Effects of canary seed on two patients with disseminated granuloma annulare.

Treatment of disseminated granuloma annulare (GA) can be challenging and there is no gold standard for treatment. We observed two cases of generalized GA that were treated successfully with canary seed milk despite being resistant to other treatments. Canary seed milk has antioxidant (contains vitamin E), anti-diabetic (DPP-4 inhibition), and anti-hypertensive (ACE inhibition) properties. Therefore, dermatologists can consider canary seed milk, also known as alpiste milk, as a sole or supplemental treatment for patients with GA with or without comorbidities such as diabetes and hypertension, who prefer alternative therapy or failed other treatments.

OnabotulinumtoxinA versus PrabotulinumtoxinA-xvfs: A Randomized, Triple-blind, Split-face Study on the Time to Onset, Rhytid Appearance, and Patient Satisfaction in Forehead and Glabellar Lines.

Background: Both onabotulinumtoxinA and prabotulinumtoxinA-xvfs are FDA-approved formulations of botulinum toxin A for the treatment of glabella and forehead rhytids. Objective: We sought to compare the onset to action and patient satisfaction of onabotulinumtoxinA and prabotulinumtoxinA-xvfs in treating dynamic rhytids of the forehead and glabella. Methods: Fifteen patients, aged 28 to 74, were enrolled and completed the study. Patients were randomly assigned to receive equal amounts of onabotulinumtoxinA and prabotulinumtoxinA-xvfs injected to opposite sides of the face in the glabella and forehead at Day 0 by a blinded injector. Glabellar and frontalis muscle onset to action and rhytid appearance were blindly evaluated using photographs at Days 0, 2, 4, 6, 8, 10 post-injection. Patients rated their satisfaction of left and right sides using a standardized scale. Results: There was no statistically significant difference in onset to action, rhytid appearance, and patient satisfaction after injection with onabotulinumtoxinA versus prabotulinumtoxinA-xvfs in the corrugator and frontalis muscles. Although not statistically significant, a trend existed towards increased patient satisfaction with onabotulinumtoxinA. Conclusion: Both onabotulinumtoxinA and prabotulinumtoxinA-xvfs are equally efficacious formulations of botulinum toxin type A for the treatment of glabellar and forehead rhytids.

Pityriasis Lichenoides-Like Mycosis Fungoides: A Case Report.

A rare subtype of mycosis fungoides (MF) known as pityriasis lichenoides-like mycosis fungoides (PL-like MF) manifests as recurrent crops of erythematous scaly papules with the histological findings of MF. We report a 64-year-old male with recurrent crops of psoriasiform papules with mild scales on his trunk and extremities. Skin biopsy results were consistent with CD8+ cutaneous T-cell lymphoma (CTCL). Our patient had clinical features of pityriasis lichenoides and histological findings consistent with CD8+ MF. A differential diagnosis of PL, lymphomatoid papulosis (LyP), and PL-like MF was considered. Counseling patients with CD8+ cutaneous T-cell lymphoma can be challenging, as there is an aggressive variant named primary cutaneous aggressive epidermotropic CD8+ CTCL. However, with the ability to recognize PL-like MF, a rare indolent type of CD8+ CTCL, physicians can counsel patients appropriately.

Use of In Vivo Imaging and Physiologically-Based Kinetic Modelling to Predict Hepatic Transporter Mediated Drug-Drug Interactions in Rats.

Gadoxetate, a magnetic resonance imaging (MRI) contrast agent, is a substrate of organic-anion-transporting polypeptide 1B1 and multidrug resistance-associated protein 2. Six drugs, with varying degrees of transporter inhibition, were used to assess gadoxetate dynamic contrast enhanced MRI biomarkers for transporter inhibition in rats. Prospective prediction of changes in gadoxetate systemic and liver AUC (AUCR), resulting from transporter modulation, were performed by physiologically-based pharmacokinetic (PBPK) modelling. A tracer-kinetic model was used to estimate rate constants for hepatic uptake (khe), and biliary excretion (kbh). The observed median fold-decreases in gadoxetate liver AUC were 3.8- and 1.5-fold for ciclosporin and rifampicin, respectively. Ketoconazole unexpectedly decreased systemic and liver gadoxetate AUCs; the remaining drugs investigated (asunaprevir, bosentan, and pioglitazone) caused marginal changes. Ciclosporin decreased gadoxetate khe and kbh by 3.78 and 0.09 mL/min/mL, while decreases for rifampicin were 7.20 and 0.07 mL/min/mL, respectively. The relative decrease in khe (e.g., 96% for ciclosporin) was similar to PBPK-predicted inhibition of uptake (97-98%). PBPK modelling correctly predicted changes in gadoxetate systemic AUCR, whereas underprediction of decreases in liver AUCs was evident. The current study illustrates the modelling framework and integration of liver imaging data, PBPK, and tracer-kinetic models for prospective quantification of hepatic transporter-mediated DDI in humans.

The Effect of Gadolinium-Based Contrast Agents on Longitudinal Changes of Magnetic Resonance Imaging Signal Intensities and Relaxation Times in the Aging Rat Brain.

OBJECTIVES: The aim of the study was to investigate the possible influence of changes in the brain caused by age on relaxometric and relaxation time-weighted magnetic resonance imaging (MRI) parameters in the deep cerebellar nuclei (DCN) and the globus pallidus (GP) of Gd-exposed and control rats over the course of 1 year. MATERIALS AND METHODS: Twenty-five Wistar-Han rats were equally subdivided into 5 groups and initially received 8 injections on 4 consecutive days per week of either 3.6 mL/kg body weight saline (group I-III) or 1.8 mmol Gd/kg body weight gadobutrol (group IV) or gadodiamide (group V). T1- and T2-weighted scans, as well as relaxation maps, were acquired at 1 week (all groups); 5, 12, 20, and 26 weeks (saline II, gadobutrol, gadodiamide); and at 35, 44, and 52 weeks (saline III, gadobutrol, gadodiamide) after the last administration. Saline I was euthanized after 1 week, saline II after 26 weeks, and the remaining groups after 52 weeks. Signal intensities (SIs) were evaluated for the DCN/pons (P) and the GP/piriform cortex (PC) ratios, and relaxation times for the DCN and the GP. Brain tissue was extracted, and the gadolinium, iron, and manganese contents were quantified with inductively coupled plasma mass spectrometry (ICP-MS) and laser ablation-ICP-MS imaging. RESULTS: T1-weighted SI ratios did not show any significant trend with age in any region. The between-group analysis at 52 weeks resulted in a significant difference for the DCN/P and GP/PC region ratio between gadodiamide and its comparators. T1 relaxation times dropped with increasing age in the GP with a 10% to 20% difference between first and last measurement for all groups, and in the DCN <10% with a significant decrease for the gadodiamide group only (DCN: P = 0.0158). Group-related differences were observed at the last measurement time point for T1 values between gadodiamide and saline III in the DCN (P = 0.0153) and gadodiamide and gadobutrol in the GP (P = 0.0287). Analysis of the SI ratios of the T2-weighted images revealed a significant increase for the DCN/P and a decrease for the GP/PC with increasing age for all groups and no differences at 52 weeks after the last injection between groups. T2 values of the GP showed a significant linear decrease over time for all groups (saline I-III: P = 0.0101; gadobutrol: P = 0.0001; gadodiamide: P = 0.0142) in the aging rat brain. Quantitative imaging of manganese and iron by laser ablation-ICP-MS showed a linear increase for the saline groups in the GP for both metals (Fe: P < 0.0001; Mn: P = 0.0306) and in the DCN for manganese only (P = 0.0187), but no differences between groups at 52 weeks. CONCLUSIONS: Extensive MRI evaluation did not reveal an indication of SI or relaxation time changes associated with multiple exposure to the macrocyclic-chelated GBCA gadobutrol in the DCN and the GP. With increasing age, a T1 and T2 shortening in the GP and an increase in T2-weighted SI ratio in the DCN/P, as well as a decrease in the GP/PC, were observed for all groups. Such age-related changes can potentially bias MRI results as an indicator for gadolinium presence in the brain.

The gut microbiota modulates brain network connectivity under physiological conditions and after acute brain ischemia.

The gut microbiome has been implicated as a key regulator of brain function in health and disease. But the impact of gut microbiota on functional brain connectivity is unknown. We used resting-state functional magnetic resonance imaging in germ-free and normally colonized mice under naive conditions and after ischemic stroke. We observed a strong, brain-wide increase of functional connectivity in germ-free animals. Graph theoretical analysis revealed significant higher values in germ-free animals, indicating a stronger and denser global network but with less structural organization. Breakdown of network function after stroke equally affected germ-free and colonized mice. Results from histological analyses showed changes in dendritic spine densities, as well as an immature microglial phenotype, indicating impaired microglia-neuron interaction in germ-free mice as potential cause of this phenomenon. These results demonstrate the substantial impact of bacterial colonization on brain-wide function and extend our so far mainly (sub) cellular understanding of the gut-brain axis.

Ex vivo gadoxetate relaxivities in rat liver tissue and blood at five magnetic field strengths from 1.41 to 7 T.

Quantitative mapping of gadoxetate uptake and excretion rates in liver cells has shown potential to significantly improve the management of chronic liver disease and liver cancer. Unfortunately, technical and clinical validation of the technique is currently hampered by the lack of data on gadoxetate relaxivity. The aim of this study was to fill this gap by measuring gadoxetate relaxivity in liver tissue, which approximates hepatocytes, in blood, urine and bile at magnetic field strengths of 1.41, 1.5, 3, 4.7 and 7 T. Measurements were performed ex vivo in 44 female Mrp2 knockout rats and 30 female wild-type rats who had received an intravenous bolus of either 10, 25 or 40 µmol/kg gadoxetate. T1 was measured at 37 ± 3°C on NMR instruments (1.41 and 3 T), small-animal MRI (4.7 and 7 T) and clinical MRI (1.5 and 3 T). Gadolinium concentration was measured with optical emission spectrometry or mass spectrometry. The impact on measurements of gadoxetate rate constants was determined by generalizing pharmacokinetic models to tissues with different relaxivities. Relaxivity values (L mmol-1 s-1 ) showed the expected dependency on tissue/biofluid type and field strength, ranging from 15.0 ± 0.9 (1.41) to 6.0 ± 0.3 (7) T in liver tissue, from 7.5 ± 0.2 (1.41) to 6.2 ± 0.3 (7) T in blood, from 5.6 ± 0.1 (1.41) to 4.5 ± 0.1 (7) T in urine and from 5.6 ± 0.4 (1.41) to 4.3 ± 0.6 (7) T in bile. Failing to correct for the relaxivity difference between liver tissue and blood overestimates intracellular uptake rates by a factor of 2.0 at 1.41 T, 1.8 at 1.5 T, 1.5 at 3 T and 1.2 at 4.7 T. The relaxivity values derived in this study can be used retrospectively and prospectively to remove a well-known bias in gadoxetate rate constants. This will promote the clinical translation of MR-based liver function assessment by enabling direct validation against reference methods and a more effective translation between in vitro findings, animal models and patient studies.

Human Neural Stem Cell Induced Functional Network Stabilization After Cortical Stroke: A Longitudinal Resting-State fMRI Study in Mice.

Most stroke studies dealing with functional deficits and assessing stem cell therapy produce extensive hemispheric damage and can be seen as a model for severe clinical strokes. However, mild strokes have a better prospect for functional recovery. Recently, anatomic and behavioral changes have been reported for distal occlusion of the middle cerebral artery (MCA), generating a well-circumscribed and small cortical lesion, which can thus be proposed as mild to moderate cortical stroke. Using this cortical stroke model of moderate severity in the nude mouse, we have studied the functional networks with resting-state functional magnetic resonance imaging (fMRI) for 12 weeks following stroke induction. Further, human neural stem cells (hNSCs) were implanted adjacent to the ischemic lesion, and the stable graft vitality was monitored with bioluminescence imaging (BLI). Differentiation of the grafted neural stem cells was analyzed by immunohistochemistry and by patch-clamp electrophysiology. Following stroke induction, we found a pronounced and continuously rising hypersynchronicity of the sensorimotor networks including both hemispheres, in contrast to the severe stroke filament model where profound reduction of the functional connectivity had been reported by us earlier. The vitality of grafted neural stem cells remained stable throughout the whole 12 weeks observation period. In the stem cell treated animals, functional connectivity did not show hypersynchronicity but was globally slightly reduced below baseline at 2 weeks post-stroke, normalizing thereafter completely. Our resting-state fMRI (rsfMRI) studies on cortical stroke reveal for the first time a hypersynchronicity of the functional brain networks. This hypersynchronicity appears as a hallmark of mild cortical strokes, in contrast to severe strokes with striatal involvement where exclusively hyposynchronicity has been reported. The effect of the stem cell graft was an early and persistent normalization of the functional sensorimotor networks across the whole brain. These novel functional results may help interpret future outcome investigations after stroke and demonstrate the highly promising potential of stem cell treatment for functional outcome improvement after stroke.

Persistent Quantitative Vitality of Stem Cell Graft Is Necessary for Stabilization of Functional Brain Networks After Stroke.

Stem cell treatment after stroke has demonstrated substantial outcome improvement. However, monitoring of stem cell fate in vivo is still challenging and not routinely performed, yet important to quantify the role of the implanted stem cells on lesion improvement; in several studies even mortality of the graft has been reported. Resting state functional magnetic resonance imaging (rs-fMRI) is a highly sensitive imaging modality to monitor the brain-wide functional network alterations of many brain diseases in vivo. We monitor for 3 months the functional connectivity changes after intracortical stem cell engraftment in large, cortico-striatal (n = 9), and in small, striatal (n = 6) ischemic lesions in the mouse brain with non-invasive rs-fMRI on a 9.4T preclinical MRi scanner with GE-EPI sequence. Graft vitality is continuously recorded by bioluminescence imaging (BLI) roughly every 2 weeks after implantation of 300 k neural stem cells. In cortico-striatal lesions, the lesion extension induces graft vitality loss, in consequence leading to a parallel decrease of functional connectivity strength after a few weeks. In small, striatal lesions, the graft vitality is preserved for the whole observation period and the functional connectivity is stabilized at values as in the pre-stroke situation. But even here, at the end of the observation period of 3 months, the functional connectivity strength is found to decrease despite preserved graft vitality. We conclude that quantitative graft viability is a necessary but not sufficient criterion for functional neuronal network stabilization after stroke. Future studies with even longer time periods after stroke induction will need to identify additional players which have negative influence on the functional brain networks.

Repeatability and reproducibility of longitudinal relaxation rate in 12 small-animal MRI systems.

BACKGROUND: Many translational MR biomarkers derive from measurements of the water proton longitudinal relaxation rate R1, but evidence for between-site reproducibility of R1 in small-animal MRI is lacking. OBJECTIVE: To assess R1 repeatability and multi-site reproducibility in phantoms for preclinical MRI. METHODS: R1 was measured by saturation recovery in 2% agarose phantoms with five nickel chloride concentrations in 12 magnets at 5 field strengths in 11 centres on two different occasions within 1-13 days. R1 was analysed in three different regions of interest, giving 360 measurements in total. Root-mean-square repeatability and reproducibility coefficients of variation (CoV) were calculated. Propagation of reproducibility errors into 21 translational MR measurements and biomarkers was estimated. Relaxivities were calculated. Dynamic signal stability was also measured. RESULTS: CoV for day-to-day repeatability (N = 180 regions of interest) was 2.34% and for between-centre reproducibility (N = 9 centres) was 1.43%. Mostly, these do not propagate to biologically significant between-centre error, although a few R1-based MR biomarkers were found to be quite sensitive even to such small errors in R1, notably in myocardial fibrosis, in white matter, and in oxygen-enhanced MRI. The relaxivity of aqueous Ni2+ in 2% agarose varied between 0.66 s-1 mM-1 at 3 T and 0.94 s-1 mM-1 at 11.7T. INTERPRETATION: While several factors affect the reproducibility of R1-based MR biomarkers measured preclinically, between-centre propagation of errors arising from intrinsic equipment irreproducibility should in most cases be small. However, in a few specific cases exceptional efforts might be required to ensure R1-reproducibility.

Functional networks are impaired by elevated tau-protein but reversible in a regulatable Alzheimer's disease mouse model.

BACKGROUND: Aggregation of tau proteins is a distinct hallmark of tauopathies and has been a focus of research and clinical trials for Alzheimer's Disease. Recent reports have pointed towards a toxic effect of soluble or oligomeric tau in the spreading of tau pathology in Alzheimer's disease. Here we investigated the effects of expressing human tau repeat domain (tauRD) with pro- or anti-aggregant mutations in regulatable transgenic mouse models of Alzheimer's Disease on the functional neuronal networks and the structural connectivity strength. METHODS: Pro-aggregant and anti-aggregant mice were studied when their mutant tauRD was switched on for 12 months to reach the stage where pro-aggregant mice show cognitive impairment, whereas anti-aggregant mice remained cognitively normal. Then, mutant tauRD was switched off by doxycycline treatment for 8 weeks so that soluble transgenic tau disappeared and cognition recovered in the pro-aggregant mice, although some aggregates remained. At these two time points, at baseline after 12 months of mutant tau expression and after 8 weeks of doxycycline treatment, resting state fMRI and diffusion MRI were used to determine functional neuronal networks and fiber connectivities. Results of the transgenic mice were compared with wildtype littermates. RESULTS: Functional connectivity was strongly reduced in transgenic animals during mutant tauRD expression, in relation to WT mice. Interestingly, transgenic mice with the non-aggregant tau mutant showed identical functional deficits as the pro-aggregant mice, even though in this case there was no cognitive decline by behavioral testing. Upon 8 weeks doxycycline treatment and transgene switch-off, functional connectivity in both transgenic groups presented complete normalization of functional connectivity strength, equivalent to the situation in WT littermates. Structural connectivity was found only marginally sensitive to mutant tau expression (both pro- and anti-aggregant tauRD) and by doxycycline treatment. CONCLUSIONS: Our in vivo investigations unravel for the first time a strong reduction of functional neuronal networks by the presence of increased soluble rather than fibrillary tau, independent of its intrinsic propensity of aggregation, which is reversible by switching tau off. Our functional MRI study thus is an unexpected in vivo validation of a novel property of tau, while previous results pointed to a role of aggregation propensity for a pathological state by histopathology and cognitive decline. Our results present further evidence for early tauopathy biomarkers or a potential early stage drug target by functional networks analysis.

Sensorimotor Functional and Structural Networks after Intracerebral Stem Cell Grafts in the Ischemic Mouse Brain.

Past investigations on stem cell-mediated recovery after stroke have limited their focus on the extent and morphological development of the ischemic lesion itself over time or on the integration capacity of the stem cell graft ex vivo However, an assessment of the long-term functional and structural improvement in vivo is essential to reliably quantify the regenerative capacity of cell implantation after stroke. We induced ischemic stroke in nude mice and implanted human neural stem cells (H9 derived) into the ipsilateral cortex in the acute phase. Functional and structural connectivity changes of the sensorimotor network were noninvasively monitored using magnetic resonance imaging for 3 months after stem cell implantation. A sharp decrease of the functional sensorimotor network extended even to the contralateral hemisphere, persisting for the whole 12 weeks of observation. In mice with stem cell implantation, functional networks were stabilized early on, pointing to a paracrine effect as an early supportive mechanism of the graft. This stabilization required the persistent vitality of the stem cells, monitored by bioluminescence imaging. Thus, we also observed deterioration of the early network stabilization upon vitality loss of the graft after a few weeks. Structural connectivity analysis showed fiber-density increases between the cortex and white matter regions occurring predominantly on the ischemic hemisphere. These fiber-density changes were nearly the same for both study groups. This motivated us to hypothesize that the stem cells can influence, via early paracrine effect, the functional networks, while observed structural changes are mainly stimulated by the ischemic event.SIGNIFICANCE STATEMENT In recent years, research on strokes has made a shift away from a focus on immediate ischemic effects and towards an emphasis on the long-range effects of the lesion on the whole brain. Outcome improvements in stem cell therapies also require the understanding of their influence on the whole-brain networks. Here, we have longitudinally and noninvasively monitored the structural and functional network alterations in the mouse model of focal cerebral ischemia. Structural changes of fiber-density increases are stimulated in the endogenous tissue without further modulation by the stem cells, while functional networks are stabilized by the stem cells via a paracrine effect. These results will help decipher the underlying networks of brain plasticity in response to cerebral lesions and offer clues to unravelling the mystery of how stem cells mediate regeneration.

Dynamic Modulation of Microglia/Macrophage Polarization by miR-124 after Focal Cerebral Ischemia.

Mononuclear phagocytes respond to ischemic stroke dynamically, undergoing an early anti-inflammatory and protective phenotype followed by the pro-inflammatory and detrimental type. These dual roles of microglia/macrophages suggest the need of subtle adjustment of their polarization state instead of broad suppression. The most abundant brain-specific miRNA, miR-124, promotes neuronal differentiation but can also modulate microglia activation and keeps them in a quiescent state. We addressed whether the intracerebral injection of miR-124 in a mouse model of ischemic stroke before or after the peak phase of the pro-inflammatory polarization modifies the pro-/anti- inflammatory balance. In the sub-acute phase, 48 h after stroke, liposomated miR-124 shifted the predominantly pro-inflammatory polarized microglia/macrophages toward the anti-inflammatory phenotype. The altered immune response improved neurological deficit at day 6 after stroke. When miR-124 was injected 10 days after stroke, the pro-/anti- inflammatory ratio was still significantly reduced although to a lower degree and had no effect on recovery at day 14. This study indicates that miR-124 administration before the peak of the pro-inflammatory process of stroke is most effective in support of increasing the rehabilitation opportunity in the sub-acute phases of stroke. Our findings highlight the important role of immune cells after stroke and the therapeutic relevance of their polarization balance.

Fenómeno de Raynaud con lesiones isquémicas digitales: tratamiento con bloqueo de ganglio estrellado: presentación de un caso / Digital ischemic lesions associated to Raynaud's phenomenon treated with stellate ganglion block: case report

El fenómeno de Raynaud consiste en la aparición paroxística de espasmo vascular, que afecta a pequeñas arterias y arteriolas cutáneas, de las extremidades. Se manifiesta con palidez extrema, que puede ir seguida de cianosis y posterior rubicundez durante la fase hiperémica. Se acompaña generalmente de disestesias y, en forma ocasional, también de dolor. Generalmente, presentan escasa repercusión sistémica asociada. Los principales desencadenantes son el frío y el estrés emocional. El bloqueo del ganglio estrellado es utilizado frecuentemente para el diagnóstico y tratamiento de múltiples sindromes dolorosos crónicos. Con el bloqueo de la actividad simpática, se produce una vasodilatación de los vasos de la extremidad superior, cabeza y cuello, siendo éste el sustrato para su utilización en cuadros de insuficiencias vasculares de las zonas inervadas. Presentamos el caso de un bloqueo de ganglio estrellado en una paciente con lesiones isquémicas digitales secundarias a un fenómeno de Raynaud primario.

The sudden onset of vascular spasm, affecting small arteries and skin arterioles of limbs is known as Raynaud's phenomenon. it includes severe paleness sometimes followed by cyanosis and redness during the hyperemic phase. Usual findings are dysestesias and ocassionally pain. Normally it causes a small systemic impact. The most relevant triggering factors are cold and emotional stress. Stellate Ganglion Block is frequently used to diagnose and treat several chronic pain syndromes. The sympathetic activity block causes the vasodilation of the arms, head and neck, and this is the substratum for using it in vascular impairment syndrome. We present a stellate ganglion block in a patient with isquemic digital lesions secondary to Raynaud phenomenon.

A 2-year stage of change evaluation of dietary fat and fruit and vegetable intake behaviors of cardiac rehabilitation patients.

PURPOSE: To track the 2-year movement of cardiac rehabilitation patients through the stages of change for dietary fat reduction and increasing fruit and vegetable intake. DESIGN: A cross-sectional, longitudinal evaluation of a convenience sample of cardiac rehabilitation patients. SETTING: Department of Pulmonary and Cardiac Rehabilitation, Moses H. Cone Memorial Hospital, Greensboro, North Carolina. SUBJECTS: Subjects (n = 118) were predominately white, overweight, married men with a history of tobacco use. INTERVENTION: Group nutrition education sessions for 12 weeks. MEASURES: Stage of change assessments for dietary fat reduction and increasing fruit and vegetable intake were performed at the start (baseline), conclusion (3 months), and 2 years after cardiac rehabilitation. RESULTS: Baseline staging demonstrated patients' efforts to reduce dietary fat intake (preparation, 10.2%; action, 35.6%; maintenance, 47.5%). The assessment at 2 years staged 87.3% of the population in the maintenance stage. In contrast, the precontemplation (30.0%), contemplation (7.6%), and preparation (49.2%) stages dominated baseline staging for modifying fruit and vegetable intake. Patients in the precontemplation and contemplation stages increased to 58.5% at 2 years. CONCLUSIONS: Cardiac rehabilitation patients are in different stages for two food behaviors linked to the same illness. Results support the appropriateness of nutrition education that emphasizes instrumental information for affecting fat reduction behaviors. Modifying fruit and vegetable intake behaviors is more appropriately addressed with noninstrumental interventions that emphasize health benefits and barriers to change.