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Biomedical subjects

P Carroll

Publications and source records attributed to P Carroll.

At least 37 records · Page 2Linked to original sources
PubMed2001

Spectroscopy in prostate cancer: hope or hype?

Clinical applications of image-based radiation therapy for the study of prostate cancer have expanded significantly over the past years. The results of recent studies of magnetic resonance imaging (MRI) combined with magnetic resonance spectroscopic imaging (MRSI) demonstrate that the MRI/MRSI exam is a unique method by which to noninvasively study the cellular metabolism and anatomy of the prostate. This technology has the potential to define the tumor volume through functional or metabolic imaging. The results of current MRI/ MRSI studies also provide evidence that the magnitude of metabolic changes in regions of cancer before therapy, as well as the extent of the time course of metabolic changes after therapy, may improve our understanding of cancer aggressiveness. Assessment of cancer spread outside the prostate can be significantly improved by combining MRI findings with estimates of metabolic abnormalities provided by MRSI. Clinically, combined MRI/MRSI has already demonstrated a potential for improved diagnosis, staging, and treatment planning for patients with prostate cancer. Additional studies will reveal both the positive aspects and clinical challenges of MRI/

Biopsy↗
PubMed2000

A single nucleotide polymorphism in the E-cadherin gene promoter alters transcriptional activities.

E-cadherin plays a critical role in many aspects of cell adhesion, epithelial development, and the establishment and maintenance of epithelial polarity. The loss of the adhesive function of E-cadherin is a critical step in the promotion of epithelial cells to a more malignant phenotype. We identified a C/A single nucleotide polymorphism at -160 from the transcriptional start site of the E-cadherin gene promoter. Transient transfection experiments showed that the A allele of this polymorphism decreased the transcriptional efficiency by 68% compared with the C allele (P<0.001). Electrophoretic mobility shift and footprinting assays revealed that the C allele had a stronger transcriptional factor binding strength than the A allele. These results indicate that the -160 C/A polymorphism has a direct effect on E-cadherin gene transcriptional regulation. This allelic variation may be a potential genetic marker that can help identify those individuals at higher risk for invasive/metastatic diseases.

Alleles↗
PubMed2000

Metastatic microcystic adnexal carcinoma in an immunocompromised patient.

BACKGROUND: Microcystic adnexal carcinoma is an uncommon, locally aggressive cutaneous neoplasm. To date, there are only two reports of histologically proven lymph node involvement with this tumor. We describe a case of a patient with microcystic adnexal carcinoma who developed multiple local metastasis in transit with histologically proven lymph node involvement and was diagnosed with chronic lymphocytic leukemia. OBJECTIVE: To describe the details of our case and to review what is currently known about this tumor. METHODS: Mohs micrographic surgery was utilized for tumor removal. RESULTS: This patient developed multiple tumors of the scalp over the period of a 1 year which were histologically proven to be microcystic adnexal carcinoma. All tumors were noncontiguous and presented on the scalp. During the histologic analysis of the last tumor removed by Mohs micrographic surgery a lymph node was resected which revealed infiltrative microcystic adnexal carcinoma. CONCLUSIONS: We present the case of an immunocompromised patient treated for microcystic adnexal carcinoma with Mohs micrographic surgery who proceeded to develop local metastasis in transit.

Aged↗
PubMed2000

Deletion of Y-chromosome specific genes in human prostate cancer.

PURPOSE: The present study is based on the hypothesis that deletion of Y-chromosome-specific genes is associated with prostate cancer. To test this hypothesis, we analyzed the deletion of six Y-chromosome-specific genes in prostate cancer samples. MATERIALS AND METHODS: Fifty human prostate cancer specimens were processed for microdissection of pure epithelial cells. DNA was extracted from these cells and amplified using PCR and analyzed for loss of six different Y-chromosome-specific genes (SRY, ZFY, BPY1, SMCY, RBM1 and BPY2). We used D8S262 primer (chromosome 8p23) for internal control to assess the quality and loading of DNA for each sample. RESULTS: Deletion was observed in most of the prostate cancer specimens with at least one Y-chromosome-specific gene. The loss of SRY gene (Yp11.32) was shown in 38% of cases whereas the other genes show 18% loss in ZFY (Yp11.31), 14% in BPY1 (Yq11.2), 52% in SMCY (Yq11.22), 32% in RBM1 (Yq11.23) and 42% in BPY2 (Yq12.1). The loss of most genes analyzed is seen more frequent in advanced stages and grades of prostate cancer. CONCLUSION: There was a significant loss of Y-chromosome-specific genes in prostate cancer. The loss of SRY and BPY2 genes was more frequent in higher stages and grades of prostate cancer. This is the first report to demonstrate that the loss of Y-chromosome-specific genes is associated with prostate cancer, suggesting their role in pathogenesis of this disease.

Chromosome Mapping↗
PubMed2000

Frequent genotype changes at -308, and 488 regions of the tumor necrosis factor-alpha (TNF-alpha) gene in patients with prostate cancer.

PURPOSE: Tumor necrosis factor-alpha (TNF-alpha) is involved in oncogenesis of several cancers. The purpose of this study was to investigate whether genotype changes of TNF-alpha promoter regions (-238, -308) and at the 488 region are associated with human prostate cancer. MATERIALS AND METHODS: The DNA from 73 cases of human prostate cancer was analyzed by allele-specific polymerase chain reaction to characterize the genotype changes of three regions of the TNF-alpha gene in prostate cancer patients. We also determined the genotype frequency in these patients. The relative risk of variant genotype was calculated by comparing with our previous data from healthy controls. RESULTS: Genetic changes were detected in 15.1% (11/73) of prostate cancer samples at 488 region of TNF-alpha. Seventy-three percent (53/73) of the patients showed genotype GA at -308 region of TNF-alpha. Genotype GA at 488 region in TNF-alpha was observed in 73% (53/73) of the cancer and 71% (52/73) of the normal tissue. The relative risks of incidence for prostate cancer was 14-fold higher in people with genotype GA at -308 region of TNF-alpha. The relative incidence for prostate cancer was a 17-fold higher in-patient with genotype GA at 488 region of TNF-alpha. Genotype GA at -308 of TNF-alpha was related to higher clinical tumor stage of prostate cancer than genotype G (p <0.05). CONCLUSIONS: The present study demonstrates, for the first time, that the genotype changes in -308 and 488 regions of TNF-alpha are associated with prostate cancer.

Alleles↗
PubMed2000

Pretreatment prostate-specific antigen and Gleason score predict the risk of extracapsular extension and the risk of failure following radiotherapy in patients with clinically localized prostate cancer.

The purpose of this study is to evaluate the use of a relatively simple equation for predicting the risk of extracapsular extension (ECE) based on the pretreatment prostate-specific antigen (PSA) and Gleason score (GS) in patients with clinically localized prostate cancer. Three hundred and seventy-four patients who underwent radical prostatectomy between 1988 and 1994 and 521 men undergoing definitive radiotherapy during a similar time period were eligible for this analysis. Surgically treated patients were considered eligible if the pathological stage, preoperative PSA, and GS were available. Among these patients, the median preoperative PSA was 8.1 ng/mL (range, 0 to 195 ng/mL), and the median preoperative GS was 6 (range, 2 to 10). The empirically derived equation tested was (1.5 x PSA + [GS - 3] x 10). For this equation, the range of calculated risk was limited to 0% to 100%. Using the empirically derived equation, patients with a low calculated risk (CR) of < or = 33% had an average calculated risk (ACR) of 21.9% and an observed incidence (OI) of ECE was 17.8%. Patients with a moderate CR of 34% to 66% had an ACR of 46.3%, and an OI of ECE was 46.7%. Patients with a CR of 67% to 100% had an ACR of 83.7% and an OI of ECE of 66.7%. Of the 21 patients who had a PSA < or = 4 and a GS < or = 4, only 1 patient (4.8%) was found to have ECE. Men with an estimated risk of ECE of <33%, 33% to 67%, and >67% had a 4-year risk of biochemical failure following radiotherapy of 29%, 56%, and 78% (P < .00001). This empirically derived data appears to be reasonably accurate at estimating the incidence of ECE in patients with at low or intermediate risk before surgery. The risk of biochemical failure following radiotherapy also correlated the risk of ECE. Future staging systems for prostate cancer should use similar approach for defining risk groups.

Biopsy↗
PubMed2000

Exploring chest drain options.

The variety of chest drainage systems now available makes it more important than ever for nurses to understand what's out there and how these systems work. Nurses are responsible for managing chest drains and need to know which drain is best suited for which situation.

Chest Tubes↗
PubMed1999

Repetitive firing deficits and reduced sodium current density in retinal ganglion cells developing in the absence of BDNF.

Previous work by Cellerino et al. has shown that chronic absence of brain-derived neurotrophic factor (BDNF) resulted in hypomyelination of the optic nerve. Since myelination is influenced by neuronal activity, it is possible that a deficiency in BDNF during early development could alter the firing properties of retinal neurons. To test this hypothesis, patch-clamp recordings were performed in retinal whole mounts from BDNF-deficient (bdnf-/-), heterozygote (bdnf+/-) or wild-type control mice (bdnf+/+). Ganglion cell layer neurons (RGNs) were tested at different age [postnatal day (P)1-11] for their ability to encode graded depolarization with variable action potential frequency. At all developmental ages examined, RGNs exhibiting frequency coding were less frequently encountered in bdnf-/- than in bdnf+/+ mice. At P1, none of the RGNs from bdnf-/- mice displayed repetitive firing compared to 50% in bdnf+/+ mice, and by P7-11, only 50% of bdnf-/- RGNs exhibited repetitive firing compared to 100% in bdnf+/+ mice. Moreover, in bdnf-/- RGNs repetitive discharge was characterized by a reduced frequency increment per current change. Acquisition of repetitive firing was paralleled by a decrease in input resistance and a steep increase of sodium current density. In bdnf-/- mice, the onset of this increase occurred at later stages of development than in wild-type controls (bdnf-/-: P6-11; bdnf+/+: P2-6). The discharge pattern of P7-11 bdnf-/- RGNs resembled that of RGNs in neonatal wild-type mice and was mimicked by acute application of a Ca(2+) channel blocker. We conclude that BDNF plays an important role in the ontogeny of repetitive firing of RGNs.

Animals↗
PubMed1999

A changing pattern of brain-derived neurotrophic factor expression correlates with the rearrangement of fibers during cochlear development of rats and mice.

The reorganization of specific neuronal connections is a typical feature of the developing nervous system. It is assumed that the refinement of connections in sensory systems requires spontaneous activity before the onset of cochlear function and selective sensory experience during the ensuing period. The mechanism of refinement through sensory experience is currently postulated as being based on the selective reinforcement of active projections by neurotrophins. We studied a presumed role of neurotrophins for rearrangement of afferent and efferent fibers before the onset of sensory function in the precisely innervated auditory end organ, the cochlea. We observed a spatiotemporal change in the localization of brain-derived neurotrophic factor (BDNF) protein and mRNA, which correlated with the reorganization of fibers. Thus, BDNF decreased in target hair cells during fiber retraction and was subsequently upregulated in neurons, target hair cells, and adjacent supporting cells concomitant with the formation of new synaptic contacts. Analysis of the innervation pattern in BDNF gene-deleted mice by immunohistochemistry and confocal microscopy revealed a failure in the rearrangement of fibers and a BDNF dependency of distinct neuronal projections that reorganize in control animals. Our data suggest that, before the onset of auditory function, a spatiotemporal change in BDNF expression in sensory, epithelial, and neuronal cells may guide the initial steps of refinement of the innervation pattern.

Afferent Pathways↗
PubMed1999

Stomatin, a MEC-2 like protein, is expressed by mammalian sensory neurons.

The molecular mechanism whereby vertebrate primary sensory neurons convert mechanical energy at their receptive fields into action potentials is unknown. In recent years, genetic screens for touch insensitive mutants of the nematode worm Caenorhabditis elegans have led to the identification of several genes required for mechanical sensitivity. A model has been proposed in which a mechanically gated ion channel is connected both to the extracellular matrix and to the cytoskeleton. Displacement of the membrane is proposed to produce a shearing force that pulls the channel open. MEC-2 is thought to play an important role in this complex by linking the ion channel to the cytoskeleton. MEC-2 is highly homologous to a vertebrate protein called stomatin. Stomatin was first isolated from erythrocytes where it is a major integral membrane protein. To date, however, no data on neuronal expression of stomatin in the peripheral nervous system (PNS) or central nervous system (CNS) is available. Here, we have used RT-PCR, in situ hybridization, Northern blotting, and immunocytochemistry to demonstrate that stomatin is expressed by all sensory neurons in mouse dorsal root ganglia. Indirect immunofluorescence together with transfection of cultured adult sensory neurons with epitope-tagged stomatin show that stomatin is localized in spots on somatic and axonal membranes. During development, stomatin begins to be expressed by sensory neurons only as target innervation occurs. The onset of expression of stomatin thus coincides with the onset of functional mechanical sensitivity. Together, our data suggest that stomatin, like the C. elegans MEC-2 gene, is expressed in an appropriate temporal and spatial manner to participate in a putative vertebrate mechanotransduction complex.

Animals↗
PubMed1999

The role of body dissatisfaction and bingeing in the self-esteem of women with type II diabetes.

This study investigated the impact of body dissatisfaction and binge eating on self-esteem in women with Type II diabetes. The relationship of body dissatisfaction and bingeing to perceived blood glucose control was also assessed. Questionnaires were completed by a total of 215 women: 125 women with Type II diabetes and 90 comparison women, who were roughly matched for age, education, and ethnicity. When actual weight (BMI) was statistically controlled, there was no difference between the groups in body dissatisfaction or bingeing behavior. The women with diabetes, however, had significantly lower self-esteem. Further, bingeing made a significant contribution to their self-esteem, in contrast to the women without diabetes. For the women with diabetes, body dissatisfaction and bingeing were also related to perceived blood glucose control, although only bingeing remained significant when both variables were entered into the regression equation. It was concluded that diabetes broadens the domains of body dissatisfaction which are related to self-esteem.

Adult↗