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.

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?
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.

Context: Although successful cochlear implantation of patients with deafness following meningitis is expected, long-term stability of electrical current requirements has not been systematically evaluated. This study evaluated changes in programming for patients deafened by bacterial meningitis and stability of auditory performance over time.', 'In this retrospective descriptive study, cochlear implant (CI) stimulation mode and performance of 14 patients deafened by meningitis were compared with those of an age-matched control group of patients deafened by other causes.', 'There were no significant differences in mean performance between the meningitis group and control group (P > 0.05). However, the postmeningitis group required progressively higher stimulation levels and higher programming modes over time as compared to the control group.\Question: Do changes in programming over time in postmeningitis cochlear implant users?
Even with deafness accompanied by labyrinthine ossification attributed to meningitis, neural elements were present and could be stimulated. Because increasing levels of stimulation were required over time, postmeningitic children with CIs, and those with cochlear ossification in particular, may need frequent programming adjustments to maintain performance.

Context: Lung morphogenesis is regulated by interactions between the canonical Wnt/-catenin and Kras/ERK/Foxm1 signaling pathways that establish proximal-peripheral patterning of lung tubules. How these interactions influence the development of respiratory epithelial progenitors to acquire airway as compared to alveolar epithelial cell fate is unknown. During branching morphogenesis, SOX9 transcription factor is normally restricted from conducting airway epithelial cells and is highly expressed in peripheral, acinar progenitor cells that serve as precursors of alveolar type 2 (AT2) and AT1 cells as the lung matures.', 'To identify signaling pathways that determine proximal-peripheral cell fate decisions, we used the SFTPC gene promoter to delete or overexpress key members of Wnt/-catenin and Kras/ERK/Foxm1 pathways in fetal respiratory epithelial progenitor cells. Activation of -catenin enhanced SOX9 expression in peripheral epithelial progenitors, whereas deletion of -catenin inhibited SOX9. Surprisingly, deletion of -catenin caused accumulation of atypical SOX9-positive basal cells in conducting airways. Inhibition of Wnt/-catenin signaling by Kras(G12D) or its downstream target Foxm1 stimulated SOX9 expression in basal cells. Genetic inactivation of Foxm1 from Kras(G12D) -expressing epithelial cells prevented the accumulation of SOX9-positive basal cells in developing airways.\Question: Are -catenin and Kras/Foxm1 signaling pathway critical to restrict Sox9 in basal cells during pulmonary branching morphogenesis?
Interactions between the Wnt/-catenin and the Kras/ERK/Foxm1 pathways are essential to restrict SOX9 expression in basal cells. Developmental Dynamics 245:590-604, 2016. ©️ 2016 Wiley Periodicals, Inc.