Recent Research Articles from UNTHSC

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Progesterone-induced neuroprotection: factors that may predict therapeutic efficacy.

Wed, 01/15/2014 - 9:41am
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Progesterone-induced neuroprotection: factors that may predict therapeutic efficacy.

Brain Res. 2013 Jun 13;1514:98-106

Authors: Singh M, Su C

Abstract
Both progesterone and estradiol have well-described neuroprotective effects against numerous insults in a variety of cell culture models, animal models and in humans. However, the efficacy of these hormones may depend on a variety of factors, including the type of hormone used (ex. progesterone versus medroxyprogesterone acetate), the duration of the postmenopausal period prior to initiating the hormone intervention, and potentially, the age of the subject. The latter two factors relate to the proposed existence of a "window of therapeutic opportunity" for steroid hormones in the brain. While such a window of opportunity has been described for estrogen, there is a paucity of information to address whether such a window of opportunity exists for progesterone and its related progestins. Here, we review known cellular mechanisms likely to underlie the protective effects of progesterone and furthermore, describe key differences in the neurobiology of progesterone and the synthetic progestin, medroxyprogesterone acetate (MPA). Based on the latter, we offer a model that defines some of the key cellular and molecular players that predict the neuroprotective efficacy of progesterone. Accordingly, we suggest how changes in the expression or function of these cellular and molecular targets of progesterone with age or prolonged duration of hormone withdrawal (such as following surgical or natural menopause) may impact the efficacy of progesterone. This article is part of a Special Issue entitled Hormone Therapy.

PMID: 23340161 [PubMed - indexed for MEDLINE]

Window of opportunity: estrogen as a treatment for ischemic stroke.

Wed, 01/15/2014 - 9:41am
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Window of opportunity: estrogen as a treatment for ischemic stroke.

Brain Res. 2013 Jun 13;1514:83-90

Authors: Liu R, Yang SH

Abstract
The neuroprotection research in the last 2 decades has witnessed a growing interest in the functions of estrogens as neuroprotectants against neurodegenerative diseases including stroke. The neuroprotective action of estrogens has been well demonstrated in both in vitro and in vivo models of ischemic stroke. However, the major conducted clinical trials so far have raised concern for the protective effect of estrogen replacement therapy in postmenopausal women. The discrepancy could be partly due to the mistranslation between the experimental stroke research and clinical trials. While predominant experimental studies tested the protective action of estrogens on ischemic stroke using acute treatment paradigm, the clinical trials have mainly focused on the effect of estrogen replacement therapy on the primary and secondary stroke prevention which has not been adequately addressed in the experimental stroke study. Although the major conducted clinical trials have indicated that estrogen replacement therapy has an adverse effect and raise concern for long term estrogen replacement therapy for stroke prevention, these are not appropriate for assessing the potential effects of acute estrogen treatment on stroke protection. The well established action of estrogen in the neurovascular unit and its potential interaction with recombinant tissue Plasminogen Activator (rtPA) makes it a candidate for the combined therapy with rtPA for the acute treatment of ischemic stroke. On the other hand, the "critical period" and newly emerged "biomarkers window" hypotheses have indicated that many clinical relevant factors have been underestimated in the experimental ischemic stroke research. The development and application of ischemic stroke models that replicate the clinical condition is essential for further evaluation of acute estrogen treatment on ischemic stroke which might provide critical information for future clinical trials. This article is part of a Special Issue entitled Hormone Therapy.

PMID: 23340160 [PubMed - indexed for MEDLINE]

Window of opportunity for estrogen and progestin intervention in brain aging and Alzheimer's disease.

Wed, 01/15/2014 - 9:41am
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Window of opportunity for estrogen and progestin intervention in brain aging and Alzheimer's disease.

Brain Res. 2013 Jun 13;1514:1-2

Authors: Singh M, Simpkins JW, Simpkins JW, Bimonte-Nelson HA, Bimonte-Nelson HA, Brinton RD, Brinton RD

PMID: 23726132 [PubMed - indexed for MEDLINE]

Therapeutic strategies in Friedreich's ataxia.

Wed, 01/15/2014 - 9:41am
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Therapeutic strategies in Friedreich's ataxia.

Brain Res. 2013 Jun 13;1514:91-7

Authors: Richardson TE, Kelly HN, Yu AE, Simpkins JW

Abstract
First established as a diagnosis by Nikolaus Friedreich in 1863, Friedreich's ataxia (FA) is an autosomal recessive progressive neurodegenerative disorder cause by a trinucleotide repeat expansion. FA begins with the functional absence of the FXN gene product frataxin, a protein whose exact function still remains unknown. This absence results in impaired intracellular antioxidant defenses, dysregulation of iron-sulfur cluster proteins, depression of aerobic electron transport chain respiration, massive mitochondrial dysfunction, and ultimately cell death in the brain, spinal cord and heart. Herein, we review the molecular and cellular pathogenesis leading to widespread organ system dysfunction, as well as current therapeutic research aimed at preventing the debilitating effects of frataxin loss and preventing the signs and symptoms associated of FA. We also discuss the ongoing treatment strategies employed by our laboratory to prevent mitochondrial damage using synergistic effects of 17β-estradiol and methylene blue, previously shown by our group and others to have protective effects in human FA fibroblasts. This article is part of a Special Issue entitled Hormone Therapy.

PMID: 23587934 [PubMed - indexed for MEDLINE]

Oxidative stress defines the neuroprotective or neurotoxic properties of androgens in immortalized female rat dopaminergic neuronal cells.

Sat, 01/11/2014 - 5:31am
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Oxidative stress defines the neuroprotective or neurotoxic properties of androgens in immortalized female rat dopaminergic neuronal cells.

Endocrinology. 2013 Nov;154(11):4281-92

Authors: Holmes S, Abbassi B, Su C, Singh M, Cunningham RL

Abstract
Males have a higher risk for developing Parkinson's disease and parkinsonism after ischemic stroke than females. Although estrogens have been shown to play a neuroprotective role in Parkinson's disease, there is little information on androgens' actions on dopamine neurons. In this study, we examined the effects of androgens under conditions of oxidative stress to determine whether androgens play a neuroprotective or neurotoxic role in dopamine neuronal function. Mitochondrial function, cell viability, intracellular calcium levels, and mitochondrial calcium influx were examined in response to androgens under both nonoxidative and oxidative stress conditions. Briefly, N27 dopaminergic cells were exposed to the oxidative stressor, hydrogen peroxide, and physiologically relevant levels of testosterone or dihydrotestosterone, applied either before or after oxidative stress exposure. Androgens, alone, increased mitochondrial function via a calcium-dependent mechanism. Androgen pretreatment protected cells from oxidative stress-induced cell death. However, treatment with androgens after the oxidative insult increased cell death, and these effects were, in part, mediated by calcium influx into the mitochondria. Interestingly, the negative effects of androgens were not blocked by either androgen or estrogen receptor antagonists. Instead, a putative membrane-associated androgen receptor was implicated. Overall, our results indicate that androgens are neuroprotective when oxidative stress levels are minimal, but when oxidative stress levels are elevated, androgens exacerbate oxidative stress damage.

PMID: 23959938 [PubMed - indexed for MEDLINE]

STRait Razor: a length-based forensic STR allele-calling tool for use with second generation sequencing data.

Thu, 01/09/2014 - 12:27pm
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STRait Razor: a length-based forensic STR allele-calling tool for use with second generation sequencing data.

Forensic Sci Int Genet. 2013 Jul;7(4):409-17

Authors: Warshauer DH, Lin D, Hari K, Jain R, Davis C, Larue B, King JL, Budowle B

Abstract
Recent studies have demonstrated the capability of second generation sequencing (SGS) to provide coverage of short tandem repeats (STRs) found within the human genome. However, there are relatively few bioinformatic software packages capable of detecting these markers in the raw sequence data. The extant STR-calling tools are sophisticated, but are not always applicable to the analysis of the STR loci commonly used in forensic analyses. STRait Razor is a newly developed Perl-based software tool that runs on the Linux/Unix operating system and is designed to detect forensically-relevant STR alleles in FASTQ sequence data, based on allelic length. It is capable of analyzing STR loci with repeat motifs ranging from simple to complex without the need for extensive allelic sequence data. STRait Razor is designed to interpret both single-end and paired-end data and relies on intelligent parallel processing to reduce analysis time. Users are presented with a number of customization options, including variable mismatch detection parameters, as well as the ability to easily allow for the detection of alleles at new loci. In its current state, the software detects alleles for 44 autosomal and Y-chromosome STR loci. The study described herein demonstrates that STRait Razor is capable of detecting STR alleles in data generated by multiple library preparation methods and two Illumina(®) sequencing instruments, with 100% concordance. The data also reveal noteworthy concepts related to the effect of different preparation chemistries and sequencing parameters on the bioinformatic detection of STR alleles.

PMID: 23768312 [PubMed - indexed for MEDLINE]

The role of p38 in mitochondrial respiration in male and female mice.

Thu, 01/09/2014 - 12:27pm
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The role of p38 in mitochondrial respiration in male and female mice.

Neurosci Lett. 2013 Jun 7;544:152-6

Authors: Ju X, Wen Y, Metzger D, Jung M

Abstract
p38 is a mitogen-activated protein kinase and mediates cell growth, cell differentiation, and synaptic plasticity. The aim of this study is to determine the extent to which p38 plays a role in maintaining mitochondrial respiration in male and female mice under a normal condition. To achieve this aim, we have generated transgenic mice that lack p38 in cerebellar Purkinje neurons by crossing Pcp2 (Purkinje cell protein 2)-Cre mice with p38(loxP/loxP) mice. Mitochondria from cerebellum were then isolated from the transgenic and wild-type mice to measure mitochondrial respiration using XF24 respirometer. The mRNA and protein expression of cytochrome c oxidase (COX) in cerebellum were also measured using RT-PCR and immunoblot methods. Separately, HT22 cells were used to determine the involvement of 17β-estradiol (E2) and COX in mitochondrial respiration. The genetic knockout of p38 in Purkinje neurons suppressed the mitochondrial respiration only in male mice and increased COX expression only in female mice. The inhibition of COX by sodium azide (SA) sharply suppressed mitochondrial respiration of HT22 cells in a manner that was protected by E2. These data suggest that p38 is required for the mitochondrial respiration of male mice. When p38 is below a normal level, females may maintain mitochondrial respiration through COX up-regulation.

PMID: 23603578 [PubMed - indexed for MEDLINE]

Neurogenesis in neurological and psychiatric diseases and brain injury: From bench to bedside.

Tue, 01/07/2014 - 5:18am
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Neurogenesis in neurological and psychiatric diseases and brain injury: From bench to bedside.

Prog Neurobiol. 2013 Dec 30;

Authors: Ruan L, Lau BW, Wang J, Huang L, Zhuge Q, Wang B, Jin K, So KF

Abstract
Researchers who have uncovered the presence of stem cells in an adult's central nervous system have not only challenged the dogma that new neurons cannot be generated during adulthood, but also shed light on the etiology and disease mechanisms underlying many neurological and psychiatric disorders. Brain trauma, neurodegenerative diseases, and psychiatric disorders pose enormous burdens at both personal and societal levels. Although medications for these disorders are widely used, the treatment mechanisms underlying the illnesses remain largely elusive. In the past decade, an increasing amount of evidence indicate that adult neurogenesis (i.e. generating new CNS neurons during adulthood) may be involved in the pathology of different CNS disorders, and thus neurogenesis may be a potential target area for treatments. Although the new neurons were shown to be a major player in mediating treatment efficacy of neurological and psychotropic drugs on cognitive functions, it is still debatable if the altered production of new neurons can cause the disorders. This review hence seeks to discuss pre and current clinical studies that demonstrate the functional impact adult neurogenesis have on neurological and psychiatric illnesses while examining the related underlying disease mechanisms.

PMID: 24384539 [PubMed - as supplied by publisher]

Menu-Labeling Usage and Its Association with Diet and Exercise: 2011 BRFSS Sugar Sweetened Beverage and Menu Labeling Module.

Tue, 01/07/2014 - 5:18am
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Menu-Labeling Usage and Its Association with Diet and Exercise: 2011 BRFSS Sugar Sweetened Beverage and Menu Labeling Module.

Prev Chronic Dis. 2014;11:E02

Authors: Bowers KM, Suzuki S

Abstract
INTRODUCTION: The primary objective of our study was to investigate the association between menu-labeling usage and healthy behaviors pertaining to diet (consumption of fruits, vegetables, sodas, and sugar-sweetened beverages) and exercise.
METHODS: Data from the 2011 Behavioral Risk Factor Surveillance System, Sugar Sweetened Beverage and Menu-Labeling module, were used. Logistic regression was used to determine the association between menu-labeling usage and explanatory variables that included fruit, vegetable, soda, and sugar-sweetened beverage consumption as well as exercise.
RESULTS: Nearly half (52%) of the sample indicated that they used menu labeling. People who used menu labeling were more likely to be female (odds ratio [OR], 2.29; 95% confidence interval [CI], 2.04-2.58), overweight (OR, 1.13; 95% CI, 1.00-1.29) or obese (OR, 1.29; 95% CI, 1.12-1.50), obtain adequate weekly aerobic exercise (OR, 1.18; 95% CI, 1.06-1.32), eat fruits (OR, 1.20; 95% CI, 1.12-1.29) and vegetables (OR, 1.12; 95% CI, 1.05-1.20), and drink less soda (OR, 0.76; 95% CI, 0.69-0.83).
CONCLUSION: Although obese and overweight people were more likely to use menu labeling, they were also adequately exercising, eating more fruits and vegetables, and drinking less soda. Menu labeling is intended to combat the obesity epidemic; however the results indicate an association between menu-labeling usage and certain healthy behaviors. Thus, efforts may be necessary to increase menu-labeling usage among people who are not partaking in such behaviors.

PMID: 24384303 [PubMed - in process]

Modulation of Cellular Signaling Pathways in P23H Rhodopsin Photoreceptors.

Sun, 01/05/2014 - 9:22am
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Modulation of Cellular Signaling Pathways in P23H Rhodopsin Photoreceptors.

Cell Signal. 2013 Dec 27;

Authors: Sizova OS, Shinde VM, Lenox A, Gorbatyuk MS

Abstract
We previously reported activation of the unfolded protein response (UPR) in P23H rhodopsin (RHO) retinas with autosomal dominant retinitis pigmentosa (ADRP). Knowing that the UPR can trigger Ca(2+) release from the endoplasmic reticulum and regulate cellular signaling we examined the level of Ca(2+)-regulated proteins. We also looked for changes in the expression of Bcl2 family proteins, autophagy proteins and the mTOR/AKT pathways, as well as for the induction of mitochondria-associated apoptosis in the P23H RHO retina. Our data demonstrated that the elevation of calpain and caspase-12 activity was concomitantly observed with a decrease in the BCL2-XL/BAX ratio and an increase in mTor levels in the P23H-3 RHO retina suggesting a vulnerability of P23H RHO photoreceptors to apoptosis. The translocation of BAX to the mitochondria, as well as the release of cytochrome C and AIF into the cytosol supports this conclusion and indicates the involvement of mitochondria-induced apoptosis in the progression of ADRP. The level of autophagy proteins in general was found to be decreased in the P21-P30 P23H RHO retina. Injections of rapamycin, however, protected the P23H RHO rod photoreceptors from experiencing physiological decline. Despite this fact, the downregulation of mTOR did not alter the level of autophagy proteins. Our results imply that in addition to activation of the UPR during ADRP progression, photoreceptors also experience alterations in major proapoptotic pathways.

PMID: 24378535 [PubMed - as supplied by publisher]

Differentially Expressed Wound Healing-Related microRNAs in the Human Diabetic Cornea.

Sun, 01/05/2014 - 9:22am
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Differentially Expressed Wound Healing-Related microRNAs in the Human Diabetic Cornea.

PLoS One. 2013;8(12):e84425

Authors: Funari VA, Winkler M, Brown J, Dimitrijevich SD, Ljubimov AV, Saghizadeh M

Abstract
MicroRNAs are powerful gene expression regulators, but their corneal repertoire and potential changes in corneal diseases remain unknown. Our purpose was to identify miRNAs altered in the human diabetic cornea by microarray analysis, and to examine their effects on wound healing in cultured telomerase-immortalized human corneal epithelial cells (HCEC) in vitro. Total RNA was extracted from age-matched human autopsy normal (n=6) and diabetic (n=6) central corneas, Flash Tag end-labeled, and hybridized to Affymetrix® GeneChip® miRNA Arrays. Select miRNAs associated with diabetic cornea were validated by quantitative RT-PCR (Q-PCR) and by in situ hybridization (ISH) in independent samples. HCEC were transfected with human pre-miR(TM)miRNA precursors (h-miR) or their inhibitors (antagomirs) using Lipofectamine 2000. Confluent transfected cultures were scratch-wounded with P200 pipette tip. Wound closure was monitored by digital photography. Expression of signaling proteins was detected by immunostaining and Western blot. Using microarrays, 29 miRNAs were identified as differentially expressed in diabetic samples. Two miRNA candidates showing the highest fold increased in expression in the diabetic cornea were confirmed by Q-PCR and further characterized. HCEC transfection with h-miR-146a or h-miR-424 significantly retarded wound closure, but their respective antagomirs significantly enhanced wound healing vs. controls. Cells treated with h-miR-146a or h-miR-424 had decreased p-p38 and p-EGFR staining, but these increased over control levels close to the wound edge upon antagomir treatment. In conclusion, several miRNAs with increased expression in human diabetic central corneas were found. Two such miRNAs inhibited cultured corneal epithelial cell wound healing. Dysregulation of miRNA expression in human diabetic cornea may be an important mediator of abnormal wound healing.

PMID: 24376808 [PubMed - in process]

Multiple biomarker panels for early detection of breast cancer in peripheral blood.

Wed, 01/01/2014 - 5:32am
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Multiple biomarker panels for early detection of breast cancer in peripheral blood.

Biomed Res Int. 2013;2013:781618

Authors: Zhang F, Deng Y, Drabier R

Abstract
Detecting breast cancer at early stages can be challenging. Traditional mammography and tissue microarray that have been studied for early breast cancer detection and prediction have many drawbacks. Therefore, there is a need for more reliable diagnostic tools for early detection of breast cancer due to a number of factors and challenges. In the paper, we presented a five-marker panel approach based on SVM for early detection of breast cancer in peripheral blood and show how to use SVM to model the classification and prediction problem of early detection of breast cancer in peripheral blood. We found that the five-marker panel can improve the prediction performance (area under curve) in the testing data set from 0.5826 to 0.7879. Further pathway analysis showed that the top four five-marker panels are associated with signaling, steroid hormones, metabolism, immune system, and hemostasis, which are consistent with previous findings. Our prediction model can serve as a general model for multibiomarker panel discovery in early detection of other cancers.

PMID: 24371830 [PubMed - in process]

Knockdown of tyrosine hydroxylase in the nucleus of the solitary tract reduces elevated blood pressure during chronic intermittent hypoxia.

Wed, 01/01/2014 - 5:32am
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Knockdown of tyrosine hydroxylase in the nucleus of the solitary tract reduces elevated blood pressure during chronic intermittent hypoxia.

Am J Physiol Regul Integr Comp Physiol. 2013 Nov 1;305(9):R1031-9

Authors: Bathina CS, Rajulapati A, Franzke M, Yamamoto K, Cunningham JT, Mifflin S

Abstract
Noradrenergic A2 neurons in nucleus tractus solitarius (NTS) respond to stressors such as hypoxia. We hypothesize that tyrosine hydroxylase (TH) knockdown in NTS reduces cardiovascular responses to chronic intermittent hypoxia (CIH), a model of the arterial hypoxemia observed during sleep apnea in humans. Adult male Sprague-Dawley rats were implanted with radiotelemetry transmitters and adeno-associated viral constructs with green fluorescent protein (GFP) reporter having either short hairpin RNA (shRNA) for TH or scrambled virus (scRNA) were injected into caudal NTS. Virus-injected rats were exposed to 7 days of CIH (alternating periods of 10% O2 and of 21% O2 from 8 AM to 4 PM; from 4 PM to 8 AM rats were exposed to 21% O2). CIH increased mean arterial pressure (MAP) and heart rate (HR) during the day in both the scRNA (n = 14, P < 0.001 MAP and HR) and shRNA (n = 13, P < 0.001 MAP and HR) groups. During the night, MAP and HR remained elevated in the scRNA rats (P < 0.001 MAP and HR) but not in the shRNA group. TH immunoreactivity and protein were reduced in the shRNA group. FosB/ΔFosB immunoreactivity was decreased in paraventricular nucleus (PVN) of shRNA group (P < 0.001). However, the shRNA group did not show any change in the FosB/ΔFosB immunoreactivity in the rostral ventrolateral medulla. Exposure to CIH increased MAP which persisted beyond the period of exposure to CIH. Knockdown of TH in the NTS reduced this CIH-induced persistent increase in MAP and reduced the transcriptional activation of PVN. This indicates that NTS A2 neurons play a role in the cardiovascular responses to CIH.

PMID: 24049117 [PubMed - indexed for MEDLINE]

Lymphatic pump treatment repeatedly enhances the lymphatic and immune systems.

Sun, 12/29/2013 - 5:26am

Lymphatic pump treatment repeatedly enhances the lymphatic and immune systems.

Lymphat Res Biol. 2013 Dec;11(4):219-26

Authors: Schander A, Padro D, King HH, Downey HF, Hodge LM

Abstract
Abstract Background: Osteopathic practitioners utilize manual therapies called lymphatic pump techniques (LPT) to treat edema and infectious diseases. While previous studies examined the effect of a single LPT treatment on the lymphatic system, the effect of repeated applications of LPT on lymphatic output and immunity has not been investigated. Therefore, the purpose of this study was to measure the effects of repeated LPT on lymphatic flow, lymph leukocyte numbers, and inflammatory mediator concentrations in thoracic duct lymph (TDL). Methods and Results: The thoracic ducts of five mongrel dogs were cannulated, and lymph samples were collected during pre-LPT, 4 min of LPT, and 2 hours post-LPT. A second LPT (LPT-2) was applied after a 2 hour rest period. TDL flow was measured, and TDL were analyzed for the concentration of leukocytes and inflammatory mediators. Both LPT treatments significantly increased TDL flow, leukocyte count, total leukocyte flux, and the flux of interleukin-8 (IL-8), keratinocyte-derived chemoattractant (KC), nitrite (NO2(-)), and superoxide dismutase (SOD). The concentration of IL-6 increased in lymph over time in all experimental groups; therefore, it was not LPT dependent. Conclusion: Clinically, it can be inferred that LPT at a rate of 1 pump per sec for a total of 4 min can be applied every 2 h, thus providing scientific rationale for the use of LPT to repeatedly enhance the lymphatic and immune system.

PMID: 24364845 [PubMed - in process]

Correction to miller et Al. (2012).

Sun, 12/29/2013 - 5:26am

Correction to miller et Al. (2012).

Psychol Addict Behav. 2013 Dec;27(4):1101

Authors: Miller MB, Leffingwell TR, Claborn K, Meier E, Walters S, Neighbors C

Abstract
Reports an error in "Personalized Feedback Interventions for College Alcohol Misuse: An Update of Walters & Neighbors (2005)" by Mary Beth Miller, Thad Leffingwell, Kasey Claborn, Ellen Meier, Scott Walters and Clayton Neighbors (Psychology of Addictive Behaviors, Advanced Online Publication, Dec 31, 2012, np). There was an error in the coding of content components in a few studies. The Carey et al. (2009, 2011), Juarez et al. (2006), Walters (2000), and Walters et al. (2000) studies did not include decisional balance content. As a result of this, the article included an error in the calculation of effect size comparisons for this intervention component. In light of these corrections, there is no significant difference between the short-term effect sizes of written interventions that included or excluded the decisional balance component. Conclusions regarding the relative efficacy of decisional balance as a component of PFI content in the article are unfounded and should be disregarded. There were also a few errors in the tables; the corrected tables appear in the correction. (The following abstract of the original article appeared in record 2012-35005-001.) Personalized drinking feedback is an evidence-based and increasingly common way of intervening with high-risk college drinking. This article extends an earlier review by Walters and Neighbors (S. T. Walters & C. Neighbors, 2005, Feedback interventions for college alcohol misuse: What, why, and for whom? Addictive Behaviors, 30, 1168-1182) by reviewing the literature of published studies using personalized feedback as an intervention for heavy drinking among college students. This article updates and extends the original review with a more comprehensive and recent set of 41 studies, most of which were not included in the original article. This article also examines within-subject effect sizes for personalized feedback interventions (PFIs) for high-risk alcohol use and examines the content of PFIs more closely to provide insight on the most essential components that will guide the future development of feedback-based interventions. In general, PFIs appear to be reliably effective at reducing harmful alcohol misuse among college students. Some components are almost universally included (i.e., drinking profile and normative comparison), precluding inferences regarding their unique contribution. Significantly larger effect sizes were observed for interventions that included decisional balance, practical costs, and strategies to limit risks. The present research provides an important empirical foundation for determining the relative contribution of individual components and facets in the efficacy of PFIs. (PsycINFO Database Record (c) 2013 APA, all rights reserved).

PMID: 24364690 [PubMed - in process]