Oxytocin is involved in the regulation of social behaviors including parental behaviors in a variety of species. Oxytocin triggers social behaviors by binding to oxytocin receptors (OXTRs) in various parts of the brain. OXTRs are present in the preoptic area (POA) where hormone-sensitive sexually dimorphic nuclei exist. The present study was conducted to examine whether sex differences exist in the distribution of neurons expressing OXTRs in the POA. Using OXTR-Venus (an enhanced variant of yellow fluorescent protein) mice, the distribution of OXTR-Venus cells in the POA was compared between sexes. The total number of OXTR-Venus cells in the medial POA (MPOA) was significantly greater in females than in males. No detectable OXTR-Venus cells were observed in the anteroventral periventricular nucleus (AVPV) within the MPOA in most of the brain sections from males. We further examined the total number of OXTR-Venus cells in the AVPV and the rest of the MPOA between the sexes. The total number of OXTR-Venus cells in the AVPV in females (615 ± 43) was significantly greater than that in males (14 ± 2), whereas the total number of OXTR-Venus cells in the rest of the MPOA did not differ significantly between the sexes. Thus, the sexually dimorphic expression of OXTR-Venus specifically occurred in the AVPV, but not in the rest of the MPOA. We also examined whether the expression of OXTR in the AVPV is driven by the female gonadal hormone, estrogen. Immunocytochemistry and single-cell RT-PCR revealed the presence of the estrogen receptor α in OXTR-Venus cells in the female AVPV. Moreover, ovariectomy resulted in the absence of OXTR-Venus expression in the AVPV, whereas estrogen replacement therapy restored OXTR-Venus expression. These results demonstrate that the expression of OXTR in the AVPV is primarily female specific and estrogen dependent. The presence of the sexually dimorphic expression of OXTR in the AVPV suggests the involvement of OXTR neurons in the AVPV in the regulation of female-specific behavior and/or physiology.

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Objective. Black thyroid is a rare pigmented change seen almost exclusively in patients upon minocycline ingestion, and the process has previously been thought to be generally benign. There have been 61 reported cases of black thyroid. We are aware of 13 cases previously reported in association with thyroid carcinoma. This paper reports six patients with black thyroid pigmentation in association with thyroid carcinoma. Design. The medical records of six patients who were diagnosed with black thyroid syndrome, all of whom underwent thyroid surgery, were reviewed. Data on age, gender, race, preoperative fine needle aspiration biopsy (FNA), thyroid function levels, and pathology reports were collected. Main Outcome. The mean age was 60 years. There were 5 females, 4 of whom were African American. All patients were clinically and biochemically euthyroid. Black pigmentation was not diagnosed in preoperative FNA, and only one patient had a preoperative diagnosis of papillary thyroid carcinoma. The other patients underwent surgery and were found to have black pigmentation of the thyroid associated with carcinoma. Conclusions. FNA does not diagnose black thyroid, which is associated with thyroid carcinoma. Thyroid glands with black pigmentation deserve thorough pathologic examination, including several sections of each specimen.

Bilirubin is an endogenous antioxidant and is the end product of heme catabolism by heme oxygenase (HO) and biliverdin reductase. Chronic angiotensin II (Ang II) infusion induces renal HO‐1 expression which is associated with renoprotective effects, and further induction of renal HO‐1 attenuates the development of hypertension in this model. To determine the effects of bilirubin on the development of Ang II‐induced hypertension, two groups of rats were studied: Ang II (n=4) and Ang II+Bilirubin (n=4). Rats were infused with Ang II (80 ng/min for 2 weeks) and bilirubin was administered simultaneously (3mg/100g BWt/48 hrs, intraperitoneally). Two weeks after Ang II infusion, systolic blood pressure significantly increased from 134±4 mmHg to 198±7 mmHg (p<0.05) in the Ang II group, and from 128±8 mmHg to 209±9 mmHg (p<0.05) in the Ang II+Bilirubin group. Relative to the Ang II group, treatment with bilirubin did not alter body weight 259±18 g vs. 275±18 g, food intake 25±3 g vs. 25±2 g, water intake 78.1±6.7 vs. 75.3±7.3 ml/day, or urine output 58.5±5.8 ml vs. 50.8±5.5 ml/day. However, urinary protein excretion was significantly lower in the Ang II+Bilirubin group (32.9±9.7 mg/day vs. 81.4±22.8 mg/day, p<0.05). We conclude that bilirubin contributes to the renoprotective effects conferred by induction of HO‐1 in Ang II‐dependent hypertension. Supported by NIH grants HL26371 and COBRE P20 RR 017659.