotide CIDEC variant (E186X) causes lipodystrophy, hypertriglyceridemia, and insulin resistance. To establish the unknown mechanistic link between CIDEC and maintenance of systemic glucose homeostasis, we generated transgenic mouse models expressing CIDEC (Ad-CIDECtg) and CIDEC E186X variant (Ad-CIDECmut) transgene specifically in the adipose tissue. Ad-CIDECtg but not Ad-CIDECmut mice were protected against high-fat diet (HFD)-induced glucose intolerance. Transcriptomics and lipidomics revealed the role of CIDEC in lipid metabolism. Serum triglycerides, cholesterol, and low-density lipoproteins were lower in HFD-fed Ad-CIDECtg mice compared to their littermate controls. Mechanistically, CIDEC regulates the enzymatic activity of ATGL via interacting with its activator, CGI-58, to reduce free fatty acid (FFA) release and lipotoxicity. We confirmed that CIDEC is indeed a vital regulator of lipolysis in adipose tissue of obese humans. Finally, treatment with recombinant CIDEC decreased triglyceride breakdown in visceral human adipose tissue. Our study unravels a central pathway whereby adipocyte-specific CIDEC plays a pivotal role in regulating adipose lipid-metabolism and whole-body glucose homeostasis. In sum, our findings identify human CIDEC as a potential 'drug' or a 'druggable' target to reverse obesity-induced lipotoxicity and glucose intolerance.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
LBSUN99 Combination Of Drosophila And Mammalian Genetics Identifies Lcorl As A Novel Regulator Of Metabolism
Authors: Elmquist Joel 
Published: November 2022

Abstract
Obesity and adult-onset diabetes result from a complex interaction of multiple genetic, environmental, and behavioral factors. The hypothalamus contains multiple nuclei required for the regulation of metabolic homeostasis. One nucleus, termed the ventromedial hypothalamus (VMH), facilitates glucose homeostasis and metabolic adaptations to challenges such as high fat diet (HFD) and exercise. Using a combination of Drosophila and mouse genetics, we uncovered a novel gene network whose function is required for VMH-regulated whole body metabolism. Using Drosophila to rapidly screen orthologs of genes enriched in the mouse VMH, we identified the gene encoding the Ecdysone Induced Protein 93F (E93; human ortholog, Ligand dependent corepressor-like, Lcorl). Adult flies with neural knockdown of E93 are obese and hyperphagic, with increased energy stores, reduced exercise endurance, and dampened circadian amplitude. These findings reveal a novel role of E93 in metabolism. We found that the knockdown of E93 specifically in myoinhibitory peptide (MIP) and GABAergic neurons are sufficient to recapitulate the phenotype seen in a pan-neuronal E93 knockdown. | In mice, we found that Lcorl, the mammalian orthologue of E93, is highly expressed throughout the entire VMH. We used CRISPR/Cas9 to generate mice harboring both a Lcorl KO and a floxed allele to investigate its function in the whole-body and in a tissue specific manner. Lcorl KO mice are viable and fertile. However, they have disruptions in growth, lipid metabolism, and circadian rhythm. Taken together these data reveal that Lcorl is as a novel regulator of energy metabolism and circadian rhythm. Additionally, this study shows the power of combined drosophila and mammalian genetics in uncovering novel regulators of metabolism.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
ODP005 Molecular Characterization of Early Adipose Tissue Remodeling and Fibrosis in a Murine Model of Diet-Induced Obesity.
Authors: Timms Katie , Winkel Emma , Ahmed Rayan , Maurice Sean , Gray Sarah 
Published: November 2022

Abstract
One of the many pathophysiological changes associated with obesity is the build up of structural and physiochemical extracellular matrix components in adipose depots, known as adipose tissue fibrosis. Like liver fibrosis, adipose tissue fibrosis occurs as a response to chronic injury and inflammation and can perpetuate inflammation and impede proper tissue functioning. Key adipose tissue fibrosis markers have been identified in obese adipose tissue, including collagen VI and its cleavage product endotrophin, however, adipose tissue fibrosis remains poorly characterized, particularly in its initiating phases. We have developed and characterized a murine model of diet-induced obesity (12 weeks of high fat feeding), insulin resistance, and early fibrotic development in both sexes. While diagnosable fibrosis was absent, as determined by picrosirius red staining, we detected elevated collagen VI, TGF-β, TNF-α, and TIMP-1 mRNA in gonadal white adipose of both sexes. TIMP-4 was decreased in males but elevated in females. Immunohistochemical analysis revealed pericellular build up of collagen VI immunoreactivity in males only, co-localized with immunoreactivity of its protease MMP-14, which is known to generate the pro-fibrotic fragment endotrophin. This work identifies key sex differences and fibrosis markers present during the initiation of adipose tissue fibrosis, earlier than diagnosable fibrosis can be detected, highlighting their potential as therapeutic targets for prevention or reversal of fibrosis in the treatment of obesity and insulin resistance.
Presentation: No date and time listed
LBSAT63 Cushing Syndrome As A Presentation Of Adrenocortical Carcinoma.Case Report
Authors: Eid Mennaallah , Zahra Tasneem , Vargas-Jerez Julia 
Published: November 2022

Abstract

Introduction
adrenocortical carcinoma is a rare endocrine malignancy (1) Case: 44 year old afro American female with no past medical history. No regular medications. Amenorrhea for 2 years. smokes cigarettes. Irrelevant family history. She presented with itchiness after cat scratch and was found to have hypertension urgency 229/123. Review of systems was positive for weight gain and easy bruises. Physical examination alert and oriented with body mass index of 31 kg/m2 heart rate 75 beats per minute normal heart sounds and clear lungs with scratch marks on left hand. bilateral lower extremities pitting edema, supraclavicular fat pad and violet abdominal striae. No facial plethora or hirsutism or lymphadenopathy or acne. Laboratory work up was remarkable for hypokalemia and metabolic alkalosis. High plasma morning cortisol level 53.6ug/dl normal between 6.2 and 29, 24hour urine cortisol and DHEAS and low ACTH FSH and LH. Estradiol 261pg/ml 17hydroxyprogesterone 49ng/dl and prolactin 31.7ng/ml. HBA1C 6.7. Normal renin aldosterone TSH and plasma and 24hour metanephrine and normetanephrine. Normal creatinine liver function and complete blood count. CT abdomen and pelvis with contrast showed large lobular heterogeneously enhancing mass in the left adrenal gland of 9. 0×10.1×10.1cm with left kidney posterior displacement and left renal vein compression. The pancreatic tail and splenic vein were draped over the mass. The right adrenal gland and other abdominal organs were unremarkable. DEXA scan showed osteopenia. CT chest showed 5mm right lower lobe nodule and compression fracture in the 7th thoracic vertebrae. Echocardiogram showed dilated left ventricle dimension with reduced ejection fraction 45%. The diagnosis was made for ACTH independent Cushing syndrome with adrenal mass. She underwent open left adrenalectomy distal pancreatectomy splenectomy and left nephrectomy in another institution. Histopathology showed 12×7.5×7 cm stage III adrenal cortical malignancy T3N0M0. Extensive necrosis and capsular invasion but negative surgical margins. Possibility of lung metastasis. Postoperative cortisol level 6. 02ug/dl. She was kept on postoperative slow tapering hydrocortisone with plan of chemotherapy and Mitotane.

Conclusion
adrenocortical carcinoma has a poor prognosis. It usually metastasizes to distant organs at time of diagnosis and rarely presents as Cushing syndrome. Surgical resection is the main management of localized tumors with controlling the effects of secreted hormones. Adjuvant therapies are chemotherapy radiotherapy and Mitotane according to the tumor stage and size. Mitotane is adrenal cytotoxic agent showed increase survival of advanced stages(1). References: 1-Stigliano A,Cerquetti L,Lardo P,Petrangeli E,Toscano V.2017 New insights and future perspectives in the therapeutic strategy of adrenocortical carcinoma(review). Oncol Rep 37: 1301-1311
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
ODP296 An unusual presentation of Glucagonoma syndrome.
Authors: Zare Ahmad , Deshmukh Mrunalini , Vemparala Pranathi 
Published: November 2022

Abstract

Introduction
Glucagonoma is an uncommon neoplasm of the pancreatic neuroendocrine islet α-cells. At least 50% of cases will have metastatic disease when diagnosed. Glucagonomas can be associated with other tumors in Multiple Endocrine Neoplasia syndrome 1 (MEN 1), but this association is rare and comprises no more than 3% of glucagonomas. Glucagonoma syndrome is a rare paraneoplastic phenomenon characterized by necrolytic migratory erythema (NME), hyperglucagonemia, diabetes mellitus, anemia, weight loss, glossitis, cheilitis, steatorrhea, diarrhea, and venous thrombosis.

Case presentation
A 55-year-old Caucasian woman was admitted for acute onset of shortness of breath and she was seen by endocrinology team for persistent hyperglycemia. Her medical history revealed a long-standing uncontrolled type 2 diabetes mellitus and an episode of left lower extremity deep-vein thrombosis. Her physical exam revealed tachycardia, otherwise unremarkable, with no skin lesions. Laboratory results showed hyperglycemia (387 mg/dl), Hemoglobin A1C, 9%, and hypoalbuminemia (3.4 g/dl). Her Hemoglobin (13 g/dl), white cell count (6100/μL), and platelet level (19.3 × 104/μL) were within normal limits. The patient underwent CT pulmonary angiogram, which showed a large saddle pulmonary embolism as well as a distal pancreatic mass measuring 4.5×3.4 cm, which contains numerous coarse calcifications. Pancreatic mass was confirmed in a CT abdomen and pelvis with contrast. CA 19-9 was elevated to 51 U/ml (normal range, 0- 35U/ml). The GI team performed an Endoscopic Ultrasound, and samples were sent for FNA and flow cytometry which revealed a 4 cm irregular heterogeneous mass with calcifications at the distal pancreatic body, positive for Pankeratin (CK), Cam 5.2, Synaptophysin, Chromogranin A, and CD56, consistent with Pancreatic neuroendocrine Tumor. Her serum glucagon level was elevated to 447 pg/mL (normal range, 50 -150 pg/mL), while her levels of other hormones, such as somatostatin or gastrin, were within normal limits. Glucagonoma of the pancreas was diagnosed, and a spleen-preserving distal pancreatectomy was performed. Histopathological examination revealed a 5.9 cm alpha-cell pancreatic tumor without lymphovascular or perineural tumor invasion. (AJCC 8th edition staging II, pT3, pN0, MX, G1). Immunohistochemical staining was strongly positive for glucagon. A gallium-68 positron emission tomography (68Ga-PET, Netspot) did not show metastasis. Post resection surveillance showed normalization in Glucagon level and no evidence of recurrence in CT abdomen.

Conclusion
The diagnosis of glucagonoma is often delayed due to unusual initial manifestations of glucagonoma. Early diagnosis provides a good chance of complete surgical removal as the only curative treatment.
Presentation: No date and time listed
ODP337 Neurenteric Cyst Apoplexy with Post-Operative Diabetes Insipidus in a 14-year-old Male
Authors: Patterson Mary 
Published: November 2022

Abstract

Background
Apoplexy of benign neurenteric cysts can present with acute onset of a severe headache. Pituitary dysfunction, such as hypothyroidism and diabetes insipidus, can occur after transsphenoidal resection of these cysts.

Clinical Case
A 14-year-old male presented to the ED with acute onset of a severe headache, nausea and emesis. He denied recent vision changes, weight changes, temperature intolerance, diarrhea, constipation, skin changes, polyuria, or polydipsia. He reported starting puberty by 13 years of age. He was treated with Zofran, Tylenol, and Dexamethasone which led to headache resolution. His MRI showed a trans-sellar structure measuring 12 by 16 mm and demonstrating internal intrinsic T1 hyper-intensity, deep T2 hypo-intensity, and mildly thickened peripheral enhancement. The lesion abuts the undersurface of the optic chiasm and the stalk enhances normally. The neurohypophysis is not well identified. The optic nerves are unremarkable, and the optic chasm is slightly bowed superiorly. His initial labs were significant for: Na 136 mmol/L, K 4 mmol/L, TSH 1.15 uIU/mL, FT4 0.81 ng/dL, IGF-1 286 ng/mL, cortisol &lt;1 ug/dL (drawn in the PM), FSH 6.23 mIU/mL, LH 2. 01 mIU/mL, PRL 7.8 ng/mL, testosterone 187 ng/dL. He was taken to surgery where a transsphenoidal resection with a mucosal graft for sellar reconstruction was completed. Pathology results showed evidence of a neurenteric cyst with glandular elements within the cyst wall. He was noted to have an increase in water intake and urine output post-operatively with intake of 6200 mL and output of 6768 mL over 24 hours (3.5 mL/kg/hr). His Na was 141 mmol/L with urine SG of 1. 002, and urine osmolality of 75 mosm/kg. He was discharged on a DDAVP dose of 0.2 mg tid. His thyroid function was reassuring post-op with a T4 of 8.4 ug/dL. He had a normal morning cortisol of 14.6 ug/dL. One month post-op, he required treatment with a DDAVP dose of 0.1 mg bid. The rest of his pituitary function appeared intact one month post-op with labs significant for LH 2.56 mIU/mL, FSH 5 mIU/mL, testosterone 261 ng/dL, PRL 7.8 ng/mL, TSH 2. 09 uIU/mL, and FT4 1 ng/dL.

Conclusion
This case demonstrates that neurenteric cyst apoplexy can occur in teenagers who present with the acute onset of a severe headache with associated nausea and emesis. This case demonstrates the importance of thoroughly investigating the patient's pituitary function at baseline and post-operatively since pituitary deficiencies, such as DI, can occur.
Presentation: No date and time listed
ODP357 The Effect of Hyperbetacarotenaemia on Pituitary Homeostasis – A Case Series
Authors: Dhatariya Ketan , Rogers Rebecca 
Published: November 2022

Abstract

Betacarotene is an antioxidant pigment found in red, orange and yellow coloured leafy fruits and vegetables. Recent studies have found that beta carotene is involved in cell cycle arrest with apoptotic effects in ACTH secreting pituitary cells. It may have desirable anti-tumorigenic effects. Hyperbetacarotenaemia is commonly caused by excess intake of carotene rich food. However, correlating the clinical picture with liver, thyroid and lipid profiling, vitamin A concentrations and exclusion of nephrotic syndrome is necessary to underpin the causative mechanism. We present two cases of hyperbetacarotenaemia with clinical manifestations of hypopituitarism.

Case 1
– A 55 year old lady presented with partial hypopituitarism. She had a history of restrictive eating disorder and excessive exercise regime. She cycled 140 miles a week and ate 4lbs of leafy vegetables a day. Her pituitary profile reflected partial hypopituitarism with inappropriately undetectable LH/FSG, low IGF-1 and central hypothyroidism. Her cortisol response to tetracosactide testing was normal. Betacarotene reached a peak of 2.7umol/L (upper reference range 1.58umol/L).

Case 2
– A 29 year old lady was diagnosed and treated for a 4mm microprolactinoma, which subsequently regressed and prolactin levels returned to normal. Despite this, she continued to experience menstrual irregularities and found to have elevated serum beta carotene levels. On direct questioning she admitted to drinking 1.5L of Lucozade® per day. Betacarotene reached a peak of 3.81umol/L. These cases illustrate the importance of taking a detailed dietary history when considering the causes of pituitary dysfunction.
Presentation: No date and time listed
ODP024 Adrenocortical Carcinoma Identified in a Patient With Familial Adenomatous Polyposis Syndrome
Authors: Park Eujean , Prasad Heranmaye 
Published: November 2022

Abstract

Background
Numerous extracolonic manifestations are associated with familial adenomatous polyposis (FAP), including benign thyroid and adrenal nodules, less commonly thyroid and adrenal cancers. We describe a case of a patient with history of FAP who was found to have malignant lesions both in the thyroid and adrenal glands.

Clinical Case
A 54 year-old female with familial adenomatous polyposis (FAP) underwent partial colectomy at age 16. Known extracolonic manifestation at initial presentation was limited to a dermoid tumor of the right breast. Upon evaluation by endocrinology, she was found to have a dominant thyroid nodule in the right lobe that eventually doubled in size and was positive for papillary thyroid cancer with a BRAF V600E mutation. Successful total thyroidectomy with central neck lymph node dissection was completed, and she is now undergoing routine surveillance for ATA low risk PTC. She maintained annual endoscopic surveillance with gastroenterology and underwent serial abdominal imaging studies for complaints of abdominal discomfort. Right adrenal adenoma was first identified in August 2017 and screening for functionality, to include pheochromocytoma, was negative. Repeat abdominal imaging in 2020 showed the lesion increased in size by 30%. CT imaging identified the nodule as indeterminate based on the washout characteristics (HU 27 pre-contrast, absolute washout = 13% and relative washout = 8%). A 2cm left adrenal mass was also noted with radiographic features consistent with a lipid poor, benign, adenoma (HU 33 pre-contrast, absolute washout = 58%, relative washout = 39%). PET-CT was performed to further characterize the right sided lesion, which was vividly FDG avid at 8.7 SUV (high probability of malignancy). The left adrenal nodule was mildly FDG avid with an SUV of 2.4. CT-guided biopsy of the right adrenal gland was performed and immunohistochemistry did not stain for chromogranin, inhibin, pankeratin or calretinin. Positive staining for MART-1 was seen, which is a typically associated with adrenal cortical cells. There was a high index of suspicion for malignancy given her hereditary cancer syndrome, and the decision was made to proceed with right adrenalectomy. Final surgical pathology confirmed a low grade adrenocortical carcinoma with two nodular lesions, both staining CD10 positive with the mitotic marker (Ki-67) 2-3% positive. The patient's left adrenal gland remains functionally intact, and there were no indications to pursue postoperative treatment or adjuvant therapy.

Conclusion
The patient presented here is representative of incidentally discovered nonfunctional adrenocortical carcinoma in the setting of a hereditary cancer syndrome. The available literature suggests that adrenocortical tumors should be considered FAP tumors, and sporadic mutations leading to adrenocortical carcinoma are less likely related to germline APC gene mutations
Presentation: No date and time listed