Body shape variation is common across all vertebrates and has important consequences for an animal's ecology, locomotion,
Divergence along the benthic-pelagic axis is one of the most widespread and repeated patterns of morphological variation in fishes, producing body shape diversity associated with ecology and swimming mechanics. This ecological shift is also the first stage of the explosive adaptive radiation of cichlid fishes in the East African Rift Lakes. We use two hybrid crosses of cichlids (Metriaclima sp. x Aulonocara sp. and Labidochromis sp. x Labeotropheus sp., >975 animals total) along the benthic-pelagic ecomorphological axis to determine the genetic basis of body shape diversification. Using a series of both linear and geometric shape measurements, we identify 55 quantitative trait loci (QTL) that underlie various aspects of body shape variation associated with benthic-pelagic divergence. These QTL are spread throughout the genome, each explain 3.0-7.2% of phenotypic variation, and are largely modular. Further, QTL are distinct both between these two crosses of Lake Malawi cichlids and compared to previously identified QTL for body shape in fishes such as sticklebacks. We find that body shape is controlled by many genes of small effects. In all, we find that convergent benthic and pelagic body phenotypes commonly observed across fish clades are most likely due to distinct genetic and molecular mechanisms.
Introduction Parathyroid crisis is a characterized by severe hypercalcemia associated with multiple organ dysfunction. Case 90 years-old Caucasian man was hospitalized for progressive confusion over 3 days and was noted to have a critically elevated serum calcium (S Ca) 16.8 mg/dl (8.6-10.0) with albumin 4.1 mg/dl. Patient had a good functional status prior to the hospitalization. On further evaluation, patient was diagnosed with primary hyperparathyroidism with a high suspicion for parathyroid cancer, with labs showing a markedly elevated PTH 1183 pg/ml (15-65) and ionized Ca >1.85 mmol/L (1.15-1.35). Of note, S Ca was normal at 9.5 mg/dl (no albumin) approximately 20 months prior to the hospitalization. Parathyroid ultrasound showed a 1.8×1.7×1.1 cm left superior parathyroid mass with ill-defined margins. Sestamibi scan confirmed a left superior parathyroid mass. CT neck/chest/abdomen/pelvis with contrast showed a 1.8×1.1×1.9 cm left superior parathyroid mass with enhancement and punctate non-obstructing right kidney stones. Hypercalcemia responded extremely well to medical management (calcitonin, 4 mg of zoledronic acid infusion and 13 days of cinacalcet 30 mg daily) resulting in normalization of S Ca. However, patient required a prolonged hospitalization for aspiration pneumonia and severe electrolyte disturbances. Since patient was not a good surgical candidate and hypercalcemia resolved on medical management, patient was discharged to a rehab facility with the plan to pursue parathyroidectomy as outpatient. S Ca worsened progressively and was 10.4 mg/dl (albumin 3.6 mg/dl) with PTH 130 pg/ml on day 15 after discharge. Cinacalcet was added when hypercalcemia further worsened to 11.7 mg/dl (albumin 3.6 mg/dl) on day 38. However, patient was hospitalized again for altered mental status, recurrent severe hypercalcemia (S Ca 15.7 mg/dl, albumin 3.8 mg/dl, PTH 1299 pg/ml), hypokalemia and urinary tract infection. In the ED, patient developed complete heart block that responded to atropine. Interestingly, hypercalcemia was recalcitrant to aggressive medical management during this hospitalization (zoledronic acid 4 mg infusion, calcitonin IM- increased up to 6 mg IM q6hr, cinacalcet- increased to 60 mg PO BID and IV fluid resuscitation with furosemide as needed). S Ca was 14.2 mg/dl (albumin 3.4 mg/dl) on day 8 of hospitalization. Therefore, urgent left superior parathyroidectomy was performed. Surgical pathology revealed a 3.1 gm parathyroid adenoma. Post-operative day#1 labs showed normal PTH 17.3 pg/ml, S Ca 12.1 mg/dl and albumin 3.2 mg/dl. S Ca and patient's mental status normalized over next few days. Discussion Urgent parathyroidectomy has shown to have excellent outcomes in patients with parathyroid crisis. Our patient's severe hypercalcemia initially responded excellently to medical management but recurred within few weeks and developed resistance to medical management. Our case highlights the importance of performing surgical exploration as soon as possible after initial medical stabilization in patients with parathyroid crisis. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
Introduction Adjuvants are substances that are commonly found in vaccines. They can enhance the efficacy and potency of a vaccine via an immunological response. However, in some susceptible individuals, these adjuvants can lead to a serious autoimmune response known as autoimmune/inflammatory syndrome induced by adjuvants (ASIA). This can lead to the onset of autoimmune disorders following vaccination. There are many case reports of the onset of autoimmune disorders following COVID-19 vaccination. However, new onset of Graves’ disease within one day after COVID-19 vaccination, is of rare occurrence. Clinical Case We present the case of a 33-year-old Caucasian male who presented to his primary care physician with chief complaints of fever ranging between 99.2F to 101.3F, palpitations and hand tremors which started one day after he received his first dose of COVID-19 vaccine. Initial laboratory evaluation included a negative throat swab for Group A Streptococcus, a negative nasal swab for Influenza A & Influenza B and a negative nasopharyngeal swab for SARS-COV-2 RNA. On physical examination, he was afebrile, pulse rate 101/min, blood pressure 125/74 mm Hg and oxygen saturation 98%. Due to persistence of tachycardia, an EKG was done which showed a normal sinus rhythm with no other abnormalities. Further laboratory testing was remarkable for a suppressed TSH 0.005 (0.300-4.00 uUI/ml), elevated FT4 2.36 (0.80-1.80 ng/dl) and an elevated TSH receptor Antibody (TRAb) 8.67 (0.00-1.75 IU/L), which confirmed the diagnosis of Graves’ disease. Subsequently, patient established care at our endocrinology clinic. Labs were repeated which showed persistence of hyperthyroidism with TSH <0.005, high normal FT4 1.56 and an elevated FT3 5.36 (2.00-4.40 pg/ml). Thyroid ultrasound was remarkable for mild thyromegaly with increased vascularity and no discrete nodules. Patient was initiated on Methimazole 10 mg daily and propranolol 10 mg twice daily. During the first follow-up visit, the dose of Methimazole was reduced to 5 mg daily based on improved labs. However, it had to be increased back to 10 mg daily due to subsequent worsening of labs. Since then, patient has been maintained on a stable dose of Methimazole 10 mg once daily and the beta-blocker has been discontinued. It has been almost 1 year since the diagnosis and the Graves’ disease specific Thyroid Stimulating Immunoglobulin (TSI) antibody is still elevated at 1.31 (0.00-0.55 IU/L). Conclusion Graves’ disease should be considered high in the differential diagnosis in a patient presenting with fever and tachycardia following COVID-19 vaccination. Our unique case supports the current literature available on the various autoimmune conditions caused by the autoimmune/inflammatory syndrome induced by adjuvants, also known as ASIA. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m., Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
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