The latest on the rapidly growing use of innovative archaeological remote sensing for anthropological applications in North America
Updating the highly praised 2006 publication Remote Sensing ...in Archaeology , edited by Jay K. Johnson, Archaeological Remote Sensing in North America: Innovative Techniques for Anthropological Applications is a must-have volume for today’s archaeologist. Targeted to practitioners of archaeological remote sensing as well as students, this suite of current and exemplary applications adheres to high standards for methodology, processing, presentation, and interpretation.
The use of remote sensing technologies to address academic and applied archaeological and anthropological research problems is growing at a tremendous rate in North America. Fueling this growth are new research paradigms using innovative instrumentation technologies and broader-area data collection methods. Increasingly, investigators pursuing these new approaches are integrating remote sensing data collection with theory-based interpretations to address anthropological questions within larger research programs.
In this indispensable volume, case studies from around the country demonstrate the technically diverse and major remote sensing methods and their integration with relevant technologies, such as geographic information systems (GIS) and global positioning systems (GPS), and include various uses of the “big four”: magnetometry, resistivity, ground-penetrating radar (GPR), and electromagnetic induction.
The study explores four major anthropological themes: site structure and community organization; technological transformation and economic change; archaeological landscapes; and earthen mound construction and composition. Concluding commentary from renowned expert Kenneth L. Kvamme overviews the practices, advances, and trends of geophysics and remote sensing in the past decade.
Rat superior cervical ganglion (SCG) neurons express low-threshold noninactivating M-type potassium channels (I-K(M)), which can be inhibited by activation of M-1 muscarinic receptors (M-1 mAChR) and ...bradykinin (BK) B-2 receptors. Inhibition by the M1 mAChR agonist oxotremorine methiodide (Oxo-M) is mediated, at least in part, by the pertussis toxin-insensitive G-protein G alpha (q) (Caulfield et al., 1994; Haley et al., 1998a), whereas BK inhibition involves G alpha (q) and/or G alpha (11) (Jones et al., 1995). G alpha (q) and G alpha (11) can stimulate phospholipase C-beta (PLC-beta), raising the possibility that PLC is involved in I-K(M) inhibition by Oxo-M and BK. RT-PCR and antibody staining confirmed the presence of PLC-beta1, - beta2, - beta3, and - beta4 in rat SCG. We have tested the role of two PLC isoforms (PLC-beta1 and PLC-beta4) using antisense-expression constructs. Antisense constructs, consisting of the cytomegalovirus promoter driving antisense cRNA corresponding to the 3'-untranslated regions of PLC-beta1 and PLC-beta4, were injected into the nucleus of dissociated SCG neurons. Injected cells showed reduced antibody staining for the relevant PLC-beta isoform when compared to uninjected cells 48 hr later. BK inhibition of I-K(M) was significantly reduced 48 hr after injection of the PLC-beta4, but not the PLC-beta1, antisense-encoding plasmid. Neither PLC-beta antisense altered M-1 mAChR inhibition by Oxo-M. These data support the conclusion of Cruzblanca et al. (1998) that BK, but not M-1 mAChR, inhibition of I-K(M) involves PLC and extends this finding by indicating that PLC-beta4 is involved.
Objective : To describe re-admission rates, identify reasons for re-admission and examine characteristics of children requiring re-admission to inpatient pulmonary rehabilitation. Methodology : ...Retrospective record review of infants and toddlers (less than three years of age) requiring oxygen or ventilator support discharged from an inpatient paediatric pulmonary rehabilitation programme between 1992 and 1999. Results : Forty-one initial admissions resulted in 45 readmissions with a mean re-admission rate of 1.1 (SD = 1.41) re-admissions per child. Children with re-admissions ( n = 22, 54%) required significantly more ventilator support ( p = 0.001) and nursing care ( p = 0.001) and were transferred to acute care more frequently ( p = 0.002) than children without re-admissions. One-half of the children re-admitted to inpatient pulmonary rehabilitation were re-admitted two or more times. Conclusions : Based on this cohort of children, dependence on supplemental oxygen and/or mechanical ventilation and medical complexity may be indicators that children will require re-admission to rehabilitation following a transfer back to acute care. Further examination of re-admission rates and reasons and children's clinical characteristics may have predictive value and provide practice improvement opportunities.
Rat superior cervical ganglion (SCG) neurons express low-threshold noninactivating M-type potassium channels (IK(M)), which can be inhibited by activation of M1 muscarinic receptors. This inhibition ...occurs via pertussis toxin-insensitive G-proteins belonging to the Galphaq family (Caulfield et al., 1994 ). We have used DNA plasmids encoding antisense sequences against the 3' untranslated regions of Galpha subunits (antisense plasmids) to investigate the specific G-protein subunits involved in muscarinic inhibition of IK(M). These antisense plasmids specifically reduced levels of the target G-protein 48 hr after intranuclear injection. In cells depleted of Galphaq, muscarinic inhibition of IK(M) was attenuated compared both with uninjected neurons and with neurons injected with an inappropriate GalphaoA antisense plasmid. In contrast, depletion of Galpha11 protein did not alter IK(M) inhibition. To determine whether the alpha or beta gamma subunits of the G-protein mediated this inhibition, we have overexpressed the C terminus of beta adrenergic receptor kinase 1 (betaARK1), which binds free beta gamma subunits. betaARK1 did not reduce muscarinic inhibition of IK(M) at a concentration of plasmid that can reduce beta gamma-mediated inhibition of calcium current (). Also, expression of beta1gamma2 dimers did not alter the IK(M) density in SCG neurons. In contrast, IK(M) was virtually abolished in cells expressing GTPase-deficient, constitutively active forms of Galphaq and Galpha11. These data suggest that Galphaq is the principal mediator of muscarinic IK(M) inhibition in rat SCG neurons and that this more likely results from an effect of the alpha subunit than the beta gamma subunits of the Gq heterotrimer.
Rat superior cervical ganglion (SCG) neurons express low-threshold noninactivating M-type potassium channels (I(K(M))), which can be inhibited by activation of M(1) muscarinic receptors (M(1) mAChR) ...and bradykinin (BK) B(2) receptors. Inhibition by the M(1) mAChR agonist oxotremorine methiodide (Oxo-M) is mediated, at least in part, by the pertussis toxin-insensitive G-protein Galpha(q) (Caulfield et al., 1994; Haley et al., 1998a), whereas BK inhibition involves Galpha(q) and/or Galpha(11) (Jones et al., 1995). Galpha(q) and Galpha(11) can stimulate phospholipase C-beta (PLC-beta), raising the possibility that PLC is involved in I(K(M)) inhibition by Oxo-M and BK. RT-PCR and antibody staining confirmed the presence of PLC-beta1, -beta2, -beta3, and -beta4 in rat SCG. We have tested the role of two PLC isoforms (PLC-beta1 and PLC-beta4) using antisense-expression constructs. Antisense constructs, consisting of the cytomegalovirus promoter driving antisense cRNA corresponding to the 3'-untranslated regions of PLC-beta1 and PLC-beta4, were injected into the nucleus of dissociated SCG neurons. Injected cells showed reduced antibody staining for the relevant PLC-beta isoform when compared to uninjected cells 48 hr later. BK inhibition of I(K(M)) was significantly reduced 48 hr after injection of the PLC-beta4, but not the PLC-beta1, antisense-encoding plasmid. Neither PLC-beta antisense altered M(1) mAChR inhibition by Oxo-M. These data support the conclusion of Cruzblanca et al. (1998) that BK, but not M(1) mAChR, inhibition of I(K(M)) involves PLC and extends this finding by indicating that PLC-beta4 is involved.
Therapies that might delay degeneration of synapses offer an appealing strategy for treatment of neurodegenerative diseases, including Alzheimer's disease and related dementias, prion diseases, ...schizophrenia and amyotrophic lateral sclerosis. Analysis of mouse mutants provides one possible avenue towards identifying relevant mechanisms. Here, we used quantitative and serial section electron microscopy to find out whether the onset and time course of pre-synaptic nerve terminal degeneration is delayed in the striatum of Wallerian degeneration slow (Wld super(s)) mutant mice. Synaptic degeneration was observed within 48 h of cortical ablation in wild-type mice but was delayed by approximately 1 week in Wld super(s) mice. However, the morphological characteristics of degenerating nerve terminals in wild-type and Wld super(s) mice were indistinguishable, in contrast to the differences reported previously in studies of the PNS. Surprisingly, the delayed onset of synaptic degeneration was accompanied by an increased incidence of complex synaptic morphologies on post-synaptic spines in the denervated Wld super(S) striatum indicating an enhanced plastic response at both injured and uninjured synapses. The data suggest that targeting Wallerian-like mechanisms of synaptic degeneration could lead to the development of new therapies for the treatment of CNS disorders where synapse loss is a primary feature.
NO and CO are small gaseous molecules that can be synthesized de novo in neuronal tissue and can diffuse readily through the plasma membrane. NOS inhibitors prevent the induction of LTP in the ...hippocampus, and studies with NOS knock-out mice and viral overexpression of mutated NOS indicate that the endothelial form of the enzyme is probably responsible for NO production in these neurons. Inhibitors of CO production can block the induction of LTP, but this does not correlate with their ability to prevent CO production in the hippocampus. LTP is normal in mice that lack HO-2 and, furthermore, there is no obvious mechanism by which HO could be activated during synaptic stimulation. NO probably diffuses out of the postsynaptic neuron and acts on neighbouring neurons and presynaptic terminals to either instigate, or assist in, the generation or stabilization of LTP, possibly by activating GC. There are NO-dependent and NO-independent forms of LTP, and both forms can be found at synapses on to the same neuron. It is therefore possible that subtle discrimination can occur between different inputs on to the same cell. NO may also participate in the induction of sensitization within the spinal cord. NOS inhibitors can prevent the development of spinal hyperalgesia due to intrathecal NMDA administration or peripheral nerve injury, and could therefore contribute to some chronic pain states.
Wallerian degeneration slow (Wld
S) mice express a chimeric protein that delays axonal degeneration. The N-terminal domain (N70), which is essential for axonal protection
in vivo, binds ...valosin-containing protein (VCP) and targets both Wld
S and VCP to discrete nuclear foci. We characterized the formation, composition and localization of these potentially important foci. Missense mutations show that the N-terminal sixteen residues (N16) of Wld
S are essential for both VCP binding and targeting Wld
S to nuclear foci. Removing N16 abolishes foci, and VCP binding sequences from ataxin-3 or HrdI restore them.
In vitro, these puncta co-localize with proteasome subunits.
In vivo, Wld
S assumes a range of nuclear distribution patterns, including puncta, and its neuronal expression and intranuclear distribution is region-specific and varies between spontaneous and transgenic Wld
S models. We conclude that VCP influences Wld
S intracellular distribution, and thus potentially its function, by binding within the N70 domain required for axon protection.
Nitric oxide synthase (NOS) inhibitors have been shown to block long-term synaptic enhancements in the mammalian hippocampus. This effect has been somewhat controversial, however, showing sensitivity ...to both temperature and stimulus strength. We have demonstrated a differential effect of the NOS inhibitor L-NG-nitroarginine (NOArg) on long-term potentiation (LTP) induced by weak and strong tetanic stimulation in slices of rat hippocampus. NOArg prevented LTP induction by a weak tetanus that produced stable potentiation in control slices, while the NOS inhibitor was without effect when strong tetani were used. These results suggest that nitric oxide (NO) produced as a result of tetanic stimulation plays a role in adjusting the threshold of LTP induction, but is not necessary for establishing synaptic enhancement under conditions of strong synaptic activation.
The Wld
s
mouse mutant demonstrates a remarkable phenotype of delayed axonal and synaptic degeneration after nerve lesion. In this study, the authors tested the hypothesis that expression of Wld ...protein is neuroprotective in an in vivo mouse model of global cerebral ischemia. This model is associated with selective neuronal degeneration in specific brain regions such as the caudate nucleus and CA2 hippocampal pyramidal cell layer. The extent of neuronal damage was quantified in Wld
s
compared to wild-type mice after an identical episode of global cerebral ischemia. The results demonstrated a significant and marked reduction in the extent of neuronal damage in Wld
s
as compared to wild-type C57Bl/6 mice. In the caudate nucleus, Wld expression significantly reduced the percentage of ischemic neuronal damage after global ischemia (Wld
s
, 27.7 ± 16.8%; wild-type mice, 58.7 ± 32.3%; P = 0.036). Similarly, in the CA2 pyramidal cell layer, there was a significant reduction of neuronal damage in the Wld
s
mice as compared to wild-type mice after ischemia (Wld
s
, 17.7 ± 23.0%; wild-type mice, 41.9 ± 28.0%; P < 0.023). Thus, these results clearly demonstrate that the Wld gene confers substantial neuroprotection after cerebral ischemia, and suggest a new role to that previously described for Wld
s
.
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