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.

Ex Input:
Context: Transforming growth factor beta 1 (TGFβ1) is strongly induced following brain injury and polarises microglia to an anti-inflammatory phenotype. Augmentation of TGFβ1 responses may therefore be beneficial in preventing inflammation in neurological disorders including stroke and neurodegenerative diseases. However, several other cell types display immunogenic potential and identifying the effect of TGFβ1 on these cells is required to more fully understand its effects on brain inflammation. Pericytes are multifunctional cells which ensheath the brain vasculature and have garnered recent attention with respect to their immunomodulatory potential. Here, we sought to investigate the inflammatory phenotype adopted by TGFβ1-stimulated human brain pericytes.', 'Microarray analysis was performed to examine transcriptome-wide changes in TGFβ1-stimulated pericytes, and results were validated by qRT-PCR and cytometric bead arrays. Flow cytometry, immunocytochemistry and LDH/Alamar Blue® viability assays were utilised to examine phagocytic capacity of human brain pericytes, transcription factor modulation and pericyte health.', 'TGFβ1 treatment of primary human brain pericytes induced the expression of several inflammatory-related genes (NOX4, COX2, IL6 and MMP2) and attenuated others (IL8, CX3CL1, MCP1 and VCAM1). A synergistic induction of IL-6 was seen with IL-1β/TGFβ1 treatment whilst TGFβ1 attenuated the IL-1β-induced expression of CX3CL1, MCP-1 and sVCAM-1. TGFβ1 was found to signal through SMAD2/3 transcription factors but did not modify nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) translocation. Furthermore, TGFβ1 attenuated the phagocytic ability of pericytes, possibly through downregulation of the scavenger receptors CD36, CD47 and CD68. Whilst TGFβ did decrease pericyte number, this was due to a reduction in proliferation, not apoptotic death or compromised cell viability.\Question: Does tGF-beta1 regulate human brain pericyte inflammatory processes involved in neurovasculature function?

Ex Output:
TGFβ1 attenuated pericyte expression of key chemokines and adhesion molecules involved in CNS leukocyte trafficking and the modulation of microglial function, as well as reduced the phagocytic ability of pericytes. However, TGFβ1 also enhanced the expression of classical pro-inflammatory cytokines and enzymes which can disrupt BBB functioning, suggesting that pericytes adopt a phenotype which is neither solely pro- nor anti-inflammatory. Whilst the effects of pericyte modulation by TGFβ1 in vivo are difficult to infer, the reduction in pericyte proliferation together with the elevated IL-6, MMP-2 and NOX4 and reduced phagocytosis suggests a detrimental action of TGFβ1 on neurovasculature.


Ex Input:
Context: Although uncommon, hearing loss after spinal anesthesia has been described. Vestibulocochlear dysfunction after spinal anesthesia in which 22-gauge and 25-gauge Quincke needles were used was investigated to determine if needle size affected hearing.', 'Patients with American Society of Anesthesiologists physical status I and II, aged 20 to 40 years, who were undergoing lower extremity surgery under spinal anesthesia were randomized into 2 groups. After intravenous hydration, 3 mL of 0.5% bupivacaine was administered for spinal anesthesia, which was performed with a 22-gauge Quincke needle in group I (n=30) patients and a 25-gauge Quincke needle in group II (n=30) patients. Before surgery and 2 days after surgery, pure-tone audiometry and tympanometry were performed. Preoperative and postoperative hearing data were obtained in the right and left ears for every frequency. Headache, nausea, and vomiting and cranial nerve III, IV, V, VI, VII, and VIII function were assessed on postoperative day 2.', 'Demographic data were not different between the groups. No hypoacousis was noted at any frequency during the entire testing period in either group. Two patients from group I experienced postdural puncture headache on postoperative day 3, and neither had hearing loss. No patient had cranial nerve dysfunction.\Question: Does hearing loss occur in young patients undergoing spinal anesthesia?

Ex Output:
We were unable to induce hearing loss in young patients undergoing spinal anesthesia by injecting the anesthetic with a 22-gauge or a 25-gauge Quincke needle.


Ex Input:
Context: Many studies have reported that hypoxia might be associated with angiogenesis and fibrogenesis, and the level of transforming growth factor-beta1 (TGF-beta1) was increased in fibrotic liver and maximal at cirrhosis. Therefore, we examined the expression of TGF-beta1, phosphorylated-Smad2/3 (p-Smad2/3) of the TGF-beta immediate down stream signaling system and hypoxic status during hepatic fibrogenesis.', 'Fibrosis of rats was induced by carbon tetrachloride. Collagens were detected with Azan stain. Immunohistochemistry and immunoblotting was used.', 'TGF-beta1 was mainly produced by hypoxic hepatocytes at cirrhosis although myofibroblasts (MFBs) and macrophages producing TGF-beta1 were decreased. Moreover, distribution of p-Smad2/3 in hepatocytes was consistent with those of hypoxic hepatocytes regardless of MFBs. Furthermore, in recovery, most MFBs disappeared, whereas positive reactions of p-Smad2/3 still existed in the hepatocytes of hypoxic areas. Therefore, TGF-beta1 expression in hepatocytes might have been associated with hypoxia.\Question: Does hypoxia potentiate transforming growth factor-beta expression of hepatocyte during the cirrhotic condition in rat liver?

Ex Output:

We put forward the hypothesis that TGF-beta1 is mainly produced by MFBs and macrophages at early and middle stages of fibrotic processes, but it is predominantly released by hypoxic hepatocytes in the last fibrotic stage or cirrhosis.