The structure of the amygdala associates with human sexual permissiveness: Evidence from voxel‐based morphometry

Sexual behavior is a critical function of human procreation. Despite previous studies that investigated the neural mechanisms of basic human physiological sexual functions, the neural mechanisms that underlie individual differences in human sexual permissiveness remain unknown. We used voxel‐based morphometry and a questionnaire (scale for sexual attitudes) to measure sexual permissiveness to investigate the gray matter and white matter structural correlates of sexual permissiveness. Sexual permissiveness was negatively correlated with regional gray matter density of the structures involving the right amygdala and surrounding areas, and positively correlated with regional white matter density of the white matter area that spread around the left amygdala to the hypothalamus area. There were no gender‐specific relationships in the neural correlates of our findings. These findings suggest that structural variations in regions that play key roles in the basic physiological aspects of human sexuality underlie individual complex sexual attitudes in social life. Hum Brain Mapp 36:440–448, 2015. © 2014 The Authors. Human Brain Mapping Published by Wiley Periodicals, Inc.     

Effect of T-cell receptor VΒ-specific monoclonal antibodies on cyclophosphamide-induced diabetes mellitus in non-obese diabetic mice

Summary The expression of specific T-cell receptor gene segments by T lymphocytes appears to be critically important for the induction of several experimental autoimmune diseases mediated by these cells. We examined whether this situation also applied to non-obese diabetic mice by using various T-cell receptor V-specific monoclonal antibodies. No significant age- or sex-related differences were observed in V usage by peripheral and splenic T lymphocytes. CD8⁺ T lymphocytes among the islet-derived mononuclear cells isolated from 20-week-old female non-obese diabetic mice showed heterogeneity of their V gene usage. In order to examine the role of T lymphocyte subsets expressing specific T-cell receptor V gene segments in the development of diabetes mellitus, T-cell receptor V-specific monoclonal antibodies were administered to 10-week-old male non-obese diabetic mice treated with cyclophosphamide. None of the antibodies used could significantly diminish the incidence of cyclophosphamide-induced diabetes and the severity of insulitis [anti-V3 (11 of 22 mice became diabetic, 50%), anti-V5 (9 of 14, 64%), anti-V8 (9 of 21, 43%), anti-V11 (12 of 23, 52%), anti-V14 (7 of 12, 58%), and anti-V5 + anti-V11 (6 of 12, 50%)] when compared with control mice (12 of 21, 57%). In addition, there were no significant differences in T-cell receptor V usage between diabetic and non-diabetic cyclophosphamide-treated mice. These results suggest that five T-lymphocyte subsets expressing different T-cell receptor V gene segments, considered to be candidates involved in the pathogenesis of autoimmune diabetes, do not individually contribute to the development of cyclophosphamide-induced diabetes in non-obese diabetic mice.     

A new glucose-6-phosphate dehydrogenase variant G6PD Sugao (826C-->T) exhibiting chronic hemolytic anemia with episodes of hemolytic crisis immediately after birth

A case of glucose-6-phosphate dehydrogenase (G6PD) deficiency associated with chronic hemolysis with episodes of hemolytic crisis immediately after birth is reported. The propositus was a 1-month-old Japanese male infant. Molecular analysis of the G6PD gene revealed a novel missense mutation (826C-->4T) in exon 8 predicting a single amino acid substitution, Pro276Ser. The mother was confirmed to be heterozygous for this mutation. We designated this novel class 1 variant as G6PD Sugao. Pro276 is a phylogenetically conserved residue that may play a significant role in dimer formation.     

Prognostic Value of Early Evaluation of Left Ventricular Dyssynchrony After Myocardial Infarction

Molecular Imaging and Biology - Dispersion in the contraction of the normally coordinate ventricular system, referred to as left ventricular (LV) dyssynchrony, is constantly observed at different...     

Evaluation of Inferior Mesenteric Vein Blood Flow Circulation with Per-Rectal Administration of Thalliuni-201 and Technetium-99m Pertechnetate

We administered both per-rectal thallinm-201 (²⁰¹TI) and technetium-99m pertechnetate (^99mTc) to patients with liver diseases in order to understand the abnormalities of inferior mesenteric vein (IMV) blood flow circulation. As ²⁰¹TI heart-to-liver uptake ratio (H:L), reflecting the degree of portal-systemic shuntings (PSS), increased, the visualization of IMV in general became poor on ^99m Tc scintigrams. ²⁰¹TI H:L in the group with no visualization of IMV on ^99m Tc scintigrams was significantly higher than in the group with clear visualization of IMV ( p < 0.001). However, there were patients who showed IMV visualization among those with high ²⁰¹ TI H:L. In these patients, it was considered that IMV blood flowed in the normograde direction, escaping mainly through PSS at the upper part of the portal system, and resulting in elevated H:L. In the patients without IMV visualization, IMV blood flowed in the retrograde direction, escaping mainly through collaterals at the lower part of IMV. Inferior vena cava (IVC) was visualized on ^99m Tc scintigrams in some patients without IMV visualization, indicating the presence of collaterals from the distal part of IMV to IVC. Per-rectal studies using these two radiotracers can afford us useful informations on the abnormalities of IMV blood flow hemodynamics in patients with liver diseases.     

Preferential acetazolamide-induced vasodilation based on vessel size and organ: confirmation of peripheral vasodilation with use of colored microspheres

When carbonic anhydrase activity decreases, the regional blood flow (rBF) in organs increases as hypercapnia develops. However, the effects of acetazolamide (AZ)-induced vasodilation have not been estimated with respect to vessel size and organs. The aim of this study was to determine the diameter of the capillaries in various organs that respond to inhibition of carbonic anhydrase activity by AZ. White rabbits were anesthetized with urethane and ketamine and infused with AZ. While the systolic blood pressure (SBP), pH, hemoglobin concentration, and base excess did not change, the partial pressure of arterial oxygen (PaO2) increased significantly and the partial pressure of arterial carbon dioxide (PaCO2) decreased significantly with AZ. The rBF was calculated by using 3 different sizes (15, 25, and 50 microm) of colored microspheres (CM). The rBF measured with 15 microm CM in the brain, kidneys, and liver increased in response to AZ, and the rBF in these organs was different with the different sizes of CM. However, the rBF calculated by using the different sizes of CM in the stomach and abdominal muscle did not change after the administration of AZ. The AZ-induced vasodilation occurred in all sizes of vessels in the liver, in the small and medium-sized vessels in kidneys, and in the larger capillaries in the brain.     

Acetazolamide-induced increase in blood flow to rabbit organs is confirmed using colored microspheres

Summary Inhibitors of carbonic anhydrase activity have been found to increase blood and organPCO₂ and to increase blood flow (BF) in individual organs. To determine whether carbonic anhydrase inhibition coordinately induces an increase in BF in several organs, we assayed the effect of the carbonic anhydrase inhibitor, acetazolamide (AZ), on BF in rabbit organs using the colored microsphere (CM) assay. Eight female white rabbits were anesthetized with ketamine and urethane, and administered three sequential doses of 4 mg/kg AZ. After each dose, the rabbits were injected with 9 × 10⁵ CMs of different colors, and arterial blood was collected. We found that AZ had no effect on blood pressure, body temperature, hemoglobin conentration, orPaCO₂. In contrast, 12 mg/kg AZ significantly increasedPaO₂ and significantly decreased base excess. When we measured organ BF, we observed, in response to 12 mg/kg AZ, an 82% increase in brain BF and a 55% increase in kidney BF, but no change in BF of the liver, stomach wall, or abdominal muscle. These findings suggest that the inhibition of carbonic anhydrase activity by AZ, which decreases the rate of CO₂ conversion to HCO ₃ ^- , causes the retention of CO₂ in tissues and organs, and thus increases BF in specific organs. Administration of carbonic anhydrase inhibitors, such as AZ, may increase BF to the brain and kidney without reducingPaO₂, thereby increasing the supply of oxygen in conditions involving hypoxia such as ischemia and shock.     

Hemodynamic changes and prognosis in patients with hypertrophic cardiomyopathy and abnormal blood pressure responses during exercise

BACKGROUND: An abnormal blood pressure response (BPR) during exercise has been proposed as a risk factor for sudden cardiac death in patients with hypertrophic cardiomyopathy (HCM). Some patients with HCM show systolic dysfunction during exercise. HYPOTHESIS: The aim of this study was to clarify the hemodynamic response during exercise and prognosis in patients with HCM and abnormal BPR. METHODS: Sixty-five patients with HCM underwent radionuclide monitoring of left ventricular function and measurement of blood pressure during supine ergometer exercise. Thereafter, cardiac events were recorded for an average period of 76 months. RESULTS: Seven of 65 patients had abnormal BPR, while the others had normal BPR. Changes of heart rate and systemic vascular resistance during exercise did not differ between the two groups. Stroke volume did not increase in the abnormal BPR group but did in the normal BPR group. During a mean follow-up period of 76 months, three of the seven patients (43%) with abnormal but only one patient (2%) with normal BPR suffered a malignant arrhythmia. CONCLUSIONS: Abnormal BPR occurred in about 11% of patients with nonobstructive HCM and was associated with a high prevalence of cardiac events. The predictor of abnormal BPR during exercise may not be an abnormal response of systemic vascular resistance and heart rate, but the lack of an appropriate increase in stroke volume.