Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Q: Context: It has been hypothesized that minichromosome maintenance (MCM) proteins, which are replicative control factors, can be used to detect tumor proliferation. The aim of the present study was to investigate the expression of MCM in colorectal cancer tissues and correlate it to clinical outcomes.', 'The study included 145 patients with colorectal cancer who underwent curative surgery, from January 2002 until December 2004, at the Kurume University Hospital in Fukuoka, Japan. The median follow-up duration was 87 months. The expression of MCM7 in tissues was studied by immuno-histochemical staining. The labeling index (LI) of MCM7 was calculated by dividing the number of positively-stained cells by the total number of cells counted. We divided samples into two groups: positive (MCM7 LI 76% or higher) and negative (MCM7 LI less than 76%).', 'In patients with Dukes A and B, there were no significant differences in either overall survival (OS) or recurrence-free survival (RFS) between patents with MCM7-positive and those with MCM7-negative disease. On the other hand, in patients with Dukes C, there was significantly worse OS and RFS for patients with MCM7-positive compared to those with MCM7-negative disease.
Answer: We found that the expression of MCM7 is an independent risk factor for RFS in patients with Dukes C colorectal cancer. Further studies are required to investigate the validity of MCM7 protein expression for its potential clinical use in colorectal cancer therapy and prognosis.

A: Is minichromosome maintenance protein 7 a risk factor for recurrence in patients with Dukes C colorectal cancer?
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Q: Context: This study was designed to examine the course of psychological distress and pain from study entry to death in 59 women with metastatic breast cancer participating in a randomized trial of the effects of group psychotherapy on psychosocial outcomes and survival. It was hypothesized that psychological distress would increase significantly before death independent of changes in pain.', 'Data were collected as part of a larger study (N = 125). Analyses were based on data from a subset of women who had died and for whom we had data from at least three assessments. Mean levels of mood, trauma symptoms, depression symptoms, well-being, and pain over three time points were examined: at baseline (T1), the second-to-last assessment before death (T2), and the last assessment before death (T3).', 'Results indicate that while psychological distress remained relatively constant or declined from T1 to T2, means on all measures significantly changed in the hypothesized direction from T2 to T3. Neither self-reported pain, nor the passage of time, appeared to account for these changes. Additionally, participation in group psychotherapy did not have a significant impact on this change in distress proximal to death.
Answer: Results suggest that specialized end-stage clinical interventions are particularly needed for cancer patients as they approach death. Moreover, intervention studies for patients with deteriorating illnesses may need to take this "spike" in psychological distress and pain proximal to death into account to avoid Type II errors in evaluations of psychological outcomes.

A: Do psychological distress and pain significantly increase before death in metastatic breast cancer patients?
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Q: Context: To fully understand the cytotoxicity of after-degradation QDs, we synthesized CdS QDs and investigated its toxicity mechanism.', 'Biomimetic method was proposed to synthesize cadmium sulfide (CdS) QDs. Thereafter MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay was conducted to evaluate their cytotoxicity. To investigate the toxicity mechanism, we subsequently conducted intracellular reactive oxygen species (ROS) measurement with DCFH-DA, glutathione (GSH) measurement with DTNB, and cellular cadmium assay using atomic absorption spectrometer. Microsized CdS were simultaneously tested as a comparison.', "MTT assay results indicated that CdS QDs are more toxic than microsized CdS especially at concentrations below 40 microg/ml. While microsized CdS did not trigger ROS elevation, CdS QDs increase ROS by 20-30% over control levels. However, they both deplete cellular GSH significantly at the medium concentration of 20 microg/ml. In the presence of NAC, cells are partially protected from CdS QDs, but not from microsized particles. Additionally, nearly 20% of cadmium was released from CdS nanoparticles within 24h, which also accounts for QDs' toxicity.
Answer: Intracellular ROS production, GSH depletion, and cadmium ions (Cd(2+)) release are possible mechanisms for CdS QDs' cytotoxicity. We also suggested that with QD concentration increasing, the principal toxicity mechanism changes from intracellular oxidative stress to Cd(2+) release.

A:
Do intracellular oxidative stress and cadmium ions release induce cytotoxicity of unmodified cadmium sulfide quantum dots?
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