TASK DEFINITION: In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.
PROBLEM: Context: The effect of inhalational anesthetics on sensory-evoked unit activity in the cerebral cortex has been controversial. Desflurane has desirable properties for in vivo neurophysiologic studies, but its effect on cortical neuronal activity and neuronal responsiveness is not known. The authors studied the effect of desflurane on resting and visual evoked unit activity in rat visual cortex in vivo.', 'Desflurane was administered to adult albino rats at steady-state concentrations at 2%, 4%, 6%, and 8%. Flashes from a light emitting diode were delivered to the left eye at 5-s intervals. Extracellular unit activity within the right visual cortex was recorded using a 49-electrode array. Individual units were identified using principal components analysis.', 'At 2% desflurane, 578 active units were found. Of these, 75% increased their firing rate in response to flash. Most responses contained early (0-100 ms) and late (150-1000 ms) components. With increasing desflurane concentration, the number of units active at baseline decreased (-13%), the number of early-responding units increased (+31%), and number of late-responding units decreased (-15%). Simultaneously, baseline firing rate decreased (-77%), the early response was unchanged, and the late response decreased (-60%).\Question: Does desflurane selectively suppress long-latency cortical neuronal response to flash in the rat?

SOLUTION: The results indicate that visual cortex neurons remain responsive to flash stimulation under desflurane anesthesia, but the long-latency component of their response is attenuated in a concentration-dependent manner. Suppression of the long-latency response may be related to a loss of corticocortical feedback and loss of consciousness.

PROBLEM: Context: Glioblastomas treated with bevacizumab may develop low-signal apparent diffusion coefficient (low-ADC) lesions, which may reflect increased tumor cellularity or atypical necrosis. The purpose of this study was to examine the relationship between low-ADC lesions and overall survival (OS). We hypothesized that growing low-ADC lesions would be associated with shorter OS.', 'We retrospectively identified 52 patients treated with bevacizumab for the first (n = 42, 81%) or later recurrence of primary glioblastoma, who had low-ADC lesions and 2 post-bevacizumab scans ≤90 days apart. Low-ADC lesion volumes were measured, and normalized 5th percentile histogram low-ADC values were recorded. Using OS as the primary endpoint, semiparametric Cox models were fitted to ascertain univariate and multivariate hazard ratios (HRs) with significance at P = .05.', 'Median OS was 9.1 months (95% CI = 7.2-14.3). At the second post-bevacizumab scan, the volume of the low-ADC lesion (median: 12.94 cm(3)) was inversely associated with OS, with larger volumes predicting shorter OS (HR = 1.014 [95% CI = 1.003-1.025], P = .009). The percent change in low-ADC volume (median: 6.8%) trended toward increased risk of death with growing volumes (P = .08). Normalized 5th percentile low-ADC value and its percent change were not associated with OS (P > .51). Also correlated with shorter OS were the pre-bevacizumab nonenhancing volume (P = .025), the first post-bevacizumab enhancing volume (P = .040), and the second post-bevacizumab enhancing volume (P = .004).\Question: Do large-volume low apparent diffusion coefficient lesions predict poor survival in bevacizumab-treated glioblastoma patients?

SOLUTION: The volume of low-ADC lesions at the second post-bevacizumab scan predicted shorter OS. This suggests that low-ADC lesions may be considered important imaging markers and included in treatment decision algorithms.

PROBLEM: Context: In a number of experimental models of nephropathy, heparin is renoprotective because it inhibits mesangial matrix synthesis and cell proliferation; in most of these models, glomerular macrophage infiltration has a pathogenic role. We investigated the hypothesis that heparin might also be renoprotective by modulating the macrophages in various ways in the chronic puromycin glomerulosclerosis model.', 'We studied the effect of a 3 month course, two different dosages of a non-anticoagulant heparin by immunohistochemical evaluation of the number of macrophages (ED-1 positive cells) in glomeruli, as well as the expression and deposition of TGF-beta and latent TGF-beta binding protein in foam cells and mesangial matrix.', 'The renoprotective effect of heparin in this model was confirmed by our observation of lower urine protein and albumin excretion, and a reduced glomerular sclerosis score. These effects were associated with the prevention of macrophage glomerular infiltration, and the inhibition of the TGF-beta axes in foam cells as shown by the reduction in cytoplasm immunostaining for TGF-beta and LTBP-1; heparin also reduced peri-macrophagic collagen IV deposition.\Question: Does heparin reduce glomerular infiltration and TGF-beta protein expression by macrophages in puromycin glomerulosclerosis?

SOLUTION:
The inhibition of TGF-beta in macrophages seems to be part of heparin general activities. The inhibitory effect of heparin on macrophage infiltration and TGF-beta synthesis in this renal disease model supports the notion that heparin and derived molecules constitute potentially useful therapeutic agents in nephropathies.