U.S. cancer mortality data derived from information recorded on death certificates are frequently relied upon as an indicator of progress against cancer. A limitation of this measure is the lack of information pertaining to the onset of disease, such as year-of-diagnosis, age-at-diagnosis, stage of disease at diagnosis and histology of lesions. However, population-based cancer registries collect these types of data and allow the calculation of an incidence-file based mortality rate. This incidence-based mortality rate allows a partitioning of mortality by variables associated with the cancer onset. Breast cancer incidence-based mortality measures are created and compared to mortality rates based on death certificates over a comparable time period. Novel mortality measures, such as mortality rates by stage-at-diagnosis, age-at-diagnosis and year-of-diagnosis, are used to illustrate the value of this approach. 相似文献
Background: It is not known whether epidural epinephrine has an analgesic effect per se. The segmental distribution of clonidine epidural analgesia and its effects on temporal summation and different types of noxious stimuli are unknown. The aim of this study was to clarify these issues.
Methods: Fifteen healthy volunteers received epidurally (L2-L3 or L3-L4) 20 ml of either epinephrine, 100 micro gram, in saline; clonidine, 8 micro gram/kg, in saline; or saline, 0.9%, alone, on three different days in a randomized, double-blind, cross-over fashion. Pain rating after electrical stimulation, pinprick, and cold perception were recorded on the dermatomes S1, L4, L1, T9, T6, T1, and forehead. Pressure pain tolerance threshold was recorded at S1, T6, and ear. Pain thresholds to single and repeated (temporal summation) electrical stimulation of the sural nerve were determined.
Results: Epinephrine significantly reduced sensitivity to pinprick at L1-L4-S1. Clonidine significantly decreased pain rating after electrical stimulation at L1-L4 and sensitivity to pinprick and cold at L1-L4-S1, increased pressure pain tolerance threshold at S1, and increased thresholds after single and repeated stimulation of the sural nerve. 相似文献
The purpose of this study was to evaluate the ability of MRI to identify a primary site of malignancy in the breast of patients who present clinically with ipsilateral lymph nodes containing metastatic carcinoma but whose physical and mammographic examination are negative. MRI of the breast was performed on four patients using a variety of imaging parameters, all with and without gadolinium contrast. All patients had biopsy-proven adenocarcinoma of the ipsilateral axilla, with negative physical and mammographic examinations. Foci of enhancement assessed visually on precontrast and postcontrast scans (n = 1) and on substraction studies (n = 3) were considered suspicious under the clinical circumstances defined for this study. Lesions identified on MRI were re-identified on ultrasound examination and either preoperative localization for excisional biopsy or tissue sampling was performed. Surgery was performed and histopathologic correlation was obtained in all cases. Primary sites of breast carcinoma were identified in all four patients, with multiple sites of malignancy identified in three of four patients. Breast conservation therapy was made possible for three of four patients based on the results of the MRI study showing sites of malignancy and no features of cancer elsewhere in the breast. Follow-up data of 1, 2, and 5 years of these patients show no evidence of recurrent disease. MRI of the breast is a useful technique for identifying primary sites of malignancy in patients presenting with ipsilateral lymph nodes positive for metastatic adenocarcinoma when the physical and mammographic examinations are negative. 相似文献
SUMMARY Elevated plasma levels of Lp(a) do seem to influence the progression of atherosclerosis. Evidence is emerging that certain apo(a) isoforms may be more atherogenic than others, and in transgenic mice free apo(a) has been shown to be associated with accelerated atherosclerosis. Currently it is not known whether treating elevated Lp(a) levels will reduce progression of atherosclerosis and, as therapeutic options are limited, mass screening of Lp(a) levels in populations is not indicated. The presence of raised Lp(a) levels, however, warrants aggressive treatment to reduce other cardiovascular risk factors. Continuing research to investigate the relationship of the apo(a) gene to other genes, including the plasminogen gene and apo(a)-related genes, will add further information pertaining to the evolution, function, regulation and clinical implications of Lp(a). 相似文献