SUMMARY Memory traces are believed to be ensembles of cells used to store memories. To visualize memory traces, we created a transgenic line that allows for the comparison between cells activated during encoding and expression of a memory. Mice re-exposed to a fear-inducing context froze more and had a greater percentage of reactivated cells in the dentate gyrus (DG) and CA3 than mice exposed to a novel context. Over time, these differences disappeared, in keeping with the observation that memories become generalized. Optogenetically silencing DG or CA3 cells that were recruited during encoding of a fear-inducing context prevented expression of the corresponding memory. Mice with reduced neurogenesis displayed less contextual memory and less reactivation in CA3 but, surprisingly, normal reactivation in the DG. These studies suggest that distinct memory traces are located in the DG and in CA3 but that the strength of the memory is related to reactivation in CA3.
R apid COVID-19 vaccine development and uptake are critical to mitigating the ongoing epidemic. Current vaccine candidates are at various stages of development and regulatory approval. These vaccines are broadly considered safe, though adverse effects have not yet been fully characterized. In this study we present the first description of thyroiditis linked to SARS-CoV-2 vaccination.A 57-year-old woman with no medical history received the first dose of the Pfizer-BioNTech SARS-CoV-2 vaccine 34 days before presentation, with associated fatigue, nausea, chills, and myalgias lasting 1.5 days. She received the second dose 13 days before presentation, and within 24 hours had recurrence of her symptoms associated with new progressive anterior neck pain and swelling. She was referred to the hospital by her outpatient provider for thyrotropin (TSH) 0.009 lU/mL, thyroxine (T4) free 2.6 ng/dL, and T4 total 17.4 mcg/dL (outpatient normal ranges [NRs] unavailable). On hospital arrival, she was febrile to 38.3°C with a pulse of 137 beats/min. Examination revealed right thyroid gland enlargement with diffuse tenderness, and no proptosis, lid lag, or periorbital edema. Laboratories showed TSH <0.008 lU/mL (NR: 0.4-4.2), free T4 1.92 ng/dL (NR: 0.8-1.5), triiodothyronine (T3) total 137 ng/dL (NR: 87-178) with thyrotropin receptor antibody <1.10 U/L (NR: 0-1.75), thyroid stimulating immunoglobulin <0.10 U/L (NR: 0-0.55), thyroid peroxidase antibody <0.5 U/mL (NR: 0-5.6), and thyroglobulin antibody 3.4 U/mL (NR: 0-4.1). Thyroid ultrasound showed an asymmetrically enlarged hypervascular heterogeneous right thyroid lobe suggestive of thyroiditis. She was treated with propranolol and ibuprofen and later started on prednisone as an outpatient.There is likely a causal relationship between this patient's thyroiditis with thyrotoxicosis and the COVID-19 mRNA vaccine, given the condition's temporal relationship with the vaccine in a previously healthy patient with no alternative suspected cause. We reviewed the Vaccine Adverse Event Reporting System for thyroid dysfunction after the COVID-19 vaccine, and there is one case (922030) of a 46-year-old woman of ''thyroiditis with hyperthyroidism,'' who developed fever, neck pain, and tachycardia 10 days postvaccine (1). Cases 1039886 and 984402 have insufficient information but may involve postvaccine hyperthyroidism. Rare reports have linked subacute thyroiditis to varying influenza vaccines (2-4), and immune dysregulation has been
Neoplasms that secrete ectopic ACTH may cause severe, life-threatening hypercortisolism. These tumors are often difficult to localize and treat, requiring a comprehensive and systematic management plan orchestrated by a multidisciplinary team. The Mount Sinai Adrenal Center hosted an interdisciplinary retreat of experts in adrenal disorders and neuroendocrine tumors with the aim of developing a clinical pathway for the management of Cushing syndrome due to ectopic ACTH production. The result was institutional recommendations for the diagnosis, localization, surgical approaches to intrathoracic tumors and bilateral adrenalectomy, perioperative and postoperative medical management of hypercortisolism and its sequelae. Specific recommendations were made regarding the timing and selection of therapies based on the considerations of our team as well as a review of the current literature. Our clinical pathway can be applied by other institutions directly or serve as a guide for institution-specific management.
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Case Presentation: A 43 year-old female was diagnosed at birth with non-salt wasting congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency and underwent clitoral reduction surgery. She was treated with hydrocortisone and had menarche at age 7 with irregular and heavy menses. At age 15 she had a D&C with removal of “something in her ovaries.” She stopped hydrocortisone at age 30 except for stress doses during illness. At age 35 she stopped oral contraceptives and thereafter has been amenorrheic. She presented with abdominal distention and constipation. On exam she had short stature, marked frontal and temporal balding, hirsutism, increased musculature and a large distended abdomen. Labs showed AM cortisol 3.1 mcg/dL (nl 10–20), ACTH 440 pg/ml (nl <46), 17-OH Progesterone 11000 ng/dL (nl <206), DHEAS 362 mcg/dl (nl <430), FSH 0.2 mIU/ml, LH 2.7 mIU/ml, testosterone 618 ng/dl (nl 10–75), and estradiol 162 pg/ml (nl post menopause <41). MRI showed a massive fibroid (30 cm), bilateral adrenal hyperplasia and a left paraaortic, retroperitoneal mass (5.9 cm). She underwent hysterectomy with removal of a 9.5 kg uterus containing degenerated fibroids, left adrenalectomy and removal of the left paraaortic mass that was initially read as oncocytic adrenal cortical neoplasm, metastatic. A similar oncocytic neoplasm was noted in the left adrenal gland and on further review with pathology the revised report read paraaortic mass, probable adrenal rest tumor. Discussion: Excess androgens and chronically elevated ACTH levels in untreated CAH can lead to adverse effects beyond adrenal insufficiency and virilization. We present a woman with untreated classic CAH who developed a large fibroid and paraaortic adrenal cortical tumor. Fibroids have been described in CAH patients, a potential consequence of elevated androgens that are converted by aromatase in the endometrium to estrogens driving growth of fibroid tumors. Chronic ACTH can further act as a growth factor, leading to adrenal hyperplasia, adrenal tumors and ectopic adrenal rest tissue. Intra-adrenal tumors in untreated CAH are generally benign with rare cases of adrenal cortical carcinoma reported. Ectopic adrenal rest tissue in untreated CAH is most commonly reported in testes. There have been rare case reports of ectopic adrenal rest tumors in the adnexa, broad ligament, and perirenal area. Our patient presents as an unusual case of ectopic adrenal rest tumor in the paraaortic region. Based on the atypical location and incomplete history available to the pathologist, it was initially read as metastatic adrenocortical carcinoma. Upon further review given the clinical information, the diagnosis was revised to indicate a pararenal adrenal rest tumor. This case highlights the importance of glucocorticoid compliance in CAH and the necessity to provide a clinical context for the pathologist in cases of extra-adrenal tumors in untreated CAH.
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