instruction:
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.
question:
Context: Transient receptor potential ankyrin 1 (TRPA1) is a membrane-associated cation channel, widely expressed in neuronal cells and involved in nociception and neurogenic inflammation. We showed recently that TRPA1 mediates cartilage degradation and joint pain in the MIA-model of osteoarthritis (OA) suggesting a hitherto unknown role for TRPA1 in OA. Therefore, we aimed to investigate whether TRPA1 is expressed and functional in human OA chondrocytes.', 'Expression of TRPA1 in primary human OA chondrocytes was assessed by qRT-PCR and Western blot. The functionality of the TRPA1 channel was assessed by Ca(2+)-influx measurements. Production of MMP-1, MMP-3, MMP-13, IL-6, and PGE2 subsequent to TRPA1 activation was measured by immunoassay.', 'We show here for the first time that TRPA1 is expressed in primary human OA chondrocytes and its expression is increased following stimulation with inflammatory factors IL-1, IL-17, LPS, and resistin. Further, the TRPA1 channel was found to be functional, as stimulation with the TRPA1 agonist AITC caused an increase in Ca(2+) influx, which was attenuated by the TRPA1 antagonist HC-030031. Genetic depletion and pharmacological inhibition of TRPA1 downregulated the production of MMP-1, MMP-3, MMP-13, IL-6, and PGE2 in osteoarthritic chondrocytes and murine cartilage, respectively.\Question: Is transient receptor potential ankyrin 1 ( TRPA1 ) functionally expressed in primary human osteoarthritic chondrocytes?
answer:
The TRPA1 cation channel was found to be functionally expressed in primary human OA chondrocytes, which is an original finding. The presence and inflammatory and catabolic effects of TRPA1 in human OA chondrocytes propose a highly intriguing role for TRPA1 as a pathogenic factor and drug target in OA.

question:
Context: To assess the relationship between congenital uterine malformations and blood pressure in pregnancy.', 'Twenty-four-hour automated ambulatory blood pressure monitoring (readings every 30 min) was performed in 16 normotensive, nonproteinuric, primigravidae with congenital uterine malformations (5 uterus septus, 9 uterus bicornis, 2 uterine didelphys) between 20 and 30 weeks. From the 24-hr blood pressure report, we calculated 24-hr mean, daytime and nighttime means. The results were compared with 16 primigravidae, matched for age and gestation, who were and remained normotensive throughout pregnancy, and tested for statistics with t-test; significance assessed at p < 0.001.', 'Although they were within the normotensive range, all blood pressure measurements considered were significantly higher in pregnant women with congenital uterine malformations, compared to normal pregnant women. Namely, 24-hr, daytime, and nighttime systolic (mean +/- SD) were 121.1 +/- 8.4, 124.4 +/- 8.8, 114.0 +/- 7.7 mmHg, respectively, in women with uterine malformations and 108.0 +/- 7.4, 109.2 +/- 7.3, 102.1 +/- 8.5 mmHg, respectively, in normal pregnant women. Twenty-four-hour diastolic, daytime, and nighttime diastolic (mean +/- SD) 74.1 +/- 10.2, 77.1 +/- 10.6, 68.1 +/- 9.2 mmHg, in women with uterine malformations and 64.1 +/- 5.7, 66.0 +/- 5.7, 58.2 +/- 6.3 mmHg, in normal pregnant women (all differences p < 0.001). Fifteen of the fetuses from women with congenital uterine malformations showed intrauterine growth retardation. No differences were found 6 months after delivery.\Question: Are congenital uterine malformations associated to increased blood pressure in pregnancy?
answer:
Although the blood pressure levels remained within the normotensive range, pregnant women with congenital uterine anomalies have a higher blood pressure than normal women. Elevated blood pressure can result from altered uterine circulation and reduced blood supply to the placenta. This pathogenesis or the poor placentation may result in a foetal growth retardation.

question:
Context: Despite of many studies conducted on toothbrushes and toothpaste to find out the culprit for abrasion, there is no clear cut evidence to pin point the real cause for abrasion.', 'An in vitro assessment of the role of different types of toothbrushes (soft/ medium/hard) in abrasion process when used in conjunction with and without a dentifrice.', 'Forty five freshly extracted, sound, human incisor teeth were collected for this study. Enamel specimens of approximately 9 mm(2) were prepared by gross trimming of extracted teeth using a lathe machine (Baldor 340 Dental lathe; Ohio, USA). They were mounted on separate acrylic bases. The specimens were divided into three groups, each group containing 15 mounted specimens. Group 1 specimens were brushed with soft toothbrush; Group 2 brushed with medium toothbrush and Group 3 with hard toothbrush. Initially, all the mounted specimens in each group were brushed using dentifrice and then the same procedure was repeated with water as control. Profilometric readings were recorded pre and post to tooth brushing and the differences in readings served as proxy measure to assess surface abrasion. These values were then compared to each other. Kruskal Wallis and Mann-Whitney U test were performed.', 'The results showed that brushing, with water alone, caused less abrasion than when toothpaste was added (p< 0.008). When brushed with water, the harder toothbrush caused more abrasion (higher Ra-value), but when toothpaste was added, the softer toothbrush caused more abrasion (p< 0.001).\Question: Do a Profilometric Study to Assess the Role of Toothbrush and Toothpaste in Abrasion Process?
answer:
Besides supporting the fact that toothpaste is needed to create a significant abrasion, this study also showed that a softer toothbrush can cause more abrasion than harder ones. The flexibility of bristles is only secondary to abrasion process and abrasivity of dentifrice has an important role in abrasion process.