Partial graft liver recipients with graft weight/recipient weight (GW/RW) ratios Ͻ 0.8% are thought to have a higher incidence of postoperative complications, including small-for-size syndrome (SFSS). We analyzed a cohort of such recipients and compared those with GW/RW Ͻ 0.8% to those with GW/RW Ն 0.8%. Between 1999 and 2008, 107 adult patients underwent partial graft liver transplants: 76 from live donors [living donor liver transplantation (LDLT)] and 31 from deceased donors [split liver transplantation (SLT)]. Of these, 22 had GW/RW Ͻ 0.8% (12 with LDLT and 10 with SLT), and 85 had GW/RW Ն 0.8% (64 with LDLT and 21 with SLT). The baseline demographics and median length of follow-up were similar. SFSS developed in 3 recipients with GW/RW Ͻ 0.8% (13.6%) and in 8 recipients with GW/RW Ն 0.8% (9.4%; P ϭ not significant). Other early complications were similar between the 2 groups. Inflow modification with splenic artery occlusion was performed in 13 recipients: 7 with GW/RW Ͻ 0.8% and 6 with GW/RW Ն 0.8%. Graft survival at 1 year post-transplant did not differ (91% versus 92%; P ϭ not significant). In conclusion, GW/RW did not appear to be the only determinant of outcome after partial liver transplantation. Using techniques such as inflow modification may help to prevent some of the problems seen with smaller grafts.
We examined a group of SPK recipients that had early (<90 d post-transplant) pancreas graft failure caused by a technical complication, and looked at outcomes of the kidney graft in these recipients. Of 289 SPK transplants, 36 (12.5%) had early pancreas graft failure because of a technical complication: thrombosis (n = 16), leak (n = 5), infection (n = 14), and pancreatitis (n = 1). Once the pancreas was lost, there was a high incidence of subsequent kidney graft failure. Kidney graft survival in these 36 recipients was 71.4% at one yr and 59.5% at three yr, significantly inferior compared to recipients that did not have early failure of the pancreas (86% at one yr and 82% at three yr, p < 0.001). Of the 36 recipients with early pancreas loss, 18 have gone on to failure of the kidney graft. Causes included thrombosis (n = 3), infection (n = 1), death with function (n = 6), chronic rejection (n = 4), ischemia (n = 1), and other (n = 3). Of the 18 kidney graft failures, nine occurred within three months after loss of the pancreas graft, usually either because of graft thrombosis, or patient death (usually from systemic sepsis). Multivariate analysis showed technical failure of the pancreas to be the most significant risk factor for kidney graft loss (HR = 2.08, p = 0.006).
This article aims to quantify the impact optical character recognition (OCR) has on the quantitative analysis of historical documents. Using Eighteenth Century Collections Online as a case study, we first explore and explain the differences between the OCR corpus and its keyed-in counterpart, created by the Text Creation Partnership. We then conduct a series of specific analyses common to the digital humanities: topic modelling, authorship attribution, collocation analysis, and vector space modelling. The article concludes by offering some preliminary thoughts on how these conclusions can be applied to other datasets, by reflecting on the potential for predicting the quality of OCR where no ground-truth exists.
Airway constriction is accompanied by folding of the mucosa to form ridges that run axially along the inner surface of the airways. The mucosa has been modeled (R. K. Lambert. J. Appl. Physiol. 71:666-673, 1991) as a thin elastic layer with a finite bending stiffness, and the contribution of its bending stiffness to airway elastance has been computed. In this study, we extend that work by including surface tension and intraluminal fluid in the model. With surface tension, the pressure on the inner surface of the elastic mucosa is modified by the pressure difference across the air-liquid interface. As folds form in the mucosa, intraluminal fluid collects in pools in the depressions formed by the folds, and the curvature of the air-liquid interface becomes nonuniform. If the amount of intraluminal fluid is small, < 2% of luminal volume, the pools of intraluminal fluid are small, the air-liquid interface nearly coincides with the surface of the mucosa, and the area of the air-liquid interface remains constant as airway cross-sectional area decreases. In that case, surface energy is independent of airway area, and surface tension has no effect on airway mechanics. If the amount of intraluminal fluid is > 2%, the area of the air-liquid interface decreases as airway cross-sectional area decreases. and surface tension contributes to airway compression. The model predicts that surface tension plus intraluminal fluid can cause an instability in the area-pressure curve of small airways. This instability provides a mechanism for abrupt airway closure and abrupt reopening at a higher opening pressure.
The parenchymal marker technique was used to measure regional tidal volumes of samples of lung parenchyma in four open-chest supine dogs. Radiopaque markers that had been implanted in the lower lobe were tracked by biplane video fluoroscopy during sinusoidal volume oscillations at tidal volumes of approximately 20% of total lung capacity and frequencies of 1-40 breaths/min before and after methacholine was administered by aerosol. The volumes of tetrahedrons with apexes at four markers were computed, and sine waves were fit to the data for volume vs. time for each tetrahedron. The ratio of mean regional volume to mean airway pressure decreased by 10-45% after exposure to methacholine. Dynamic lung elastance and resistance of the constricted lungs were larger than control, and both were frequency dependent. Regional elastance and resistance varied considerably among tetrahedrons, and these were also frequency dependent. The data were fit by a model in which tissue elastance was uniform and nearly equal to elastance in the control state, but small-airway resistance was high and variable. We conclude that the lung contracts under bronchoconstriction but that the increased dynamic elastance and resistance of the constricted lung may be primarily the result of nonuniform increased airway resistance at the level of the terminal bronchioles.
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