Evaluation of the SCA instrument for measuring patient satisfaction with cancer care administered via paper or via the Internet.

BACKGROUND: Patients' perspectives provide valuable information on quality of care. This study evaluates the feasibility and validity of Internet administration of Service Satisfaction Scale for Cancer Care (SCA) to assess patient satisfaction with outcome, practitioner manner/skill, information, and waiting/access. PATIENTS AND METHODS: Primary data collected from November 2007 to April 2008. Patients receiving cancer care within 1 year were recruited from oncology, surgery, and radiation clinics at a tertiary care hospital. An Internet-based version of the 16-item SCA was developed. Participants were randomised to Internet SCA followed by paper SCA 2 weeks later or vice versa. Seven-point Likert scale responses were converted to a 0-100 scale (minimum-maximum satisfaction). Response distribution, Cronbach's alpha, and test-retest correlations were calculated. RESULTS: Among 122 consenting participants, 78 responded to initial SCA. Mean satisfaction scores for paper/Internet were 91/90 (outcome), 95/94 (practitioner manner/skill), 89/90 (information), and 86/86 (waiting/access). Response rate and item missingness were similar for Internet and paper. Except for practitioner manner/skill, test-retest correlations were robust r = 0.77 (outcome), 0.74 (information), and 0.75 (waiting/access) (all P < 0.001). CONCLUSIONS: Internet SCA administration is a feasible and a valid measurement of cancer care satisfaction for a wide range of cancer diagnoses, treatment modalities, and clinic settings.

Mice with altered alpha-actinin-4 expression have distinct morphologic patterns of glomerular disease.

Mutations in ACTN4, encoding the actin-binding protein alpha-actinin-4, cause a form of familial focal segmental glomerulosclerosis. We had developed two strains of transgenic mice with distinct alterations in the expression of alpha-actinin-4. One strain carried a human disease-associated mutation in murine Actn4, whereas the other knockout strain did not express alpha-actinin-4 protein. Most adult homozygous Actn4 mutant and knockout mice developed collapsing glomerulopathy. Homozygous Actn4 mutant mice also exhibited actin and alpha-actinin-4-containing electron-dense cytoplasmic structures, that were present but less prominent in heterozygous Actn4 mutant mice and not consistently seen in wild-type or knockout mice. Heterozygous Actn4 mutant mice did not develop glomerulosclerosis, but did exhibit focal glomerular hypertrophy and mild glomerular ultrastructural changes. The ultrastructural abnormalities seen in heterozygous Actn4 mutant mice suggest low-level glomerular damage, which may increase susceptibility to injury caused by genetic or environmental stressors. Our studies show that different genetic defects in the same protein produce a spectrum of glomerular morphologic lesions depending on the specific combination of normal and/or defective alleles.

The glomerular filter: Biologic and genetic complexity.

The list of known genes that, when altered, cause proteinuric renal disease continues to increase. Recent mouse and human genetic studies, including that by Hasselbacher et al., are refocusing our attention on glomerular basement membrane components as critical to the barrier to protein filtration.

E2F4 is essential for normal erythrocyte maturation and neonatal viability.

The retinoblastoma protein (pRB) plays a key role in the control of normal development and proliferation through the regulation of the E2F transcription factors. We generated a mutant mouse model to assess the in vivo role of the predominant E2F family member, E2F4. Remarkably, loss of E2F4 had no detectable effect on either cell cycle arrest or proliferation. However, E2F4 was essential for normal development. E2f4-/- mice died of an increased susceptibility to opportunistic infections that appeared to result from craniofacial defects. They also displayed a variety of erythroid abnormalities that arose from a cell autonomous defect in late stage maturation. This suggests that E2F4 makes a major contribution to the control of erythrocyte development by the pRB tumor suppressor.

E2f3 is critical for normal cellular proliferation.

E2F is a family of transcription factors that regulate both cellular proliferation and differentiation. To establish the role of E2F3 in vivo, we generated an E2f3 mutant mouse strain. E2F3-deficient mice arise at one-quarter of the expected frequency, demonstrating that E2F3 is important for normal development. To determine the molecular consequences of E2F3 deficiency, we analyzed the properties of embryonic fibroblasts derived from E2f3 mutant mice. Mutation of E2f3 dramatically impairs the mitogen-induced, transcriptional activation of numerous E2F-responsive genes. We have been able to identify a number of genes, including B-myb, cyclin A, cdc2, cdc6, and DHFR, whose expression is dependent on the presence of E2F3 but not E2F1. We further show that a critical threshold level of one or more of the E2F3-regulated genes determines the timing of the G(1)/S transition, the rate of DNA synthesis, and thereby the rate of cellular proliferation. Finally, we show that E2F3 is not required for cellular immortalization but is rate limiting for the proliferation of the resulting tumor cell lines. We conclude that E2F3 is critical for the transcriptional activation of genes that control the rate of proliferation of both primary and tumor cells.