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Pubertal male Syrian hamsters (Mesocricetus auratus) treated with anabolic/androgenic steroids (AASs) during adolescence (P27-P56) display a highly intense aggressive phenotype that shares many behavioral similarities with pathological aggression in youth. Anticonvulsant drugs like valproate that enhance the activity of the γ-aminobutyric acid (GABA) neural system in the brain have recently gained acceptance as a primary treatment for pathological aggression. This study examined whether valproate would selectively suppress adolescent AAS-induced aggressive behavior and whether GABA neural signaling through GABAA subtype receptors in the latero-anterior hypothalamus (LAH; an area of convergence for developmental and neuroplastic changes that underlie aggression in hamsters) modulate the aggression-suppressing effect of this anticonvulsant medication. Valproate (1.0-10.0 mg/kg, intraperitoneal) selectively suppressed the aggressive phenotype in a dose-dependent fashion, with the effective anti-aggressive effects beginning at 5 mg/kg, intraperitoneally. Microinfusion of the GABAA receptor antagonist bicuculline (7.0-700 ng) into the LAH reversed valproate's suppression of AAS-induced aggression in a dose-dependent fashion. At the 70 ng dose of bicuculline, animals expressed the highly aggressive baseline phenotype normally observed in AAS-treated animals. These studies provide preclinical evidence that the anticonvulsant valproate selectively suppresses adolescent, AAS-induced aggression and that this suppression is modulated, in part, by GABA neural signaling within the LAH.

The mouse cerebral cortex contains neurons that express choline acetyltransferase (ChAT) and are a potential local source of acetylcholine. However, the neurotransmitters released by cortical ChAT+ neurons and their synaptic connectivity are unknown. We show that the nearly all cortical ChAT+ neurons in mice are specialized VIP+ interneurons that release GABA strongly onto other inhibitory interneurons and acetylcholine sparsely onto layer 1 interneurons and other VIP+/ChAT+ interneurons. This differential transmission of ACh and GABA based on the postsynaptic target neuron is reflected in VIP+/ChAT+ interneuron pre-synaptic terminals, as quantitative molecular analysis shows that only a subset of these are specialized to release acetylcholine. In addition, we identify a separate, sparse population of non-VIP ChAT+ neurons in the medial prefrontal cortex with a distinct developmental origin that robustly release acetylcholine in layer 1. These results demonstrate both cortex-region heterogeneity in cortical ChAT+ interneurons and target-specific co-release of acetylcholine and GABA.

The cerebral cortex contains neurons that express choline acetyltransferase (ChAT) and are a potential local source of acetylcholine. However, the neurotransmitters released by cortical ChAT+ neurons and their synaptic connectivity are unknown. We show that the nearly all cortical ChAT+ neurons are specialized VIP+ interneurons that release GABA strongly onto other inhibitory interneurons and acetylcholine sparsely onto layer 1 interneurons and other VIP+/ChAT+ interneurons. This differential transmission of ACh and GABA based on the postsynaptic target neuron is reflected in VIP+/ChAT+ interneuron pre-synaptic terminals, as quantitative molecular analysis shows that only a subset of these are specialized to release acetylcholine. In addition, we identify a separate, sparse population of non-VIP ChAT+ neurons in the medial prefrontal cortex with a distinct developmental origin that robustly release acetylcholine in layer 1. These results demonstrate both cortex-region heterogeneity in cortical ChAT+ interneurons and target-specific co-release of acetylcholine and GABA.

The mouse cerebral cortex contains neurons that express choline acetyltransferase (ChAT) and are a potential local source of acetylcholine. However, the neurotransmitters released by cortical ChAT+ neurons and their synaptic connectivity are unknown. We show that the nearly all cortical ChAT+ neurons in mice are specialized VIP+ interneurons that release GABA strongly onto other inhibitory interneurons and acetylcholine sparsely onto layer 1 interneurons and other VIP+/ChAT+ interneurons. This differential transmission of ACh and GABA based on the postsynaptic target neuron is reflected in VIP+/ChAT+ interneuron pre-synaptic terminals, as quantitative molecular analysis shows that only a subset of these are specialized to release acetylcholine. In addition, we identify a separate, sparse population of non-VIP ChAT+ neurons in the medial prefrontal cortex with a distinct developmental origin that robustly release acetylcholine in layer 1. These results demonstrate both cortex-region heterogeneity in cortical ChAT+ interneurons and target-specific co-release of acetylcholine and GABA.

Dental disease is a frequent finding on head and neck images, especially in the context of emergencies, and can be a challenge for radiologists who are inexperienced with findings of dental trauma or disease. Dental abnormalities can be subtle and therefore must be included in the systematic approach to these images. Although dedicated dental images are not acquired in most emergency cases, the teeth are included on many different images of the head and neck, and their initial evaluation seldom requires a specific protocol. The high prevalence of craniofacial trauma, sinus infection, and maxillomandibular procedures, among other conditions, frequently requires interpretation of dental images in daily emergency practice. The imaging findings can be categorized into infection, trauma, and complications of procedures, although sometimes these categories can overlap. Such categories can help the radiologist decide which imaging protocol and dynamic maneuvers should be used and are also useful when reading images and proposing differential diagnoses. Familiarity with the imaging findings of dental emergencies improves the radiologist's diagnostic confidence and role in guiding patient care, avoiding progression to life-threatening conditions, and reducing aesthetic problems, dental loss, and related conditions. Information about the imaging protocols is provided, the relevant anatomy of the teeth and related structures is reviewed, and the key imaging findings of dental emergencies are presented.©RSNA, 2019.

The modulation of cortex by acetylcholine (ACh) is typically thought to originate from long-range projections arising in the basal forebrain. However, a subset of VIP interneurons express ChAT, the synthetic enzyme for ACh, and are a potential local source of cortical ACh. Which neurotransmitters these VIP/ChAT interneurons (VCINs) release is unclear, and which post-synaptic cell types these transmitters target is not known. Using quantitative molecular analysis of VCIN pre-synaptic terminals, we show expression of the molecular machinery to release both ACh and GABA, with ACh release restricted to a subset of boutons. A systematic survey of potential post-synaptic cell types shows that VCINs release GABA primarily onto other inhibitory interneuron subtypes, while ACh neurotransmission is notably sparse, with most ACh release onto layer 1 interneurons and other VCINs. Therefore, VCINs are an alternative source of cortical ACh signaling that supplement GABA-mediated disinhibition with highly targeted excitation through ACh.

This Conference is the fifth of a series of Workshops on High Energy Gamma- ray Experiments, following the Conferences held in Perugia 2003, Bari 2004, Cividale del Friuli 2005, Elba Island 2006. This year the focus was on the use of gamma-ray to study the Dark Matter component of the Universe, the origin and propagation of Cosmic Rays, Extra Large Spatial Dimensions and Tests of Lorentz Invariance., Comment: 328 pages, 7.8Mb, Proceedings of the 5th SCINEGHE Workshop, June 18-20, 2007 http://www.roma2.infn.it/SciNeGHE07/

Among the adverse effects possibly associated with the use of erythropoietin (EPO) in hemodialysis patients is an increased incidence of thrombosis of the vascular access. However, little is known about the effect of EPO on the stenotic lesion in the venous outflow system, which is the leading cause of fistula thrombosis. This study was designed to explore the long-term effects of EPO treatment on progressive fistula stenosis and the plasma concentrations of some potential mediators of neointimal hyperplasia. A cross-sectional and 3-yr prospective, placebo-controlled, pilot study was performed in 30 hemodialysis patients with native arteriovenous fistula. Sixteen patients received EPO and 14 received a placebo. Venous dialysis pressure, urea recirculation, color Doppler sonography, and angiography were used to monitor vascular access patency. Compared with 60 healthy subjects, the hemodialysis patients had elevated plasma levels of platelet-derived growth factor, monocyte chemoattractant protein-1, and interleukin 6, three proteins that might be involved in the neointima formation regulating the proliferation of vascular smooth muscle cells. In addition, these patients had numerous endothelial and hemostatic abnormalities that indicated a thrombophilic state. Eleven patients, six (37.5%) receiving EPO and five (35.7%) taking placebo, developed a progressive stenosis in the venous circuit of the fistula. There was no significant difference in the vascular access, event-free survival over 36 mo between patients receiving EPO therapy and placebo. EPO induced a significant decrease in the plasma values of platelet-derived growth factor and vascular cell adhesion molecule-1 and an increase of monocyte chemoattractant protein-1 concentration. After EPO withdrawal, these parameters returned to pretreatment levels. In conclusion, long-term EPO therapy does not increase the risk of progressive stenosis of native arteriovenous fistula. The use of erythropoietin does not induce any prothrombotic change in hemostatic parameters, and further studies are required to elucidate the theoretically beneficial effects on the plasma concentration of some potential mediators of neointimal formation.

Vascular access dysfunction is an important cause of morbidity for dialysis patients and a major contributor to hemodialysis cost. Thrombosis is a leading cause of vascular access failure, and usually results from stenotic lesions in the venous outflow system. This study was designed to explore the impact of serum levels of various risk factors for thrombosis and accelerated fibrointimal hyperplasia on progressive stenosis, and the subsequent thrombosis of hemodialysis fistula. A cross-sectional and 2-yr prospective pilot study was performed in 30 nondiabetic hemodialysis patients with primary arteriovenous fistula. Venous dialysis pressure, urea recirculation, color Doppler sonography, and angiography were used to monitor vascular access patency. Eleven patients (37%) developed a progressive stenosis in the venous circuit, which was complicated by thrombosis in three patients. Compared with the patients without fistula dysfunction, these patients had higher serum levels of monocyte chemoattractant protein-1 and interleukin-6, two cytokines that regulate the proliferation of vascular smooth muscle cells, which is the key mechanism in the pathogenesis of fistula stenosis. In addition, they had hyperinsulinemia, hyperlipidemia, and increased plasma levels of two hemostasis-derived risk factors for thrombosis: plasminogen activator inhibitor type 1 and factor VII. Monocyte chemoattractant protein-1, interleukin-6, plasminogen activator inhibitor type 1, factor VII, triglycerides, and the ratios for cholesterol/HDL-cholesterol, apolipoprotein (apo) A-I/ apo C-III, apo A-I/apo B, and glucose/insulin were independent predictors of fistula dysfunction. This study demonstrates the influece of cytokines, hemostasis-derived vascular risk factor, hyperinsullnemia, and abnormallties of lipids and apolipoproteins on primary fistula survival. The assessment of these factors might be useful for the identification of the patients at risk of fistula stenosis and thrombosis.

Una lettura di taglio psicoanalitico di Barbarella di Roger Vadim.