instruction:
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.
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Context: The membrane protein CD46, a ubiquitous cell surface pathogen receptor, can bind Streptococcus to trigger cell autophagy, which is a critical step in the control of infection.', 'In this study, we found a new splice variant designated CD46 transcript variant (CD46-TV). The splice variant is characterized by the retention of a 48\xa0bp sequence from intron 8 of the bovine CD46 gene, which encodes a putative protein enlarged by 16 amino acids. CD46-TV mRNA was found to be over expressed in mastitis-infected mammary gland tissues relative to healthy tissues. A single nucleotide polymorphism (c. 1033\u2009+\u20092184 C\u2009>\u2009T) in the exonic splicing enhancer (ESE) motif region was shown to result in the CD46-TV aberrant splice variant through constructing alternative alleles using the pSPL3 exon capturing vector and transfecting these into 293\xa0T cells. Allelic frequency in 56,682 individuals belonging to 112 Bos taurus, Bos indicus, Bos javanicus, Bos grunniens and Bos mutus, etc. suggests that the C allele (80.09%) is the ancestral allele. Association analysis found that the mean genomic estimated breeding values (gEBV) for milk somatic cell score and the occurrence of clinical mastitis, as well as the milk somatic cell score of Chinese Holsteins with the CT genotype was lower than those of individuals with either the CC or TT genotypes. The mean gEBV for udder health synthesis for the TT genotype was greater than those for the CC or CT genotypes.
Answer: Our findings suggest that the CD46 gene likely plays a critical role in the risk of mastitis caused by Streptococcus in dairy cows via an alternative splicing mechanism caused by a functional mutation in intron 8. Our data also underline the importance of variation within ESEs in regulating transcript processing.
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Does a SNP in intron 8 of CD46 cause a novel transcript associated with mastitis in Holsteins?


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Context: To assess the accuracy of the clinically estimated blood loss (EBL) when compared with the actual blood loss (ABL) in replacement surgeries.', "This prospective study was done in Sri Ramachandra Medical Centre from April 2011 to April 2013. Altogether 140 patients undergoing total hip replacement or total knee replacement were included with the inclusion criteria being patients with haemoglobin higher than 100 g/ml and coagulation profile within normal limits. Exclusion criteria were intake of anti-platelet drug or anti-coagulant, bleeding disorders, thrombotic episode, and haematological disorders. There were 65 men and 75 women. In this study, the consultants were free to use any clinical method to estimate the blood loss, including counting the blood-soaked mops and gauze pieces (estimating the volume of blood carried in all the mops and gauzes), measuring blood lost to suction bottles and blood in and around the operative field. The ABL was calculated based on a modification of the Gross's formula using haematocrit values.", 'In 42 of the 140 cases, the EBL exceeded the ABL. These cases had a negative difference in blood loss (or DIFF-BL<0) and were included in the overestimation group, which accounted for 30% of the study population. Of the remaining 98 cases (70%), the ABL exceeded the EBL. Therefore they were put into the underestimation group who had a positive difference in blood loss (DIFF-BL>0). We found that when the average blood loss was small, the accuracy of estimation was high. But when the average blood loss exceeded 500 ml, the accuracy rate decreased significantly. This suggested that clinical estimation is inaccurate with the increase of blood loss.
Answer: This study has shown that using clinical estimation alone to guide blood transfusion is inadequate. In this study, 70% of patients had their blood loss underestimated, proving that surgeons often underestimate blood loss in replacement surgeries.
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Do surgeons often underestimate the amount of blood loss in replacement surgeries?


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Context: Checkpoint adaptation (entry into mitosis with damaged DNA) is a process that links arrest at the G2/M cell cycle checkpoint and cell death in cancer cells. It is not known, however, whether cells treated with the genotoxic agent, cisplatin, undergo checkpoint adaptation or if checkpoint adaptation is a major pathway leading to cell death or not. Therefore, we investigated the relationship between treatment with cisplatin and cytotoxicity in cancer cells.', 'Treatment of HT-29 human colorectal adenocarcinoma cells with cisplatin can induce cell death by one of two different mechanisms. Cells treated with a cytotoxic 30 μM amount of cisplatin died after undergoing checkpoint adaptation. Before dying, however, almost all treated cells were positive for histone γH2AX staining and contained high levels of cyclin B1. Rounded cells appeared that were positive for phospho-Ser10 histone H3, with low levels of phospho-Tyr15 cyclin-dependent kinase 1, high levels of cyclin-dependent kinase 1 activity, and checkpoint kinase 1 that was not phosphorylated on Ser345. These cells were in mitosis with damaged DNA. Strikingly, with 30 μM cisplatin, 81% of cells had entered mitosis before dying. By contrast, after treatment with 100 μM cisplatin, nearly all cells died but only 7% of cells had entered mitosis. Instead, these cells died by apoptosis; they were positive for annexin-V staining, contained cleaved caspase 3, cleaved caspase 9 and cleaved PARP and did not contain Mcl-1.
Answer: Our data demonstrate that cancer cells treated with cisplatin can undergo one of two modes of cell death depending upon concentration used. These findings suggest that checkpoint adaptation is likely a primary pathway in genotoxic cell death at pharmacological concentrations of cisplatin.
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Do cytotoxic amounts of cisplatin induce either checkpoint adaptation or apoptosis in a concentration-dependent manner in cancer cells?