Representativeness of breast cancer cases in an integrated health care delivery system.

BackgroundIntegrated health care delivery systems, with their comprehensive and integrated electronic medical records (EMR), are well-poised to conduct research that leverages the detailed clinical data within the EMRs. However, information regarding the representativeness of these clinical populations is limited, and thus the generalizability of research findings is uncertain.MethodsUsing data from the population-based California Cancer Registry, we compared age-adjusted distributions of patient and neighborhood characteristics for three groups of breast cancer patients: 1) those diagnosed within Kaiser Permanente Northern California (KPNC), 2) non-KPNC patients from NCI-designated cancer centers, and 3) those from all other hospitals.ResultsKPNC patients represented 32 % (N = 36,109); cancer center patients represented 7 % (N = 7805); and all other hospitals represented 61 % (N = 68,330) of the total breast cancer patients from this geographic area during 1996-2009. Compared with cases from all other hospitals, KPNC had slightly fewer non-Hispanic Whites (70.6 % versus 74.4 %) but more Blacks (8.1 % versus 5.0 %), slightly more patients in the 50-69 age range and fewer in the younger and older age groups, a slightly lower proportion of in situ but higher proportion of stage I disease (41.6 % versus 38.9 %), were slightly less likely to reside in the lowest (4.2 % versus 6.5 %) and highest (36.2 % versus 39.0 %) socioeconomic status neighborhoods, and more likely to live in suburban metropolitan areas and neighborhoods with more racial/ethnic minorities. Cancer center patients differed substantially from patients from KPNC and all other hospitals on all characteristics assessed. All differences were statistically significant (p < .001).ConclusionsAlthough much of clinical research discoveries are based in academic medical centers, patients from large, integrated medical centers are likely more representative of the underlying population, providing support for the generalizability of cancer research based on electronic data from these centers

Pretreatment of citrus by-products affects polyphenol recovery:a review

A large amount of citrus waste is generated annually. This waste is of great economic worth, since it contains high levels of polyphenols, which have attracted scientific interest due to their potent antimicrobial and antiradical activities. Pretreatment is a crucial step that precedes the extraction process and influences the yields and quality of polyphenols. This review emphasizes the effect of different drying processes, such as freeze drying, hot-air drying, vacuum drying, microwave drying, infrared drying, and high-speed drying, on the polyphenol retention in citrus by-products. Further treatments of the dried citrus by-products for assisting the liberation of bound polyphenols are also provided and comprehensively discussed

Photoionization from the ground and excited vibrational states of H+2 and its deuterated isotopologues

Photoionization cross sections and rate coefficients have been calculated for all bound vibrational levels of the 1s$\sigma_{\mathrm{g}}$ state of H$_{2}^{+}$, HD$^{+}$, and D$_{2}^{+}$. The Born-Oppenheimer approximation is employed in our calculation of vibrationally-resolved photoionization cross sections. Vibrationally-resolved and local thermal equilibrium photoionization rate coefficients are presented for photon temperatures less than $50\,000$ K and are found to be several orders of magnitude larger than previous results in the literature. Analytic fits for the vibrationally-resolved and local thermal equilibrium photoionization rate coefficients are provided. Near threshold oscillations in the vibrationall-resolved photoionization are observed. A benchmark set of photoionization cross sections are presented. Fixed-nuclei photoionization cross sections are calculated using two-center true continuum wave functions and are verified by comparison with previous calculations and are found to be in excellent agreement in all cases. Data files for our set of benchmark cross sections, rate coefficients, and fitting parameters for H$_{2}^{+}$, HD$^{+}$, and D$_{2}^{+}$ are available on Zenodo under an open-source Creative Commons Attribution license: https://doi.org/10.5281/zenodo.8304060 .Comment: Accepted in ApJ

Regulation of Intracellular Calcium Concentration by Nanosecond Pulsed Electric Fields

Changes in [Ca2+]i response of individual Jurkat cells to nanosecond pulsed electric fields (nsPEFs) of 60 ns and field strengths of 25, 50, and 100 kV/cm were investigated. The magnitude of the nsPEF-induced rise in [Ca2+]i was dependent on the electric field strength. With 25 and 50 kV/cm, the [Ca2+]i response was due to the release of Ca2+ from intracellular stores and occurred in less than 18 ms. With 100 kV/cm, the increase in [Ca2+]i was due to both internal release and to influx across the plasma membrane. Spontaneous changes in [Ca2+]i exhibited a more gradual increase over several seconds. The initial, pulse-induced [Ca2+]i response initiates at the poles of the cell with respect to electrode placement and co-localizes with the endoplasmic reticulum. The results suggest that nsPEFs target both the plasma membrane and subcellular membranes and that one of the mechanisms for Ca2+ release may be due to nanopore formation in the endoplasmic reticulum

Benchmark Calculations of Electron Impact Electronic Excitation of the Hydrogen Molecule

We present benchmark integrated and differential cross-sections for electron collisions with H$_2$ using two different theoretical approaches, namely, the R-matrix and molecular convergent close-coupling (MCCC). This is similar to comparative studies conducted on electron-atom collisions for H, He and Mg. Electron impact excitation to the $b \ ^3\Sigma_u^+$, $a \ ^3\Sigma_g^+$, $B \ ^1\Sigma_u^+$,$c \ ^3\Pi_u$,$EF \ ^1\Sigma_g^+$,$C \ ^1\Pi_u$,$e \ ^3\Sigma_u^+$,$h \ ^3\Sigma_g^+$,$B' \ ^1\Sigma_u^+$and$d \ ^3\Pi_u$excited electronic states are considered. Calculations are presented in both the fixed nuclei and adiabatic nuclei approximations, where the latter is shown only for the$b \ ^3\Sigma_u^+$ state. Good agreement is found for all transitions presented. Where available, we compare with existing experimental and recommended data.Comment: 21 pages, 25 figure

Synthesis and Cytotoxicity of Cyanoborane Adducts of N 6 -Benzoyladenine and 6-Triphenylphosphonylpurine

N 6 -Benzoyladenine-cyanoborane (2), and 6-triphenylphosphonylpurine-cyanoborane (3) were selected for investigation of cytotoxicity in murine and human tumor cell lines, effects on human HL-60 leukemic metabolism and DNA strand scission to determine the feasibility of these compounds as clinical antineoplastic agents. Compounds 2 and 3 both showed effective cytotoxicity based on ED50 values less than 4 μg/ml for L1210, P388, HL-60, Tmolt3, HUT-78, HeLa-S3 uterine, ileum HCT-8, and liver Hepe-2. Compound 2 had activity against ovary 1-A9, while compound 3 was only active against prostate PL and glioma UM. Neither compound was active against the growth of lung 549, breast MCF-7, osteosarcoma HSO, melanoma SK2, KB nasopharynx, and THP-1 acute monocytic leukemia. In mode of action studies in human leukemia HL-60 cells, both compounds demonstrated inhibition of DNA and protein syntheses after 60 min at 100 μM. These compounds inhibited RNA synthesis to a lesser extent. The utilization of the DNA template was suppressed by the compounds as determined by inhibition of the activities of DNA polymerase α, m-RNA polymerase, r-RNA polymerase and t-RNA polymerase, which would cause adequate inhibition of the synthesis of both DNA and RNA. Both compounds markedly inhibited dihydrofolate reductase activity, especially in compound 2. The compounds appeared to have caused cross-linking of the DNA strands after 24 hr at 100 μM in HL-60 cells, which was consistent with the observed increased in ct-DNA viscosity after 24 hr at 100 μM. The compounds had no inhibitory effects on DNA topoisomerase I and II activities or DNA-protein linked breaks. Neither compound interacted with the DNA molecule itself through alkylation of the nucleotide bases nor caused DNA interculation between base pairs. Overall, these antineoplastic agents caused reduction of DNA and protein replication, which would lead to killing of cancer cells