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Oxidative modification of hepatic mitochondria protein thiols: effect of chronic alcohol consumption.

Redox modification of mitochondrial proteins is thought to play a key role in regulating cellular function, although direct evidence to support this hypothesis is limited. Using an in vivo model of mitochondrial redox stress, ethanol hepatotoxicity, the modification of mitochondrial protein thiols was examined using a proteomics approach. Specific labeling of reduced thiols in the mitochondrion from the livers of control and ethanol-fed rats was achieved by using the thiol reactive compound (4-iodobutyl)triphenylphosphonium (IBTP). This molecule selectively accumulates in the organelle and can be used to identify thiol-containing proteins. Mitochondrial proteins that have been modified are identified by decreased labeling with IBTP using two-dimensional SDS-PAGE followed by immunoblotting with an antibody directed against the triphenylphosphonium moiety of the IBTP molecule. Analyses of these data showed a significant decrease in IBTP labeling of thiols present in specific mitochondria matrix proteins from ethanol-fed rats compared with their corresponding controls. These proteins were identified as the low-K(m) aldehyde dehydrogenase and glucose-regulated protein 78. The decrease in IBTP labeling in aldehyde dehydrogenase was accompanied by a decrease in specific activity of the enzyme. These data demonstrate that mitochondrial protein thiol modification is associated with chronic alcohol intake and might contribute to the pathophysiology associated with hepatic injury. Taken together, we have developed a protocol to chemically tag and select thiol-modified proteins that will greatly enhance efforts to establish posttranslational redox modification of mitochondrial protein in in vivo models of oxidative or nitrosative stress.

Aldehyde Dehydrogenase↗

Chronic beta-adrenoreceptor activation increases cardiac cavity size through chamber remodeling and not via modifications in myocardial material properties.

Chronic beta-adrenoreceptor (beta-AR) activation increases left ventricular (LV) cavity size by promoting a rightward shift in LV diastolic pressure-volume (P-V) relations in association with increases in low-tensile strength myocardial (non-cross-linked) collagen concentrations. Because diastolic P-V relations are determined by chamber remodeling as well as by myocardial material properties (indexed by myocardial stiffness), both of which are associated with modifications in myocardial collagen cross-linking, we evaluated whether chamber remodeling or alterations in myocardial material properties govern beta-AR-mediated modifications in diastolic P-V relations. The effects of chronic administration of isoproterenol (Iso; 0.04 mg.kg(-1).day(-1) from 12 to 19 mo of age) to spontaneously hypertensive rats (SHRs) on LV cavity dimensions, LV diastolic P-V relations, myocardial collagen characteristics, myocardial stiffness constants [e.g., the slope of the LV diastolic stress-strain relation (k)], and LV chamber and myocardial systolic function were assessed. SHRs at 19 mo of age had normal LV diastolic P-V relations, marked myocardial fibrosis (using a pathological score), increased myocardial cross-linked (insoluble to cyanogen bromide digestion) type I and type III collagen concentrations, and enhanced myocardial k values. Iso administration to SHRs resulted in enlarged LV cavity dimensions mediated by a rightward shift in LV diastolic P-V relations, increased volume intercept of the LV diastolic P-V relation, decreased LV relative wall thickness despite a tendency to augment LV hypertrophy, and increased non-cross-linked type I and type III myocardial collagen concentrations. Iso administration resulted in reduced pump function without modification of intrinsic myocardial systolic function. However, despite increasing myocardial non-cross-linked concentrations, Iso failed to alter myocardial k in SHRs. These results suggest that beta-AR-mediated rightward shifts in LV diastolic P-V relations, which induce decreased pump function, are mediated by chamber remodeling but not by modifications in myocardial material properties.

Animals↗

Perinatal nutritional modification of weanling rat heart contractile protein.

The present study ascertained the influence of litter-size-induced perinatal nutritional modification on cardiac contractile protein enzymatic activity and isomyosin composition. Myofibrillar enzyme activities for Mg2+ -ATPase, Ca2+ -ATPase, and creatine kinase (CK) in the weanling heart were unaltered by nutritional modification. However, these enzyme activities were all significantly augmented in the adult heart. Hill plot analyses of Mg2+ -ATPase activities indicated that myofibrillar calcium regulation was not influenced by either nutritional modification or the weanling-to-adult developmental progression. Isomyosin V1 composition (90 +/- 1%) correlated with plasma thyroid hormone level in normal-growth (8/litter) weanlings. Undernutrition retarded conversion of V3 isomyosin to the V1 species while overnutrition enhanced isomyosin conversion. Isomyosin composition in weanling rats subjected to perinatal nutritional modification was independent of thyroid status. In the adult rat, plasma thyroxine levels were increased, whereas V1 isomyosin remained unchanged (88 +/- 2%) compared with that of the weanling groups. Discrepancies in the relationship between contractile protein enzymatic activities, myosin composition, and heart function are apparent between both the litter-size-adjusted weanling rats and between weanling and adult animals. These discrepancies indicate the complex relationship between heart function and contractile protein properties.

Animals↗

Biological significance of nitric oxide-mediated protein modifications.

Nitric oxide (NO), despite an apparently simple diatomic structure, has a wide variety of functions in both physiology and pathology and within every major organ system. It has become an increasingly important scientific challenge to decipher how this wide range of activity is achieved. To this end a number of investigators have begun to explore how NO-mediated posttranslational modifications of proteins may represent mechanisms of cellular signaling. These modifications include: 1). binding to metal centers; 2). nitrosylation of thiol and amine groups; 3). nitration of tyrosine, tryptophan, amine, carboxylic acid, and phenylalanine groups; and 4). oxidation of thiols (both cysteine and methionine residues) and tyrosine. However, two particular modifications have recently received much attention, nitrosylation of thiols to produce S-nitrosothiol and nitration of tyrosine residues to produce nitrotyrosine. It is the purpose of this review to examine the possibility that these modifications may play a role in NO-mediated signaling.

Humans↗

Behavioral, plasma, and calorimetric changes related to food texture modification in men.

We hypothesized that food texture modifications might alter anticipatory reflexes, feeding behavior, and the postabsorptive consequences of ingestion. Two sets of complete meals with different textures but the same macronutrient composition were prepared. The first set was either a soup containing chunks of food (mixture) or the same soup blended until smooth (purée). The second set was either a rusk (R), a sandwich loaf (SL), or a liquid rusk meal (LR). We measured hunger and fullness feelings after ingestion of each food in a calibrated lunch, the ingestion rate, the duration between lunch and a spontaneous dinner request, the energy value, and the macronutrient composition of the ad libitum dinner. We also studied plasma modifications and respiratory gas exchanges from lunch to dinner. Feelings of hunger and fullness were not affected by texture modifications. The purée soup was consumed faster than the mixture (P < 0.05), and insulin, triacylglycerol, and energy expenditure were greater with the purée (P < 0.05). LR was less palatable than the other rusk lunch versions (P < 0.001), and R was ingested more slowly (P < 0.05). The lowest increase in plasma glucose occurred with SL, and the highest energy expenditure was seen with LR (P < 0.05). In humans, food texture modification affects not only eating patterns and palatability of ingestants but also metabolic management.

Adult↗

Motor cortical activity during voluntary gait modifications in the cat. I. Cells related to the forelimbs.

1. The discharge patterns of 91 identified pyramidal tract neurons (PTNs), located within the forelimb region of area 4 of the cat motor cortex, were recorded during the voluntary modifications of gait needed to step over obstacles attached to a moving treadmill belt. Recordings were made simultaneously from flexor and extensor muscles acting around the shoulder, elbow, wrist, and digits of the forelimb contralateral to the recording site. 2. Analysis of the changes in electromyographic (EMG) activity during the gait modification showed increases in the activity of most flexor muscles of the shoulder and elbow, as well as in the wrist and digit dorsiflexors, when the contralateral forelimb was the first to pass over the obstacle. This period of augmented activity could be subdivided into two parts: one associated with the initial flexion of the limb that was needed to bring it above and over the obstacle (phase I), and the second associated with increased wrist dorsiflexor muscle activity before foot contact (phase II). 3. The discharge frequency of a total of 57/91 (63%) of the recorded PTNs was significantly increased during the gait modification when the limb contralateral to the recording site was the first to step over the obstacle; six of these neurons also showed a significant decrease in their discharge in a different part of the step cycle. In a further 21/91 (23%) neurons, discharge frequency was only decreased, whereas the remaining 13/91 (14%) PTNs showed similar patterns of activity both during control walking and during the gait modifications. 4. Most of those neurons (47/57) in which significant increases in firing frequency were observed, discharged maximally during the period of increased activity of the physiological flexor muscles. Twenty-three of these cells (23/47) discharged maximally in phase I, and 12 (12/47) in phase II. A third population of PTNS (12/47) started to increase their discharge in the stance phase of the step cycle immediately preceding the modified cycle. Seven (7/57) PTNs increased their discharge during the stance phase of the modified cycle, and the remaining three could not be classified as being preferentially related to any one part of the step cycle. 5. The frequency modulation of 41/57 PTNs was less when the leg contralateral to the recording site was the second to encounter the obstacle. In many neurons there was also an appreciable change in the time in the step cycle that peak discharge occurred. These changes in amplitude and timing paralleled the changes observed in the temporal relationships of the muscles.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Corticoreticular pathways in the cat. II. Discharge activity of neurons in area 4 during voluntary gait modifications.

We propose that the descending command from area 4 that is responsible, in part, for the change in limb trajectory required to step over an obstacle in one's path also plays a role in triggering the anticipatory postural modifications that accompany this movement. To test this hypothesis, we recorded the discharge characteristics of identified classes of corticofugal neurons in area 4 of the cat. Neurons were identified either as: pryamidal tract neurons (PTNs) if their axon projected to the caudal pyramidal tract (PT) but not to the pontomedullary reticular formation (PMRF); as corticoreticular neurons (CRNs) if their axon projected to the PMRF but not to the PT; and as PTN/CRNs if their axon projected to both structures. Altogether, the discharge properties of 212 corticofugal neurons (109 PTNs, 66 PTN/CRNs, and 37 CRNs) within area 4 were recorded during voluntary gait modifications. Neurons in all three classes showed increases in their discharge frequency during locomotion and included groups that increased their discharge either during the swing phase of the modified step, during the subsequent stance phase, or in the stance phase of the cycle preceding the step over the obstacle. A slightly higher percentage of CRNs (39%) discharged in the stance phase prior to the gait modification than did the PTNs or PTN/CRNs (20% and 17% respectively). In 37 electrode penetrations, we were able to record clusters of 3 or more neurons within 500 micro(m) of each other. In most cases, PTN/CRNs recorded in close proximity to PTNs had similar receptive fields and discharged in a similar, but not identical, manner during the gait modifications. Compared with adjacent PTNs, CRNs normally showed a more variable pattern of activity and frequently discharged earlier in the step cycle than did the PTNs or PTN/CRNs. We interpret the results as providing support for the original hypothesis. We suggest that the collateral branches to the PMRF from corticofugal neurons with axons that continue at least as far as the caudal PT provide a signal that could be used to trigger dynamic postural responses that are appropriately organized and scaled for the movements that are being undertaken. We suggest that the more variable and earlier discharge activity observed in CRNs might be used to modify the postural support on which the movements and the dynamic postural adjustments are superimposed.

Animals↗

Role of oxidative modifications in atherosclerosis.

This review focuses on the role of oxidative processes in atherosclerosis and its resultant cardiovascular events. There is now a consensus that atherosclerosis represents a state of heightened oxidative stress characterized by lipid and protein oxidation in the vascular wall. The oxidative modification hypothesis of atherosclerosis predicts that low-density lipoprotein (LDL) oxidation is an early event in atherosclerosis and that oxidized LDL contributes to atherogenesis. In support of this hypothesis, oxidized LDL can support foam cell formation in vitro, the lipid in human lesions is substantially oxidized, there is evidence for the presence of oxidized LDL in vivo, oxidized LDL has a number of potentially proatherogenic activities, and several structurally unrelated antioxidants inhibit atherosclerosis in animals. An emerging consensus also underscores the importance in vascular disease of oxidative events in addition to LDL oxidation. These include the production of reactive oxygen and nitrogen species by vascular cells, as well as oxidative modifications contributing to important clinical manifestations of coronary artery disease such as endothelial dysfunction and plaque disruption. Despite these abundant data however, fundamental problems remain with implicating oxidative modification as a (requisite) pathophysiologically important cause for atherosclerosis. These include the poor performance of antioxidant strategies in limiting either atherosclerosis or cardiovascular events from atherosclerosis, and observations in animals that suggest dissociation between atherosclerosis and lipoprotein oxidation. Indeed, it remains to be established that oxidative events are a cause rather than an injurious response to atherogenesis. In this context, inflammation needs to be considered as a primary process of atherosclerosis, and oxidative stress as a secondary event. To address this issue, we have proposed an "oxidative response to inflammation" model as a means of reconciling the response-to-injury and oxidative modification hypotheses of atherosclerosis.

Animals↗

Modification of lipoproteins in uremia: oxidation, glycation and carbamoylation.

Lipoprotein modification occurs in uremic patients and in patients with end stage kidney disease under chronic renal replacement therapy. Forms of lipoprotein modification include lipid peroxidation, glycation, and carbamoylation. In this short review, we discuss the presence of these forms of lipoprotein modification and their association with various renal diseases. Methods to analyze lipoprotein modification are introduced, and functional consequences related to vascular and renal function are presented.

Arteriosclerosis↗

The role of lifestyle modification in dysmetabolic syndrome management.

Lifestyle modification should be the primary therapeutic intervention in individuals with the dysmetabolic syndrome, given the fact that obesity, unhealthy diet, and physical inactivity are primary underlying risk factors for its development. Most individuals with the dysmetabolic syndrome need to lose weight through dietary changes and increases in physical activity. Modest weight losses may significantly improve all aspects of the syndrome. Because individuals differ in their lifestyles, tailoring interventions to meet the specific needs of each person will maximize the chances of success. Assessment of the individual with the dysmetabolic syndrome involves quantification of obesity, diets and dietary patterns, physical activity, emotional problems, and motivation. To help individuals make lifestyle changes, a number of behavior modification strategies have shown good efficacy. These strategies include a tailored problem-solving intervention, involving goal-setting, self-monitoring, stimulus control, cognitive restructuring, stress management, relapse prevention, social support, and contracting. The frequency of self-monitoring is an especially important strategy for continued success. Research studies have clearly demonstrated the power of lifestyle modification for long-term behavioral change. Lifestyle modification appears effective in delaying or preventing the development of the dysmetabolic syndrome.

Cognitive Behavioral Therapy↗

Subunit interactions of the nerve and epidermal growth factor complexes: protection of the biological subunit from proteolytic modification.

The nerve growth factor dimer (beta NGF) can undergo two proteolytic modifications, one near the amino terminus where a unique histidine/methionine bond is cleaved and the other at the carboxy terminus releasing the terminal arginine residue. The modification near the amino terminus, releasing the first eight amino acids as an octapeptide, occurs as the result of the action of a specific endopeptidase present in the submaxillary gland. This same enzyme was found to be present in high concentration in epinephrine-stimulated saliva (20 mM) and was isolated from this source. The subunit interactions in 7S NGF were considered by assessing the protection afforded by each subunit, individually and in combination, against these two proteolytic modifications. Similar experiments were attempted with high molecular weight epidermal growth factor (HMW-EGF), an analogous growth factor complex that can experience a single modification, the release of arginine by carboxypeptidase B from the carboxy terminus of its biological subunit, low molecular weight EGF (LMW-EGF). The amino terminal octapeptide of beta NGF is protected by both the alpha and gamma subunits of 7S NGF and its loss has no effect on 7S NGF complex stabilization by zinc. The carboxy terminal arginine is protected only by the gamma subunit. A scheme depicting the subunit interactions in 7S NGF is presented.

Animals↗

Modification of protein moiety of human low density lipoprotein by hypochlorite generates strong platelet agonist.

Conflicting reports exist about the effects of mildly or extensively oxidized low density lipoproteins (LDLs) on the reactivity of human platelets. This platelet response is mainly caused by modification of the protein and lipid moiety, giving rise to very differently modified species with hardly predictable properties. The aim of this study was to prepare oxidized LDL with modifications essentially restricted to the protein moiety and to determine the eventual platelet responses. We treated LDL at 0 degrees C for 10 minutes with a 60- to 1000-fold molar excess of sodium hypochlorite in borate buffer in the presence of the radical scavenger butylated hydroxytoluene. Under these conditions, neither fragmentation of apolipoprotein B-100 nor formation of LDL aggregates was observed, and lipid oxidation products did not exceed the amount present in untreated LDLs. The degree of modification and the respective effects on platelet function were highly reproducible. Hypochlorite-modified LDLs act as strong platelet agonists, inducing morphological changes, dense granule release, and irreversible platelet aggregation. The evoked platelet effects are completely suppressed by inhibitors of the phosphoinositide cycle but not by EDTA or acetylsalicylic acid. Most likely, these effects are transmitted via high-affinity binding to a single class of sites, which does not recognize native or acetylated LDL. Obviously, modified lysines, and the secondary lipid modifications derived from them, are not essential for this interaction. We conclude that bioactive oxidized lipids are not directly involved in the stimulation of platelets by hypochlorite-modified LDLs.

Adenosine Diphosphate↗

Oxidative modification of beta-very low density lipoprotein. Potential role in monocyte recruitment and foam cell formation.

Oxidative modification of low density lipoprotein (LDL) generates a form that is degraded much more rapidly by macrophages and may thus be more atherogenic than unoxidized LDL. Recently, we provided evidence that oxidative modification of LDL may play a significant role in the generation of fatty streaks in the LDL receptor-deficient rabbit. The major lipoprotein in cholesterol-fed animals is the beta-very low density lipoprotein (beta-VLDL). Since beta-VLDL is avidly taken up by macrophages, it could lead to foam cell formation without the need for oxidative modification or modification of other kinds. However, the present studies show that beta-VLDL can be oxidized by incubation with endothelial cells or with copper ions. Oxidized beta-VLDL was degraded by macrophages at about twice the rate of unoxidized beta-VLDL, and it stimulated cholesterol esterification twice as much as unoxidized beta-VLDL. The degradation of oxidized beta-VLDL was inhibited either by oxidized beta-VLDL itself or by oxidized LDL, but not by unoxidized beta-VLDL. beta-VLDL was chemotactic for human monocytes and contained significant amounts of lysophosphatidylcholine, previously shown to be a chemotactic agent. In summary, oxidized LDL is degraded by macrophages proportionately more than oxidized beta-VLDL as compared to the unmodified lipoproteins. However, the twofold increase may, nevertheless, be significant in the atherogenicity of beta-VLDL.

Animals↗

Atrioventricular node modification in patients with chronic atrial fibrillation: role of morphology of RR interval variation.

BACKGROUND: This study evaluates the role of RR interval distribution pattern as an outcome predictor of radiofrequency (RF) modification of atrioventricular (AV) node in chronic atrial fibrillation (AF) and attempts to elucidate the likely mechanism of rate control. METHODS AND RESULTS: Sixty-five patients with chronic AF underwent AV node modification. The RR interval distribution pattern was derived from 24-hour ECG recordings obtained before and after the procedure. The preablation pattern was bimodal (B) in 36 patients (55%) and unimodal (U) in 29 patients (45%). After the modification procedure, the B pattern shifted to U (78%) or became modified B (22%). The mean number of RF pulses delivered and the fluoroscopy time were n=8+/-5 and 24+/-11 minutes, respectively, in patients with B pattern versus n=18+/-7 and 45+/-17 minutes in patients with U pattern (P<0.001 for both). The location of successful ablation was posteroseptal and lower midseptal in 26 patients (81%) with B pattern versus 2 (13%) with U pattern (P<0.001). Mean and maximal ventricular rates and heart rate at peak exercise were reduced after the procedure in both groups (P<0.001 for all). Long-term success rate, AV block incidence, and pacemaker implantation rate were 89%, 0%, and 8%, respectively, in patients with B pattern versus 52% (P<0.001), 21% (P=0.006), and 48% (P<0.001) in patients with U pattern. CONCLUSIONS: RF modification of the AV node is expected to be more effective, safe, and expeditious in patients with chronic AF and B RR interval distribution pattern. Posterior atrionodal input ablation may be the prevailing mechanism of rate control in these patients, whereas U-pattern patients may benefit from partial injury to the AV node.

Adult↗

Mechanism of ventricular rate control after radiofrequency modification of atrioventricular conduction in patients with atrial fibrillation.

BACKGROUND: Modification of atrioventricular (AV) conduction during atrial fibrillation (AF) may be achieved by radiofrequency ablation in the posteroseptal region of the tricuspid annulus. We tested the hypothesis that elimination of the posterior atrionodal input rather than direct damage to the compact AV node accounts for the decrease in ventricular rate after AV nodal modification. METHODS AND RESULTS: Twenty-four patients with the typical form of AV nodal reentrant tachycardia (AVNRT) underwent selective radiofrequency ablation of the slow AV nodal pathway in the posteroseptal tricuspid annulus. AF was induced before ablation (phase 1), 30 minutes after ablation (phase 2), and during follow-up 24 hours after ablation (phase 3), both with and without concurrent infusion of isoproterenol (4 micrograms/min). Successful elimination of AVNRT was achieved in all patients. During phase 3, 11 patients (46%) had residual dual pathway physiology. AV nodal Wenckebach cycle length (AVNW-CL) increased progressively during each phase of the protocol (356 +/- 72 versus 371 +/- 78 ms versus 432 +/- 104 ms, P < .0001), as did the effective refractory period of the AV node (279 +/- 60 versus 304 +/- 67 ms versus 372 +/- 56 ms, P < .0001). Minimal, mean, and maximal RR intervals during AF progressively increased immediately after ablation and 24 hours later (485 +/- 88 versus 533 +/- 116 ms versus 637 +/- 142 ms for mean RR, P < .0001). The changes in AVNW-CL, AV nodal effective refractory period, and ventricular response during AF were independent of residual dual pathway physiology after ablation. Similar observations were observed during isoproterenol infusion. CONCLUSIONS: Modification of AV nodal conduction during AF by radiofrequency ablation in the posteroseptal tricuspid annulus is independent of the presence or absence of a residual slow AV nodal pathway. On the basis of these observations, the mechanism of AV nodal modification is consistent with elimination of the posterior atrionodal input.

Adult↗

A new antiinflammatory compound, leumedin, inhibits modification of low density lipoprotein and the resulting monocyte transmigration into the subendothelial space of cocultures of human aortic wall cells.

Addition of leumedin, N-[9H-(2,7-dimethylfluorenyl-9-methoxy) carbon]-L-leucine at 30-60 microM together with LDL almost completely prevented the induction of monocyte chemotactic protein mRNA, reduced monocyte chemotactic protein 1 levels by 84%, and inhibited monocyte migration into the subendothelial space of cocultures of human aortic wall cells by < or = 98%. LDL incubated with leumedin formed a stable complex that remained intact even after refloating in an ultracentrifuge. Leumedin at 50 microM did not change conjugated diene formation during coculture modification of LDL or Cu++ catalyzed oxidation of LDL. Unlike LDL from control rabbits, LDL isolated from rabbits that were injected with 20 mg/kg leumedin was remarkably resistant to modification by the coculture and did not induce monocyte migration to a significant degree. Moreover, HDL isolated from rabbits injected with leumedin was far more effective in protecting against LDL modification by the artery wall cocultures than HDL from control rabbits. We conclude that leumedins can associate with lipoproteins in vivo, rendering LDL resistant to biological modification and markedly amplifying the protective capacity of HDL against in vitro LDL oxidation by artery wall cells.

Animals↗

Respiratory psychophysiology and behavior modification.

This article was written as an introduction to a special issue of Behavior Modification dedicated to studies in the field of respiratory psychophysiology. Although the invited articles that constitute this special issue cover a fairly broad range of topics, priority was given to articles that focus on the role of respiration in panic disorder. Attention is directed to the fundamental role of breathing in applied psychophysiology and to the encouragement of research in the modification of breathing behavior. The connection between respiratory psychophysiology and behavior modification is explained by reference to (a) a recent article on Pavlovian and operant control of breathing behavior and (b) four published volumes of selected articles dedicated exclusively to the field of respiratory psychophysiology. The present special issue of Behavior Modification marks the fifth volume.

Arousal↗

A health and demographic profile of noninstitutionalized older Americans residing in environments with home modifications.

OBJECTIVES: In this analysis the authors investigate the demographic characteristics, the health conditions/events, and the disabilities of community-dwelling Americans 70 years of age and older that are associated with residing in environments with specific home modifications. METHODS: Data from a large population-based study of the elderly are used to estimate logistic regression equations that reveal profiles of older individuals who are likely to have distinct home modifications. RESULTS: Having diseases such as diabetes and stroke, having experienced a hip fracture, a fall or a joint replacement, and having greater limitations with activities of daily living raise the likelihood of having home modifications. Low income, Hispanic, and African American elderly appear underrepresented among those with modifications. DISCUSSION: The authors conclude that specialized housing alternatives will be an increasingly important issue in the future as individuals aim to achieve and maintain the delicate balance between their functional ability and their living environment.

Activities of Daily Living↗