100,850 research outputs found

    Letter, [Author unclear] to Paulina T. Merritt

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    Handwritten letter to Paulina Merritt from an unknown author, October 1, 1876.

    Ontogeny of cardiac beta-adrenoceptor desensitization mechanisms: agonist treatment enhances receptor/G-protein transduction rather than eliciting uncoupling.

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    In the fetus and neonate, beta-adrenoceptor stimulation fails to produce physiological desensitization. The current study explores the mechanisms underlying the response pattern in neonatal rats. Homologous cardiac beta-adrenergic desensitization caused by isoproterenol treatment in vivo was demonstrable in adult rats by the immediate (2h) and specific loss of the ability of isoproterenol, but not glucagon, to stimulate adenylyl cyclase in vitro. Homologous desensitization was absent when the same treatment was given to neonates. By 12 h post-treatment, the adults showed heterologous desensitization (loss of the response to glucagon), an effect which was once again absent in the immature rats. The absence of desensitization in neonates did not reflect a deficiency in the activity or subcellular distribution of beta ARK1, the enzyme that initiates the phosphorylation and consequent desensitization of beta-adrenoceptors. On the other hand, neonates showed relatively poor receptor-Gs transduction as assessed by the GTP-induced shift in receptor ligand binding. Repeated isoproterenol treatment of adult rats led to uncoupling of receptor-G-protein transduction but the same treatment in neonates enhanced transduction. Furthermore, neonatal sympathectomy with 6-OHDA interfered with the ontogenetic rise in beta-adrenoceptor-Gs interactions. These results indicate that the maintenance of agonist responses in the face of neonatal adrenergic stimulation does not reflect simply an absence of the ability to elicit homologous or heterologous desensitization but rather represents an active regulatory mechanism in which neural input exerts a positive trophic role at the level of G-protein function

    Tectonic and metamorphic discontinuities in the Freater Himalayan Sequence in Central Himalaya: insights from natural examples and numerical modelling

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    The Greater Himalayan Sequence (GHS) is the main metamorphic unit of the Himalayan belt, stretching for ~ 2400 km, bounded to the South by the Main Central Thrust (MCT) and to the North by the South Tibetan Detachment (STD) whose contemporanous activity controlled its exhumation between 23 and 17 Ma (Godin et al., 2006). Several shear zones and/or faults have been recognized within the GHS, usually regarded as out of sequence thrusts. Recent multitechniques investigations in the GHS in Central-Eastern Himalaya allowed the Authors to identify two different levels of tectonic and metamorphic discontinuities, above the MCT, both characterized by a top-to-the SW sense of shear (Carosi et al., 2010; Montomoli et al., 2013; Montomoli et al., 2014, Iaccarino et al, 2015): a higher (Kalopani and Tiyar shear zones) and a lower tectono-metamorphic discontinuity (Higher Himalayan Discontinuity: Montomoli et al., 2014). U-Th-Pb in situ monazite ages provide ages of initiation at ~ 36 Ma of the upper tectonic and metamorphic discontinuity and at 26-24 Ma for the lower one, continuing up to ~ 17 Ma. Data on the P and T evolution testify that these shear zones affected the tectono-metamorphic evolution of the belt and different P and T conditions have been recorded in the hanging-wall and footwall of the discontinuities. The GHS is consequently divided into three tectonic sub-units and peak metamorphism were reached in different times in each sub-unit. When the mid unit underwent prograde meamorphism the upper one underwent exhumation by activation of the upper discontinuity. When mid unit was exhumed by activation of the lower discontinuity the lower one underwent prograde metamorphism. All the GHS underwent exhumation during the activation of the MCT. The actual proposed models of exhumation of the GHS, based exclusively on the MCT and STD activities and considering the GHS as a single tectonic unit, are not able to explain the occurrence of the Higher Himalayan Discontinuity and other older in-sequence shear zones. Any model of the tectonic and metamorphic evolution of the GHS should account for the occurrence of the tectonic and metamorphic discontinuities within the GHS and its consequences on the metamorphic path. The channel flow model proposed by Beaumont et al. (2001) implies a coherent exhumation of the GHS due to the focused monsoonal erosion acting on the southern flank of the Himalayas. However, channel flow model is not consistent with the occurrence of the several tectono-metamorphic discontinuites within the GHS, indicating a sequential exhumation of different GHS sub-units (Montomoli et al., 2013, 2014; Iaccarino et al., 2015). We have numerically simulated the interaction between surface and exhumation processes in post-subduction collisional orogens. Two kinds of collisional orogens are obtained: asymmetric and symmetric ones. Asymmetric collisional orogens feature the occurrence of a channel flow-like behaviour, high crustal temperatures and exhumation of partially molten rocks, while symmetric orogens features lower crustal temperatures and different patterns of exhumation. The asymmetric models have been chosen to test the influence of surface processes. By taking a fixed value of focused erosion rate, the timing of the focused erosion and sedimentation rate are independently varied. The results give several insights: 1) focused erosion is not a necessary condition for the exhumation of the partially molten rocks; 2) timing of the focused erosion controls the dynamics of the channel flow and, consequently, the exhumation processes; 3) the sedimentation rate may induce first order modifications on the evolution of the orogeny; 4) sequential exhumation of high grade metamorphic sub-units is achieved when the focused erosion is activated at the final stage of the collision

    Cerebrospinal fluid T cell receptor gamma/delta+ lymphocyte subsets in patient with AIDS-dementia complex

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    A subset of peripheral T cells, whose physiological function is little known, expresses a distinct CD3-associated receptor composed of gamma and delta chains. We used two monoclonal antibodies to characterize the TcR gamma/delta lymphocytes (TcR delta 1+) and their fraction (TcS delta 1+) in peripheral blood and cerebrospinal fluid of patients affected by AIDS dementia complex (ADC). Thirty patients with ADC and a control group of twenty individuals with other non-inflammatory neurological diseases (OND) were recruited. Our results demonstrate that the TcR gamma/delta cells were also present in cerebrospinal fluid of ADC patients, but we did not find any statistical difference between the two groups

    Cerebrospinal fluid T cell receptor gamma/delta+ lymphocyte subsets in patient with AIDS-dementia complex.

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    A subset of peripheral T cells, whose physiological function is little known, expresses a distinct CD3-associated receptor composed of gamma and delta chains. We used two monoclonal antibodies to characterize the TcR gamma/delta lymphocytes (TcR delta 1+) and their fraction (TcS delta 1+) in peripheral blood and cerebrospinal fluid of patients affected by AIDS dementia complex (ADC). Thirty patients with ADC and a control group of twenty individuals with other non-inflammatory neurological diseases (OND) were recruited. Our results demonstrate that the TcR gamma/delta cells were also present in cerebrospinal fluid of ADC patients, but we did not find any statistical difference between the two groups
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