A Novel Nomogram to Identify Candidates for Extended Pelvic Lymph Node Dissection Among Patients with Clinically Localized Prostate Cancer Diagnosed with Magnetic Resonance Imaging-targeted and Systematic Biopsies

Background

Available models for predicting lymph node invasion (LNI) in prostate cancer (PCa) patients undergoing radical prostatectomy (RP) might not be applicable to men diagnosed via magnetic resonance imaging (MRI)-targeted biopsies.

Correlation between amount of retinal afferents to the pretectal nucleus of the optic tract and dorsal terminal accessory optic nucleus and performance of horizontal optokinetic reflex in rat.

Intraocular kainic acid injection in Long-Evans rats induces loss of retinal afferents to subcortical visual centers as assessed by the axoplasmic transport of [14C]valine. The optical terminal fields of the pretectal nucleus of the optic tract (NOT), superior colliculus and accessory optic system (AOS) nuclei appear particularly affected. Since NOT and the AOS dorsal terminal nucleus (DTN) represent the first relay station of the visuomotor pathway mediating horizontal optokinetic nystagmus (HOKR), we have studied the characteristics of HOKR after various degrees of retinal deafferentation of these nuclei induced by intraocular KA injection. Taking advantage of the arrangement of the primary optic projections to NOT-DTN, that in rats are almost entirely crossed, in each animal, monocular HOKR induced by stimulation of the injected eye was compared to monocular HOKR elicited by stimulation of the intact, ipsilateral eye. Following NOT-DTN optic denervation, HOKR gain always worsened, and in a way, that the greater the deficits of retinal afferents, the greater the HOKR inability to compensate for visual motion. Furthermore, for any given retinal denervation the higher the stimulus velocity, the greater the HOKR deficit. While the correlation between HOKR gain and the amount of retinal afferents to NOT-DTN would seem to indicate a functional homogeneity of the retinal ganglion cells sending axons to these nuclei, the finding that the extent of HOKR impairment also varied with velocity might not support the above view.     

Epilepsy syndromes associated with hypothalamic hamartomas.

PURPOSE: Hypothalamic hamartoma (HH) related epilepsy presents with gelastic seizures (GS), other seizure types and cognitive deterioration. Although seizure origin in GS has been well established, non-GS are poorly characterized. Their relationship with the HH and cognitive deterioration remains poorly understood. We analyzed seizure type, spread pattern in non-GS and their relationship with the epileptic syndrome in HH. METHODS: We documented all current seizure types in six adult patients with HH-epilepsy with video-EEG monitoring, characterized clinical-electrographic features of gelastic and non-gelastic seizures and correlated these findings with cognitive profile, as well as MRI and ictal SPECT data. RESULTS: Only four seizure types were seen: GS, complex partial (CPS), tonic seizures (TS) and secondarily generalized tonic-clonic seizures (sGTC). An individual patient presented either CPS or TS, but not both. GS progressed to CPS or TS, but not both. Ictal patterns in GS/TS and in GS/CPS overlapped, suggesting ictal spread from the HH to other cortical regions. Ictal SPECT patterns also showed GS/TS overlap. Patients with GS-CPS presented a more benign profile with preserved cognition and clinical-EEG features of temporal lobe epilepsy. Patients with GS-TS had clinical-EEG features of symptomatic generalized epilepsy, including mental deterioration. CONCLUSIONS: Video-EEG and ictal SPECT findings suggest that all seizures in HH-related epilepsy originate in the HH, with two clinical epilepsy syndromes: one resembling temporal lobe epilepsy and a more catastrophic syndrome, with features of a symptomatic generalized epilepsy. The epilepsy syndrome may be determined by HH size or by seizure spread pattern.     

Effects of calcitonin gene-related peptide on extrapyramidal motor system.

The effects of central administration of calcitonin gene-related peptide (CGRP, 1 or 100 ng/rat) on behavioral and biochemical parameters related to the extrapyramidal motor system were investigated in male rats. The peptide-induced catalepsy occurred only at the dose of 100 ng/rat and hypomotility at both doses used. Calcitonin gene-related peptide increased haloperidol-induced catalepsy and decreased apomorphine-induced hypermotility at the doses of 1 and 100 ng/rat. Although these behaviors are related to dopamine, no significant change of striatal DA or DOPAC concentration were observed after central administration of the peptide. Other neurotransmitters may be directly or indirectly involved in these behavioral effects of CGRP.     

Nicotine reinforcement in rats with histories of cocaine self-administration

Few reports have described conditions under which nicotine self-administration occurs in rats. In this study, rats which initially lever pressed for cocaine infusion (0.05 mg/kg) during 1 h experimental sessions continued to obtain similar infusion numbers when nicotine (0.03 mg/kg) was available. When saline was substituted for nicotine, infusions decreased from 11.8±4.5/h to 5.4±1.1/h but returned to pre-saline levels when it was reintroduced (12.0±5.5/h). These results indicate that nicotine can serve as a positive reinforcer for rats under the historical and schedule conditions described.