Activational levels of androgens influence risk assessment behaviour but do not influence stress-induced suppression in hippocampal cell proliferation in adult male rats.

Adult male, but not female, rats demonstrate a suppression in hippocampal cell proliferation in response to an acute predator odour stress. The present study examined the effect of activational levels of androgens on stress-induced changes in hippocampal cell proliferation and defensive and non-defensive behaviours in adult male rats. Adult male Sprague-Dawley rats were castrated and exposed to trimethylthiazoline (TMT, the main component of fox feces). Androgen status did not significantly affect TMT-induced suppression in hippocampal cell proliferation or expression of defensive burying. However, castrated males did not show an increase in duration of stretch attends (a risk assessment behaviour) in response to TMT. The results of this study suggest that activational levels of androgens in the male rat do not directly regulate the sex difference in stress-induced suppression of hippocampal cell proliferation but do regulate risk assessment behaviour.

Primary pulmonary synovial sarcoma: a case report with unique and impressive computed tomography findings.

Primary pulmonary synovial sarcoma (PPSS) is a rare malignancy. Its etiology, imaging features and optimal treatment are not well understood. Pulmonary pseudoaneurysms and lymphadenopathy are rare complications of synovial sarcomas. A 40-year-old woman with mild hemoptysis and thoracic back pain underwent a computed tomography scan that revealed multiple pulmonary lesions, paraesophageal lymphadenopathy and incidental bilateral pulmonary emboli. A diagnosis of PPSS was made through the identification of an SS18 translocation by fluorescence in situ hybridization. She was started on adriamycin, ifosfamide and mesna chemotherapy. Over the subsequent two months, she developed three pulmonary artery pseudoaneurysms, ultimately requiring endovascular coiling. Seven months after starting treatment, the patient was asymptomatic. The lesions and lymphadenopathy decreased in size. The present case highlights complications of a rare malignancy and demonstrates positive response to ifosfamide-based chemotherapy in the setting of PPSS.

Delayed-onset hypoparathyroidism in an adolescent with chromosome 22Q11 deletion syndrome.

OBJECTIVE: To describe the first case of established chromosome 22q11 deletion syndrome with late onset presentation of hypocalcemia secondary to hypoparathyroidism. METHODS: We present the history, clinical and laboratory investigations, and management of a 17-year-old adolescent boy who presented with 3 separate seizures secondary to hypocalcemia. This patient had an established diagnosis of chromosome 22q11 deletion syndrome at the time of the seizure presentations, but had previously normal calcium levels. RESULTS: Hypocalcemia was noted during each seizure, with corrected calcium levels ranging from 6.64 to 7.76 mg/dL (reference range, 8.52 to 10.52 mg/dL). The hypocalcemia was secondary to hypoparathyroidism, with parathyroid hormone levels < 2.75 pg/mL (reference range, 22.9 to 68.75 pg/mL). He was treated with calcitriol, 0.5 µg daily, and calcium carbonate, 2,400 mg daily, leading to normalization of serum calcium and resolution of seizures. CONCLUSION: Chromosome 22q11 deletion syndrome is a relatively common genetic disorder with a wide variety of phenotypic manifestations including cardiac abnormalities, abnormal facies, thymic dysfunction, cleft palate, and hypocalcemia. This case shows that medical practitioners should be aware that hypocalcemia can present after an established diagnosis, which has implications for the management of this disorder.

Endocannabinoids modulate stress-induced suppression of hippocampal cell proliferation and activation of defensive behaviours.

The endocannabinoid system has been shown to regulate both the hypothalamic-pituitary-adrenal (HPA) axis and emotionality. The present experiment was designed to examine whether pharmacological modulation of the endocannabinoid system would affect the suppression of hippocampal cell proliferation and increase in defensive behaviours seen following exposure to predator odour (trimethylthiazoline; TMT) stress. Rats were administered either an endocannabinoid uptake inhibitor (AM404; 2 mg/kg) or a cannabinoid CB1 receptor antagonist (AM251; 5 mg/kg) 30 min prior to exposure to TMT. Exposure to TMT reduced cell proliferation in the dentate gyrus and increased the expression of defensive burying. Administration of AM404 significantly inhibited defensive burying, and attenuated the reduction in cell proliferation in response to TMT exposure. Administration of AM251 alone significantly increased cell proliferation; however, pretreatment with AM251 prevented neither the stress-induced suppression of cell proliferation nor the stress-induced increase in behavioural responses. These results support previous research demonstrating that augmentation of endocannabinoid signalling can suppress stress-responsive systems. They also suggest that endocannabinoids may play a complex role in the regulation of neurogenesis via cell proliferation in the hippocampus.