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: Bacteria often form multicellular, organized communities known as biofilms, which protect cells from a variety of environmental stresses. During biofilm formation, bacteria secrete a species-specific matrix; in Bacillus subtilis biofilms, the matrix consists of protein polymers and exopolysaccharide. Many domesticated strains of B. subtilis have a reduced ability to form biofilms, and we conducted a two-month evolution experiment to test whether laboratory culturing provides selective pressure against biofilm formation in B. subtilis.', 'Bacteria grown in two-month-long batch culture rapidly diversified their biofilm-forming characteristics, exhibiting highly diverse colony morphologies on LB plates in the initial ten days of culture. Generally, this diversity decreased over time; however, multiple types of colony morphology remained in our final two-month-old populations, both under shaking and static conditions. Notably, while our final populations featured cells that produce less biofilm matrix than did the ancestor, cells overproducing biofilm matrix were present as well. We took a candidate-gene approach to identify mutations in the strains that overproduced matrix and found point mutations in the biofilm-regulatory gene sinR. Introducing these mutations into the ancestral strain phenocopied or partially phenocopied the evolved biofilm phenotypes.
Answer: Our data suggest that standard laboratory culturing conditions do not rapidly select against biofilm formation. Although biofilm matrix production is often reduced in domesticated bacterial strains, we found that matrix production may still have a fitness benefit in the laboratory. We suggest that adaptive specialization of biofilm-forming species can occur through mutations that modulate biofilm formation as in B. subtilis.

A: Is sinR a mutational target for fine-tuning biofilm formation in laboratory-evolved strains of Bacillus subtilis?
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Q: Context: Concomitant thyroid nodules are the most common reason for false-positive ultrasonography (US) results in primary hyperparathyroidism. The aims of this prospective clinical study were to evaluate false-positive US results according to the characteristics of concomitant thyroid nodules and to determine which characteristics of thyroid nodules are important.', 'This prospective study included 120 consecutive patients with primary hyperparathyroidism. The patients were divided into 2 groups according to preoperative US results. Group 1 consisted of 32 patients with false-positive US results and group 2 consisted of 88 patients with true-positive US results.', 'The risk for false-positive US result was increased 25-fold for patients with parathyroid adenoma weight of more than 500 mg (odds ratio [OR], 25; 95% confidence interval [CI], 8.6-74.5), 75-fold for more than 1 posteriorly located thyroid (OR, 75; 95% CI, 19.3-293.4), 358-fold for the presence of exophytic thyroid nodules (OR, 358; 95% CI, 42.3-3036), and 423-fold for the presence of posteriorly located thyroid nodules (OR, 423; 95% CI, 49-3662).
Answer: Although there was no particular characteristic of concomitant thyroid nodules that contributes to false-positive US results, the posteriorly located thyroid nodules were the strongest correlate for the false-positive US results to other features.

A: Do the characteristics of concomitant thyroid nodules cause false-positive ultrasonography results in primary hyperparathyroidism?
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Q: Context: Recurrence and subsequent acquired chemoresistance to platinum-based treatments constitute major hurdles to ovarian carcinoma therapy. Our objective was to examine the involvement of Bcl-xL anti-apoptotic protein in resistance to cisplatin.', 'We described the effect of cisplatin on cell cycle and apoptosis induction in sensitive (IGROV1 and OAW42) and resistant (IGROV1-R10 and SKOV3) ovarian carcinoma cell lines. We correlated it with Bcl-xL mRNA and protein expression after exposure to cisplatin. We then used bcl-xS gene transfer to impede Bcl-xL activity.', 'Our study showed that Bcl-xL basal expression was high in both sensitive and resistant cell lines, as well as in all the studied ovarian tumor samples. Thus, Bcl-xL basal expression could not allow to predict sensitivity. Wondering whether variation of Bcl-xL level in response to cisplatin could be a better determinant of sensitivity, we investigated the expression of this protein in the cell lines after treatment. Cisplatin-induced down-regulation of Bcl-xL was strictly associated with apoptosis and absence of recurrence in vitro. Conversely, the maintenance of Bcl-xL expression in response to cisplatin appeared as a sine qua non condition to escape to treatment. To try to sensitize SKOV3 cells by impeding anti-apoptotic activity of Bcl-xL, we transfected bcl-xS gene in these cells. Bcl-xS exogenous expression was only slightly cytotoxic on its own, but highly sensitized SKOV3 resistant cells to cisplatin-induced apoptosis, and delayed recurrence.
Answer: This work thus provides one more argument to put Bcl-xL forward as a pertinent target of inhibition to overcome chemoresistance of epithelial ovarian carcinoma.

A:
Is absence of Bcl-xL down-regulation in response to cisplatin associated with chemoresistance in ovarian carcinoma cells?
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