Deposition of general ellipsoidal particles

We present a systematic overview of granular deposits composed of ellipsoidal particles with different particle shapes and size polydispersities. We study the density and anisotropy of such deposits as functions of size polydispersity and two shape parameters that fully describe the shape of a general ellipsoid. Our results show that, while shape influences significantly the macroscopic properties of the deposits, polydispersity plays apparently a secondary role. The density attains a maximum for a particular family of non-symmetrical ellipsoids, larger than the density observed for prolate or oblate ellipsoids. As for anisotropy measures, the contact forces show are increasingly preferred along the vertical direction as the shape of the particles deviates for a sphere. The deposits are constructed by means of an efficient molecular dynamics method, where the contact forces are efficiently and accurately computed. The main results are discussed in the light of applications for porous media models and sedimentation processes.Comment: 7 pages, 8 figure

Enzymic degradation of luteinizing hormone-releasing hormone (LH-RH) by hypothalamic tissue.

Synthetic luteinizing hormone-releasing hormone (LH-RH) lost both its immunore-activity and hormonal activity on incubation with hypothalamic or cerebrocortical slices or homogenates. This inactivation was shown to be due to degradation of the decapeptide by soluble enzyme(s) present in the 100,000 × g supernatant fraction of the homogenates. The supernatant derived from one rat hypothalamus was capable of destroying 1 μg of exogenous LH-RH within 5 min. The hexapeptide pGlu-His-Trp-Ser-Tyr-Gly was identified as the major radioactive breakdown product of [pGlu-3-3H] LH-RH, and tentative evidence for the formation of the tetrapeptide Leu-Arg-Pro-Gly-NH2 was obtained by sequential electrophoresis and paper chromatography. These findings suggest that the Gly-Leu bond may be the preferred site of cleavage. © 1974

Entorhinal and ventromedial prefrontal cortices abstract and generalize the structure of reinforcement learning problems

Knowledge of the structure of a problem, such as relationships between stimuli, enables rapid learning and flexible inference. Humans and other animals can abstract this structural knowledge and generalize it to solve new problems. For example, in spatial reasoning, shortest-path inferences are immediate in new environments. Spatial structural transfer is mediated by cells in entorhinal and (in humans) medial prefrontal cortices, which maintain their co-activation structure across different environments and behavioral states. Here, using fMRI, we show that entorhinal and ventromedial prefrontal cortex (vmPFC) representations perform a much broader role in generalizing the structure of problems. We introduce a task-remapping paradigm, where subjects solve multiple reinforcement learning (RL) problems differing in structural or sensory properties. We show that, as with space, entorhinal representations are preserved across different RL problems only if task structure is preserved. In vmPFC and ventral striatum, representations of prediction error also depend on task structure

Phase I trial of procarbazine as a 5-day continuous infusion in children with central nervous system tumors.

Seven children with previously treated brain tumors were enrolled in a phase I trial of 5-day continuous-infusion procarbazine at 360, 480, and 638 mg/m2/day. Vitamin B6 levels were monitored. Myelosuppression was moderate though occasionally delayed, and nausea and vomiting were mild. At the highest dose level, a patient experienced severe psychosis that persisted for several weeks. From that dose-limiting toxicity and the degree of myelosuppression, the recommended dose for phase II trials in children is the same as for adults, 450 mg/m2/day

Therapeutic modalities for central nervous system involvement by granulocytic sarcoma (chloroma) in children with acute nonlymphocytic leukemia.

Four cases of central nervous system involvement by granulocytic sarcoma (three intracranial and one paraspinal) in children with acute nonlymphocytic leukemia (FAB M1 or M2 subtype) are presented, and therapeutic modalities are discussed. All tumors were noted at initial presentation with diagnosis being made on clinical and radiological findings without biopsy. All patients had karyotypic abnormalities: three had translocation of chromosomes 8 and 21, and one had an unspecified hypodiploid clone. The three patients who developed intracranial tumors responded well to triple agent (cytosine arabinoside, hydrocortisone, and methotrexate) intrathecal chemotherapy and systemic chemotherapy, with or without local irradiation, as evidenced by rapid disappearance of the tumors. Two children are disease-free after 17 and 57 months. One patient with paraspinal tumor failed to achieve a systemic remission but had no evidence of granulocytic sarcoma at autopsy. Thus, the prognosis of CNS granulocytic sarcoma is not uniformly gloomy if treated aggressively by combined modalities. The value of surgical intervention in terms of primary management, however, is limited

Corticotropin-releasing hormone (CRH) downregulates the function of its receptor (CRF1) and induces CRF1 expression in hippocampal and cortical regions of the immature rat brain.

In addition to regulating the neuroendocrine stress response, corticotropin-releasing hormone (CRH) has been implicated in both normal and pathological behavioral and cognitive responses to stress. CRH-expressing cells and their target neurons possessing CRH receptors (CRF1 and CRF2) are distributed throughout the limbic system, but little is known about the regulation of limbic CRH receptor function and expression, including regulation by the peptide itself. Because CRH is released from limbic neuronal terminals during stress, this regulation might play a crucial role in the mechanisms by which stress contributes to human neuropsychiatric conditions such as depression or posttraumatic stress disorder. Therefore, these studies tested the hypothesis that CRH binding to CRF1 influenced the levels and mRNA expression of this receptor in stress-associated limbic regions of immature rat. Binding capacities and mRNA levels of both CRF1 and CRF2 were determined at several time points after central CRH administration. CRH downregulated CRF1 binding in frontal cortex significantly by 4 h. This transient reduction (no longer evident at 8 h) was associated with rapid increase of CRF1 mRNA expression, persisting for >8 h. Enhanced CRF1 expression-with a different time course-occurred also in hippocampal CA3, but not in CA1 or amygdala, CRF2 binding and mRNA levels were not altered by CRH administration. To address the mechanisms by which CRH regulated CRF1, the specific contributions of ligand-receptor interactions and of the CRH-induced neuronal stimulation were examined. Neuronal excitation without occupation of CRF1 induced by kainic acid, resulted in no change of CRF1 binding capacity, and in modest induction of CRF1 mRNA expression. Furthermore, blocking the neuroexcitant effects of CRH (using pentobarbital) abolished the alterations in CRF1 binding and expression. These results indicate that CRF1 regulation involves both occupancy of this receptor by its ligand, as well as "downstream" cellular activation and suggest that stress-induced perturbation of CRH-CRF1 signaling may contribute to abnormal neuronal communication after some stressful situations