TASK DEFINITION: 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.
PROBLEM: Context: Helicobater (H.) pylori eradication rates with standard first-line triple therapy have declined to unacceptable levels. To date, amoxicillin-resistant H. pylori strains have rarely been detected. Whether increasing the dosage of amoxicillin in a standard 7 days eradicating regimen may enhance its efficacy is not known. The aim of this paper is to compare the efficacy of a 7 days high-dose amoxicillin based first-line regimen with sequential therapy.', 'We have retrospectively analyzed data from 300 sex and age matched patients, who underwent 3 different therapeutic schemes: (1) standard LCA, lansoprazole 30 mg bid, clarithromycin 500 mg bid and amoxicillin 1000 mg bid for 7 days; (2) high dose LCA (HD-LCA), lansoprazole 30 mg bid, clarithromycin 500 mg bid and amoxicillin 1000 mg tid for 7 days; (3) sequential LACT, lansoprazole 30 mg bid plus amoxicillin 1000 mg bid for 5 days, followed by lansoprazole 30 mg bid, clarithromycin 500 mg bid and tinidazole 500 mg bid for 5 days. Eradication was confirmed by 13C-urea breath test. Compliance and occurrence of adverse effects were also assessed.', 'Eradication rates were: 55% for LCA, 75% for HD-LCA and 73% for LACT. Eradication rates were higher in HD-LCA group compared to LCA (p<0.01), while no significant differences were observed in HD-LCA group compared to LACT (p=ns). Compliance and occurrence of adverse effects were similar among groups.\Question: Is high dose amoxicillin-based first line regimen equivalent to sequential therapy in the eradication of H. pylori infection?

SOLUTION: High-dose amoxicillin based eradicating treatment is superior to standard triple therapy and equivalent to sequential therapy; compared to the latter, the shorter duration may represent an advantage.

PROBLEM: Context: Transforming growth factor beta 1 (TGF1) is strongly induced following brain injury and polarises microglia to an anti-inflammatory phenotype. Augmentation of TGF1 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 TGF1 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 TGF1-stimulated human brain pericytes.', 'Microarray analysis was performed to examine transcriptome-wide changes in TGF1-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.', 'TGF1 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-1/TGF1 treatment whilst TGF1 attenuated the IL-1-induced expression of CX3CL1, MCP-1 and sVCAM-1. TGF1 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, TGF1 attenuated the phagocytic ability of pericytes, possibly through downregulation of the scavenger receptors CD36, CD47 and CD68. Whilst TGF 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?

SOLUTION: TGF1 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, TGF1 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 TGF1 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 TGF1 on neurovasculature.

PROBLEM: Context: Posttraumatic stress symptoms are common after intensive care treatment. The influence of anxiety during critical illness on the development of posttraumatic stress symptoms needs to be investigated.', 'To determine the association between anxiety during critical illness (state and trait components) and posttraumatic stress symptoms over six months after ICU discharge.', 'Prospective study including 141 patients admitted 24h to a closed mixed adult ICU in a tertiary hospital. State anxiety was assessed with the Faces Anxiety Scale during ICU stay. Trait anxiety was measured with the State-Trait Anxiety Inventory Form Y-2. Posttraumatic stress symptoms were measured at three and six months after ICU discharge using the Post-Traumatic Stress Symptoms 10-Question Inventory. Clinical and demographical data were also collected. Mixed effect regression models were used to determine if state and trait anxiety were factors significantly associated with posttraumatic stress symptoms over time.', 'Moderate to severe levels of state anxiety in ICU were reported by 81 (57%) participants. Levels of trait anxiety (median 36 IQR: 29-47) were similar to the Australian population. High levels of posttraumatic stress symptoms occurred at three (n=19, 19%) and six months (n=15, 17%). Factors independently associated with posttraumatic stress symptoms were trait anxiety (2.2; 95% CI, 0.3-4.1; p=0.02), symptoms of anxiety after ICU discharge (0.6; 95% CI, 0.2-1.1; p=0.005), younger age (-1.4; 95% CI, -2.6 to -0.2; p=0.02) and evidence of mental health treatment prior to the ICU admission (5.2; 95% CI, 1.5-8.9; p=0.006).\Question: Is in ICU state anxiety associated with posttraumatic stress symptoms over six months after ICU discharge : A prospective study?

SOLUTION:
Posttraumatic stress symptoms occurred in a significant proportion of ICU survivors and were significantly associated with higher levels of trait anxiety, younger age, mental health treatment prior to the ICU admission and more symptoms of anxiety after ICU discharge. Early assessment and interventions directed to reduce state and trait anxiety in ICU survivors may be of benefit.