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This article summarizes the proceedings of an NIH workshop on timing, intensity, and duration of rehabilitation for acute stroke and hip fracture. Participants concentrated on methodological issues facing investigators and suggested priorities for future research in this area.
BACKGROUND: Patients with posttraumatic stress disorder (PTSD) exhibit smaller regional brain volumes in commonly reported regions including the amygdala and hippocampus, regions associated with fear and memory processing. In the current study, we have conducted a voxel-based morphometry (VBM) meta-analysis using whole-brain statistical maps with neuroimaging data from the ENIGMA-PGC PTSD working group. METHODS: T1-weighted structural neuroimaging scans from 36 cohorts (PTSD n = 1309; controls n = 2198) were processed using a standardized VBM pipeline (ENIGMA-VBM tool). We meta-analyzed the resulting statistical maps for voxel-wise differences in gray matter (GM) and white matter (WM) volumes between PTSD patients and controls, performed subgroup analyses considering the trauma exposure of the controls, and examined associations between regional brain volumes and clinical variables including PTSD (CAPS-4/5, PCL-5) and depression severity (BDI-II, PHQ-9). RESULTS: PTSD patients exhibited smaller GM volumes across the frontal and temporal lobes, and cerebellum, with the most significant effect in the left cerebellum (Hedges' g = 0.22, pcorrected = .001), and smaller cerebellar WM volume (peak Hedges' g = 0.14, pcorrected = .008). We observed similar regional differences when comparing patients to trauma-exposed controls, suggesting these structural abnormalities may be specific to PTSD. Regression analyses revealed PTSD severity was negatively associated with GM volumes within the cerebellum (p corrected  = .003), while depression severity was negatively associated with GM volumes within the cerebellum and superior frontal gyrus in patients (p corrected  = .001). CONCLUSIONS: PTSD patients exhibited widespread, regional differences in brain volumes where greater regional deficits appeared to reflect more severe symptoms. Our findings add to the growing literature implicating the cerebellum in PTSD psychopathology.
A 6-month randomized controlled trial examined the effect of walking and stretching/toning activity on changes in self-efficacy to overcome barriers and engage in incremental periods of activity in older, formerly sedentary adults (N = 174, M age = 65.5 years). Additionally, we were interested in the extent to which social, affective, and behavioral influences contributed to self-efficacy at the end of the 6-month program. Multiple sample latent growth curve analyses revealed a nonsignificant curvilinear growth pattern for barriers efficacy with increases in efficacy occurring from baseline to 2 months and then declining at 4 and 6 months. In the case of efficacy related to continued activity participation, there was a significant growth pattern demonstrating declines in efficacy over the 4 time points. Structural modeling analyses revealed significant direct effects of physical activity, affect experienced during activity, and exercise social support on both types of self-efficacy. These relationships were not significantly different between modes of activity. The findings are discussed in terms of the need to target sources of efficacy information prior to program end and the implications that such an approach might have for long-term maintenance of physical activity in older adults.
BACKGROUND: Physical activity has been effective in enhancing quality of life (QOL) of older adults over relatively short periods of time. However, little is known about the long-term effects of physical activity and even less about the possible mediators of this relationship. PURPOSE: We examined the mediating effects of psychological variables on the relationship between physical activity and global QOL (satisfaction with life) in older adults over a 4-year period. METHODS: Participants (N = 174, M age = 66.7 years) completed a battery of psychosocial measures at 1 and 5 years following enrollment in a 6-month randomized controlled exercise trial. RESULTS: Panel analysis conducted within a covariance modeling framework indicated that physical activity was related to self-efficacy, physical self-esteem, and positive affect at 1 year, and in turn, greater levels of self-efficacy and positive affect were associated with higher levels of QOL. Analyses indicated that changes in physical activity over the 4-year period were related to increases in physical self-esteem and positive affect, but only positive affect directly influenced improvements in QOL. CONCLUSIONS: The findings lend support to the position that physical activity effects on QOL are in part mediated by intermediate psychological outcomes and that physical activity can have long-term effects on well-being.
BACKGROUND: Studies examining physical activity levels have used samples primarily composed of non-Latino Whites and have focused on leisure time physical activity (LTPA). Additionally, few studies have investigated differences in physical activity between Latino men and Latina women, or the relationship between acculturation and activity. PURPOSE: To examine the subjective and objective physical activity of Latinos and gender differences in physical activity and the extent to which LTPA and non-LTPA were predictive of overall accelerometer physical activity. An additional objective was to examine the relationship between acculturation and different types of physical activity. METHODS: Data were obtained from 155 Latinos (n = 86 female, n = 69 male). Comparisons were made between Latino men and women. RESULTS: Latino men participated in significantly greater occupational and overall objective and subjective physical activity than Latina women; however, women participated in greater household activity. Regression analyses demonstrated that recreational, occupational, and household activity were significant predictors of overall accelerometer physical activity for the complete sample. Among women, recreational and household activity were significant predictors; however, overall accelerometer physical activity was not significantly predicted in men. Additionally, it was demonstrated that acculturation was related to occupational activity, but not to recreational activity. CONCLUSIONS: These results suggest that gender differences in physical activity are present among Latinos and that acculturation may be a correlate of various types of physical activity.
In this study, exercise self-efficacy was manipulated in a laboratory setting and its effects on feeling state responses were examined. A sample consisting largely of Non-Latina White and Latina women (N = 59) were randomly assigned to a low- or high-efficacy condition, and efficacy was manipulated by provision of false feedback and computer data. Feeling state responses were assessed before and after exercise. Efficacy was successfully manipulated, and participants in the high-efficacy condition reported more positive well-being and energy and less psychological distress and fatigue than those in the low-efficacy condition. There were no significant differences between the two ethnic groups for self-efficacy and feeling state responses. In addition, no clear pattern of relations emerged between efficacy and feeling state responses. The results support structuring exercise treatments in such a way that mastery experiences and positive feedback are maximized to enhance self-efficacy and improve subjective experiences.
The adrenal gland is highly vascularized with tightly regulated blood flow that is closely correlated with steroidogenesis. Mechanisms involved in the regulation of adrenal blood flow and vascular tone are largely unknown. The present study characterizes the contractile responses of isolated small cortical arteries from bovine adrenal glands. In endothelium-intact arteries, K(+), the thromboxane mimetic U46619, 5-hydroxytryptamine (5-HT), and endothelin-1 (ET-1) induced concentration-dependent contractions, whereas phenylephrine, norepinephrine, and ACTH were without effect. The EC(50)s for K(+), U46619, 5-HT, and ET-1 were 45 +/- 3 mm, 150 +/- 24 nm, 370 +/- 38 nm, and 2.8 +/- 0.8 nm, respectively. Contractions induced by U46619, 5-HT, and ET-1 were blocked by the thromboxane receptor antagonist SQ 29,548, the 5-HT(2A) receptor antagonist ketanserin, and the ET(A) receptor antagonist BQ 123, respectively. Removal of the endothelium caused a marked leftward shift of concentration responses to high K(+), U46619, 5-HT, and ET-1, and revealed contractile responses to phenylephrine and norepinephrine. In U46619-preconstricted arteries, BQ 123 converted ET-1-induced contractions to relaxations (maximal relaxation of 57 +/- 8%), which were subsequently blocked by the ET(B) receptor antagonist BQ 788. The ET(B)-mediated relaxations were endothelium dependent and inhibited by the nitric oxide synthase inhibitor N-nitro-l-arginine, the cytochrome P450 inhibitor SKF 525A, and high extracellular K(+), but not by the cyclooxygenase inhibitor indomethacin. These results demonstrate that small adrenal cortical arteries are highly responsive to various vasoconstrictor agents. The forceful contractile responses of these arterioles are consistent with their potential role in the regulation of adrenal blood flow.
The present study characterizes the vascular responses of isolated small bovine adrenal cortical arteries to acetylcholine, an endogenous neurotransmitter in the adrenal gland. Acetylcholine (10(-10) to 10(-6) m) elicited a concentration-dependent relaxation, with a maximal relaxation of 96 +/- 1% and EC50 of 4.2 nm. The relaxation was abolished by endothelial removal and attenuated by the nitric oxide synthase inhibitor N-nitro-L-arginine (L-NA, 30 microm) but not by the cyclooxygenase inhibitor indomethacin (10 microm). The maximal relaxation and EC50 of acetylcholine in the presence of L-NA were 87 +/- 4% and 22 nm, respectively. The acetylcholine-induced, indomethacin- and L-NA-resistant relaxation was eliminated by high K+ and markedly inhibited by the cytochrome P450 inhibitors SKF 525A (10 microm) and miconazole (10 microm). The maximal relaxations and EC50s with SKF 525A and miconazole were 56 +/- 8 and 72 +/- 2% and 0.8 and 0.5 microm, respectively. In indomethacin- and L-NA-treated arteries, acetylcholine induced a smooth muscle hyperpolarization, which was blocked by SKF 525A (3 +/- 1 mV vs. 15 +/- 2 mV of control). Arachidonic acid (10(-9) to 10(-5) m) and 14,15-epoxyeicosatrienoic acid (14,15-EET, 10(-9) to 10(-5) m), a cytochrome P450 metabolite of arachidonic acid, also evoked relaxations in small adrenal arteries, with maximal relaxations of 56 +/- 4 and 90 +/- 5%, respectively. The arachidonic acid-induced relaxation was blocked by SKF 525A. Using high-pressure liquid chromatography and gas chromatography/mass spectrometry analysis, EETs were identified in small adrenal arteries. These results demonstrate that acetylcholine is a potent vasodilator of small adrenal cortical arteries. The acetylcholine-induced relaxation is largely mediated by an endothelium-dependent hyperpolarization mechanism, presumably through cytochrome P450 metabolites of arachidonic acid.
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Fibroglycan (syndecan-2) is a member of a family of cell surface heparan sulfate proteoglycans that interact with adhesion molecules, growth factors and a variety of other effector systems that support the shaping, maintenance and repair of an organism. To investigate this apparent redundancy of proteoglycans at the cell surface, we have studied the expression of fibroglycan in the mouse embryo and compared this expression with that of syndecan-1. The characterisation of mouse embryo cDNA clones that crosshybridized to human fibroglycan-cDNA predicted that murine and human fibroglycan were highly similar in structure. Consistently, the analysis of transfectant cells, murine cell lines and embryo extracts indicated that the murine proteoglycan reacted specifically with monoclonal antibody 10H4 developed against the human protein. Fibroglycan, as detected by monoclonal antibody 10H4 in sections of embryonic tissues, occurred exclusively on mesenchymal cells that represented the putative precursors of the hard and connective tissue cells. No fibroglycan was detected in epithelia or in muscle cells. Areas where fibroglycan was particularly abundant were sites of high morphogenetic activity where intense cell-cell and cell-matrix interactions are known to occur (e.g. the epithelial-mesenchymal interfaces, the prechondrogenic and preosteogenic mesenchymal condensations). The expression of fibroglycan was weak in the early embryo, culminated during the morphogenetic phase and at the moment of cell lineage differentiation, and persisted in the perichondrium, periosteum and connective tissue cells. Syndecan-1, in contrast, was primarily detected in epithelia, and transiently in some mesenchymal cells, with mesenchymal localisations that did not or only partially overlap with those of fibroglycan. In situ hybridization analyses confirmed these expression patterns at the transcriptional level, identifying mesenchymal cells as the major source of fibroglycan production. These data indicate that the expression of fibroglycan occurs along unique and developmentally regulated patterns, and suggest that fibroglycan and syndecan-1 may have distinctive functions during tissue morphogenesis and differentiation.
The present article provides a brief review of the human and animal literature that has investigated the relationship between fitness training and brain and cognitive function. The animal research clearly suggests that improvements in fitness can lead to both morphological and functional changes in the brains of older animals. Results of a recent meta-analysis suggest that fitness training can also have beneficial effects on human cognition, particularly on tasks requiring executive control processing. These effects are also moderated by a number of factors, including the proportion of men and women in the intervention studies, the length of training sessions, the age of the participants, and the combination of fitness training regimes. The article also discusses preliminary results that link, for the first time, fitness training and differences in human brain structure and function. Finally, we discuss the important issue of participant adherence to fitness training programs and the factors that influence fitness participation.
The inappropriate expression/activation of cell-cycle-related molecules is associated with neuron death in many experimental paradigms and human neuropathologic conditions. However, the means whereby this links to the core apoptotic machinery in neurons have been unclear. Here, we show that the pro-apoptotic Bcl-2 homology 3 domain-only molecule Bcl-2 interacting mediator of cell death (Bim) is a target of a cell-cycle-related apoptotic pathway in neuronal cells. Induction of Bim in NGF-deprived cells requires expression and activity of cyclin-dependent kinase 4 (cdk4) and consequent de-repression of E2 promoter binding factor (E2F)-regulated genes including members of the myb transcription factor family. The Bim promoter contains two myb binding sites, mutation of which abolishes induction of a Bim promoter-driven reporter by NGF deprivation or E2F-dependent gene de-repression. NGF deprivation significantly increases endogenous levels of C-myb and its occupancy of the endogenous Bim promoter. These findings support a model in which apoptotic stimuli lead to cdk4 activation, consequent de-repression of E2F-regulated mybs, and induction of pro-apoptotic Bim.
Activation of cell cycle elements plays a required role in neuronal apoptosis associated with both development and neurodegenerative disorders. We demonstrated previously that neuron survival requires gene repression mediated by the cell cycle transcription factor E2F (E2 promoter binding factor) and that apoptotic stimuli lead to de-repression of E2F-regulated genes and consequent death. However, the downstream mediators of such death have been unclear. The transcription factors B- and C-myb are E2F-regulated genes that are induced in neurons by apoptotic stimuli. Here, we examine the role of B- and C-myb induction in neuron death. Antisense and siRNA constructs that effectively block the upregulation of B- and C-myb provide substantial protection against death of cultured neuronal PC12 cells, sympathetic neurons, and cortical neurons elicited by either NGF withdrawal or DNA damage. There is also significant protection from death induced by direct E2F-dependent gene de-repression. Our findings thus establish required roles for B- and C-myb in neuronal apoptosis.
We examined the impact of multidisciplinary clinical management of the Parkinson's Disease Research, Education, and Clinical Center program on Parkinson's disease progression. Initial and follow-up scores on the Part III Motor Examination subscale of the Unified Parkinson's Disease Rating Scale (UPDRS) were examined. Overall, 37 (75.5%) of the 49 patients demonstrated stable or improved UPDRS motor scores at 1- to 3-year follow-up; in the 1-year group (n = 28), 22 patients (78.6%) improved, while 6 (21.4%) worsened. In the 2-year group (n = 15), 10 (66.7%) improved, while 5 (33.3%) worsened. In the 3-year group (n = 6), 5 (83.3%) improved, while 1 (16.7%) worsened. Multidisciplinary interventions included neurology (95.9% of patients), physiatry (93.9%), nursing (87.8%), psychology (42.9%), medication changes (59.2% increases, 18.4% decreases), rehabilitation therapies (physical, occupational, speech-language, 67.3%), functional diagnostic testing (18.4%), support group (16.3%), home exercise instruction (85.7%), and disease and wellness education (81.6%). Improved and worsened patients did not significantly differ on the individual program components. Clinical implications and study limitations are discussed.
This study examined the frequency and degree of caregiver burden in persons with parkinsonism, a group of disorders with four primary symptoms that include tremor, rigidity, postural instability, and bradykinesia. We assessed associations between perceived caregiver burden and physical, cognitive, and functional impairments using well-established tools for persons with parkinsonism. The 49 individuals with parkinsonism ranged in age from 61 to 87 (mean = 75), while their caregivers (N = 49) ranged in age from 48 to 83 (mean = 70). The caregivers were predominantly either wives (82%) or daughters (6%), with other family members, friends, and/or neighbors (12%) making up the rest. The caregivers reported a relatively high ability for coping (mean scores = 4.6/6). Caregiver burden was significantly negatively associated with activities of daily living and motoric difficulties as measured on the Unified Parkinson's Disease Rating Scale (UPDRS). Likewise, caregiver burden was negatively associated with caregiver self-reported sleep and coping ability. Results did not demonstrate an association on the UPDRS among mentation, behavior, and mood. We found a significant negative correlation for mentation between the Folstein Mini-Mental Status Examination and caregiver burden measures; however, we did not find this association with the Dementia Rating Scale-2. Patient's self-reported pain and caregiver burden were not associated.
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BACKGROUND: Exercise is integral to the management of type 2 diabetes. Unfortunately, the majority of adults with type 2 diabetes do not engage in regular exercise. METHODS: Three hundred patients with type 2 diabetes were randomly selected from a patient pool of diabetic patients encountered in 1996 at the Department of Veterans Affairs Medical Center in New Orleans, Louisiana. Medical records from October 1996 to June 1999 were reviewed. Information about exercise, alcohol intake, smoking, medications, laboratory results, and other variables was extracted from medical records. Patients with mean glycosylated hemoglobin (HbA1c) < 8.0 (good diabetic control) were compared with those who had poor diabetic control (mean (HbA1c) > or = 8.0). The effect of exercise in the management of type 2 diabetes was assessed. RESULTS: After adjustment for other variables, patients without exercise had an odds ratio of 2.71 (95% CI, 1.38-5.32) for poor diabetic control compared with patients with exercise. CONCLUSIONS: These findings suggest that exercise by itself is important for type 2 diabetes management.