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.

[EX Q]: Context: Downstream effects of muscarinic receptor stimulation in intestinal smooth muscle include contraction and intestinal transit. We thought to determine whether classic transient receptor potential (TRPC) channels integrate the intracellular signaling cascades evoked by the stimulated receptors and thereby contribute to the control of the membrane potential, Ca-influx, and cell responses.', 'We created trpc4-, trpc6-, and trpc4/trpc6-gene-deficient mice and analyzed them for intestinal smooth muscle function in vitro and in vivo.', 'In intestinal smooth muscle cells TRPC4 forms a 55 pS cation channel and underlies more than 80% of the muscarinic receptor-induced cation current (mI(CAT)). The residual mI(CAT) depends on the expression of TRPC6, indicating that TRPC6 and TRPC4 determine mI(CAT) channel activity independent of other channel subunits. In TRPC4-deficient ileal myocytes the carbachol-induced membrane depolarizations are diminished greatly and the atropine-sensitive contraction elicited by acetylcholine release from excitatory motor neurons is reduced greatly. Additional deletion of TRPC6 aggravates these effects. Intestinal transit is slowed down in mice lacking TRPC4 and TRPC6.
Answer: In intestinal smooth muscle cells TRPC4 and TRPC6 channels are gated by muscarinic receptors and are responsible for mI(CAT). They couple muscarinic receptors to depolarization of intestinal smooth muscle cells and voltage-activated Ca(2+)-influx and contraction, and thereby accelerate small intestinal motility in vivo.
[EX A]: Does deletion of TRPC4 and TRPC6 in mice impair smooth muscle contraction and intestinal motility in vivo?

[EX Q]: Context: Tinnitus can adversely affect patients' quality of life. Transcutaneous electrical nerve stimulation (TENS) may be effective in the management of tinnitus. No study has investigated the efficacy of TENS for the management of tinnitus by means of quality of life measures. In this study, we evaluated the efficacy of TENS for the management of tinnitus symptoms by using the visual analogue scale (VAS), tinnitus handicap inventory test, Nottingham health profile (NHP) and short form-36 (SF-36) questionnaires.", 'Twenty-two patients were included in this study (male/female, 16/6; mean age, 48.04 +/- 15.57 years). Nine patients had unilateral and 13 patients had bilateral tinnitus.', 'After TENS, improvement measured by VAS was only marginally significant (p = 0.059). However, after TENS, there were statistically significant improvements regarding tinnitus severity scores, tinnitus handicap inventory scores, NHP fatigue, social isolation and emotional problems scores, and many parameters measured by the SF-36 (physical functioning, general health, vitality, social functioning, role limitations due to emotional problems, and mental health)(p < 0.05).
Answer: Transcutaneous electrical nerve stimulation is a useful method to improve the quality of life of patients with tinnitus.
[EX A]: Does treatment of tinnitus with transcutaneous electrical nerve stimulation improve patients ' quality of life?

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