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School counselors frequently face ethical dilemmas. These dilemmas often involve relationships with principals, parents, and other stakeholders. School counselors may confront complex ethical issues involving confidentiality, student safety, parental rights,and social media. The American School Counselor Association recommends following an ethical decision-making model when dealing with complex ethical issues. An explanatory case study is provided along with sample dilemmas to illustrate how an ethical decision-making model might be used within the school setting.

School counselors' perceptions of the efficacy and satisfaction of their experiential training in group work were investigated. An exploratory factor analysis (n = 304) revealed four salient factors: leader characteristics, leader responsibilities, child/adolescent group leadership and adult group leadership. A majority of participants indicated they were not satisfied with their experiential training and supervision in group work. A multiple regression analysis showed a statistically significant relationship between experiential training and utilization of psycho-educational groups in schools. Implications for school counselor preparation programs are discussed. (Contains 1 table.)

This study examined school counselors' and principals' perceptions of their relationship and the effectiveness of their respective professional preparation programs. An exploratory factor analysis (n = 615) revealed three salient factors: relationship quality, campus leadership and training satisfaction. Kruskal-Wallis tests revealed statistically significant differences in all three factors across the four groups (elementary counselors and principals, and secondary counselors and principals). Mann Whitney "U" post hoc tests indicated more statistically significant differences among secondary counselors and principals than elementary. Implications for school counselors and improvements in preparation programs for counselors and principals are included. (Contains 1 table.)

This national exploratory study examined the perceptions of secondary school counselors' (n = 81) understanding of non-suicidal self-injury (NSSI). Two one-way ANOVAs revealed no statistically significant differences between middle and high school counselors on their perceptions of the prevalence of NSSI. Descriptive analyses revealed that a majority of participants lacked confidence in providing information about NSSI to school personnel. Recommendations for school counselors are provided. (Contains 1 table.)

This exploratory study examined the importance of a mentoring program using a purposeful sample of 16 first-year elementary school counselors. A qualitative analysis revealed the importance of support that participants received from their mentors and mentoring cohort group. Participants also indicated an increase in self-efficacy as a result of the mentoring program. Implications for counselor induction and preparation are discussed.

The authors conducted a meta-analysis and systematic review that examined 23 studies evaluating the effectiveness of child centered play therapy (CCPT) conducted in elementary schools. Meta-analysis results were explored using a random effects model for mean difference and mean gain effect size estimates. Results revealed statistically significant effects for outcome constructs, including externalizing problems (d = 0.34), internalizing problems (d = 0.21), total problems (d = 0.34), self-efficacy (d = 0.29), academic (d = 0.36), and other behaviors (d = 0.38). Further, a systematic review was conducted on all studies compared with Outcome Research Coding Protocol criteria. Results indicated that CCPT studies provided quantitative support and qualitatively promising to strong evidence in support of its use in the schools.

A visitor to a random sampling of Modern World History classes in the United States will find that the subject of "revolution" is a favorite for many students. Reading about and researching individuals and topics such as Tsar Nicholas II, Rasputin, Marie Antoinette and guillotines is never boring. Unfortunately, in too many classrooms, revolutions are studied in complete isolation of each other; a student might study the French Revolution near the beginning of the school year and the Russian Revolution several months later and make absolutely no connection between the two events. In the twentieth and twenty-first centuries, numerous political scientists and historians have written about the connections between various revolutions, discovering common patterns, structures, and characteristics of both historical and contemporary revolutions. This article will review important general theories of revolution written in the modern era that have influenced the study of revolutions. They will be presented in a format that enables any Modern World History teacher to understand them and utilize them with his or her classes without much difficulty. (Contains 26 notes.)

The effectiveness of group sandtray therapy was examined using a pretest-posttest control group design with young adolescent girls (n = 37) identified as having low self-esteem. A split-plot analysis of variance (SPANOVA) revealed statistically significant differences between participants in the treatment and control groups in self-esteem on five of the six subscales of the Self-Perception Profile for Children. The implications of the findings are discussed. (Contains 1 table and 2 figures.)

The feature film "12 Angry Men" focuses on an organizational task group that demonstrates the dynamics of a working group. The film is discussed as an effective tool for illuminating group process. The authors describe their experiences using the movie as a teaching tool and provide examples of how it can be used to depict critical incidents, the recognition and understanding of group process, and interpersonal learning. This paper also describes how group instructors can use a feature film to facilitate an in-depth experience for group counseling trainees. It captures the immediacy of here-and-now feedback and confrontation, which gives trainees an experience that is unavailable in training films and role-playing.

When elementary school counselors have a solid developmental understanding of children, play therapy might be one counseling intervention that they use with their students. Landreth (2002) has promoted the use of play therapy in schools by explaining that its objective is to help children get ready to profit from what teachers have to offer. Play therapy is an approach that may help school counselors to effectively assist children in their developmental growth. This study surveyed elementary school counselors who were members of the American School Counselor Association regarding play therapy practices in the schools. Participants (N = 381) were surveyed regarding their training in play therapy, their use of play therapy, their belief system regarding play therapy, and their perceived limitations to the use of play therapy in the schools. Although school counselors appear to believe in the utility of play therapy in the schools, certain barriers were found to exist that were detrimental to its implementation. Counselors identified lack of time available with students and lack of training in play therapy as the primary limitations to its use in the schools.

Gonadotropin-releasing hormone (GnRH) acts via seven transmembrane receptors to stimulate gonadotropin secretion. Sustained stimulation desensitizes GnRH receptor (GnRHR)-mediated gonadotropin secretion, and this underlies agonist use in hormone-dependent cancers. Since type I mammalian GnRHR do not desensitize, agonist-induced internalization and downregulation may underlie desensitization of GnRH-stimulated gonadotropin secretion; however, research focus has recently shifted to anterograde trafficking, with the finding that human (h)GnRHR are mostly intracellular. Moreover, there is little direct evidence for agonist-induced trafficking of hGnRHR, and whether or not type 1 mammalian GnRHR show agonist-induced internalization is controversial. Here we use automated imaging to monitor expression and internalization of hemagglutinin (HA)-tagged hGnRHRs, mouse (m) GnRHR, Xenopus (X) GnRHRs, and chimeric receptors (hGnRHR with added XGnRHR COOH tails, h.XGnRHR) expressed by adenoviral transduction in HeLa cells. We find that agonists stimulate downregulation and/or internalization of mGnRHR and XGnRHR, that GnRH stimulates trafficking of hGnRHR and can stimulate internalization or downregulation of hGnRHR when steps are taken to increase cell surface expression (addition of the XGnRHR COOH tail or pretreatment with pharmacological chaperone). Agonist effects on internalization (of h.XGnRHR) and downregulation (of hGnRHR and h.XGnRHR) were not mimicked by a peptide antagonist and were prevented by a mutation that prevents GnRHR signaling, demonstrating dependence on receptor signaling as well as agonist occupancy. Thus agonist-induced internalization and downregulation of type I mammalian GnRHR occurs in HeLa cells, and we suggest that the high throughput imaging systems described here will facilitate study of the molecular mechanisms involved. seven transmembrane receptor; trafficking; G protein-coupled receptor

This article provides a framework for social skills homework in special education; an example of a social skills assignment; and a continuum for the involvement of parents, teachers, peers, and others in the homework process. Practicing social skills in natural settings is felt to assist in generalization and maintenance. (JDD)

Abstract Background Current protocols for the treatment of ovarian cancer include combination chemotherapy with a platinating agent and a taxane. However, many patients experience relapse of their cancer and the development of drug resistance is not uncommon, making successful second line therapy difficult to achieve. The objective of this study was to develop and characterize a cell line resistant to both carboplatin and docetaxel (dual drug resistant ovarian cell line) and to compare this cell line to cells resistant to either carboplatin or docetaxel. Methods The A2780 epithelial endometrioid ovarian cancer cell line was used to select for isogenic carboplatin, docetaxel and dual drug resistant cell lines. A selection method of gradually increasing drug doses was implemented to avoid clonal selection. Resistance was confirmed using a clonogenic assay. Changes in gene expression associated with the development of drug resistance were determined by microarray analysis. Changes in the expression of selected genes were validated by Quantitative Real-Time Polymerase Chain Reaction (QPCR) and immunoblotting. Results Three isogenic cell lines were developed and resistance to each drug or the combination of drugs was confirmed. Development of resistance was accompanied by a reduced growth rate. The microarray and QPCR analyses showed that unique changes in gene expression occurred in the dual drug resistant cell line and that genes known to be involved in resistance could be identified in all cell lines. Conclusions Ovarian tumor cells can acquire resistance to both carboplatin and docetaxel when selected in the presence of both agents. Distinct changes in gene expression occur in the dual resistant cell line indicating that dual resistance is not a simple combination of the changes observed in cell lines exhibiting single agent resistance.

Learning disabled and mentally retarded elementary and secondary students (N=343) exhibited significant differences on scores of three tests designed to measure the same area of achievement. Results suggested that specific abilities of pupils interact with aspects of the test items. (CL)

Five elementary level males with learning disabilities read material at two levels of difficulty in a multi-element design. Findings suggested that oral reading rate and reading comprehension performance are more strongly linked than previously suggested. (CL)

The relationship between teacher-perceived brightness/dullness and classroom interactions was investigated with 96 intermediate-grade children. Positive interactions were distributed unevenly between "bright" and "dull" children; no differences were indicated in the distributions of negative and neutral interactions. (Author/GDC)

A survey was conducted with 114 junior high, middle grade, and high school LD teachers concerning various aspects of mathematics disabilities in students. The most common deficit areas included division of whole numbers, basic operations involving fractions, decimals, percent, fraction terminology, multiplication of whole numbers, and place value. (Author/SEW)

The article focuses on some discussion in historical and museum circles on why Connecticut schools don't teach more about Connecticut and local communities. Topics include the some claim schools are ignoring many of the incredibly valuable resources that the state offers, and the social studies/history curriculum in each district and school is NOT dictated by a curriculum created at the state level: what is taught in every subject is created by educators in that district.

The article reviews the music score "B-Minor Ballade" by Franz Liszt.

Guanine nucleotide binding protein (G protein)-coupled receptors (GPCRs) function in complexes with a range of molecules and proteins including ligands, G proteins, arrestins, ubiquitin, and other receptors. Elements of these complexes may interact constitutively or dynamically, dependent upon factors such as ligand binding, phosphorylation, and dephosphorylation. They may also be allosterically modulated by other proteins in a manner that changes temporally and spatially within the cell. Elucidating how these complexes function has been greatly enhanced by biophysical technologies that are able to monitor proximity and/or binding, often in real time and in live cells. These include resonance energy transfer approaches such as bioluminescence resonance energy transfer (BRET) and fluorescence resonance energy transfer (FRET). Furthermore, the use of fluorescent ligands has enabled novel insights into allosteric interactions between GPCRs. Consequently, biophysical approaches are helping to unlock the amazing diversity and bias in G protein-coupled receptor signaling. [ABSTRACT FROM AUTHOR]

Arginine vasopressin (AVP) is released from the posterior pituitary and controls water homeostasis. AVP binding to vasopressin V2 receptors (V2Rs) located on kidney collecting duct epithelial cells triggers activation of Gs proteins, leading to increased cAMP levels, trafficking of aquaporin-2 water channels, and consequent increased water permeability and antidiuresis. Typically, loss-of-function V2R mutations cause nephrogenic diabetes insipidus (NDI), whereas gain-of-function mutations cause nephrogenic syndrome of inappropriate antidiuresis (NSIAD). Here we provide further characterization of two mutant V2Rs, R181C and M311V, reported to cause complete and partial NDI respectively, together with a V266A variant, in a patient diagnosed with NSIAD. Our data in HEK293FT cells revealed that for cAMP accumulation, AVP was about 500- or 30-fold less potent at the R181C and M311V mutants than at the wild-type receptor respectively (and about 4000- and 60-fold in COS7 cells respectively). However, in contrast to wild type V2R, the R181C mutant failed to increase inositol phosphate production, while with the M311V mutant, AVP exhibited only partial agonism in addition to a 37-fold potency decrease. Similar responses were detected in a BRET assay for β-arrestin recruitment, with the R181C receptor unresponsive to AVP, and partial agonism with a 23-fold decrease in potency observed with M311V in both HEK293FT and COS7 cells. Notably, the V266A V2R appeared functionally identical to the wild-type receptor in all assays tested, including cAMP and inositol phosphate accumulation, β-arrestin interaction, and in a BRET assay of receptor ubiquitination. Each receptor was expressed at comparable levels. Hence, the M311V V2R retains greater activity than the R181C mutant, consistent with the milder phenotype of NDI associated with this mutant. Notably, the R181C mutant appears to be a Gs protein-biased receptor incapable of signaling to inositol phosphate or recruiting β-arrestin. The etiology of NSIAD in the patient with V266A V2R remains unknown. [ABSTRACT FROM AUTHOR]

Heteromerization can play an important role in regulating the activation and/or signal transduction of most forms of receptors, including receptor tyrosine kinases (RTKs). The study of receptor heteromerization has evolved extensively with the emergence of resonance energy transfer based approaches such as bioluminescence resonance energy transfer (BRET). Here, we report an adaptation of our Receptor-Heteromer Investigation Technology (Receptor-HIT) that has recently been published as the G protein-coupled receptor (GPCR) Heteromer Identification Technology (GPCR-HIT). We now demonstrate the utility of this approach for investigating RTK heteromerization by examining the functional interaction between the epidermal growth factor (EGF) receptor (EGFR; also known as erbB1/HER1) and heregulin (HRG) receptor 3 (HER3; also known as erbB3) in live HEK293FT cells using recruitment of growth factor receptor-bound protein 2 (Grb2) to the activated receptors. We found that EGFR and HER3 heteromerize specifically as demonstrated by HRG inducing a BRET signal between EGFR/Rluc8 and Grb2/Venus only when HER3 was co-expressed. Similarly, EGF stimulation promoted a specific BRET signal between HER3/Rluc8 and Grb2/Venus only when EGFR was co-expressed. Both EGF and HRG effects on Grb2 interaction are dose-dependent, and specifically blocked by EGFR inhibitor AG-1478. Furthermore, truncation of HER3 to remove the putative Grb2 binding sites appears to abolish EGF-induced Grb2 recruitment to the EGFR-HER3 heteromer. Our results support the concept that EGFR interacts with Grb2 in both constitutive and EGF-dependent manners and this interaction is independent of HER3 co-expression. In contrast, HER3-Grb2 interaction requires the heteromerization between EGFR and HER3. These findings clearly indicate the importance of EGFR-HER3 heteromerization in HER3-mediated Grb2-dependent signaling pathways and supports the central role of HER3 in the diversity and regulation of HER family functioning. [ABSTRACT FROM AUTHOR]

Gonadotropin-releasing hormone (GnRH) acts via G-protein-coupled receptors on gonadotrophs to stimulate synthesis and secretion of luteinizing hormone and follicle-stimulating hormone. It is secreted in pulses, and its effects depend on pulse frequency, but decoding mechanisms are unknown. Here we have used an extracellular signal regulated kinase-green fluorescent protein (ERK2-GFP) reporter to monitor GnRH signaling. GnRH caused dose-dependent ERK2-GFP translocation to the nucleus, providing a live-cell readout for activation. Pulsatile GnRH caused dose- and frequency-dependent ERK2-GFP translocation. These responses were rapid and transient, showed only digital tracking, and did not desensitize under any condition tested (dose, frequency, and receptor number varied). We also tested for the effects of cycloheximide (to prevent induction of nuclear-inducible MAPK phosphatases) and used GFP fusions containing ERK mutations (D319N, which prevents docking domain-dependent binding to MAPK phosphatases, and K52R, which prevents catalytic activity). These manipulations had little or no effect on the translocation responses, arguing against a role for MAPK phosphatases or ERK-mediated feedback in shaping ERK activation during pulsatile stimulation. GnRH also caused dose- and frequency-dependent activation of the α-gonadotropin subunit-, luteinizing hormone β-, and follicle-stimulating hormone β-luciferase reporters, and the latter response was inhibited by ERK1/2 knockdown. Moreover, GnRH caused frequency-dependent activation of an Egrlluciferase reporter, but the response was proportional to cumulative pulse duration. Our data suggest that frequency decoding is not due to negative feedback shaping ERK signaling in this model. [ABSTRACT FROM AUTHOR]

Gonadotropin-releasing hormone (GnRH) acts via 7 transmembrane region receptors on gonadotrophs to stimulate synthesis and secretion of the luteinizing hormone and follicle-stimulating hormone. It is secreted in pulses, and its effects depend on pulse frequency, but decoding mechanisms are unknown. Here we have used (nuclear factor of activated T-cells 2 (NFAT2)-emerald fluorescent protein) to monitor GnRH signaling. Increasing [Ca2+]i causes calmodulin/calcineurin-dependent nuclear NEAT translocation, a response involving proteins (calmodulins and NFATs) that decode frequency in other systems. Using live cell imaging, pulsatile GnRH caused dose- and frequency-dependent increases in nuclear NFAT2-emerald fluorescent protein, and at low frequency, translocation simply tracked GnRH exposure (albeit with slower kinetics). At high frequency (30-mm intervals), failure to return to basal conditions before repeat stimulation caused integrative tracking, illustrating how the relative dynamics of up- and downstream signals can increase efficiency of GnRH action. Mathematical modeling predicted desensitization of GnRH effects on [Ca2+]i and that desensitization would increase with dose, frequency, and receptor number, but no such desensitization was seen in HeLa and/or LβT2 cells possibly because pulsatile GnRH did not reduce receptor expression (measured by immunofluorescence). GnRH also caused dose- and frequency-dependent activation of αGSU, luteinizing hormone β, and follicle-stimulating hormone β luciferase reporters, effects that were blocked by calcineurin inhibition. Pulsatile GnRH also activated an NEAT-responsive luciferase reporter, but this response was directly related to cumulative pulse duration. This together with the lack of desensitization of translocation responses suggests that NEAT may mediate GnRH action but is not a genuine decoder of GnRH pulse frequency. [ABSTRACT FROM AUTHOR]

Although many stimuli activate extracellular signal-regulated kinases 1 and 2 (ERK1/2), the kinetics and compartmentalization of ERK1/2 signals are stimulus-dependent and dictate physiological consequences. ERKs can be inactivated by dual specificity phosphatases (DUSPs), notably the MAPK phosphatases (MKPs) and atypical DUSPs, that can both dephosphorylate and scaffold ERK1/2. Using a cell imaging model (based on knockdown of endogenous ERKs and add-back of wild-type or mutated ERK2-GFP reporters), we explored possible effects of DUSPs on responses to transient or sustained ERK2 activators (epidermal growth factor and phorbol 12,13-dibutyrate, respectively). For both stimuli, a D319N mutation (which impairs DUSP binding) increased ERK2 activity and reduced nuclear accumulation. These stimuli also increased mRNA levels for eight DUSPs. In a short inhibitory RNA screen, 12 of 16 DUSPs influenced ERK2 responses. These effects were evident among nuclear inducible MKP, cytoplasmic ERK MKP, JNK/p38 MKP, and atypical DUSP subtypes and, with the exception of the nuclear inducible MKPs, were paralleled by corresponding changes in Egr-1 luciferase activation. Simultaneous removal of all JNK/p38 MKPs or nuclear inducible MKPs revealed them as positive and negative regulators of ERK2 signaling, respectively. The effects of JNK/p38 MKP short inhibitory RNAs were not dependent on protein neosynthesis but were reversed in the presence of JNK and p38 kinase inhibitors, indicating DUSP-mediated cross-talk between MAPK pathways. Overall, our data reveal that a large number of DUSPs influence ERK2 signaling. Together with the known tissue- specific expression of DUSPs and the importance of ERK1/2 in cell regulation, our data support the potential value of DUSPs as targets for drug therapy. [ABSTRACT FROM AUTHOR]

A micro-dilution technique with changes in optical density (OD) used to measure bacterial growth over 72h in culture media containing 0, 5, 10, 20, 40, 80 and 160μg OTC (oxytetracycline)ml−1 was applied to determine growth inhibition (GI) in mixed bacterial strains cultured from samples of marine sediments and salmon feed pellets. Growth of control cultures (Aeromonas salmonicida) was inhibited at all OTC concentrations. Some feed pellet samples and under-cage sediments from salmon aquaculture sites in the Bay of Fundy showed GI up to ≥160μg OTCml−1. Lower values (40 to 80μg OTCml−1) occurred in subsurface (5–18cm) sediments, >100m from salmon pens and adjacent to sewage outfalls in Halifax Harbour. GI values <20μg OTCml−1 in sediment from reference locations in Halifax Harbour and mussel aquaculture sites are considered to reflect natural background levels for OTC resistance. [Copyright &y& Elsevier]

Gonadotropin-releasing hormone (GnRH) is secreted in brief pulses that stimulate synthesis and secretion of pituitary gonadotropin hormones and therebymediate control of reproduction. It acts via G-protein-coupled receptors to stimulate effectors, including ERK. Information could be encoded in GnRH pulse frequency, width, amplitude, or other features of pulse shape, but the relative importance of these features is unknown. Here we examine this using automated fluorescence microscopy and mathematical modeling, focusing on ERK signaling. The simplest scenario is one in which the system is linear, and response dynamics are relatively fast (compared with the signal dynamics). In this case integrated system output (ERK activation or ERK-driven transcription) will be roughly proportional to integrated input, but we find that this is not the case. Notably, we find that relatively slow response kinetics lead to ERK activity beyond the GnRH pulse, and this reduces sensitivity to pulse width. More generally, we show that the slowing of response kinetics through the signaling cascade creates a system that is robust to pulse width. We, therefore, show how various levels of response kinetics synergize to dictate system sensitivity to different features of pulsatile hormone input. We reveal the mathematical and biochemical basis of a dynamic GnRH signaling system that is robust to changes in pulse amplitude and width but is sensitive to changes in receptor occupancy and frequency, precisely the features that are tightly regulated and exploited to exert physiological control in vivo. [ABSTRACT FROM AUTHOR]

TTLL5/STAMP (tubulin tyrosine ligase-like family member 5) has multiple activities in cells. TTLL5 is one of 13 TTLLs, has polyglutamylation activity, augments the activity of p160 coactivators (SRC-1 and TIF2) in glucocorticoid receptor-regulated gene induction and repression, and displays steroid-independent growth activity with several cell types. To examine TTLL5/ STAMPfunctions in whole animals, mice were prepared with an internal deletion that eliminated several activities of the Stamp gene. This mutation causes both reduced levels of STAMP mRNA and C-terminal truncation of STAMP protein. Homozygous targeted mutant (Stamptm/tm) mice appear normal except for marked decreases in male fertility associated with defects in progressive sperm motility. Abnormal axonemal structures with loss of tubulin doublets occur in most Stamptm/tm sperm tails in conjunction with substantial reduction in β-tubulin polyglutamylation, which closely correlates with the reduction in mutant STAMP mRNA. The axonemes in other structures appear unaffected. There is no obvious change in the organs for sperm development ofWTversus Stamptm/tm males despite the levels of WTSTAMP mRNA in testes being 20-fold higher than in any other organ examined. This defect in male fertility is unrelated to other Ttll genes or 24 genes previously identified as important for sperm function. Thus, STAMP appears to participate in a unique, tissue-selective TTLL-mediated pathway for β-tubulin polyglutamylation that is required for sperm maturation and motility and may be relevant for male fertility. [ABSTRACT FROM AUTHOR]

We have provided the first evidence for specific heteromerization between the α1A-adrenoceptor (α1AAR) and CXC chemokine receptor 2 (CXCR2) in live cells. α1AAR and CXCR2 are both expressed in areas such as the stromal smooth muscle layer of the prostate. By utilizing the G protein-coupled receptor (GPCR) heteromer identification technology on the live cell-based bioluminescence resonance energy transfer (BRET) assay platform, our studies in human embryonic kidney 293 cells have identified norepinephrine-dependent β-arrestin recruitment that was in turn dependent upon co-expression of α1AAR with CXCR2. These findings have been supported by co-localization observed using confocal microscopy. This norepinephrine-dependent β-arrestin recruitment was inhibited not only by the α1AR antagonist Terazosin but also by the CXCR2-specific allosteric inverse agonist SB265610. Furthermore, Labetalol, which is marketed for hypertension as a nonselective β-adrenoceptor antagonist with α1AR antagonist properties, was identified as a heteromer-specific-biased agonist exhibiting partial agonism for inositol phosphate production but essentially full agonism for β-arrestin recruitment at the α1AAR-CXCR2 heteromer. Finally, bioluminescence resonance energy transfer studies with both receptors tagged suggest that α1AAR-CXCR2 heteromerization occurs constitutively and is not modulated by ligand. These findings support the concept of GPCR heteromer complexes exhibiting distinct pharmacology, thereby providing additional mechanisms through which GPCRs can potentially achieve their diverse biological functions. This has important implications for the use and future development of pharmaceuticals targeting these receptors. [ABSTRACT FROM AUTHOR]