The effect of a synthetic analogue of CCK (Thr4,Nle7CCK-9) on growth of SW-1990 human pancreatic cancer was examined in two experimental models. Nude mice bearing SW-1990 pancreatic cancer xenografts were injected with CCK (5, 15, or 25 micrograms/kg) or vehicle twice daily for 20 days. Animals were then sacrificed and tumor volume, weight, protein, and deoxyribonucleic acid (DNA) content were evaluated. SW-1990 cells were grown in vitro and the effects of CCK, secretin, vasoactive intestinal peptide (VIP), and proglumide (a CCK-receptor antagonist) on cell number and DNA synthesis were determined. The highest dose of CCK, 25 micrograms/kg, significantly increased tumor weight, protein content, and DNA content (P less than 0.005). In vitro, CCK caused significant increases in cell counts of up to 47% at six days and 66% at 12 days compared to control. Graded concentrations of CCK had a biphasic effect on DNA synthesis with significant increases of up to 65% (P less than 0.005). CCK-induced cell proliferation was inhibited by proglumide. Secretin slightly increased cancer cell growth, although not as potently as CCK, VIP or secretin in combination with CCK did not show potentiation. These results indicate that growth of some human pancreatic cancers may be influenced by gastrointestinal peptides, of which CCK is the most potent.
The SF-36 has satisfactory to good psychometric properties in pain patients, the NHP item selection has to be improved. The FLZ-M weighting can be eliminated. The shortcomings of the SF-36 can be overcome by adding short scales on role functioning and pain (modular approach).
ObjectivesIncreasing evidence suggests that hearing loss may be linked to cognitive decline, and that cochlear implantation may lead to improvements in cognition. The goal of this study was to examine the effects of severe‐to‐profound hearing loss and cochlear implantation in post‐lingually deafened adults, compared with age‐matched normal‐hearing (NH) peers. Participants were tested on several non‐auditory measures of cognition: working memory (WM) (digit span, object span, symbol span), non‐verbal reasoning (Raven's progressive matrices), information‐processing speed and inhibitory control (Stroop test), speed of phonological and lexical access (Test of Word Reading Efficiency), and verbal learning and memory (California Verbal Learning Test). Demographic measures were also collected.MethodsCohort study at tertiary neurotology center. Forty‐three post‐lingually deafened experienced CI users, 19 post‐lingually deafened CI candidates, and 40 age‐matched NH controls with no cognitive impairment were enrolled. Comparisons among the groups on the cognitive measures were performed.ResultsAdult CI users and CI candidates demonstrated worse (or a trend towards worse) performance as compared with NH peers on non‐verbal reasoning, information‐processing speed, speed of lexical access, and verbal learning and memory. However, after controlling for gender, socioeconomic status (SES), and vocabulary knowledge among groups, some of these differences were no longer significant. Similarly, large differences were not found in most cognitive abilities between experienced CI users and CI candidates.ConclusionsAdult CI users, CI candidates, and NH peers generally demonstrated equivalent non‐auditory cognitive abilities, after controlling for gender, SES, and vocabulary knowledge. These findings provide support for a link between cognitive decline and hearing loss, but this association may be partly attributable to group differences in SES and vocabulary knowledge.Level of Evidence2b.
An alarming trend of declining applications to otolaryngology-head and neck surgery has surfaced over the past 3 years. There are many possible explanations for this decline, and a recent publication has implicated "impossible" qualifications as the reason for this decline. While these qualifications may deter a significant number of potential applicants, they have not changed significantly in the past 5 years and do not seem to explain a sudden decline. This commentary argues that the program-specific paragraph, which was introduced in 2015, may be at least in part responsible.
The effects of a high-fat diet and the CCK-receptor antagonist, L364,718, were examined on growth of human pancreas cell line SW-1990 xenografted to nude mice. Sixty animals were fed either low-fat (4.3%) or high-fat (20.25%) diet. Fifteen mice in each diet group were treated with L364,718 (2 mg/kg) subcutaneously twice daily for 23 days. On day 24 the animals were sacrificed. Tumor and animal pancreases were dissected and evaluated for weight, protein, and DNA content. When comparing within each diet group, L364,718 significantly decreased tumor volume, weight, protein, and DNA content compared to untreated mice (P less than 0.005). Tumor volume and protein content were significantly larger in untreated animals on the high-fat diet (P less than 0.05) compared to the low-fat diet. Mouse pancreatic weight, protein, and DNA content per kilogram of animal weight were all significantly lower (P less than 0.005) in mice on the low-fat diet treated with L364,718. Pancreatic DNA content was also decreased in both groups of animals on the high-fat diet compared to untreated mice on the low-fat diet. These findings suggest that diets high in unsaturated fat promote the growth of human pancreatic cancer. Since both tumor and pancreas growth are inhibited by the specific CCK-antagonist, L364,718, it is possible that endogenous CCK promotes the growth.
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