The first of these established the neurodevelopmental view of schizophrenia, now widely accepted throughout the field. This model provides the logic of early intervention. The second tradition is far more empirical, and is based on increasing evidence that early treatment, initiated as close after onset of psychosis as possible, appears to improve outcome. It thus follows from these findings that treatment started before onset might be better still. The neurodelopmental model The currently

accepted view of schizophrenia holds that it is a gradually unfolding illness, one that Inhibitors,research,lifescience,medical has its roots in prenatal development. Though the evidence is indirect, it is believed that a genetic error of some kind (most likely in interaction with other biological and environmental factors) leads to subtle abnormalities in the evolving brain. The

resulting pathophysiology is not, in itself, schizophrenia, but rather a susceptibility or vulnerability to the disorder. Subtle vulnerability indicators can be detected Inhibitors,research,lifescience,medical throughout late childhood and early adolescence (eg, cognitive impairments, social difficulties), but the underlying disturbance begins to fulminate toward midadolescence, when clinical warning signs (ie, attenuated Inhibitors,research,lifescience,medical positive symptoms) become increasingly apparent. A number of models, differing from each other mainly in details, have been derived from this basic set of assumptions.2-10 The neurodevelopmental model is widely supported by both genetic high-risk prospective and birth cohort follow-back studies. In particular, Inhibitors,research,lifescience,medical genetic high-risk studies have implicated early cognitive and social skill deficits

in young at-risk offsprings of schizophrenic parents who later become ill.11-14 Follow-back studies, such as the British15,16 and Finnish birth cohorts,17 and the large population Swedish conscripts18,19 and Israeli Inhibitors,research,lifescience,medical army studies,7 have consistently reported a diversity of cognitive, social, and other developmental precursors to schizophrenia. The application of the neurodevelopmental view to prevention is threefold: first, this model depicts the clinical illness as a long-term, developmental process. As a result, intervention is viewed as being possible well before psychosis sets in, and thus, as having the potential Adenylyl cyclase to stop continued Fostamatinib datasheet progression to illness. Second, the proposed presence of a detectable, biological vulnerability provides the mechanism for early detection. In order to begin preventive treatment prior to illness onset, there must be a way to identify who is in need of intervention. Prodromal vulnerability indicators provide the means to identify those individuals who are at risk for illness. It should be noted that this represents a major advance, since risk has traditionally been a group construct, not definable on an individual level.

3% versus 22.6%, P = 0.0042; median PFS 9.2 months versus 7.5 months; HR = 0.73, P = 0.017) and partially sensitive disease with median

PFS of 7.4 months versus 5.5 months in PLD/TRAB versus PLD arm (HR = 0.65, P = 0.0152). An unplanned hypothesis-generating analysis adjusting for the PFI imbalance and other prognostic factors suggested an improvement in OS associated with the trabectedin/PLD arm (HR = 0.82; 95% CI: 0.69–0.98; P = 0.0285). In another unplanned exploratory analysis, the subset of patients with a PFI of 6–12 months Inhibitors,research,lifescience,medical had the largest difference in OS (HR = 0.64; 95% CI: 0.47–0.86; P = 0.0027). Data showed a longer time to the following platinum therapy, and Inhibitors,research,lifescience,medical this imbalance in platinum-free interval was suggested as a possible cause of the increased OS [78]. Thus, these data suggest that the treatment with an effective nonplatinum combination may artificially prolong the platinum-free interval giving more chance of activity to further platinum therapy. This hypothesis will be investigated in a phase III trial, called INNOVATYION. As expected the combination Inhibitors,research,lifescience,medical regimen of TRAB/PLD has been associated to a

greater haematological toxicity (grade 3/4 anaemia 14%, neutropenia and thrombocytopenia 63%). Among other toxicities, short-lived grade 3/4 hypertransaminasemia (38%) and HFS were documented in 4% of the PLD/TRAB arm compared to 20% in the PLD alone arm [79]. In September 2009, based on these results, which support the PLD/TRAB combination as the most effective nonplatinum-based combination in platinum-sensitive disease, the PLD (30mg/m2) and TRAB (1.1mg/m2) association every 3 weeks has Inhibitors,research,lifescience,medical been approved by the EMA for treatment of patients with relapsed platinum-sensitive OvCa [80]. Based on the phase-II trials in platinum-sensitive OvCa the combination of PLD/carboplatin has Inhibitors,research,lifescience,medical been explored in phase-III trials [53]. Markman et al. compared single-agent carboplatin to

its combination with PLD in recurrent ovarian cancer, showing a statistically significant improvement of PFS with carboplatin/PLD, without an overall survival benefit. Interestingly, for unknown reasons, the association drastically reduced the rate of hypersensitivity reactions compared to carboplatin alone (9% versus 0%, P = 0.0008) [53]. Later on the results of the CALYPSO trial have been reported [81, 82]. This international open-label phase-III trial compared carboplatin Edoxaban PLD (CD) with carboplatin-paclitaxel (CP) in patients with platinum-sensitive recurrent ovarian cancer (ROC). A total of 976 recurrent patients relapsing >6 months after first- or second-line therapy were randomized to receive CD or CP for six cycles. Designed as a noninferiority trial, CALYPSO Daporinad nmr demonstrated that the combination of CD was not only noninferior to CP in terms of PFS, but indeed it was more effective (HR = 0.82, P = 0.005) in patients with platinum-sensitive recurrent ovarian cancer.

e., “red” printed in red ink) and incongruent stimuli (i.e., “green” in red ink) and measures interference between cognitive processes by requiring the participant to name the color (“red”) regardless of the word (“red” or “green”; Stroop 1935). It is hypothesized that the slower the speed of color-naming during incongruent stimuli, the more important the cognitive interference component. Consequently, in the Drug Stroop, the slower the speed of color-naming during stimuli associated with drug cues, the stronger the attentional bias toward

the drug-related stimuli (Cox et al. 2006). Inhibitors,research,lifescience,medical For example, 24-h abstinent smokers showed higher attentional bias for smoking cues than current smokers (Waters and Feyerabend 2000). The Dot Probe task also measures attentional bias toward drug-related stimuli. Here, two stimuli (one drug-related and one neutral) are presented side by side, after which Inhibitors,research,lifescience,medical the images disappear and a dot appears for a short time. Fast responding toward the dot where a drug-related stimulus was previously shown is a measure for increased attentional bias. Smokers showed Inhibitors,research,lifescience,medical greater attentional bias toward smoking-cues than nonsmokers during a Dot Probe task (Ehrman et al. 2002). In addition, compared with current smokers, 12-h abstinent smokers showed increased attentional bias for smoking cues (Gross et al. 1993),

and ex-smokers showed an intermediate level of attentional bias compared with current smokers and nonsmokers measured with the Dot Probe task (Ehrman et al. 2002). Using a related measure, abstinent crack-cocaine dependent patients had faster eye-movements toward cocaine-related pictures Inhibitors,research,lifescience,medical as compared to neutral pictures, Inhibitors,research,lifescience,medical and this correlated with self-reported intensity of cocaine craving (Rosse et al. 1997). It should

be noted that the drug Stroop and the Dot Probe task both measure selective attention (i.e., to drug stimuli), but the Stroop task requires more cognitive effort and flexibility, which might be responsible for PFT�� order different findings when using these different first paradigms. Cue-reactivity is also an import aspect of drug addiction and refers to the physiological and related subjective reactions (craving) that occur in the presence of drug-related stimuli, and can ultimately lead to relapse. Cue-reactivity is generally investigated using a cue-exposure or cue-reactivity task. Unlike other neurocognitive tasks, cue-reactivity paradigms employed during functional imaging only require the participant to watch drug-related pictures or videos (without any cognitive effort), although some cue-reactivity tasks include easy binary tasks to control for attention differences, in which baseline trials are usually incorporated requiring similar motor responses.

32,40,41 Conversely, reducing histone acetylation by overexpressing certain HDACs, or knockdown of the HAT, CBP, results in less sensitivity to cocaine.32,34,40 Two reports have extended these findings in rat models of cocaine self-administration, where animals are trained to press levers to receive the drug. Interestingly, delivery of the HDAC inhibitor, sodium butyrate, potentiates drug-taking42 while delivery of the HDAC inhibitor, trichostatin Inhibitors,research,lifescience,medical A, attenuates it.43 The explanation for these different observations is unclear, but it may involve experimental differences with the self-administration paradigm

or the HDAC inhibitor used. Cocaine alters histone acetylation through many enzymes in the NAc, but one particular HDAC, HDAC5, responds uniquely to chronic cocaine administration, raising the interesting 3-MA concentration possibility Inhibitors,research,lifescience,medical that this HDAC is involved in the behavioral transitions which occur between acute and chronic cocaine exposure (eg, drug experimentation to compulsive

drug use). Chronic cocaine administration increases the phosphorylation Inhibitors,research,lifescience,medical of IIDAC5 and shuttles it out of the nucleus, permitting hyperacetylation of histones at target genes for HDACS (Figure 2).40 This phosphorylation reaction may be mediated by Ca2+/calmodulin-dependent protein kinase II (CaMKII), since ex vivo inhibition of CaMKII reduces the activity-induced phosphorylation of HDAC5. Consistent with its regulation by cocaine, mice deficient for HDACS display normal rewarding responses to initial cocaine exposures, but become hypersensitive when treated with a Inhibitors,research,lifescience,medical chronic course of cocaine.40 Thus, pharmacological and genetic manipulations that increase histone acetylation Inhibitors,research,lifescience,medical appear to potentiate behavioral responses to cocaine and suggest that altered histone acetylation may contribute to establishment of an addicted state. Histone H3 phosphorylation and phosphoacetylation also appear to play key roles in drug-regulated behaviors. Global levels of

histone H3 phosphorylation at serine 10 are induced by acute Sclareol cocaine in striatum, a process which requires the kinase MSKl.19,32 The function of MSK1 is behaviorally important, as mice lacking this kinase have attenuated locomotor responses to cocaine. Cocaine-induced inhibition of protein phosphatase-1 also plays an important role in IB phosphorylation in striatum (Figure 2). Dopamine D1 receptor activation alters the phosphorylation of dopamine-regulated and cyclic-AMP-regulated phosphoprotein of 32kD (DARPP-32) at particular serine residues; the protein then accumulates in the nucleus to inhibit protein phosphatase-1 from dephosphorylating histone H3.20 The simultaneous activation of an H3 kinase and inhibition of an H3 phosphatase results in the robust increase in H3 phosphorylation after acute cocaine exposure.

This paper seeks to address this gap. The paper reports on one element of a broader study which set out to investigate issues of choice and decision making in end of life care (EOLC) from the perspective of patients, their family members and HCPs involved in their care. One of the key objectives in our study related to the Preferred Place of Care (PPCa) tool. This originated as part of a District Nurse education programme [15-17] to encourage discussion of ACP. The study aimed to explore if, when and how PPC was used to facilitate conversations about patients’ preferences (for place Inhibitors,research,lifescience,medical of care and death) and how these were documented. Discussion

and recording of these preferences is seen as an important means of supporting and enabling

patient choice, currently a central aspect of EOLC policy in England [18]. PPC is one of three interventions that were rolled out in England in the first phase of the National End of Life Care Programme between 2004–2007. In addition, the Gold Standards Inhibitors,research,lifescience,medical Framework was developed as a grass roots initiative to improve palliative care within primary care Inhibitors,research,lifescience,medical settingsb. The Liverpool Care Pathway is an integrated care pathway used at the bedside to deliver sustained quality of care for the dying in the last hours and days of lifec. The End of Life Care Strategy (EOLCS) for England Inhibitors,research,lifescience,medical [19] was published in 2008. This further emphasised the government’s core commitment to making excellent EOLC universally available through the realisation of patient choice about the manner and, particularly, the place of dying. It sets out an EOLC Pathway, the first step of which highlights that discussions about, and recording of, preferences for future care

between CYC202 manufacturer people approaching the end of life, Inhibitors,research,lifescience,medical their family members and health and social care staff are central to the delivery of good EOLC. ACP was highlighted as a key area within the Strategy and it has subsequently become more clearly defined in policy and guidanced[19,20]. ACP has been defined as a ‘voluntary process of discussion and review to help an individual Bay 11-7085 who has capacity to anticipate how their condition may affect them in the future and, if they wish, set on record: choices about their care and treatment and / or an advance decision to refuse a treatment in specific circumstances, so that these can be referred to by those responsible for their care or treatment (whether professional staff or family carers) in the event that they lose capacity to decide once their illness progresses’ [20]. The EOLC Strategy has identified the lack of open communication between people approaching the end of life, their family members and health and social care staff as one of the key barriers to the delivery of good EOLC. Poor communication about EOLC is a common and enduring complaint [21].

Section 2.3 is devoted to exploring the distribution of essentiality classes and established topological categories across three-node subgraphs of the reaction-centric metabolic network. In Section 4 we interpret the findings from Section 2.2 and Section 2.3 and use them to topologically characterize a typical reaction displaying medium-dependent essentiality. See Table 1 for a summary

of model, reaction category, activity, and essentiality statistics. Table 1 Summarizing statistics of reaction categories and essentialities. 2. Results 2.1. Relative Essentiality Analysis In order to subdivide the metabolic reactions into essentiality Inhibitors,research,lifescience,medical classes, namely non-essential, conditional lethal, and essential, we quantify the relative essentiality of a reaction by computing optimal, i.e., maximizing biomass production, steady-state flux distributions for over more than 7 × 104 combinatorial minimal media conditions. Furthermore, all subsequent single reaction knockouts of active (non-zero flux carrying) reactions are performed to identify for each medium Inhibitors,research,lifescience,medical condition

the set of essential reactions (see Methods for details). An illustrative example of this concept, involving E. coli central carbon metabolism Inhibitors,research,lifescience,medical [31], is provided in the supplementary materials. The relative essentiality of a particular reaction is then defined as the number of lethal outcomes due to its removal divided by the number of environmental conditions under which it has been active. An alternative definition of relative essentiality would be to normalize the number of lethal outcomes to the total number of media sampled. In this case, however, essential reactions that Inhibitors,research,lifescience,medical are rarely active would

give an unrealistically low essentiality value. Figure 2a shows the sorted relative essentiality profile of all reactions in the E. coli model, which have been active at least once during the FBA simulations; blocked reactions [32] have thus been eliminated; see also Methods). In Figure 2a the three essentiality classes Inhibitors,research,lifescience,medical are clearly visible: The removal of most reactions has no or only small consequences for the SCH727965 production of biomass (non-essential). Some reactions are globally essential (essential) and a third set is only medium-dependent essential (conditional lethal). Excluding non-essential reactions, Figure 2b depicts the relative essentiality profile in a semilog plot. The stepwise appearance of the conditional Oxalosuccinic acid lethal curve indicates three major groups of reactions that exhibit very similar relative essentiality scores, connected by some intermediate reactions. Figure 2 Outcome of combinatorial minimal media simulations. (a) Sorted relative essentiality profile determined by the simulation of reaction deletions under 72468 combinatorial minimal media conditions. The three different essentiality classes are indicated … Almaas et al. [21] reported a high, global essentiality for MC reactions. This finding suggests a higher essentiality for more active reactions.

Brain activity detection through EEG A BCI system needs an input from the user’s brain and these signals are converted in external operations; for this reason, brain signals have to be detected. EEG usually uses small ROCK inhibitors for glaucoma electrodes placed directly on the scalp at standardized positions. When a neuron is activated, a local current flow is produced and weak potential differences (5–100 μV) between electrodes are measured.

Inhibitors,research,lifescience,medical A large population of active neurons must be involved to generate electrical activity that can be detected with EEG over the scalp (Srinivasan et al. 1998). The electrodes record brain activity that is converted into digital signals and a sequence of steps translate this signals into commands. A limiting issue with EEG recording is its low spatial resolution, ranging between 2 and 3 cm. Moreover, EEG is deduced from apical Inhibitors,research,lifescience,medical dendrites of cortical pyramidal cells (Teplan 2002), thus

activity of deeper structures can only be studied indirectly. Because of the fluid, bone, and skin that separate the electrodes from the electrical activity, signals tend to be smoothed and noisy. This makes it difficult to locate the exact source of the oscillation. Inhibitors,research,lifescience,medical Nevertheless, EEG-based BCI have been shown to support a high performance, EEG is the predominant technology in BCI studies and most of clinical applications of BCI in patients with severe motor disorders have been demonstrated using EEG (e.g., Kubler et al. 2005; Vaughan et al. 2006; Nijboer et al. 2008). The changes in power of four frequency bands are used as control signals for BCI systems: delta (1–3 Hz), theta (4–7 Hz),

alpha (8–12 Inhibitors,research,lifescience,medical Hz), and beta (13–30 Hz). Four groups of electrophysiological Inhibitors,research,lifescience,medical signals in a BCI system As mentioned above, different noninvasive electrophysiological signals can be used as input for BCI systems. Therefore, BCIs can be classified into four groups based on the electrophysiological signals they use. Visual evoked potentials (VEP) VEPs are evoked electrophysiological potential that can be recorded throughout the visual system; they are extracted, using signal averaging, from the electroencephalographic activity recorded at the scalp. VEPs are elicited by visual stimuli such as flashes of light or flickering illumination presented on a screen. Users are presented with a panel whatever with different items and they have to fix their gaze on the item they want to select. The items on the screen are activated sequentially to elicit a visual evoked potential. BCI detects the VEP elicited by the stimulus where the subject looked at and the waveform of the VEPs depends upon the temporal frequency of the stimulus. In patients with neurological disease such as ALS, Sutter (Sutter 1992), for example, described communication problem with BCI due to artifacts caused by fasciculations.

Symptom score improvements seemed to be sufficient and durable (Figure 11). The company has initiated an international, multicenter, randomized, sham-controlled (randomization 3:1 active vs sham) trial that has just started in the United States. The data from this trial will determine whether the technology will be submitted for approval to the FDA.101 Figure 11 International Inhibitors,research,lifescience,medical Prostate Symptom Score (IPSS), benign prostatic hyperplasia (BPH) II, and quality of life (QoL) measures demonstrate sustained reduction through 3 years of follow-up.

(P < .05 for all displayed values). Reproduced with permission ... Overall, the 2011 AUA Annual Meeting in Washington, DC, provided an opportunity to learn more about the basic science, Inhibitors,research,lifescience,medical epidemiology, and natural history of LUTS and BPH as well as a host of medical and device treatments with their respective outcomes. In addition, LUTS and BPH are also conditions often examined in the sessions on cost-effectiveness and practice patterns. [Claus G. Roehrborn, MD, FACS]
Injury to the lower urinary tract is relatively uncommon in the setting of blunt trauma. However, it is particularly susceptible to those forces that produce sufficient energy to

cause pelvic ring disruption. As a result, at least 85% of bladder ruptures are associated with pelvic fracture.1,2 Urethral disruption has been reported in 3.5% to 28.8% of patients with pelvic fractures, almost exclusively in Inhibitors,research,lifescience,medical men. In Inhibitors,research,lifescience,medical Victoria, lower urinary tract injuries occurred in 1.5% of major trauma patients in 2009 (data from the Victorian State Trauma Outcomes Registry). It is well recognized that prompt recognition and early management of these urological injuries can significantly reduce morbidity and mortality. Difficulties arise in the severely injured multitrauma patient when lifesaving measures or damage-control surgery may delay the diagnosis and treatment of lower urinary tract injuries. As management strategies have become more conservative, particular attention has been given to defining patients

who would benefit most from intervention. This article describes the management of lower urinary tract Inhibitors,research,lifescience,medical injuries as practiced at Australia’s busiest below trauma center. Bladder The bladder is a muscular organ which, when empty, lies protected by the anterior bony pelvis. It is located extraperitoneally in the adult with peritoneum covering the superior surface. The dome is the most mobile and weakest part of the bladder, leaving it susceptible to rupture when the bladder is full. Associated injuries in bladder trauma are common and include pelvic fractures (93%–97%), long bone injuries (50%–53%), and central nervous system (28%–31%) and thoracic injuries (28%–31%).3,4 The mortality related to bladder trauma can be as high as 34% and is largely a consequence of associated injuries rather than bladder perforation find more itself. Mechanism Bladder perforation is seen most commonly in blunt trauma and infrequently as a result of penetrating injuries.

The scopolamine model was used in cognitive research to study the clinical correlates of ACh deficiency (see reference 21 for a review). It was applied to elderly subjects

and AD patients22-33 as a marker of cholinergic sensitivity, with the purpose of improving the diagnosis and staging of the disease. It failed, however, to predict cognitive decline on the basis of the subjects’ sensitivity.34 Calcitriol in vitro Animal studies assessing the reversal of scopolamineinduced memory impairment by various compounds are too numerous to be cited exhaustively. This approach has also been used in humans with the following molecules: Inhibitors,research,lifescience,medical physostigmine,35-40 velnacrine,40 choline,41 RO 15-1788,39 moclobemide,42,43 RU 41656,44 L-α-glycerylphosphoryleholine,45 Inhibitors,research,lifescience,medical oxiracetam,46 aniracetam and piracetam,47 tenilsetam,48 BMY 21502,49 D-cycloserine,50 SDZ ENS-163,51 and ZK-93426.52 However, the scopolamine model has not become a standard tool in the early assessment of drugs. One reason for this is that the cognitive

changes induced by scopolamine do not really mimic the AD picture. The details Inhibitors,research,lifescience,medical of the differences listed in Figure 1 (based on references 28, 40, and 53-63) are open to discussion, but there is a general agreement on the fact that, as Wesnes40 wrote, all the scopolamine-induced deficiencies are also observed Inhibitors,research,lifescience,medical in AD, while the reverse is not always true. The same is observed in neurological investigations. The electrophysiological effects of scopolamine (reviewed in reference 64) are close on EEG and similar on visual evoked potentials to those of AD. In PET65-68 and single photon emission computed tomography (SPECT)69 studies, scopolamine induces cerebral blood flow (CBF) and glucose metabolism changes, which are sometimes Inhibitors,research,lifescience,medical divergent and region-specific, but in all cases different from the pattern observed in AD. Figure 1. Memory dysfuction in Alzheimer’s disease (AD) and after scopolamine or ketamine The ketamine model Ketamine is a noncompetitive

N-methyl-D-aspartate (NMDA) receptor antagonist.70-71 Its administration in order to produce a model is the correlate of the glutamatergic hypothesis of AD (reviewed in reference 72). Two, apparently opposite, glutamatergic hypotheses have been proposed. The excitotoxic hypothesis states that there is a glutamatergic hyperactivity enough in AD. Domoic acid poisoning in humans was responsible for irreversible memory loss.73 Neuronal74 and astroglial75 glutamate transporter dysfunction in AD could result in excess glutamate in the synaptic cleft and in excitotoxic neuronal damage. This hypothesis is consistent with the beneficial effects of memantine76 and lamotrigine77 in AD patients. Some findings provide a link with the histopathological lesions that are the hallmarks of AD.

102-104 One systematic review concluded that individually tailored behavior management therapy over at least six sessions successfully reduced caregiver distress and burden in both the short and

longer term, but support for the effectiveness of group therapy teaching general principles of behavior management was lacking.104 Mittelman and colleagues105 demonstrated that individually tailored individual, family, and ad-hoc counseling sessions covering topics specific to individual caregivers successfully reduced caregiver depression scores Inhibitors,research,lifescience,medical over 2 years. Pinquart and Sorenson103 determined that longer interventions were more successful at reducing depression and the risk of institutionalization than shorter or “one-off” support or information sessions. Inhibitors,research,lifescience,medical A meta-analysis by Brodaty et al102

reported that the strongest predictor of success for an intervention was involving the patient in addition to the caregiver in a structured program, such as teaching the caregiver how to manage problem behaviors. The metaanalysis by Brodaty et al102 found a small significant overall effect of intervention on caregiver burden Inhibitors,research,lifescience,medical in addition to effects on knowledge/abilities, psychological health of caregivers, subjective wellbeing, and care receiver symptoms due to the inclusion of more recent studies which Inhibitors,research,lifescience,medical were found to have stronger effects on burden. The Seattle Protocols Stem Cell Compound Library provide a systematic, structured yet individualized approach to training

family caregivers to reduce behavioral and psychiatric disturbances in people with Alzheimer’s disease by teaching caregivers to monitor problems, identify possible events that trigger disturbances, and develop more effective responses.106 It has been successfully used to improve caregivers’ quality of life, reduce subjective burden and reactive responses to dementia care recipients’ problem Inhibitors,research,lifescience,medical behaviors,106 and to reduce dementia-related problems including depression,107 agitation108 and sleep disturbance.109 The Resources for Enhancing Alzheimer’s Caregiver Health (REACH) multi-site, multicomponent intervention included information provision, didactic instruction, role-playing, problem-solving, skills training, stress management techniques, Cell press and telephone support.110 The randomized, controlled trial involving 642 caregivers in ethnically diverse populations in the US resulted in significantly lower depression, burden, and care recipient problem behaviors, and higher self-care and social support in Caucasian and Hispanic caregivers as compared with controls but not for African- American caregivers, apart from better spousal caregiver quality of life.110 Caregiver interventions can delay nursing-home placement.