Cure kinetics of composites using video imaging

PURPOSE: To study the rate of curing, three composites, Heliomolar (Vivadent), Z100 (3M), and Renew (Bisco) were investigated METHODS: Volumetric shrinkage was measured at 25 degrees C using the Acuvol with an RG610 red filter. The dynamic measurements were made in the single view mode. RESULTS: Detailed kinetic studies for Renew determined the effect of varying the light intensity (100mW - 500mW) and irradiation time (3 seconds - 30 seconds) on the rate of curing. A measurement of the gel time of composites and a kinetic constant is reported. ANOVA followed by a Fisher's LSD test and a Kruskall-Wallis test were used for analysis of the data. The gel times follow the order of Heliomolar > Renew > Z100 at 20 seconds and 500 mW. Irradiation time had no significant effect on the gel time of Renew. Light intensity had a significant effect on the gel time of Renew.     

Breast conserving surgery versus mastectomy: the influence of comorbidities on choice of surgical operation in the Department of Defense health care system

Background

Studies on the effect of comorbidities on breast cancer operation have been limited and inconsistent. This study investigated whether pre-existing comorbidities influenced breast cancer surgical operation in an equal access health care system.

Methods

This study was based on linked Department of Defense cancer registry and medical claims data. The study subjects were patients diagnosed with stage I to III breast cancer during 2001 to 2007. Logistic regression was used to determine if comorbidity was associated with operation type and time between diagnosis and operation.

Results

Breast cancer patients with comorbidities were more likely to receive mastectomy (odds ratio [OR] = 1.27; 95% confidence interval [CI], 1.14 to 1.42) than breast conserving surgery plus radiation. Patients with comorbidities were also more likely to delay having operation than those without comorbidities (OR = 1.27; 95% CI, 1.14 to 1.41).

Conclusions

In an equal access health care system, comorbidity was associated with having a mastectomy and with a delay in undergoing operation.     

CD4 T cell control primary measles virus infection of the CNS: regulation is dependent on combined activity with either CD8 T cells or with B cells: CD4, CD8 or B cells alone are ineffective

Measles virus (MV), one of the most infectious of human pathogens, still infects over 30 million humans and causes over 500,000 deaths each year [Griffin, D., 2001. Measles virus. In: Fields, B., Knipe, D., Howley, P. (Eds.), Fields Virology. Lippincott-Raven, Philadelphia, pp. 1401-1442; ]. Death is primarily due to secondary microbial infections associated with the immunosuppression caused by MV. Studies of humans with genetic or acquired deficiencies of either the humoral or cellular arm of the immune system, and rodent models have implicated T cells in the control of the ongoing MV infection but the precise role and activities of the specific T cell subset or the molecules they produce is not clear. Using a transgenic mouse model in conjunction with depletion and reconstitution of individual B and T cell subsets alone or in combination, we show that neither CD4, CD8 nor B cells per se control acute MV infection. However, combinations of either CD4 T cells and B cells, or of CD4 and CD8 T cells are essential but CD8 T with B cells are ineffective. Interferon-gamma and neutralizing antibodies, but neither perforin nor TNF-alpha alone are associated with clearance of MV infection. TNF-alpha combined with interferon-gamma is more effective in protection than interferon alone. Further, the lack of an interferon-gamma response leads to persistence of MV.     

Molecular analysis of WFDC1/ps20 gene in prostate cancer

BACKGROUND: WFDC1/ps20 protein has been previously established as a growth suppressor of the prostate cancer cell line PC3. It maps to chromosome 16q23.1, a region of frequent loss of heterozygosity, familial association, and genomic loss in prostate cancer. We, therefore, chose to examine WFDC1/ps20 for mutations and expression changes in prostate cancer. METHODS: DNA from 21 prostate cancer patients and 5 prostate cancer cell lines was screened for mutations in the WFDC1/ps20 gene by sequencing PCR products of each exon. An SphI polymorphism in the 5' UTR was screened in 23 tumors, 22 normal adjacent prostate tissue samples, and 35 control DNAs. Expression of WFDC1/ps20 in different tissue types was examined by Northern blot and by PCR across a multi-tissue cDNA panel. Expression patterns of WFDC1/ps20 in primary tumors were examined by full-length RT-PCR and products were cloned and sequenced to identify novel splice forms. Quantitative RT-PCR analysis of WFDC1/ps20 was performed in a separate cohort of matched tumor/benign tissues. RESULTS: No tumor-associated mutations were identified in the coding region of WFDC1/ps20. A novel polymorphism was found in exon 6 in DNA from cell lines, tumors, and normal adjacent benign tissue. A novel splice form completely deleted for exon 3 was found in tumor and normal prostate RNA. Quantitative RT-PCR demonstrated significant down regulation of WFDC1/ps20 in prostate tumors. Subdivision of normal tissue into stromal and epithelial compartments showed that WFDC1/ps20 expression correlates exponentially with the amount of stroma present. CONCLUSIONS: WFDC1/ps20 is down regulated but not frequently mutated in prostate cancer. It is expressed predominantly in the normal stroma of the prostate. We, therefore, propose that WFDC1/ps20 may not be a classical tumor suppressor gene, but might play a role in the maintenance of the normal extra cellular matrix milieu in the prostate.     

Race-ing Time: Clinical Temporalities and Inequality in Public Prenatal Care

ABSTRACT

Analysis of clinical temporalities, or the social organization of time in the clinic, offers insights into how racism coheres in pregnant bodies and institutions, with implications for health care experiences for patients and providers. Based on research at a public prenatal clinic, I argue that long patient wait-times and pressure on providers to speed up are temporal instantiations of the same racist structures that shape public health care in the US. Through these temporal experiences, racialized patient populations and staff who work in racialized systems of public health care encounter the lesser value assigned to their time, bodies, and labor.     

Targeting pain catastrophization in patients with fibromyalgia using virtual reality exposure therapy: a proof-of-concept study

[Purpose] Pain catastrophizing is a key predictor of poor compliance to exercises among patients with fibromyalgia syndrome. Alteration of pain catastrophizing in this group is thus warranted. This study aimed to provide proof-of-concept of a novel virtual reality exposure therapy program as treatment for exercise-related pain catastrophizing in patients with fibromyalgia syndrome. [Subjects and Methods] An exploratory, case-controlled study was conducted (fibromyalgia syndrome group and matched control group). Functional magnetic resonance imaging was used to acquire neural correlates. The functional magnetic resonance imaging task consisted of two stimuli: active (exercise activity visuals) and passive (relaxing visuals). Structural images and blood-oxygenation-level-dependent contrasts were acquired for the conditions and compared within subjects/groups and between groups. Statistic images were thresholded using corrected clusters (determined by Z>2.3; level of significance: 0.05). [Results] Thirteen fibromyalgia syndrome subjects and nine healthy matched controls were included. The right inferior frontal gyrus, right middle frontal gyrus, right posterior cerebellum, left thalamus, and left supramarginal gyrus were activated in the fibromyalgia syndrome subjects. [Conclusion] The study results provide preliminary proof indicating that exposing patients with fibromyalgia syndrome to visuals of exercises elicits neurophysiological changes in functional brain areas associated with pain catastrophization and add to the current body of knowledge regarding the possibility of objectively identifying cognitive behavioral strategies like pain catastrophization.Key words: Fibromyalgia, Pain catastrophizing, Exercise     

Genetic variation in PRL and PRLR, and relationships with serum prolactin levels and breast cancer risk: results from a population-based case-control study in Poland

Introduction

Studies suggest that high circulating levels of prolactin increase breast cancer risk. It is unclear if genetic variations in prolactin (PRL) or prolactin receptor (PRLR) genes also play a role. Thus, we examined the relationship between single nucleotide polymorphisms (SNPs) in PRL and PRLR, serum prolactin levels and breast cancer risk in a population-based case-control study.

Methods

We genotyped 8 PRL and 20 PRLR tag SNPs in 1965 breast cancer cases and 2229 matched controls, aged 20-74, and living in Warsaw or Łódź, Poland. Serum prolactin levels were measured by immunoassay in a subset of 773 controls. Odds ratios (ORs) and 95% confidence intervals (CIs) for genotype associations with breast cancer risk were estimated using unconditional logistic regression, adjusted for age and study site. Geometric mean prolactin levels were estimated using linear regression models adjusted for age, study site, blood collection time, and menstrual cycle day (premenopausal women).

Results

Three SNPs were associated with breast cancer risk: in premenopausal women, PRLR rs249537 (T vs. C per-allele OR 1.39, 95% CI 1.07 - 1.80, P = 0.01); and in postmenopausal women, PRLR rs7718468 (C vs. T per-allele OR 1.16, 95% CI 1.03 - 1.30, P = 0.01) and PRLR rs13436213 (A vs. G per-allele OR 1.13 95% CI 1.01 - 1.26, P = 0.04). However, mean serum prolactin levels for these SNPs did not vary by genotype (P-trend > 0.05). Other SNPs were associated with serum prolactin levels: PRLR rs62355518 (P-trend = 0.01), PRLR rs10941235 (P-trend = 0.01), PRLR rs1610218 (P-trend = 0.01), PRLR rs34024951 (P-trend = 0.02), and PRLR rs9292575 (P-trend = 0.03) in premenopausal controls and PRL rs849872 (P-trend = 0.01) in postmenopausal controls.

Conclusions

Our data provide limited support for an association between common variations in PRLR and breast cancer risk. Altered serum prolactin levels were not associated with breast cancer risk-associated variants, suggesting that common genetic variation is not a strong predictor of prolactin-associated breast cancer risk in this population.