Citations

Abstract Vertebral fractures are more strongly associated with specific bone density, structure, and strength parameters than with areal BMD, but all of these variables are correlated. Introduction: It is unclear whether the association of areal BMD (aBMD) with vertebral fracture risk depends on bone density per se, bone macro- or microstructure, overall bone strength, or spine load/bone strength ratios. Materials and Methods: From an age-stratified sample of Rochester, MN, women, we identified 40 with a clinically diagnosed vertebral fracture (confirmed semiquantitatively) caused by moderate trauma (cases; mean age, 78.6 ± 9.0 yr) and compared them with 40 controls with no osteoporotic fracture (mean age, 70.9 ± 6.8 yr). Lumbar spine volumetric BMD (vBMD) and geometry were assessed by central QCT, whereas microstructure was evaluated by high-resolution pQCT at the ultradistal radius. Vertebral failure load (∼strength) was estimated from voxel-based finite element models, and the factor-of-risk (ϕ) was determined as the ratio of applied spine loads to failure load. Results: Spine loading (axial compressive force on L3) was similar in vertebral fracture cases and controls (e.g., for 90° forward flexion, 2639 versus 2706 N; age-adjusted p = 0.173). However, fracture cases had inferior values for most bone density and structure variables. Bone strength measures were also reduced, and the factor-of-risk was 35–37% greater (worse) among women with a vertebral fracture. By age-adjusted logistic regression, relative risks for the strongest fracture predictor in each of the five main variable categories were bone density (total lumbar spine vBMD: OR per SD change, 2.2; 95% CI, 1.1–4.3), bone geometry (vertebral apparent cortical thickness: OR, 2.1; 95% CI, 1.1–4.1), bone microstructure (none significant); bone strength (“cortical” [outer 2 mm] compressive strength: OR, 2.5; 95% CI, 1.3–4.8), and factor-of-risk (ϕ for 90° forward flexion/overall vertebral compressive strength: OR, 3.2; 95% CI, 1.4–7.5). These variables were correlated with spine aBMD (partial r, −0.32 to 0.75), but each was a stronger predictor of fracture in the logistic regression analyses. Conclusions: The association of aBMD with vertebral fracture risk is explained by its correlation with more specific bone density, structure, and strength parameters. These may allow deeper insights into fracture pathogenesis.

Mucins are the major glycoprotein component of respiratory tract secretions. Little is known about their expression in the upper respiratory tract. In order to define this expression, in situ hybridization was performed on 19 normal and 4 vasomotor rhinitis (VMR) inferior turbinates to identify mucin mRNA. MUC1, MUC2, MUC4, MUC5AC, MUC5B, and MUC7 were expressed in both the normal and VMR turbinates. MUC 4 and MUC5AC were the most highly expressed mucins. MUC1, MUC2, MUC4, and MUC5AC were expressed mainly by the epithelial border, whereas MUC5B and MUC7 were expressed by the submucosal glands. MUC1 and MUC4 exhibited a diffuse expression by multiple cell types along the mucosal border, whereas MUC2 and MUC5AC expression appeared to be limited to a subpopulation of epithelial cells, most likely goblet cells. Although MUC1, MUC4, and MUC5AC showed sporadic submucosal glandular expression, MUC5B and MUC7 appeared to be the predominant submucosal gland mucins in the inferior turbinates. MUC3 and MUC6 expression, which have been found primarily in the gastric mucosa, were not seen in any of the inferior turbinate samples examined. The only difference seen between normal and VMR turbinates was a slight decrease in MUC1 expression in the VMR group. The variety of mucins expressed and the diversity of their expression patterns may have significance in terms of the rheologic and particle clearance properties of nasal secretions. Understanding the expression patterns in normal turbinates will serve as the foundation for further study of these mucins in disease states.

Background and Purpose— Stroke symptoms in the absence of recognized stroke are common, but potential associated dysfunctions have not been described. Methods— We assessed quality-of-life measures using the Physical and Mental Component Summary scores of the Short Form 12 (PCS-12 and MCS-12) in the REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort. Differences in mean PCS-12 and MCS-12 scores were assessed among participant groups symptoms-free (n=16 090); history of stroke symptoms but free of stroke/transient ischemic attack (n=3404); history of stroke (n=1491); and history of transient ischemic attack (n=818). Results— Participants with symptoms (but no diagnosis) had average PCS-12 scores 5.5 (95% CI: 5.2 to 5.9) points lower than those without symptoms, a difference similar to transient ischemic attack (6.0; 95% CI: 5.3 to 6.7) and over one half the effect of stroke (8.4; 95% CI: 8.0 to 9.0). MCS-12 scores were 2.7 (95% CI: 2.4 to 3.0) points lower for those with symptoms, −0.5 for transient ischemic attack (95% CI: 0.0 to −1.1), and −1.6 for stroke (95% CI: −1.2 to −2.0). Differences in demographic and vascular risk factors, health behaviors, physiological measures, and indices of socioeconomic status did not fully explain these differences. Those reporting history of weakness or numbness had larger current decrements in physical functioning, and those reporting history of inability to express themselves or understand language had larger current decrements in mental functioning. Conclusions— Individuals with clinically consistent symptoms but no stroke diagnosis have a lower quality of life than those without symptoms. The difference in physical functioning is substantial with a smaller decline in mental functioning. Apart from so-called “silent stroke,” there appear to be many individuals with possibly symptomatic cerebrovascular disease—either stroke or transient ischemic attack—who are not being diagnosed. Furthermore, these symptomatic but undiagnosed strokes may not be benign.

Background— Quality improvement efforts have focused on strategies to improve the timeliness of reperfusion therapy in ST-elevation myocardial infarction patients who present to hospitals with and without percutaneous coronary intervention (PCI) capability. We implemented and evaluated a protocol to optimize the timeliness of reperfusion therapy and to coordinate systems of care for a PCI center and 28 regional hospitals located up to 150 miles away across 3 states. Methods and Results— The present study focused on a prospective, observational cohort of 597 patients who presented with ST-segment elevation and within 12 hours of symptom onset to Saint Marys Hospital and 28 regional hospitals up to 150 miles away between May 2004 and December 2006. The Mayo Clinic ST-elevation myocardial infarction protocol implemented strategies to improve timeliness of reperfusion therapy and to coordinate systems of care for transfer between hospitals. The study sample consisted of 258 patients who presented to Saint Marys Hospital and were treated with primary PCI (group A), 105 patients who presented to a regional hospital with symptom onset >3 hours and then were transferred for primary PCI (group B), and 131 patients who presented to a regional hospital with symptom onset <3 hours and were treated with full-dose fibrinolytic therapy (group C). For groups A and B, median door-to-balloon times were 71 and 116 minutes, respectively. Door-to-balloon time <90 minutes was achieved in 75% of group A and 12% of group B. Median door-to-needle time was 25 minutes for group C, and 70% had door-to-needle time <30 minutes. Conclusions— The Mayo Clinic ST-elevation myocardial infarction protocol demonstrates the feasibility of implementing strategies to optimize the timeliness of reperfusion therapy and the times that can be achieved through coordinated systems of care for ST-elevation myocardial infarction patients presenting to a PCI center (Saint Marys Hospital) and 28 regional hospitals without PCI capability located up to 150 miles away across 3 states.

Abstract Current users of postmenopausal hormones (PMH) have ∼30% to 40% lower risk of colorectal cancer (CRC), although associations with specific types of hormones have been inconsistent. Further, it is not clear whether some tumor types have a different risk. We conducted a case-control study to examine the relationship between PMH and CRC. Cases (n = 1,004), ages 50 to 74 years, were identified from the Surveillance Epidemiology and End Results registry in Washington from 1998 to 2002; controls (n = 1,062) were randomly selected from population lists. Case tissue samples were obtained for microsatellite instability (MSI) analyses. Interviews collected risk-factor data for CRC, including detailed information on PMH. Multivariable logistic regression models estimated odds ratios (OR) and 95% confidence intervals (95% CI). Current use of any PMH was associated with a 20% reduction in CRC risk (95% CI 0.6–0.9). This reduction in risk was limited to women who had taken estrogen plus progestin (EP) preparations only (OR = 0.6, 95% CI 0.5–0.9); there was no association with estrogen-only (E alone) use (OR = 0.9, 95% CI 0.7–1.1). For women with MSI-low or MSI-stable tumors, there was a statistically significant 40% reduction in CRC risk associated with EP use (95% CI 0.4–0.9); there was no clear association with MSI-high tumors. EP use was associated with a decreased risk of CRC; however, there seemed to be no association with E alone data that are consistent with the recent Women's Health Initiative findings. Progestin may enhance the estrogenic effect of conjugated estrogen so the combination may be more biologically active in the colon than E alone. [Cancer Res 2007;67(15):7534–9]

Humans have a large variability in body fat distribution, which has tremendous implications for metabolic health. Obese individuals with an upper-body-fat distribution have increased health complications such as dyslipidemia, hypertension, insulin resistance, and type 2 diabetes in comparison with lower-body-obese individuals. Additionally, females have more body fat, a greater proportion of fat in their lower body, and much less visceral fat than do lean males at the same body mass index. The reasons for these differences in body fat distribution have not been clearly identified but could be important. Herein we review what has been learned about regional differences in triglyceride storage capacity and lipolysis as they relate to the causes and consequences of regional fat accumulation. Both sex and site differences in regional fat storage have been described. In contrast, with the exception of variations between men and women in the contribution of visceral adipose tissue to hepatic FFA delivery, most studies have failed to show important sex differences in regional lipolysis in vivo.

Purpose To document and describe in detail the occurrence of apraxia of speech (AOS) in a group of individuals with a diagnosis of motor neuron disease (MND). Method Seven individuals with MND and AOS were identified from among 80 patients with a variety of neurodegenerative diseases and AOS (J. R. Duffy, 2006). The history, presenting complaints, neurological findings, and speech-language findings were documented for each case. Results Spastic or mixed spastic-flaccid dysarthria was present in all 7 cases. The AOS was judged as worse than the dysarthria in 4 cases. Nonverbal oral apraxia was eventually present in all cases. Aphasia was present in 2 cases and equivocally present in another 2. Dementia was present in 1 case and equivocally present in 2. Conclusions AOS can occur in MND, typically also with dysarthria, but not invariably with aphasia or other cognitive deficits. Thus, a diagnosis of MND does not preclude the presence of AOS. More importantly, MND should be a diagnostic consideration when AOS is a prominent sign of degenerative disease.