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CONTEXT: Despite advances in early detection and prevention of cervical cancer, women living in rural areas, and particularly in Appalachia, the rural South, the Texas/Mexico border, and the central valley of California, have had consistently higher rates of cervical cancer mortality than their counterparts in other areas during the past several decades. METHODS: This paper reviews the published literature from 1966 to July 2002 to assess three potential pathways underlying this excess mortality--high human papilloma virus (HPV) prevalence, lack of or infrequent screening and advanced disease at diagnosis, and under-use of recommended treatment and shorter survival. FINDINGS: Living in rural areas may impose barriers to cervical cancer control, including lack of transportation and medical care infrastructures. Population characteristics that place women at greater risk for developing and dying from cervical cancer, such as low income, lack of health insurance, and physician availability, are concentrated in rural areas. Published data, however, are insufficient to identify the key reasons for the observed mortality patterns. CONCLUSIONS: At this time, given the lack of definitive evidence in the published literature, decisions about priorities in areas with high rates of cervical cancer mortality will depend on knowledge of current levels of screening, incidence, and stage distribution; and service delivery infrastructures, resources, and acceptability of interventions to the target population.  相似文献   
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Background

Several methods have been developed to determine a person’s physical activity level. However, there is limited evidence in determining whether someone is physically active or not. This study aims to determine the level of physical activity and to compare the usage of short version International Physical Activity Questionnaire (IPAQ-SF) and pedometer among overweight and obese women who were involved in the My Body is Fit and Fabulous at home (MyBFF@home) study.

Methods

Baseline and sixth month data from the MyBFF@home study were used for this purpose. A total of 169 of overweight and obese respondents answered the IPAQ-SF and were asked to use a pedometer for 7 days. Data from IPAQ-SF were categorised as inactive and active while data from pedometer were categorised as insufficiently active and sufficiently active by standard classification. Data on sociodemographic and anthropometry were also obtained. Cohen’s kappa was applied to measure the agreement of IPAQ-SF and pedometer in determining the physical activity level. Pre-post cross tabulation table was created to evaluate the changes in physical activity over 6 months.

Results

From 169 available respondents, 167 (98.8%) completed the IPAQ-SF and 107 (63.3%) utilised the pedometer. A total of 102 (61.1%) respondents were categorised as active from the IPAQ-SF. Meanwhile, only 9 (8.4%) respondents were categorised as sufficiently active via pedometer. Cohen’s κ found there was a poor agreement between the two methods, κ?=?0.055, p?>?0.05. After sixth months, there was +?9.4% increment in respondents who were active when assessed by IPAQ-SF but ??1.3% reductions for respondents being sufficiently active when assessed by pedometer. McNemar’s test determined that there was no significant difference in the proportion of inactive and active respondents by IPAQ-SF or sufficiently active and insufficiently active by pedometer from the baseline and sixth month of intervention.

Conclusion

The IPAQ-SF and pedometer were both able to measure physical activity. However, poor agreement between these two methods were observed among overweight and obese women.
  相似文献   
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Patients with aneurysmal subarachnoid hemorrhage (SAH) frequently have deficits in learning and memory that may or may not be associated with detectable brain lesions. We examined mediators of long-term potentiation after SAH in rats to determine what processes might be involved. There was a reduction in synapses in the dendritic layer of the CA1 region on transmission electron microscopy as well as reduced colocalization of microtubule-associated protein 2 (MAP2) and synaptophysin. Immunohistochemistry showed reduced staining for GluR1 and calmodulin kinase 2 and increased staining for GluR2. Myelin basic protein staining was decreased as well. There was no detectable neuronal injury by Fluoro-Jade B, TUNEL, or activated caspase-3 staining. Vasospasm of the large arteries of the circle of Willis was mild to moderate in severity. Nitric oxide was increased and superoxide anion radical was decreased in hippocampal tissue. Cerebral blood flow, measured by magnetic resonance imaging, and cerebral glucose metabolism, measured by positron emission tomography, were no different in SAH compared with control groups. The results suggest that the etiology of loss of LTP after SAH is not cerebral ischemia but may be mediated by effects of subarachnoid blood such as oxidative stress and inflammation.  相似文献   
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