Development and validation of a nutrition screening tool for hospitalized cancer patients

Background & aims

Although various nutrition screening tools are used, they are not specific for the screening of malnourished cancer patients. The objective of this study was to develop a nutrition screening tool that could be used to identify cancer patients at risk for malnutrition.

Methods

Of 3010 cancer patients admitted to the National Cancer Center of Korea between April 1 and June 2, 2008, the nutritional status of 1057 patients was assessed by the Scored Patient-Generated Subjective Global Assessment (PG-SGA). Variables used in current nutrition screening tools were analyzed to select indices for a developing malnutrition screening tool for cancer patients (MSTC). The equation for the MSTC was established using receiver operating characteristics curves. Sensitivities and specificities of the MSTC were calculated using the PG-SGA as gold standard.

Results

The MSTC was calculated as follows: [MSTC = −0.116 + (1.777 × intake change) + (1.304 × Eastern Cooperative Oncology Group performance status) + (1.568 × weight loss) + (−0.187 × body mass index)]. The MSTC had a sensitivity of 94.0%, a specificity of 84.2%, and high agreement (κ = 0.70, P < 0.0001) with the PG-SGA.

Conclusions

The MSTC appears to be a valid nutrition screening tool for determining nutritional risk in hospitalized cancer patients.     

Acoustic modulation of electrically evoked otoacoustic emission in chickens

Electrically evoked otoacoustic emissions (EEOAEs) can be elicited from the chicken inner ear. Since lesion studies implicate hair cells are the source of EEOAEs, we hypothesized that acoustic stimuli would modulate EEOAE amplitude at cochlear locations where the acoustic and electrical stimuli overlap. To assess this interaction, EEOAEs were measured as the frequency and amplitude of the acoustic stimuli were varied. EEOAEs, evoked by AC current (3-250 microA rms) delivered to the round window had a broad band pass response (1-6 kHz) with a peak between 3 and 4 kHz and maximum amplitude of 27 dB SPL. EEOAE suppression/enhancement tuning curves were measured at 2, 3, 4 and 6 kHz by varying the frequency of a 70 dB SPL tone and measuring the change in EEOAE amplitude. EEOAE tuning curves were characterized by a tip; a narrow range of frequencies where EEOAE amplitude was suppressed by as much as 5 dB, and by sidebands, a range of frequencies above and below the tip where EEOAE amplitude was enhanced by as much as 1.5 dB. The best suppression frequency, or characteristic frequency, was close to the frequency of the EEOAE elicited by the 3- or 4-kHz electric stimulus. However, the characteristic frequency was displaced towards higher frequencies for the 2-kHz electric stimulus, and towards lower frequencies for the 6-kHz electric stimulus. EEOAE suppression increased approximately linearly with acoustic level. These results suggest that EEOAEs evoked by round window stimulation are predominantly generated by hair cells near the 3- to 4-kHz region of the cochlea.     

Danthron inhibits the neurotoxicity induced by various compounds causing oxidative damages including beta-amyloid (25-35) in primary cortical cultures

Oxidative stress caused by an elevation in reactive oxygen species (ROS) plays an important role in Alzheimer's disease and other neurodegenerative diseases. In this study, we examined the neuroprotective effect of danthron (1,8-dihydroxyanthraquinone) against neurotoxicities induced by beta-amyloid (25-35), excitotoxins, apoptosis, and oxidative stress in primary cortical cultures. Danthron dose-dependently reduced neuronal injury induced by 30 microM beta-amyloid (25-35). Danthron significantly inhibited oxidative injury induced by 100 microM Fe(3+) and decreased membrane lipid peroxidation induced by 100 microM Fe(3+) as measured by thiobarbituric-acid-reactive substance (TBARS). Danthron (0.5-50 microM) ameliorated the effects of buthionine sulfoximine (BSO, 1 mM), which depletes endogenous glutathione by 10-73%. Danthron also dose-dependently inhibited neuronal injury mediated by nitric oxide (NO) radicals, but failed to inhibit injury due to superoxide radicals (O(2-)). These results suggest danthron treatment may, in part, reduce neurotoxicity related to beta-amyloid protein by both dominant inhibitory effects on membrane lipid peroxidation and glutathione deprivation.     

Structure-related cytotoxicity and anti-hepatofibric effect of asiatic acid derivatives in rat hepatic stellate cell-line, HSC-T6

The structural relationship of 16 asiatic acid (AA) derivatives, including AA and asiaticoside (AS) to cytotoxicity and anti-hepatofibrotic activity in HSC-T6 cells, were investigated. Cytotoxicities of AA derivatives varied from 5.5 microM to over 2000 microM of IC50 depending on AA functional group modifications. Substituting the hydroxyl group at the C(2) to N[triple bond]C and substituting bulky groups for dihydroxyl groups at (3), (23) of the A-ring increased the cytotoxicity, but keto group at C(11) and benzoyl ester at C(2) were greatly reduced it. Modification of the carboxylic acid group at C28 also reduced the cytotoxicity. The collagen synthesis determined by hydroxyproline content in the cells was inhibited from a maximum of 48% (Zlx-i-85 and 87) to 15% (AS) by AA derivatives. The anti-hepatofibrotic effect of these compounds might be due to the reduced expression of prolyl 4-hydroxylase alpha and beta subunits and TIMP2. However, the inhibition of collagen by asiaticoside derivatives did not show any structural-activity relationship.     

Increased expression of phospholipase D in the heart with experimental autoimmune myocarditis in Lewis rats

The expression of phospholipase D (PLD) in the hearts of rats with experimental autoimmune myocarditis (EAM) was studied to elucidate the functional role of PLD in the pathogenesis of EAM. Western blot analysis showed that the level of the PLD1 isoform was significantly increased in the hearts of rats with EAM on days 14, 17 and 21 postimmunization (pi) (P < 0.01; control vs EAM at 14 pi, 17 pi and 21 pi). The phenotypes of cells exhibiting increased PLD1 expression were primarily inflammatory cells, including ED1 positive macrophages, in the inflammatory EAM lesions. Some cardiomyocytes also showed increased PLD1 immunoreaction in and around EAM lesions. Some PLD1-positive cells were also positive for proliferating cell nuclear antigen in some cardiomyocytes or terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling in some macrophages, suggesting that PLD1 positive cells have a capacity for proliferation or apoptosis depending on cell types in the target organ. Thus, it is postulated that increased expression of PLD1 in EAM may support an early inflammatory response in proliferating inflammatory cells, and its expression in cardiomyocytes may help them to survive by activation of survival factors in hearts with EAM.     

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