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: The aim of this study is to establish follow-up protocols for adult patients with common variable immunodeficiency (CVID) in a recently founded adult immunology clinic in the Central Anatolia Region of Turkey, where a clinical immunology center for adults was not available previously.', 'A total of 25 patients with CVID aged 18 years and older were included in this study. The file format consisted of 13 pages and was developed for the purpose of the study. Separate sections were designated for identity information, medical history, disease course, previous and current laboratory and imaging studies, follow-up plans, detection and management of complications/comorbidities, and treatment results.', 'The mean age of the patients was 36.6 ± 13.4 years. The delay in diagnosis was 107 ± 95.6 months. In 92% of patients, initial symptoms resulting in admission to healthcare facilities were infections. Seventeen of 25 patients (68%) had bronchiectasis at the beginning of follow-up.\Question: Does common variable immunodeficiency in adults require reserved protocols for long-term follow-up?
Early identification of complications and comorbidities in patients with CVID will significantly improve quality of life and survival. Close observation and standardized protocols for follow-up are essential components of management.

Context: Chronic inflammation is hypothesized to influence prostate cancer development, although a definitive link has not been established.', 'Prostate cancer cases (N = 191) detected on a for-cause (clinically indicated) or end-of-study (protocol directed) biopsy, and frequency-matched controls (N = 209), defined as negative for cancer on an end-of-study biopsy, were sampled from the placebo arm of the Prostate Cancer Prevention Trial. Inflammation prevalence and extent in benign areas of biopsy cores were visually assessed using digital images of hematoxylin and eosin-stained sections. Logistic regression was used to estimate associations.', 'Of note, 86.2% of cases and 78.2% of controls had at least one biopsy core (of three assessed) with inflammation in benign areas, most of which was chronic. Men who had at least one biopsy core with inflammation had 1.78 [95% confidence interval (CI), 1.04-3.06] times the odds of prostate cancer compared with men who had zero cores with inflammation. The association was stronger for high-grade disease (Gleason sum 7-10, N = 94; OR, 2.24; 95% CI, 1.06-4.71). These patterns were present when restricting to cases and controls in whom intraprostatic inflammation was the least likely to have influenced biopsy recommendation because their prostate-specific antigen (PSA) was low (<2 ng/mL at biopsy).\Question: Is chronic inflammation in benign prostate tissue associated with high-grade prostate cancer in the placebo arm of the prostate cancer prevention trial?
Inflammation, most of which was chronic, was common in benign prostate tissue, and was positively associated with prostate cancer, especially high grade. The association did not seem to be due to detection bias.

Context: Declines in skeletal muscle structure and function are found in various clinical populations, but the intramuscular proteolytic pathways that govern declines in these individuals remain relatively poorly understood. The nematode Caenorhabditis elegans has been developed into a model for identifying and understanding these pathways. Recently, it was reported that UNC-105/degenerin channel activation produced muscle protein degradation via an unknown mechanism.', 'Generation of transgenic and double mutant C.\u2009elegans, RNAi, and drug treatments were utilized to assess molecular events governing protein degradation. Western blots were used to measure protein content. Cationic dyes and adenosine triphosphate (ATP) production assays were utilized to measure mitochondrial function.', 'unc-105 gain-of-function mutants display aberrant muscle protein degradation and a movement defect; both are reduced in intragenic revertants and in let-2 mutants that gate the hyperactive UNC-105 channel. Degradation is not suppressed by interventions suppressing proteasome-mediated, autophagy-mediated, or calpain-mediated degradation nor by suppressors of degenerin-induced neurodegeneration. Protein degradation, but not the movement defect, is decreased by treatment with caspase inhibitors or RNAi against ced-3 or ced-4. Adult unc-105 muscles display a time-dependent fragmentation of the mitochondrial reticulum that is associated with impaired mitochondrial membrane potential and that correlates with decreased rates of maximal ATP production. Reduced levels of CED-4, which is sufficient to activate CED-3 in vitro, are observed in unc-105 mitochondrial isolations.\Question: Does degenerin channel activation cause caspase-mediated protein degradation and mitochondrial dysfunction in adult C. elegans muscle?

Constitutive cationic influx into muscle appears to cause caspase degradation of cytosolic proteins as the result of mitochondrial dysfunction, which may be relevant to ageing and sarcopenia.