bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Effect of the Synergy Between Opiates and Prolactin on the Growth of Chickens
Authors: Abdulateef Salwan M , Al-Hamdani Adel , Al-Ani Mohammed , Mosa Baraa 
Published: May 2021

Abstract
It is generally admitted that opioids can stimulate the release of both prolactin (PRL), the opiates induced hyperprolactinemia via dopamine receptor blockade. Prolactin hormone (PRL) plays an important role in conjunction with some hormones such as GH, PTH, ACTH, and T4 to stimulating body growth. The prolactin hormone has an important role in feeding behavior, as its role is evidenced by its effect on metabolism. In migratory birds, fat is stored in its body before migration, and the hormone prolactin activates the process of building and storing fats lipogenesis and Deposition of Fats. The hypothesis of this study is to investigate the role of natural stimuli such as sound in stimulating peptide hormones in the body and thus weight gain in chickens. 100 birds of 1 day old were used it was divided into two treatments, each treatment with 5 replications. The chicks heard different sounds and it was as follows: the first the control without sound CS, the second hen sound (mother sound) HS. The sound was heard from the one old day to 14 days, at a rate of 3 times a day, in the morning, in the afternoon and at night, for an hour each time. Chicks were raising to 42 day. The hormone was estimated in three stages, before exposure to sound 30 minutes during exposure directly after exposure for 30 minutes, and the prolactin hormone concentration was calculated each time, the results show: Significant increase (P&lt;0.05) in live body weight cumulative, weight gain cumulative, relative growth rate cumulative, and total feed conversion ratio to HS compared with CS. Significant improvement (P&lt;0.05) in the concentration of the hormone prolactin of HS in the period after exposure to sound 30 minutes during exposure directly after exposure for 30 minutes at the age of 14 days (the end of the exposure to the sound of the period). As mentioned above, the opioids stimulate prolactin, but the question here who is responsible for stimulating the opioids? Opioids secretion is linked to the body’s sense of well-being and well-being, as it is secreted naturally to aid in rest and relaxation, and this is often noticed on the organism when it feels safe and comfortable. Chicks, when it hearing her mother’s sound, gives it a powerful stimulus, and they become more active and more and less fearful and amazement. This will release the opioid, which in turn stimulates prolactin. PRL and GH are secreted from the anterior pituitary gland and affect a wide variety of physiological functions in birds. Similarly, a relationship between plasma GH concentration and body growth is well documented. There is a chemical similarity between prolactin hormone and growth hormone, so there is a similarity in biological functions, as prolactin stimulates physical growth and weight gain in birds, reptiles and mammals due to its similarity with growth hormone as the injection of prolactin causes a significant increase in body weight.
The Role of Microglia in the Polycystic Ovary Syndrome (PCOS)-Like Brain
Authors: Sati Aisha , Prescott Melanie , Jasoni Christine Louise , Desroziers Elodie , Campbell Rebecca Elaine 
Published: May 2021

Abstract
Polycystic ovary syndrome (PCOS) is the most common cause of anovulatory infertility, affecting roughly 1 in 8 women of reproductive age. Accumulating evidence from animal models suggests that the brain plays a key role in the development and maintenance of PCOS. In a well-characterised prenatally androgenised (PNA) mouse model of PCOS, aberrant neuronal wiring associated with PCOS deficits in adulthood are detected as early as postnatal day (P) 25, prior to disease onset. However, the mechanisms by which prenatal androgen exposure alters brain wiring remains unknown. Microglia, the immune cells of the brain, are active sculptors of neuronal wiring across development, mediating both the formation and removal of neuronal inputs. Therefore, microglia may play an important role in driving the abnormal neuronal wiring that leads to PCOS-like features in the PNA brain. Here, to assess whether microglia are altered in the brain of PNA mice, microglia number and morphology-associated activation states were quantified in two hypothalamic regions implicated in fertility regulation. Microglia were identified by immunolabelling for the microglia-specific marker, Iba-1, across developmental timepoints, including embryonic day 17.5, P0, P25, P40 and P60 (n = 7–14/group). At P0, PNA mice had significantly fewer “activated” amoeboid microglia compared to controls (P &lt; 0.05). Later in development at P25, PNA mice exhibited significantly fewer “sculpting” microglia (P &lt; 0.001), whereas at P60, PNA mice possessed a greater number of “activated” amoeboid microglia relative to controls (P &lt; 0.01). This study demonstrates time-specific changes in the number and morphology of microglia in a mouse model of PCOS and suggests a role for microglia in driving the brain wiring abnormalities associated with PCOS. These findings support the need for future functional experiments to determine the relative importance of microglia function in shaping the PCOS-like brain and associated reproductive dysfunction.
Transcriptome of Distinct LH and FSH Cells Reveals Different Regulation Unique to Each Cell Type
Authors: Hollander-Cohen Lian , Golan Matan , Levavi-Sivan Berta 
Published: May 2021

Abstract
From mammals to fish, gametogenesis and sexual maturation are driven by LH and FSH, the two gonadotropic hormones temporally secreted from the pituitary. Teleost fish are an excellent model for addressing the unique regulation and function of each gonadotropin hormone since, unlike mammals; they synthesize and secrete LH and FSH from distinct cells. By performing cell specific transcriptome analysis of double-labelled transgenic Nile tilapia (Oreochromis niloticus) expressing GFP and RFP in LH or FSH cells, respectively, we identified genes specifically enriched in each cell type. Though GnRH is considered the main neuropeptide regulating LH and FSH, we found that each LH and FSH cell express unique GPCR signature that reveals the direct regulation of additional metabolic and homeostatic hormones (like cholecystokinin, somatostatin and glutamate). Moreover, some of those GPCRs were conserved also in gonadotrophs of mammals (like PACAP receptor, Adropin receptor and GABBA receptor). Next, we had exploited the unique behavior of Nile tilapia where a behavioral hierarchy is created between males, to compare the gene expression in the pituitary and brain of dominant (reproducing) males to a subordinate (non-reproducing) males. By combining the two transcriptome sets we had identified novel players in the hypothalamic regulation of the HPG axis, and revealed how brain aromatase (cyp19a1b), that is enriched specifically in LH cells, is the key factor in regulating the activity of LH and FSH cells in dominant reproducing fish. Thereby, unraveling novel mechanisms in the differential regulation of LH and FSH. The research was funded by the Israel Science Foundation (ISF) no. 1540/17.
A Case of Acute Psychosis as Manifestation of Ectopic ACTH Producing Pancreatic Neuroendocrine Tumor
Authors: Motazedi Banafsheh , Cowen Laura E , Jonklaas Jacqueline 
Published: May 2021

Abstract
Introduction: Ectopic adrenocorticotrophic hormone (ACTH) producing Pancreatic Neuroendocrine Tumor (p-NET) are extremely rare with incidence of 1.2% and confer a poor prognosis (5-year survival &lt;20%).
Case Report: 31-year old female with diabetes mellitus type 2 (DM-2) and hypertension (HTN) was found to be severely hypokalemic on routine labs and was sent to the Emergency Department for potassium replacement. Vitals; BP:139/87 mmHg, HR:108 bpm, RR:18, T:37°C and saturating 98% on ambient air. Examination revealed cushingoid features; hyperpigmented face, bilateral upper extremity pigmented papules, proximal muscle weakness, acanthosis nigricans, violaceous abdominal striae, truncal obesity, ecchymoses, bilateral lower extremity edema, memory impairment and anxiety. Initial labs; BG: 289 mg/dL, HbA1c: 9.5%, K: 2 mmol/L (N 3.5-5.2), WBC: 12.5 k/μL (N 4-10.8), Cortisol &gt;150 mcg/dL (N 5-23), TSH: 0.325 μIU/mL (N 0.45-4.5), and FT4: 0.69 ng/dL (N 0.82-1.77). Diagnosis of Cushing’s syndrome was made based on elevated cortisol level and confirmed with elevated 24-hour urinary free cortisol: 13,294 μg (N&lt;45), midnight salivary cortisol &gt;15 ug/dL (N 0.09-1.5) and 1 mg dexamethasone suppression test (Cortisol &gt;150 mcg/dL, ACTH: 621 pg/ml). Additional labs showed Chromogranin A: 717 ng/mL (N 0-160). She was started on prophylactic Enoxaparin & Trimethoprim/Sulfamethoxazole and treated with Spironolactone, Basal/Bolus insulin, and Ketoconazole for hypercortisolemia. Pituitary MRI was negative for pituitary adenoma. Abdominal/Pelvic CT scan demonstrated a solid 5 cm pancreatic head mass with innumerable haptic metastases consistent with metastatic p-NET which was confirmed on PET-CT Ga68 Dotatate scan. Liver biopsy was positive for a well differentiated p-NET with ki-67 &lt;5% and negative ACTH staining. Hospital course was complicated by fluctuating cortisol levels with intermittent psychotic manifestations despite up-titration of Ketoconazole, addition of Octreotide as well as anti-psychotics. She later developed transaminitis on maximum dose of Ketoconazole and thus underwent laparoscopic total adrenalectomy for treatment of her hypercortisolemia. Post-operatively, she was started on Hydrocortisone & Fludrocortisone and Spironolactone was discontinued. She was transitioned to monthly Lanreotide and treated with Capecitabine and Temozolomide with adequate therapeutic response and subsequent down trending of her Chromogranin A: 188 ng/mL and ACTH: 228 pg/ml levels. Currently, she is doing well with significant improvement of her DM-2, HTN, psychiatric symptoms and overall clinical status.
Conclusions: Symptoms of ectopic Cushing’s syndrome may be delayed, however given the rare and aggressive nature of ACTH producing p-NET, timely diagnosis, prophylaxis and individualized treatment approach is crucial in achieving favorable prognosis.
A Case of Ectopic Cushing’s Syndrome From a Large Cell Neuroendocrine Lung Tumor With Small Cell Component/Features
Authors: Sallar Anthony Selase , Childress Richard Dale 
Published: May 2021

Abstract
Background: Endogenous Cushing’s syndrome is uncommon in clinical practice. Survival of patients with new onset ectopic Cushing’s syndrome at relapse of small cell lung cancer has been found to be poor, with death occurring within an average of 27.3 days.
Case Report: A 61-year-old African American male was seen by endocrinology service for inpatient evaluation of refractory hypokalemia of three months duration requiring recurrent potassium replacement with oral and intravenous therapy. He was inpatient for depressive symptoms and suicidal ideation. His admission lab showed hypokalemia of 2.7 mmol/L associated with elevated serum ACTH and serum cortisol. Past medical history is significant for unresectable large cell neuroendocrine neoplasm of the lung with small cell components/features diagnosed two years prior during lung cancer screening. He received chemotherapy with cisplatin/etoposide at diagnosis. He however had recurrence one year later with distant metastases. He was re-treated with cisplatin/etoposide in addition to palliative radiation therapy to painful bone met in his right hand. Three months prior to admission, imaging showed progression of the cancer with presence of new lesions in the liver for which he received one cycle of Nivolumab monotherapy. Social history was significant for 30-pack year smoking history. Physical exam findings were significant for: elevated blood pressure 167/96 mmHg, tachycardia of 107 bpm, oxygen saturation of 95% on 3-liters of intranasal oxygen, cachexia, absent buffalo hump, absent striae and decreased power in both lower limbs. Lab on supplementation showed serum potassium of 3.6, Serum magnesium of 2.0 and creatinine clearance greater than 60 Serum cortisol was 116.1 (5-25) mcg/dl and ACTH was 268.0 (9-52) pg/ml. An MRI by the referring team did not show a pituitary lesion. Patient was diagnosed with Cushing’s syndrome due to ectopic ACTH-production from a large cell neuroendocrine lung tumor with small cell component/features. Chart review showed his onset of hypokalemia occurred at the same time that imaging showed progression of the tumor three months prior. He was started on Ketoconazole and his cortisol level reduced to 14.0 within forty-eight hours with associated correction and stabilization of hypokalemia. The plan was to “block and replace” cortisol so that oncology could re-start chemotherapy. However, the patient developed acute respiratory decompensation requiring continuous BiPAP. Chest imaging showed progression of lung lesions with post obstructive pneumonia. The patient’s family opted for comfort measures and he was transferred to hospice care where he passed on ten days later.
Conclusion: In the setting of lung cancer, new onset paraneoplastic Cushing’s syndrome may have prognostic implications. Clinicians should be aware of this, provide treatment for hypercortisolism and refer early to palliative care.
A Rare Case of Metastatic Transformation to Pituitary Carcinoma
Authors: Woznick Walter K , Engel Ashley , Maas Diana 
Published: May 2021

Abstract
Background: Pituitary carcinomas are rare and comprise less than 0.5% of pituitary tumors and frequently arise from previously resected and/or radiated infiltrating adenomas.1 Radiation therapy is used to prevent regrowth but does not have significant data supporting improved prognosis.2 True pituitary carcinomas requires the presence of craniospinal and/or systemic metastases. Here, we present a case of benign pituitary adenoma that had progressed to a metastatic tumor and responded to radiation therapy. Clinical Case: Our patient was first diagnosed in 1982 with a pituitary mass after undergoing an MRI due to right eye blindness. He ultimately had a transcranial resection of the tumor and post-operative external radiation to residual tumor. Final pathology was consistent with a nonsecretory tumor. Additionally, he was diagnosed with panhypopituitarism and he was treated accordingly. Due to barriers of patient adherence, only one post-operative MRI was obtained, and he was lost to endocrine follow up. In 2007, he was again referred to endocrinology for new vision loss in the left eye. An MRI revealed a 3.0 x 3.8 x 4.4 cm tumor that compressed the optic chiasm. Additionally, multiple lesions were seen within the dural and leptomeningeal extra-axial areas including the largest left frontal lesion of 2.4 cm and a 1.7 cm lesion posterior to the cord within the foramen magnum. The patient underwent endonasal transsphenoidal resection of the sellar mass and biopsy of the frontal lesion in October 2007. Pathology showed pituitary adenocarcinoma in both the sellar and frontal lesions and immunoperoxidase staining was negative for all hormones. He completed salvage radiation to the sellar and craniospinal lesions in December 2007. MRI scans completed 7 months later showed stable residual pituitary and metastatic lesions. The patient received 6-month MRI screening exams for the first 2 years and then annually thereafter, as well as PET scanning, without significant progression or new metastatic lesions. Conclusion: We present a case of benign pituitary adenoma which transformed following resection to a malignant tumor with metastatic lesions in the brain and spinal cord that was treated with radiation with relative success. Despite the often-aggressive nature of these metastatic tumors, the patient has experienced a successful treatment course with minimal side effects and without progression 13 years after initial treatment of the metastatic pituitary carcinoma.
Acute Transient Central Diabetes Insipidus: A Rare Case of DI Secondary to Vasopressin Withdrawal
Authors: Cobb Crystal , Osakwe Ibitoro Nnenna 
Published: May 2021

Abstract
Introduction: Transient Central Diabetes Insipidus (tCDI) induced by vasopressin withdrawal is a rare condition which is possibly under recognized. It occurs in very sick, often critically ill patients and usually complicates an already complex clinical picture, so early recognition and treatment are critical to reduce morbidity.
Case Description: A 47-y/o male with a PMH of Coffin Lowry syndrome, atrial fibrillation, and GERD presented with abdominal pain and flu like symptoms. His home medications were metoprolol, loratadine and colestipol. Work up revealed bowel perforation for which he was taken to the OR for repair. Intraoperatively he developed septic shock requiring pressor support with norepinephrine and vasopressin. He was weaned off norepinephrine on post-op day (POD)1, and vasopressin on POD 2. Approximately three hours after withdrawal of vasopressin support his urine output increased dramatically up to a peak of 350 cc/hour with a recorded 24hr urine volume of &gt;5L. Concurrently, his serum sodium was found to have increased from 147 mmol/L to 173 mmol/L (n 135-145) over the course of 13 hours. Clinically, he became increasingly lethargic with abnormal eye movements. His sodium did not improve with fluid management with D5W. His other laboratory values included a urine osmolality of 141 mOsm/kg, urine sodium of 60 mmol/L and a peak serum sodium of 177mmol/L. He was administered 1mcg desmopressin and his D5W rate was increased. His urine output dropped gradually to ~150cc/hr, his serum sodium level started to trend down to 168 mmol/L and his urine osmolality increased to 439 mOsm/kg five hours after desmopressin administration, with improvement in mental status. The patient received a total of two doses of desmopressin and continued support with IV fluids. His sodium eventually normalized, and his polyuria did not return.
Discussion: This patient’s clinical picture is consistent with tCDI secondary to discontinuation of vasopressin. Transient Central diabetes insipidus due to vasopressin withdrawal is a phenomenon that is not well understood, but there is a strong male preponderance, and it tends to occur more commonly in patients with underlying neurological conditions, as did our patient. Current proposed mechanisms include decreased production and release of exogenous ADH due to negative feedback, down regulation of the V2 receptors, and hypoperfusion to the posterior pituitary. This condition deserves more investigation to better understand the incidence, risk factors and pathophysiological mechanisms.
An Atypical Case of TSH-Secreting Pituitary Adenoma in a Patient Presenting With Low Libido and Insomnia
Authors: Popli Rakesh , Endo Mayumi 
Published: May 2021

Abstract
Background: TSH-secreting pituitary adenoma is an incredibly rare cause of hyperthyroidism. Most patients with TSHomas present with clinical hyperthyroidism, but some patients may have atypical signs. Here we present the case of a patient who had been suffering from low libido and insomnia who was found to have secondary hyperthyroidism from a TSH-secreting pituitary adenoma.
Clinical Case: A 47-year-old man presented with complaints of progressive headache, fatigue, depression, insomnia, low libido and erectile dysfunction. After questioning, he noted the presence of intentional tremor for more than 5 years. He denied anxiety, palpitations, heat intolerance, hyper defecation, proximal muscle weakness, local compressive symptoms of the neck and ocular symptoms. Physical exam was notable for fine tremor and mild thyromegaly, but otherwise patient had no evidence of anxiety, exophthalmos, hyperreflexia or diaphoresis. The patient was found to have a normal free testosterone (46 pg/mL, n 30-140 pg/mL) but had an elevated TSH (6.302 IU/mL, n 0.4-5 IU/mL), elevated Free T4 (3.6 ng/dL, n 0.6-1.2 ng/dL) and an elevated T3 (422 ng/dL, n 73-178 ng/dL). Further lab work revealed elevated alpha-subunit (4.4 ng/mL, n &lt;0.5 ng/mL) suggestive of TSH-secreting pituitary adenoma. Prolactin and IGF-1 levels were normal. Patient had an MRI pituitary which showed a 2.3 cm sellar mass abutting the optic chiasm without involvement of the cavernous sinus. Patient proceeded to trans-sphenoidal resection. Post-operatively, TSH had dropped from 6.534 to 0.002 IU/mL (n 0.4-5 IU/mL) and Free T4 had dropped from 3.1 to 0.5 ng/dL (n 0.6-1.2 ng/dL). Interestingly, immunohistochemical staining was negative for TSH but the specimen did show histologic features characteristic of TSH-producing adenoma including extensive stromal fibrosis and nuclear pleomorphism. Patient was seen in clinic post-operatively where he noted a dramatic improvement in his headache and insomnia. He did show signs of hypothyroidism including constipation and weight gain. Patient was started on levothyroxine 75 mcg PO daily.
Conclusion: This demonstrates the case of a patient with a TSH-secreting pituitary adenoma who presented with minimal thyrotoxic symptoms despite elevated thyroid hormones. Patients with this condition may present with atypical symptoms, thus requiring clinicians to have a high index of suspicion for this rare tumor.
References: (1) Beck-Peccoz, P., Lania, A., Beckers, A. et al. 2013 European thyroid association guidelines for the diagnosis and treatment of thyrotropin-secreting pituitary tumors. Eur Thyroid J 2013; 2:76. (2) Cossu, G., Daniel, R.T., Pierzchala, K. et al. Thyrotropin-secreting pituitary adenomas: a systematic review and meta-analysis of postoperative outcomes and management. Pituitary 2019; 22:79.
An Unusual Case of Hypopituitarism in a 68 Year Old Man With a Normal Appearing Pituitary Gland and a Remote History of Severe Headache Attributed to Possible Apoplexy
Authors: Reddy Sai Rohit , Reddy Sravani Konatham , Mirza Lubna 
Published: May 2021

Abstract
A 66-year-old previously healthy man was admitted to the hospital with severe hypotension and gastroenteritis symptoms, which were attributed to food poisoning. No one else who ate with him got sick. Random morning cortisol was found to be 0.6, which was followed by the Cortrosyn stimulation test. Baseline cortisol was 0.9, which went up to 2.0 mcg/dL in 30 minutes after Cortrosyn stimulation and 2.9 mcg per dl after an hour. He was treated with high dose steroids during his inpatient stay and sent home on physiologic steroid doses. He followed up in the Endocrinology clinic after hospital discharge. A review of old records showed he was prescribed testosterone about ten years prior for symptoms of hypogonadism, but he never took it. Detailed workup revealed hypopituitarism. Serum prolactin, growth hormone, IGF-1, LH, FSH, Testosterone, TSH, and free T4 were all decreased. Brain/pituitary MRI, however, showed no pituitary abnormalities. All pituitary hormones were checked multiple times and were found to be consistently low. He was given hormone replacement therapy with levothyroxine and testosterone in addition to continuing steroids resulting in marked improvement. He gave a remote history of the worst headache of his life about twenty years ago. He stayed awake all night but never went to the hospital for an evaluation. A possible pituitary apoplexy several years ago was suspected in this case. We have not found any such case in the medical literature with hypopituitarism with a completely normal-appearing pituitary gland. This case illustrates the importance of detailed history, physical examination, hormonal testing, and appropriate hormone replacement in patients where an obvious acute cause may not be ascertained.