Abstract
Advances in ultrafast laser technology and nanofabrication have enabled a new class of particle accelerator based upon miniaturized laser-driven photonic structures. However, developing a ...useful accelerator based on this approach requires control of the particle dynamics at field intensities approaching the damage limit. We measure acceleration in a fused silica dielectric laser accelerator driven by fields of up to 9 GV m
−1
and observe a record 1.8 GV m
−1
in the accelerating mode. At these intensities the dielectric is driven beyond its linear response and self-phase modulation changes the phase velocity of the accelerating mode, reducing the average gradient to 850 MeV m
−1
. We show that free-space optics can be used to compensate this dephasing and demonstrate that tailoring the laser phase and amplitude can facilitate optimization of the beam dynamics. This could enable MeV scale energy gain in a single stage and pave the way towards applications in scientific, industrial, and medical fields.
Compact, table-top sized accelerators are key to improving access to high-quality beams for use in industry, medicine and academic research. Among laser-based accelerating schemes, the inverse ...free-electron laser (IFEL) enjoys unique advantages. By using an undulator magnetic field in combination with a laser, GeV m(-1) gradients may be sustained over metre-scale distances using laser intensities several orders of magnitude less than those used in laser wake-field accelerators. Here we show for the first time the capture and high-gradient acceleration of monoenergetic electron beams from a helical IFEL. Using a modest intensity (~10(13) W cm(-2)) laser pulse and strongly tapered 0.5 m long undulator, we demonstrate >100 MV m(-1) accelerating gradient, >50 MeV energy gain and excellent output beam quality. Our results pave the way towards compact, tunable GeV IFEL accelerators for applications such as driving soft X-ray free-electron lasers and producing γ-rays by inverse Compton scattering.
Abstract Background context Vertebral cement augmentation, including kyphoplasty, has been shown to be a successful treatment for pain relief for vertebral compression fracture (VCF). Patients can ...sustain additional symptomatic VCFs that may require additional surgical intervention. Purpose To examine the prevalence and predictors of patients who sustain additional symptomatic VCFs that were treated with kyphoplasty. Study design A retrospective review of patients who previously underwent kyphoplasty for VCFs and had additional VCFs that were treated with kyphoplasty. Patient sample A total of 256 patients underwent kyphoplasty for VCFs from 2000 to 2007 at a single medical center. Outcome measures The outcome measure of interest was the need for an additional kyphoplasty procedure for a symptomatic VCF. Methods Risk factors such as age, sex, smoking status, and steroid use were assessed, as well as bisphosphonate use. Sagittal spinal alignment via Cobb angles for thoracic, thoracolumbar, and lumbar regions was assessed. Results About 22.2% of the patients had an additional symptomatic VCF that was treated with a kyphoplasty procedure. Steroid use was the only significant risk factor for predicting patients with additional symptomatic VCFs who underwent additional kyphoplasty. The average time to the second VCF was 33 days. Adjacent-level VCFs were most common in the thoracic and thoracolumbar spine. Bisphosphonate use was not shown to be protective of preventing additional VCFs during this follow-up period. Conclusion This is the first single-center review of a large cohort of patients who underwent additional-level kyphoplasty for symptomatic VCFs after an index kyphoplasty procedure. Our results suggest that patients with a VCF who use chronic oral steroids should be carefully monitored for the presence of additional symptomatic VCFs that may need surgical intervention. Patients with prior thoracic VCFs who have additional back pain should be reevaluated for a possible adjacent-level fracture.
Hematomas in Tiger Territory Teso, Desarom; Rogoway, Benjamin J.; Vea, Yolanda L. ...
Innovations (Philadelphia, Pa.),
11/2017, Letnik:
12, Številka:
6
Journal Article
Recenzirano
A 26-year-old man presented with gunshot wound to the epigastrium. At surgery, he was hemodynamically stable and had a tense hematoma with thrill in zone 2 (right side) and porta triad. After liver ...injury was controlled, he underwent percutaneous stenting of a renal artery-vena cava fistula and the hepatic artery injury was followed. Historically, penetrating injury to zone 2 has mandated operative exploration. However, with the advent of endovascular options, in stable patients, catheter-based options offer a reasonable alternative with less risk of blood loss and possible nephrectomy. Renal artery stenting has been advocated for renal artery cava fistulas. The role of timing, hybrid operating suites, and traditional operative exposure will vary based on presentation and institutional capabilities.
1
The degradation of tritiated and unlabelled neurotensin (NT) following close intra‐arterial infusion of the peptides in ileal segments of anaesthetized dogs was examined.
2
Intact NT and its ...catabolites recovered in the venous effluents were purified by chromatography on Sep‐Pak columns followed by reverse‐phase h.p.l.c. and identified by their retention times or by radioimmunoassay.
3
The half‐life of neurotensin was estimated to be between 2 and 6 min. Four labelled catabolites, corresponding to free tyrosine, neurotensin (1–8), neurotensin (1–10) and neurotensin (1–11), were detected.
4
Neurotensin (1–11) was mainly generated by a phosphoramidon‐sensitive cleavage, probably elicited by endopeptidase 24–11.
5
Two endopeptidase 3.4.24.16 inhibitors, phosphodiepryl 03 and the dipeptide Pro‐Ile, dose‐dependently potentiated the recovery of intact neurotensin. Furthermore, both agents inhibited the formation of neurotensin (1–10), the product that results from the hydrolysis of neurotensin by purified endopeptidase 3.4.24.16. In contrast, the endopeptidase 3.4.24.15 inhibitor Cpp‐AAY‐pAB neither protected neurotensin from degradation nor modifed the production of neurotensin (1–10).
6
Our study is the first evidence to indicate that endopeptidase 3.4.24.16 contributes to the catabolism of neurotensin, in vivo, in the dog intestine.
The presence of a cholinergic innervation of arterioles within the gut wall is suggested by pharmacological studies of nerve mediated vasodilatation, but attempts to identify nerve cells that give ...rise to cholinergic vasodilator fibres have yielded discrepant results. In the present work, antibodies to the vesicular acetylcholine transporter protein (VAChT) were used to investigate the relationships of immunoreactive nerve fibres to submucosal arterioles. Comparison was made with cerebral arteries, which are known to be cholinergically innervated. Double labelling immunohistochemical techniques revealed separate VAChT and tyrosine hydroxylase (TH) immunoreactive (IR) fibres innervating all sizes of arteries of the submucosa of the stomach, ileum, proximal colon, distal colon and rectum as well as the cerebral arteries. Arterioles of all digestive tract regions had greater densities of TH‐IR innervation than VAChT‐IR innervation. In the ileum, double labelling for VAChT‐IR and VIP‐IR or calretinin‐IR showed more VAChT‐IR than either VIP‐IR or calretinin‐IR fibres. Calretinin‐IR and VAChT‐IR were colocalised in a majority of calretinin‐IR axons, but VIP‐IR and VAChT‐IR were not colocalised. All calretinin‐IR nerve cells in submucous ganglia were immunoreactive for choline acetyltransferase, but only 1–2% of VIP‐IR nerve cells were immunoreactive. Extrinsic denervation of the ileum did not alter the distribution of VAChT‐IR fibres, but it eliminated TH‐IR fibres. Removal of myenteric ganglia (myectomy) did not alter the distribution of fibres with VAChT or TH‐IR. This work thus provides evidence for cholinergic innervation of intrinsic arterioles throughout the digestive tract and indicates that the fibres in the small intestine originate from submucosal nerve cells.
In canine ileum we investigated the distribution of pituitary adenylate cyclase-activating peptide (PACAP), using immunofluorescence and radioimmunoassay and the binding of
I-PACAP-27 to membranes. ...Nerve profiles immunoreactive to PACAP-27, and often to vasoactive intestinal polypeptide (VIP) as well, were found in all plexi, but PACAP was present in ∼100-fold lesser amounts than VIP. High-performance liquid chromatography analysis of deep muscular plexus (DMP) synaptosomes suggested the presence of PACAP-38, PACAP-27, and a third unidentified molecular form. High- and low-affinity
I-PACAP-27 binding sites were found in DMP synaptosomes and circular smooth muscle (CM) plasma membranes. In competition studies with DMP membranes, high (H)- and low (L)-affinity dissociation constants ( K
) and maximal binding capacities (B
) were as follows: K
= 66.9 pM, B
= 101 fmol/mg; K
= 2.18 nM, B
= 580 fmol/mg protein. The binding of
I-PACAP-27 was fast. Dissociation was slow and incomplete in the presence of unlabeled PACAP-27 but accelerated by pretreatment with guanosine 5'- O-(3-thiotriphosphate) (GTPγS). GTPγS or cholera toxin treatment eliminated high-affinity binding in both membranes. VIP had ∼100-fold lower affinity than PACAP-27 in both membranes. Cross-linking studies identified an ∼70-kDa PACAP receptor in each membrane. Thus PACAP coexists with VIP in ileal enteric nerves and acts on PACAP-preferring, possibly G
-coupled, receptors in DMP synaptosomes and CM membranes.
Glucagon-like peptide-1 (GLP-1) modulates glucose levels following a meal, including by inhibition of gastric emptying and intestinal transport. Intra-arterial injection of GLP-1 into the gastric ...corpus, antrum, or pylorus of anesthetized dogs had no effect on the contractile activity of the resting or neurally activated stomach. GLP-1 injected intra-arterially inhibited intestinal segments when activated by enteric nerve stimulation but not by acetylcholine. Isolated ileum segments were perfused intra-arterially, instrumented with strain gauges to record circular muscle activity and with subserosal electrodes to stimulate enteric nerves. GLP-1 caused concentration-dependent inhibition of nerve-stimulated phasic but not tonic activity. This was absent during TTX-induced activity and partly prevented by N(G)-nitro-L-arginine. Exendin-(9-39), the GLP-1 antagonist, had no intrinsic activity and did not affect the actions of GLP-1. Capsaicin mimicked the effects of GLP-1 and may have reduced the effect of subsequent GLP-1. GLP-1 may mediate paracrine action on afferent nerves in the canine ileal mucosa using an unusual receptor.
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