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“Objective: We sought to determine
the effect of neoadjuvant chemoradiotherapy followed by surgical intervention on health-related quality of life in patients with esophageal cancer.
Methods: Health-related quality of life was evaluated in a prospective phase II study of neoadjuvant chemoradiotherapy followed by esophagectomy in 52 patients with carcinoma of the esophagus. Esophagectomy was performed 6 weeks after completion of induction. Functional Assessment of Cancer Therapy-Esophageal scoring was performed before treatment, 7 weeks after initiation of neoadjuvant therapy, before resection, and at 1, 3, and 6 months and 1 year after resection.
Results: Forty-three patients completed the entire treatment protocol. Functional Assessment of Cancer Therapy-Esophageal scores decreased significantly after chemoradiation at week 7 (120 vs 127 this website at baseline, P = .04) but returned to baseline levels before surgical intervention (127). Similarly, scores decreased significantly after surgical intervention (115 at 1 month, P = .02) but returned to baseline levels by 3 months postoperatively (127). At 1 year postoperatively, there was a statistically significant improvement in scores compared with those at baseline (139,
P = .003). Functional Assessment of Cancer Therapy- Esophageal scores continued to increase over time for patients who were alive at least 1 year after the operation with or without disease but were observed to significantly decrease in those who died within 1 year after the operation (P = .0001). An increase in quality of life was associated with a significantly lower risk Calpain of death (P = .04).
Conclusion: Neoadjuvant therapy has a significant effect on health-related quality of life, but this is transient, with recovery to baseline within 5 to 7 weeks after completion of induction therapy. Health-related quality of life decreases again after surgical intervention but returns to baseline levels
within 3 months.”
“Alzheimer’s disease (AD) is characterized by the pathological deposition of amyloid-P protein in the aged brain. Inefficient clearance of amyloid-beta from brain tissue is believed to play a major role in the pathogenesis of these deposits. Since amyloid-P clearance likely involves activation of microglial cells via toll-like receptors and since these receptors and their signaling pathways are regarded as potential therapeutic targets, we have studied the expression of toll-like receptor (tlr) mRNAs in an animal model of AD (APP23 transgenic mice). Laser microdissection was used to harvest plaques, tissue surrounding plaques and plaque-free tissue from cortex of aged APP23 transgenic mice and age-matched controls. Real-time RT-PCR was employed to quantify expression levels of different tlr mRNAs in these tissues. This revealed a strong upregulation of tlr2, tlr4.