σ-Arsolido complexes.

The σ-stannyl complexes [M(SnnBu3)(CO)n(η5-C5H5)] (n = 3, M = Mo, W; n = 2, M = Fe) serve as mild reagents for the installation of σ-arsolyl ligands in transmetallation reactions with As-chloro-arsoles ClAsC4R4 (R = Me, Ph) to afford [M(σ-AsC4R4)(CO)n(η5-C5H5)]. The reaction of [Cr(SnnBu3)(CO)3(η5-C5H5)] with ClAsC4Ph4 most likely proceeds in a similar manner but is immediately followed by rapid formation of (AsC4Ph4)2 and [Cr2(CO)6(η5-C5H5)2]. The reaction of [Mo(SnnBu3)(CO)3(η5-C5H5)] with ClAsC4(SiMe3)-2,5-Me2-3,4 is accompanied by monodesilylation to afford [Mo{σ-AsC4(SiMe3)-2-Me2-3,4}(CO)3(η5-C5H5)]. The slow reaction of [Fe(SnnBu3)(CO)2(η5-C5H5)] with ClAsC4Me4 produced only traces of [Fe(σ-AsC4Me4)(CO)2(η5-C5H5)] due to competition with the Diels-Alder type dimerisation of the haloarsole. Although attempts to decarbonylate the σ-arsolyl complexes were unsuccessful, computational analysis suggests that the trigonal 'XL' arsolenium coordination mode is viable.

Electrophilic As-functionalisation of σ-arsolido complexes.

The σ-arsolido complex [Mo(AsC4Me4)(CO)3(η5-C5H5)] is alkylated at arsenic by MeOTf to afford the pentamethylarsole complex [Mo(MeAsC4Me4)(CO)3(η5-C5H5)](OTf) while iodomethane affords a mixture of [Me2AsC4Me4]I, [MoMe(CO)3(η5-C5H5)], [MoI(CO)3(η5-C5H5)] and the arsole complexes cisoid- and transoid-[MoI(MeAsC4Me4)(CO)2(η5-C5H5)] and transoid-[Mo{C(O)Me}(MeAsC4Me4)(CO)2(η5-C5H5)], The arsole ligand in [Mo(MeAsC4Me4)(CO)3(η5-C5H5)](OTf) is readily liberated by NaI in acetone to afford free MeAsC4Me4 and [MoI(CO)3(η5-C5H5)]. In a similar manner, the reaction of [Mo(AsC4Ph4)(CO)3(η5-C5H5)] with MeI affords MeAsC4Ph4 and [MoI(CO)3(η5-C5H5)], while [Mo{AsC4(SiMe3)-2-Me2-3,4}(CO)3(η5-C5H5)] with MeOTf affords [Mo{MeAsC4(SiMe3)-2-Me2-3,4}(CO)3(η5-C5H5)](OTf). The reaction of [Mo(AsC4Me4)(CO)3(η5-C5H5)] with activated alkynes (RCCR: R = CF3, CO2Me) does not proceed via [4 + 2] cyclo-addition but rather electrophilic attack at arsenic followed by metallacyclisation with incorporation of a carbonyl ligand in the spirocyclic complexes [Mo{As(C4Me4)CRCRCO}(CO)2(η5-C5H5)].

Poly(imidazolyliden-yl)borato Complexes of Tungsten: Mapping Steric vs. Electronic Features of Facially Coordinating Ligands.

A convenient synthesis of [HB(HImMe)3](PF6)2 (ImMe = N-methylimidazolyl) is decribed. This salt serves in situ as a precursor to the tris(imidazolylidenyl)borate Li[HB(ImMe)3] pro-ligand upon deprotonation with nBuLi. Reaction with [W(≡CC6H4Me-4)(CO)2(pic)2(Br)] (pic = 4-picoline) affords the carbyne complex [W(≡CC6H4Me-4)(CO)2{HB(ImMe)3}]. Interrogation of experimental and computational data for this compound allow a ranking of familiar tripodal and facially coordinating ligands according to steric (percentage buried volume) and electronic (νCO) properties. The reaction of [W(≡CC6H4Me-4)(CO)2{HB(ImMe)3}] with [AuCl(SMe2)] affords the heterobimetallic semi-bridging carbyne complex [WAu(µ-CC6H4Me-4)(CO)2(Cl){HB(ImMe)3}].

Free and coordinated biarsolyls.

A trace side product from the reaction of [Mo(AsC4Me4)(CO)3(η-C5H5)] with [Mn(THF)(CO)2(η5-C5H4Me)] was identified as the biarsolyl complex [Mn2{µ-(AsC4Me4)2}(CO)4(C5H4Me)2] on the basis of a strategic synthesis from [Mn(THF)(CO)2(η5-C5H4Me)] and the pre-formed and structurally characterised biarsolyl (AsC4Me4)2. Crystallographic and computational data for this first example of a biarsolyl complex and free biarsolyls are discussed in the context of those for free biarsolyls.

Bridging arsolido complexes.

The σ-arsolyl complex [Mo(AsC4Me4)(CO)3(η-C5H5)] serves as a metallo-ligand for the strategic construction of µ-arsolido bridged heterobimetallic complexes [MoCr(µ-AsC4Me4)(CO)8(η5-C5H5)], [MoMn(µ-AsC4Me4)(CO)5(η5-C5H5)(η5-C5H4Me)], [MoAu(µ-AsC4Me4)(C6F5)(CO)3(η5-C5H5)] and [MoFe(µ-AsC4Me4)(CO)5(η5-C5H5)2]PF6via reactions with [Cr(THF)(CO)5], [Au(C6F5)(THT)], [Mn(THF)(CO)2(η5-C5H4Me)] and [Fe(THF)(CO)2(η5-C5H5)]PF6, respectively. The reaction of [Mo(AsC4Me4)(CO)3(η-C5H5)] with [Co3(µ3-CH)(CO)9] affords the tetrametallic species [MoCo3(AsC4Me4)(µ3-CH)(CO)11(η-C5H5)]. Crystallographic and computational data for all products are discussed.

Evaluation of the orally bioavailable 4-phenylbutyrate-tethered trichostatin A analogue AR42 in models of spinal muscular atrophy.

Proximal spinal muscular atrophy (SMA) is a leading genetic cause for infant death in the world and results from the selective loss of motor neurons in the spinal cord. SMA is a consequence of low levels of SMN protein and small molecules that can increase SMN expression are of considerable interest as potential therapeutics. Previous studies have shown that both 4-phenylbutyrate (4PBA) and trichostatin A (TSA) increase SMN expression in dermal fibroblasts derived from SMA patients. AR42 is a 4PBA-tethered TSA derivative that is a very potent histone deacetylase inhibitor. SMA patient fibroblasts were treated with either AR42, AR19 (a related analogue), 4PBA, TSA or vehicle for 5 days and then immunostained for SMN localization. AR42 as well as 4PBA and TSA increased the number of SMN-positive nuclear gems in a dose-dependent manner while AR19 did not show marked changes in gem numbers. While gem number was increased in AR42-treated SMA fibroblasts, there were no significant changes in FL-SMN mRNA or SMN protein. The neuroprotective effect of this compound was then assessed in SMNΔ7 SMA (SMN2+/+;SMNΔ7+/+;mSmn-/-) mice. Oral administration of AR42 prior to disease onset increased the average lifespan of SMNΔ7 SMA mice by ~ 27% (20.1 ± 1.6 days for AR42-treated mice vs. 15.8 ± 0.4 days for vehicle-treated mice). AR42 treatment also improved motor function in these mice. AR42 treatment inhibited histone deacetylase (HDAC) activity in treated spinal cord although it did not affect SMN protein expression in these mice. AKT and GSK3ß phosphorylation were both significantly increased in SMNΔ7 SMA mouse spinal cords. In conclusion, presymptomatic administration of the HDAC inhibitor AR42 ameliorates the disease phenotype in SMNΔ7 SMA mice in a SMN-independent manner possibly by increasing AKT neuroprotective signaling.

A transcriptional constraint mechanism limits the homeostatic response to activity deprivation in mammalian neocortex.

Healthy neuronal networks rely on homeostatic plasticity to maintain stable firing rates despite changing synaptic drive. These mechanisms, however, can themselves be destabilizing if activated inappropriately or excessively. For example, prolonged activity deprivation can lead to rebound hyperactivity and seizures. While many forms of homeostasis have been described, whether and how the magnitude of homeostatic plasticity is constrained remains unknown. Here, we uncover negative regulation of cortical network homeostasis by the PARbZIP family of transcription factors. In cortical slice cultures made from knockout mice lacking all three of these factors, the network response to prolonged activity withdrawal measured with calcium imaging is much stronger, while baseline activity is unchanged. Whole-cell recordings reveal an exaggerated increase in the frequency of miniature excitatory synaptic currents reflecting enhanced upregulation of recurrent excitatory synaptic transmission. Genetic analyses reveal that two of the factors, Hlf and Tef, are critical for constraining plasticity and for preventing life-threatening seizures. These data indicate that transcriptional activation is not only required for many forms of homeostatic plasticity but is also involved in restraint of the response to activity deprivation.

The human brain is made up of billions of nerve cells called neurons which receive and send signals to one another. To avoid being over- or under-stimulated, neurons can adjust the strength of the inputs they receive by altering how connected they are to other nerve cells. This process, known as homeostatic plasticity, is thought to be necessary for normal brain activity as it helps keep the outgoing signals of neurons relatively constant. However, homeostatic plasticity can lead to seizures if it becomes too strong and overcompensates for weak input signals. Regulating this process is therefore central to brain health, but scientists do not understand if or how it is controlled. To address this, Valakh et al. analyzed the genes activated in neurons lacking incoming signals to find proteins that regulate homeostatic plasticity. This revealed a class of molecules called transcription factors (which switch genes on or off) that constrain the process. In brain samples from mice without these regulatory proteins, neurons received twice as much input, leading to an increase in brain activity resembling that observed during seizures. Valakh et al. confirmed this finding using live mice, which developed seizures in the absence of these transcription factors. These findings suggest that this type of regulation to keep homeostatic plasticity from becoming too strong may be important. This could be especially vital as the brain develops, when the strength of connections between neurons changes rapidly. The discovery of the transcription factors involved provides a potential target for activating or restraining homeostatic plasticity. This control could help researchers better understand how the process stabilizes brain signaling.

Arsolyl-supported intermetallic dative bonding.

The first examples of late transition metal η5-arsolyls (L = CO, P(OMe)3; R = Ph, Me, Et, SiMe3; R' = Ph, H, Me, Et, Me) serve as ditopic donors to extraneous metal centres (M = PtII, AuI, HgII) through both conventional As → M and polar-covalent (dative) Co → M interactions.

Heterocyclic arsinocarbynes via tandem transmetallation.

Gold(i)-catalysed tandem transmetallation (Sn→Au→As) of the stannylcarbyne [W(≡CSnnBu3)(CO)2(Tp*)] (Tp* = hydrotris-(dimethylpyrazolyl)borate) with haloarsines gives direct access to a range of novel arsinocarbyne complexes, LnM≡CAsR2, including unusual heterocyclic phenarsazininyl and arsolyl examples.

Lacking Advanced Degrees are not a Barrier to Entry into Academic Surgery Leadership.

BACKGROUND: Undergraduate and graduate medical education offerings continue to create opportunities for medical students to pursue MD+ degree education. These educational endeavors provide formal education in fields related to surgery, which gives trainees and surgeons diverse perspectives on surgical care. This study sought to assess current prevalence of additional advanced degrees among leaders in academic surgery to assess the relationship between dual degree attainment and holding various leadership positions within surgical departments. METHODS: The Association for Program Directors in Surgery database was used to identify academic surgical programs, which comprised our study population. Each department of surgery website in the APDS database was interrogated for departmental leaders and their reported academic degrees. RESULTS: Among 3223 identified surgeon leaders, 14.6% (470/3223) were found to possess MD+ degrees. Most common degrees possessed included MBA, MPH, and PhD. In comparing different types of surgeon leaders such as chairs, program directors, and division chiefs, no group was found to have a significantly higher prevalence of MD+ degrees than others. CONCLUSION: Prevalence of MD+ degrees among current academic surgery leaders is low, and the lack of an advanced degree should not be considered a barrier to entry into leadership positions. We hypothesize that these findings are likely to evolve as larger proportions of trainees obtain MD+ degrees during medical school and academic development time throughout residency.

Effects of clonidine on progressive ratio schedule performance in Fmr1 knockout mice.

RATIONALE: Fragile X syndrome (FXS), the most prevalent genetic form of intellectual disability, is characterized by intellectual impairment, impaired sociability, aggression, self-injury, hyperactivity, and attention deficits. A consequence of the hyperactivity and attention deficits is that individuals with FXS are frequently diagnosed with attention deficit hyperactivity disorder (ADHD) and treated with medications approved for ADHD (e.g., the α2-agonist clonidine). The pharmacotherapy of FXS is often accompanied with behavioral therapies that rely on positive reinforcement and other operant principles. Despite the commonplace mixture of drug and behavioral therapy, little attention has been paid to the observation that clonidine or other psychotropic drugs may alter operant processes. OBJECTIVES: In the present progressive ratio study, we used a knockout mouse model to test the effects of the fragile X genotype, the α2-agonist clonidine, and the fragile X genotype and clonidine together on operant processes in a positive reinforcement task. RESULTS: We found that clonidine decreased the progressive ratio breakpoint, increased the length of post-reinforcement pauses, and slowed the run rate. None of these effects varied by genotype. The effect on breakpoint suggests that clonidine alters motivation, but analysis using mathematical principles of reinforcement (MPR) did not rule out motor parameters as a contributor. CONCLUSIONS: Our findings show that clonidine alters operant behavior and serve as a caution for combining clonidine with behavioral therapies that rely on positive reinforcement. Further research using different murine behaviors (e.g., touchscreen tasks) or different animal models (e.g., knockout rats) is needed to explore the interaction between pharmaco- and behavioral therapy.

Analysis of retention of gadolinium by brain, bone, and blood following linear gadolinium-based contrast agent administration in rats with experimental sepsis.

PURPOSE: It is important to identify populations that may be vulnerable to the brain deposition of gadolinium (Gd) from MRI contrast agents. At intervals from 24 hours to 6 weeks following injection of a linear Gd contrast agent, the brain, blood and bone content of Gd were compared between control rats and those with experimental endotoxin-induced sepsis that results in neuroinflammation and blood-brain barrier disruption. METHODS: Male rats were injected intraperitoneally with 10 mg/kg lipopolysaccharide. Control animals received no injection. Twenty-four hours later, 0.2 mmol/kg of gadobenate dimeglumine was injected intravenously. Brain, blood, and bone Gd levels were measured at 24 hours, 1 week, 3 weeks, and 6 weeks by inductively coupled plasma mass spectroscopy. RESULTS: Blood Gd decreased rapidly between 24 hours and 1 week, and thereafter was undetectable, with no significant difference between lipopolysaccharide and control rats. Brain levels of Gd were significantly higher (4.29-2.36-fold) and bone levels slightly higher (1.35-1.11-fold) in lipopolysaccharide than control rats at all time points with significant retention at 6 weeks. CONCLUSION: Experimental sepsis results in significantly higher deposition of Gd in the brain and bone in rats. While blood Gd clears rapidly, brain and bone retained substantial Gd even at 6 weeks following contrast injection.

Lipopolysaccharide exposure in a rat sepsis model results in hippocampal amyloid-ß plaque and phosphorylated tau deposition and corresponding behavioral deficits.

Sepsis is a severe systemic inflammatory response to infection associated with acute and chronic neurocognitive consequences, including an increased risk of later-life dementia. In a lipopolysaccharide-induced rat sepsis model, we have demonstrated neuroinflammation, cortical amyloid-beta plaque deposition, and increased whole brain levels of phosphorylated tau. Hippocampal abnormalities, particularly those of the dentate gyrus, are seen in Alzheimer's disease and age-related memory loss. The focus of this study was to determine whether Aß plaques and phosphorylated tau aggregates occur in the hippocampus as a consequence of lipopolysaccharide administration, and whether behavioral abnormalities related to the hippocampus, particularly the dentate gyrus, can be demonstrated. Male Sprague Dawley rats received an intraperitoneal injection of 10 mg/kg of lipopolysaccharide endotoxin. Control animals received a saline injection. Seven days post injection, Aß plaques and phosphorylated tau in the hippocampus were quantified following immunostaining. Behavioral tests that have previously been shown to result in specific deficits in dentate gyrus-lesioned rats were administered. Lipopolysaccharide treatment results in the deposition of beta amyloid plaques and intracellular phosphorylated tau in the hippocampus, including the dorsal dentate gyrus. Lipopolysaccharide treatment resulted in behavioral deficits attributable to the dorsal dentate gyrus, including episodic-like memory function that primarily involves spatial, contextual, and temporal orientation and integration. Lipopolysaccharide administration results in hippocampal deposition of amyloid-beta plaques and intracellular phosphorylated tau and results in specific behavioral deficits attributable to the dorsal dentate gyrus. These findings, if persistent, could provide a basis for the higher rate of dementia in longitudinal studies of sepsis survivors.

Lipopolysaccharide endotoxemia induces amyloid-ß and p-tau formation in the rat brain.

Amyloid beta (Aß) plaques are not specific to Alzheimer's disease and occur with aging and neurodegenerative disorders. Soluble brain Aß may be neuroprotective and increases in response to neuroinflammation. Sepsis is associated with neurocognitive compromise. The objective was to determine, in a rat endotoxemia model of sepsis, whether neuroinflammation and soluble Aß production are associated with Aß plaque and hyperphosphorylated tau deposition in the brain. Male Sprague Dawley rats received a single intraperitoneal injection of 10 mg/kg of lipopolysaccharide endotoxin (LPS). Brain and blood levels of IL-1ß, IL-6, and TNFα and cortical microglial density were measured in LPS-injected and control animals. Soluble brain Aß and p-tau were compared and Aß plaques were quantified and characterized. Brain uptake of [18F]flutemetamol was measured by phosphor imaging. LPS endotoxemia resulted in elevations of cytokines in blood and brain. Microglial density was increased in LPS-treated rats relative to controls. LPS resulted in increased soluble Aß and in p-tau levels in whole brain. Progressive increases in morphologically-diffuse Aß plaques occurred throughout the interval of observation (to 7-9 days post LPS). LPS endotoxemia resulted in increased [18F]flutemetamol in the cortex and increased cortex: white matter ratios of activity. In conclusion, LPS endotoxemia causes neuroinflammation, increased soluble Aß and Aß diffuse plaques in the brain. Aß PET tracers may inform this neuropathology. Increased p-tau in the brain of LPS treated animals suggests that downstream consequences of Aß plaque formation may occur. Further mechanistic and neurocognitive studies to understand the causes and consequences of LPS-induced neuropathology are warranted.

The effects of C5-substituted 2,4-diaminoquinazolines on selected transcript expression in spinal muscular atrophy cells.

C5-substituted 2,4-diaminoquinazolines (2,4-DAQs) ameliorate disease severity in SMA mice. It is uncertain, however, that these compounds increase SMN protein levels in vivo even though they were identified as activators of the SMN2 promoter. These compounds also regulate the expression of other transcripts in neuroblastoma cells. In this study, we investigate the mechanism by which the 2,4-DAQs regulate the expression of SMN2 as well as other targets. D156844, D158872, D157161 and D157495 (RG3039) increased SMN2 promoter-driven reporter gene activity by at least 3-fold in NSC-34 cells. These compounds, however, did not significantly increase SMN2 mRNA levels in type II SMA fibroblasts nor in NSC-34 cells, although there was a trend for these compounds increasing SMN protein in SMA fibroblasts. The number of SMN-containing gems was increased in SMA fibroblasts in response to 2,4-DAQ treatment in a dose-dependent manner. ATOH7 mRNA levels were significantly lower in type II SMA fibroblasts. 2,4-DAQs significantly increased ATOH7, DRNT1 and DRTN2 transcript levels in type II SMA fibroblasts and restored ATOH7 levels to those observed in healthy fibroblasts. These compounds also increase Atoh7 mRNA expression in NSC-34 cells. In conclusion, 2,4-DAQs regulate SMN2 by increasing protein levels and gem localization. They also increase ATOH7, DRNT1 and DRNT2 transcript levels. This study reveals that the protective effects of 2,4-DAQs in SMA may be independent of SMN2 gene regulation. These compounds could be used in concert with a proven SMN2 inducer to develop a multi-faceted approach to treating SMA.

The ventral dentate gyrus mediates pattern separation for reward value.

Rats with ventral dentate gyrus (DG) lesions, sham lesions, and controls were run in a runway for 20 pellets of food. After reaching running speed asymptote, the number of pellets was reduced to 1, 9, or 17 pellets. The purpose of the present experiment was to determine whether the ventral DG subregion of the hippocampus plays a role in pattern separation for reward value. The results indicated that sham lesioned and control rats displayed a graded decrease in runway velocities, supporting a pattern separation process. In contrast, ventral DG lesioned rats continued to maintain runway velocities regardless of the reward-value shifts. The ventral DG lesion results do not appear to be due to hyperactivity but could be based on the idea that the ventral DG is part of a decision-making circuitry to predict goal-relevant reward outcomes. (PsycINFO Database Record

Increasing the efficiency of a targeted methicillin-resistant Staphylococcus aureus screening program.

An interdisciplinary team implemented a screening program targeting patients with a history of methicillin-resistant Staphylococcus aureus (MRSA), to reduce unnecessary contact isolation. After converting from a 2-step culture-based protocol to single polymerase chain reaction (PCR) testing, we increased the efficiency of the screening program from 77% to 100%. Despite the higher cost of PCR-based testing, this program remained cost-saving.

Naloxone injections into CA3 disrupt pattern completion associated with relapse from cocaine seeking.

The goal of the present research was to assess the degree to which a pattern completion process operates in cue-induced relapse to cocaine-seeking behavior. Using a novel cue-preference version of the place preference task, rats were administered cocaine or saline, which resulted in a preference for the cocaine-paired cues. After 21 days of abstinence and prior to the preference test, for one group, PBS or naloxone was injected into the CA3 subregion of the hippocampus and for a second group, saline or naloxone was injected systemically. The results indicated that infusions of naloxone into CA3 or systemic injections produced a marked disruption for one and two cues, but had minimal disruptive effect for three or four cues, suggesting that naloxone injections disrupt CA3 function and trigger a deficit in a pattern completion process. Thus, it appears that cue-based activation of the dorsal CA3 might be a critical trigger via a pattern completion process. Based on additional analyses it appears that there is a disruption primarily for object touches for one cue naloxone injections into the CA3 or systemic injections, but no effect on time (spatial context). © 2016 Wiley Periodicals, Inc.

Dentate gyrus supports slope recognition memory, shades of grey-context pattern separation and recognition memory, and CA3 supports pattern completion for object memory.

In order to examine the role of the dorsal dentate gyrus (dDG) in slope (vertical space) recognition and possible pattern separation, various slope (vertical space) degrees were used in a novel exploratory paradigm to measure novelty detection for changes in slope (vertical space) recognition memory and slope memory pattern separation in Experiment 1. The results of the experiment indicate that control rats displayed a slope recognition memory function with a pattern separation process for slope memory that is dependent upon the magnitude of change in slope between study and test phases. In contrast, the dDG lesioned rats displayed an impairment in slope recognition memory, though because there was no significant interaction between the two groups and slope memory, a reliable pattern separation impairment for slope could not be firmly established in the DG lesioned rats. In Experiment 2, in order to determine whether, the dDG plays a role in shades of grey spatial context recognition and possible pattern separation, shades of grey were used in a novel exploratory paradigm to measure novelty detection for changes in the shades of grey context environment. The results of the experiment indicate that control rats displayed a shades of grey-context pattern separation effect across levels of separation of context (shades of grey). In contrast, the DG lesioned rats displayed a significant interaction between the two groups and levels of shades of grey suggesting impairment in a pattern separation function for levels of shades of grey. In Experiment 3 in order to determine whether the dorsal CA3 (dCA3) plays a role in object pattern completion, a new task requiring less training and using a choice that was based on choosing the correct set of objects on a two-choice discrimination task was used. The results indicated that control rats displayed a pattern completion function based on the availability of one, two, three or four cues. In contrast, the dCA3 lesioned rats displayed a significant interaction between the two groups and the number of available objects suggesting impairment in a pattern completion function for object cues.

Clinical, patient experience and cost impacts of performing active surveillance on known methicillin-resistant Staphylococcus aureus positive patients admitted to medical-surgical units.

BACKGROUND: There is a large and growing body of evidence that methicillin-resistant Staphylococcus aureus (MRSA) screening programs are cost effective, but such screening represents a significant cost burden for hospitals. This study investigates the clinical, patient experience and cost impacts of performing active surveillance on known methicillin-resistant S aureus positive (MRSA+) patients admitted to 7 medical-surgical units of a large regional hospital, specifically to allow discontinuation of contact isolation. METHODS: We conducted mixed-methods retrospective evaluation of a process improvement project that screened admitted patients with known MRSA+ status for continued MRSA colonization. RESULTS: Of those eligible patients on our institution's MRSA+ list who did complete testing, 80.2% (130/162) were found to be no longer colonized, and only 19.8% (32/162) were still colonized. Forty-one percent (13/32) of interviewed patients in contact isolation for MRSA reported that isolation had affected their hospital stay, and 28% (9/32) of patients reported emotional distress resulting from their isolation. Total cost savings of the program are estimated at $101,230 per year across the 7 study units. CONCLUSION: Our findings provide supporting evidence that a screening program targeting patients with a history of MRSA who would otherwise be placed in isolation has the potential to improve outcomes and patient experience and reduce costs.