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.

Q: Context: The PINK1-Parkin pathway is known to play important roles in regulating mitochondria dynamics, motility, and quality control. Activation of this pathway can be triggered by a variety of cellular stress signals that cause mitochondrial damage. How this pathway senses different levels of mitochondrial damage and mediates cell fate decisions accordingly is incompletely understood.', 'Here, we present evidence that PINK1-Parkin has both cytoprotective and proapoptotic functions. PINK1-Parkin operates as a molecular switch to dictate cell fate decisions in response to different cellular stressors. Cells exposed to severe and irreparable mitochondrial damage agents such as valinomycin can undergo PINK1-Parkin-dependent apoptosis. The proapoptotic response elicited by valinomycin is associated with the degradation of Mcl-1. PINK1 directly phosphorylates Parkin at Ser65 of its Ubl domain and triggers activation of its E3 ligase activity through an autocatalytic mechanism that amplifies its E3 ligase activity toward Mcl-1.\Question: Does pINK1 trigger autocatalytic activation of Parkin to specify cell fate decisions?

A: Autocatalytic activation of Parkin bolsters its accumulation on mitochondria and apoptotic response to valinomycin. Our results suggest that PINK1-Parkin constitutes a damage-gated molecular switch that governs cellular-context-specific cell fate decisions in response to variable stress stimuli.
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Q: Context: Matrix metalloprotease-2 (MMP-2) and matrix metalloprotease-9 (MMP-9) play a key role in tissue remodelling after processes such as joint destruction in rheumatoid arthritis. Their expression may reflect the disease activity and they could therefore represent a useful marker to assess the efficacy of therapy. In this study MMP-2 and MMP-9 serum were evaluated in patients with chronic arthritis during therapy with the anti-TNFalpha mAb, infliximab.', 'Fifty patients with chronic arthritis, 26 with rheumatoid arthritis and 24 with undifferentiated chronic arthritis, were recruited and treated with infliximab (3 mg/kg). Serum concentrations of MMP-2 and MMP-9 were serially measured by gelatine zymography at baseline and after two and fourteen weeks of infliximab therapy. DAS-28 and ACR response criteria were applied to assess disease activity and clinical improvement. Twenty-four healthy donors were included in the study as controls.', 'Although therapy with infliximab induced a statistically significant reduction of the DAS-28 score and improvement of the ACR clinical response, MMP-2 and MMP-9 serum concentrations were not modulated during therapy with infliximab.\Question: Does infliximab therapy modify MMP-2 and MMP-9 serum concentrations in chronic arthritis?

A: Our study provides further evidence that blocking TNFalpha by infliximab is a powerful tool in the management of chronic arthritis. Nevertheless, infliximab does not seem to be able to modify the serum expression of MMP-2 and MMP-9, probably because modification of these enzymes is restricted to the site of joint inflammation and serum detection can not truly mirror the local situation. Additional soluble factors correlating with joint damage should be investigated as possible markers for monitoring anti-TNFalpha therapy.
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Q: Context: This study aimed to investigate the effects of branched-chain amino acid (BCAA) supplementation on recovery of power-producing ability following a strength training (ST) session.', 'Eleven resistance-trained males, performed baseline measures of a countermovement jump (CMJ) and a seated shot-put throw (SSPT). In a counterbalanced fashion, participants were provided with either 20-g of BCAA or a placebo. Each dose was divided into two equal quantities and consumed before and after a ST session consisting of various multi-joint barbell exercises. For both conditions, the CMJ and SSPT were repeated at 24-h post-ST, in addition participants attributed their perceived muscle soreness level via a 200-mm visual analogue scale.', 'Following ST there were significant decrements in CMJ (Baseline; 55.2 ± 7.4-cm, BCAA; 52.8 ± 5.9-cm Placebo; 50.6 ± 7.3-cm) and SSPT (Baseline; 4.55 ± 0.56-m, BCAA; 4.37 ± 0.61-m, Placebo; 4.22 ± 0.64- m) for both conditions in comparison to baseline values (P < 0.05). However, BCAA was shown to attenuate the decrements in CMJ and SSPT performance compared to placebo (P < 0.05). Muscle soreness was significantly increased following ST for both conditions, however there were no differences in attributed values following BCAA and placebo ingestion.\Question: Does branched-chain amino acid supplementation attenuate a decrease in power-producing ability following acute strength training?

A:
BCAA administered acutely before and following intensive ST attenuates a decrease in power-producing ability experienced by resistance-trained males. The apparent small but significant effects on functional power suggest that BCAA is an effective ergogenic aid for athletes who require augmented recovery of power-producing ability following intensive ST.
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