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PubMed2005

Dosimetric comparison of the specific anthropomorphic mannequin (SAM) to 14 anatomical head models using a novel definition for the mobile phone positioning.

This paper presents new definitions for obtaining reproducible results in numerical phone dosimetry. Numerous numerical dosimetric studies have been published about the exposure of mobile phone users which concluded with conflicting results. However, many of these studies lack reproducibility due to shortcomings in the description of the phone positioning. The new approach was tested by two groups applying two different numerical program packages to compare the specific anthropomorphic mannequin (SAM) to 14 anatomically correct head models. A novel definition for the positioning of mobile phones next to anatomically correct head models is given along with other essential parameters to be reported. The definition is solely based on anatomical characteristics of the head. A simple up-to-date phone model was used to determine the peak spatial specific absorption rate (SAR) of mobile phones in SAM and in the anatomically correct head models. The results were validated by measurements. The study clearly shows that SAM gives a conservative estimate of the exposure in anatomically correct head models for head only tissue. Depending on frequency, phone position and head size the numerically calculated 10 g averaged SAR in the pinna can be up to 2.1 times greater than the peak spatial SAR in SAM. Measurements in small structures, such as the pinna, will significantly increase the uncertainty; therefore SAM was designed for SAR assessment in the head only. Whether SAM will provide a conservative value for the pinna depends on the pinna SAR limit of the safety standard considered.

Adolescent↗
PubMed1995

SAM: a system for iteratively building marker maps.

SAM (system for assembling markers) is a system which supports man-machine problem solving for iteratively ordering a set of markers. SAM aids the user in partially ordering a set of markers based on incomplete and uncertain data. As data is added and modified, SAM aids the user in updating the previously assembled maps. The input is a file of clones and for each clone, a list of the markers contained within it. The objective is to order the set of markers such that the markers contained in each clone are consecutive. The user directs the map building by selecting functions to assemble a region of markers, order the clones to fit the order of the markers and position new markers within an ordered set of markers. The user can edit the input data, edit the assembled map and add clones to the map based on their marker content. The results are displayed graphically and can be saved in a solution file. Based on the partial map, the user designs new experiments or edits the existing data to fill gaps and resolve ambiguities. When a previously assembled map is loaded into SAM, it is automatically updated with the new or altered data. SAM treats all markers as points, but has special features for multiple copy and long markers so that they can be used in the map building process. This system has supported the building of a YAC map of human chromosome 22 at the Sanger Centre, where use of Alu-PCR product markers is a major component in determining clone overlap and where we have an on-going effort to accumulate data from various sources. SAM is also being used at various other laboratories.

Algorithms↗
PubMedDate not supplied

Unique mutations in mitochondrial DNA of senescence-accelerated mouse (SAM) strains.

Mitochondrial DNA (mtDNA) is exclusively inherited maternally and hence could offer a good method for tracing the lineage of mouse strains. We examined the mtDNA sequence of senescence-accelerated mouse (SAM) strains as well as other laboratory strains of inbred mice to deduce the ancestral strain of SAM. Four unique mutations were identified at bases 2256, 10,847, 11,181, and 13,053 in SAM strains. The mutations were not found in other mouse strains including AKR/J, one of the parental strains of SAM. Comparison of the mtDNA sequences also led to the consensus mtDNA sequence of laboratory strains of inbred mice. The seven laboratory strains of common inbred mice showed polymorphisms at base 9348, thymine repeat from base 9818, and adenine repeat from base 9821, and could be classified into five types by combination of the differences. Although we could not identify mouse strains with the same type of mtDNA as SAM in this study, the polymorphisms would provide a promising clue to ascertain the ancestral strain(s) of SAM. The polymorphism in mtDNA could be used to ascertain the genealogy of other mouse strains as well.

Aging↗
PubMed1993

Control of BEK and K-SAM splice sites in alternative splicing of the fibroblast growth factor receptor 2 pre-mRNA.

The fibroblast growth factor receptor 2 gene pre-mRNA can be spliced by using either the K-SAM exon or the BEK exon. The exon chosen has a profound influence on the ligand-binding specificity of the receptor obtained. Cells make a choice between the two alternative exons by controlling use of both exons. Using fibroblast growth factor receptor 2 minigenes, we have shown that in cells normally using the K-SAM exon, the BEK exon is not used efficiently even in the absence of the K-SAM exon. This is because these cells apparently express a titratable repressor of BEK exon use. In cells normally using the BEK exon, the K-SAM exon is not used efficiently even in the absence of a functional BEK exon. Three purines in the K-SAM polypyrimidine tract are at least in part responsible for this, as their mutation to pyrimidines leads to efficient use of the K-SAM exon, while mutating the BEK polypyrimidine tract to include these purines stops BEK exon use.

Alternative Splicing↗
PubMed2004

Mutations in the SAM domain of the ETV6-NTRK3 chimeric tyrosine kinase block polymerization and transformation activity.

The 12p13 ETV6 (TEL) gene is frequently targeted by chromosomal translocations in human malignancies, resulting in the formation of oncogenic ETV6 gene fusions. Many of the known partner genes encode protein tyrosine kinases (PTKs), generating fusion proteins that function as chimeric PTKs. ETV6-NTRK3 (EN), comprised of the ETV6 SAM domain fused to the NTRK3 PTK, is unique among ETV6 chimeric oncoproteins, as it is expressed in cancers of multiple lineages. We initially hypothesized that, similar to other ETV6-PTK chimeras, SAM-mediated dimerization of EN leads to constitutive activation of the PTK and downstream signaling cascades. However, when the EN SAM domain was replaced with an inducible FK506 binding protein (FKBP) dimerization system, resulting FKBP-NTRK3 chimeras failed to transform NIH 3T3 cells even though PTK activation was preserved. It was recently shown that the ETV6 SAM domain has two potential interacting surfaces, raising the possibility that this domain can mediate protein polymerization. We therefore mutated each EN SAM binding interface in a manner shown previously to abolish self-association of wild-type ETV6. Each mutation completely blocked the ability of EN to polymerize, to activate its PTK, and to transform NIH 3T3 cells. Furthermore, EN itself formed large polymeric structures within cells while mutant EN proteins were present only as monomers. Finally, we observed a dominant negative effect on the transformation of isolated SAM domains coexpressed in EN-transformed cells. Taken together, our results suggest that higher-order polymerization may be a critical requirement for the transformation activity of EN and possibly other ETV6-PTK fusion proteins.

Animals↗
PubMed1995

SAM prevents impairment of glucose-stimulated insulin secretion caused by hexose deprivation or starvation.

Succinic acid monomethyl ester (SAM) was recently proposed as an insulinotropic tool in non-insulin-dependent diabetes mellitus. Three models were now used to investigate whether SAM protects the B-cell against the impairment of glucose-stimulated insulin release caused by either glucose deprivation or starvation. In the first model, preincubation of the islets for 180 min at low glucose concentration in the presence of SAM prevented the decrease in the secretory response to D-glucose otherwise observed during a subsequent incubation. In the second model, an impaired secretory response to D-glucose was observed after 3-day culture at low (2.8 or 5.6 mM) as distinct from high (11.1 mM) hexose concentration and the presence of SAM in the culture medium again protected against this anomaly. In the third model, the infusion of SAM for 3 days to starved rats restored the secretory potential of isolated islets to a level comparable to that otherwise found in fed rats. Thus, during glucose deprivation or starvation, SAM is indeed able to maintain B-cell responsiveness to D-glucose.

Animals↗
PubMed2005

Improved profile HMM performance by assessment of critical algorithmic features in SAM and HMMER.

BACKGROUND: Profile hidden Markov model (HMM) techniques are among the most powerful methods for protein homology detection. Yet, the critical features for successful modelling are not fully known. In the present work we approached this by using two of the most popular HMM packages: SAM and HMMER. The programs' abilities to build models and score sequences were compared on a SCOP/Pfam based test set. The comparison was done separately for local and global HMM scoring. RESULTS: Using default settings, SAM was overall more sensitive. SAM's model estimation was superior, while HMMER's model scoring was more accurate. Critical features for model building were then analysed by comparing the two packages' algorithmic choices and parameters. The weighting between prior probabilities and multiple alignment counts held the primary explanation why SAM's model building was superior. Our analysis suggests that HMMER gives too much weight to the sequence counts. SAM's emission prior probabilities were also shown to be more sensitive. The relative sequence weighting schemes are different in the two packages but performed equivalently. CONCLUSION: SAM model estimation was more sensitive, while HMMER model scoring was more accurate. By combining the best algorithmic features from both packages the accuracy was substantially improved compared to their default performance.

Algorithms↗
PubMed2006

Cloning and characterization of mr-s, a novel SAM domain protein, predominantly expressed in retinal photoreceptor cells.

BACKGROUND: Sterile alpha motif (SAM) domains are approximately 70 residues long and have been reported as common protein-protein interaction modules. This domain is found in a large number of proteins, including Polycomb group (PcG) proteins and ETS family transcription factors. In this work, we report the cloning and functional characterization of a novel SAM domain-containing protein, which is predominantly expressed in retinal photoreceptors and the pineal gland and is designated mouse mr-s (major retinal SAM domain protein). RESULTS: mr-s is evolutionarily conserved from zebrafish through human, organisms through which the mechanism of photoreceptor development is also highly conserved. Phylogenetic analysis suggests that the SAM domain of mr-s is most closely related to a mouse polyhomeotic (ph) ortholog, Mph1/Rae28, which is known as an epigenetic molecule involved in chromatin modifications. These findings provide the possibility that mr-s may play a critical role by regulating gene expression in photoreceptor development. mr-s is preferentially expressed in the photoreceptors at postnatal day 3-6 (P3-6), when photoreceptors undergo terminal differentiation, and in the adult pineal gland. Transcription of mr-s is directly regulated by the cone-rod homeodomain protein Crx. Immunoprecipitation assay showed that the mr-s protein self-associates mainly through the SAM domain-containing region as well as ph. The mr-s protein localizes mainly in the nucleus, when mr-s is overexpressed in HEK293T cells. Moreover, in the luciferase assays, we found that mr-s protein fused to GAL4 DNA-binding domain functions as a transcriptional repressor. We revealed that the repression activity of mr-s is not due to a homophilic interaction through its SAM domain but to the C-terminal region. CONCLUSION: We identified a novel gene, mr-s, which is predominantly expressed in retinal photoreceptors and pineal gland. Based on its expression pattern and biochemical analysis, we predict that mr-s may function as a transcriptional repressor in photoreceptor cells and in pinealocytes of the pineal gland.

Animals↗
PubMed2002

Native interface of the SAM domain polymer of TEL.

BACKGROUND: TEL is a transcriptional repressor containing a SAM domain that forms a helical polymer. In a number of hematologic malignancies, chromosomal translocations lead to aberrant fusions of TEL-SAM to a variety of other proteins, including many tyrosine kinases. TEL-SAM polymerization results in constitutive activation of the tyrosine kinase domains to which it becomes fused, leading to cell transformation. Thus, inhibitors of TEL-SAM self-association could abrogate transformation in these cells. In previous work, we determined the structure of a mutant TEL-SAM polymer bearing a Val to Glu substitution in center of the subunit interface. It remained unclear how much the mutation affected the architecture of the polymer, however. RESULTS: Here we determine the structure of the native polymer interface. To accomplish this goal, we introduced mutations that block polymer extension, producing a heterodimer with a wild-type interface. We find that the structure of the wild-type polymer interface is quite similar to the mutant structure determined previously. With the structure of the native interface, it is possible to evaluate the potential for developing therapeutic inhibitors of the interaction. We find that the interacting surfaces of the protein are relatively flat, containing no obvious pockets for the design of small molecule inhibitors. CONCLUSION: Our results confirm the architecture of the TEL-SAM polymer proposed previously based on a mutant structure. The fact that the interface contains no obvious potential binding pockets suggests that it may be difficult to find small molecule inhibitors to treat malignancies in this way.

Biopolymers↗
PubMedDate not supplied

Maintenance of certification for family physicians (MC-FP) self assessment modules (SAMs): the first year.

INTRODUCTION: In 2000, the American Board of Medical Specialties adopted Maintenance of Certification (MOC) to replace intermittent, periodic recertification. MOC consists of 4 components: demonstration of professionalism (part I); commitment to life-long learning (part II); demonstration of cognitive expertise (part III); and evaluation of performance in practice (part IV). The American Board of Family Medicine (ABFM) implemented Maintenance of Certification for Family Physicians (MC-FP) in 2004, with its MC-FP part II self-assessment modules (SAMs) as the focus of the first year's activities. METHODS: The SAMs use materials and resources provided at the ABFM's website (www.theabfm.org). As of April 2005, approximately 7000 Diplomates had successfully completed SAMs in essential hypertension (N = 2351) and type 2 diabetes mellitus (N = 4648). Participants completed categorical modified Likert scale evaluations to receive continuing education credit, and many offered unstructured free-text comments regarding the clinical simulation component. These free-text comments were entered into the AnSWR qualitative analysis program from the Centers for Disease Control and Prevention. Text coding was performed by 2 authors (MDH, DJI). As no inferential analyses or comparisons were anticipated, the authors conducted no studies of inter-rater consistency. Results are reported as means (SD) and medians for continuous data, and as frequencies for count data. RESULTS: Likert-scale ratings indicated generally favorable responses (predominantly 5 to 6 on a 6-point scale) to the hypertension and diabetes SAMs. In addition, over half (ie, 55% for hypertension and 54% for diabetes participants) of the respondents indicated that the experience would lead to changes in their practices. Navigation and system operation issues predominated in the free-text comments offered for the diabetes and hypertension simulations. CONCLUSION: The MC-FP SAMs received generally favorable ratings in the program's first year. The SAMs underwent a number of modifications and improvements during the first year, largely in response to feedback and suggestions from ABFM Diplomates.

Certification↗
PubMed1998

The SAM domain of polyhomeotic, RAE28, and scm mediates specific interactions through conserved residues.

The SAM (sterile alpha motif) domain is a 65- to 70-amino acid sequence found in many diverse proteins whose functions range from signal transduction to transcriptional repression. We show that the SAM domain of the Drosophila Polycomb group protein, polyhomeotic (ph), is capable of binding to itself in vitro. We test a number of near relatives of the ph SAM domain from fruit fly, mouse, and yeast and show that all are capable of self-binding. Heterologous interactions are seen among a subset of SAM domains, including ph, Scm, and RAE28. Several conserved amino acid residues were mutated in the ph SAM domain, and the effects on self-binding and heterologous association were demonstrated. L33, L41, and 162 are shown to be important determinants of the binding interface, while W1 and G50 are likely essential for the structure of the domain.

Amino Acid Sequence↗
PubMed2001

Preconditioning Gold Substrates Influences Organothiol Self-assembled Monolayer (SAM) Formation.

Self-assembled monolayer (SAM) formation of alkanethiols with ionic, hydrophilic terminal functionalities onto various O(2) plasma/ethanol pretreated gold substrates was characterized to explore the effect of gold surface oxide on the SAM packing quality. Oxygen adsorption induced by the Au(2)O(3) surface residuals are observed on the plasma-oxidized and O(2) plasma/ethanol-rinsed pretreated Au surfaces while no obvious adsorbed oxygen is found on freshly coated and O(2) plasma/ethanol sonication pretreated Au substrates. A model for the formation of hydrophilic terminated SAMs, -OH, -COOH, and -PO(3)H(2) is proposed. According to this model, the ionic and/or other binding interactions between the surface Au(2)O(3) and the alkanethiol hydrophilic terminal end as well as the interactions between the terminal SAM functionalities could cause the packing disorder found on these three SAMs formed on Au substrates containing Au(2)O(3) surface species. Copyright 2001 Academic Press.

Journal Article↗
PubMed1986

Periodic acid-Schiff (PAS)-positive, granular structures increase in the brain of senescence accelerated mouse (SAM).

Abnormal granular structures, which stained positively with periodic acid-Schiff (PAS-positive granular structures; PGS), were observed in the brain of senescence accelerated mouse (SAM). They were small, round to ovoid, homogeneous structures measuring up to 5 microns in diameter and usually grouped in clusters. PGS were localized in the hippocampus, piriform cortices, olfactory tubercle, nucleus of the trapezoid body, and cerebellar cortices. Quantitative analysis revealed that PGS remarkably increased in the hippocampus of SAM-P/8, a substrain of SAM, with advancing age, although a few PGS also appeared in the aged control mice, SAM-R/1 and DDD. Their histochemical nature, morphological features and distribution pattern were different from those of corpora amylacea and other similar bodies. A close anatomical relationship between PGS and glial fibrillary acidic protein-positive astrocytes was inferred from immunohistochemical studies. PGS is considered to be one of the morphological manifestations of senescence in mice brains, and are found to occur more numerously in the brains of learning or memory deficit mice, SAM-P/8.

Aging↗
PubMed1989

Behavioral characteristics of the SAM-P/8 strain in Sidman active avoidance task.

The behavior of the senescence-accelerated mouse (SAM-P/8) at the age of 1, 2, 4 and 10-11 months in Sidman active avoidance learning was analyzed, and compared to findings in the controls (SAM-R/1). At the age of 1 and 2 months, learning was comparable in these two strains. At the age of 4 and 10-11 months, SAM-P/8 but not SAM-R/1 learned active avoidance. We propose that SAM-P/8 can serve as a valid model of deficits in learning and memory.

Aging↗
PubMed1996

Comparing assessments of DSM-IV substance dependence disorders using CIDI-SAM and SCAN.

The main question addressed by this paper is whether DSM-IV substance dependence diagnoses obtained from two different instruments (the semi-structured WHO Schedules for Clinical Assessment in Neuropsychiatry, SCAN and the highly structured WHO Composite International Diagnostic Interview--Substance Abuse Module, SAM) are as consistent as diagnoses obtained from a single instrument (SAM) administered twice. Such comparisons of results from the two different instruments provide some measure of validity of the lay-administered SAM and of the underlying diagnostic concepts. Chance-corrected concordance was estimated using the kappa coefficient for SAM/SCAN (test/validation) and SAM/SAM (test/retest) comparisons. Analyses of agreement between SAM and SCAN for DSM-IV dependence diagnoses indicated good agreement for alcohol and cocaine, and fair agreement for opiates and cannabis. SAM/SAM (test/retest) agreement was excellent for alcohol and opiate dependence, good for cocaine dependence, and fair for cannabis dependence. Agreement on individual dependence criteria was generally consistent with overall diagnostic agreement though more variable. Notable was the poor agreement for cannabis criteria in the SAM/SCAN protocol. This may indicate that the dependence syndrome is less applicable to cannabis, while the consistency of agreement for alcohol, opiate, and cocaine dependence criteria supports the validity of these dependence syndromes. Finally, these data indicate that both the clinical (SCAN) and non-clinical (SAM) interviews can be used effectively for a variety of substances and dependence diagnoses.

Adolescent↗
PubMed1996

Expression of FGFR2 BEK and K-SAM mRNA variants in normal and malignant human breast.

The expression of mRNA encoding alternative forms of fibroblast growth factor receptor 2 (FGFR2) differing in the carboxy terminal half of their third immunoglobulin-like domain, was investigated in 77 human breast cancer tissues, 12 non-malignant breast biopsies and 29 cell lines, using a reverse transcriptase (RT) polymerase chain reaction (PCR) method. RNA from the two tissue groups yielded PCR product corresponding to both the BEK and the K-SAM form; amounts normalised to glyceraldehyde phosphate dehydrogenase product were similar in both groups. The level of either variant or of the total FGFR2 product was essentially unrelated to prognosis or clinical status except that patients with advanced clinical T staging had a higher proportion of BEK to K-SAM (P = 0.01). RNA from 1/2 normal breast derived and 8/10 breast cancer cell lines expressed exclusively or predominantly the K-SAM form; 2/10 had significant amounts of both BEK and K-SAM mRNA. Of 12 other epithelial lines, seven expressed mainly K-SAM mRNA, four expressed BEK and one was negative. Of five non-epithelial lines, one was negative, two expressed only BEK mRNA and two had significant amounts of both variants. We conclude that tissue levels of FGFR2 mRNA are unaltered in breast cancer extracts and that the splicing mechanism for this exon selection appears not to be significantly disrupted.

Adult↗
PubMed2002

Keratinocyte growth factor regulates proliferation and differentiation of hematopoietic cells expressing the receptor gene K-sam.

OBJECTIVE: The aim of this study was to establish a new method to overcome the problems of gene therapy targeting hematopoietic cells, namely low transduction efficiency and induction of differentiation during cytokine treatment. MATERIALS AND METHODS: The K-sam gene encoding the receptor for keratinocyte growth factor (KGF) was transduced to three factor-dependent hematopoietic cell lines (Ba/F3, 32Dcl3, and UT-7/GM) using retroviral vector, and their proliferation, differentiation, and intracellular signaling were studied. This gene also was transduced to murine bone marrow cells, and proliferation of colony-forming cells (CFCs) by KGF stimulation was examined. RESULTS: Although KGF is known to target only epithelial cells, all of the three cell lines transduced with K-sam proliferated due to KGF stimulation. Morphologic observation showed that KGF induced proliferation but did not cause significant differentiation of 32D/K-sam cells. KGF treatment increased phosphorylation of ERK1/2 but did not activate STAT molecules. Granulocyte colony-stimulating factor transduced the differentiation signal with the phosphorylation of STAT3 without significant ERK1/2 activation. Proliferation by KGF of murine primary bone marrow cells transduced with K-sam then was examined in liquid culture. KGF treatment significantly increased production of CFCs derived from K-sam-transduced bone marrow cells without causing the exhaustion of immature CFCs. CONCLUSIONS: KGF could efficiently induce proliferation of hematopoietic cells expressing the K-sam gene without obvious induction of differentiation or exhaustion of immature progenitor cells. The in vitro data are important for further preclinical in vivo study.

Animals↗
PubMedDate not supplied

Senescence-accelerated mouse (SAM): a novel murine model of senescence.

The Senescence-Accelerated Mouse (SAM) has been under development by our research team at Kyoto University since 1970 through the selective inbreeding of the AKR/J strain of mice donated by the Jackson Laboratory in 1968, based on a graded score for senescence, life span, and pathologic phenotype. At present, there are 12 lines of SAM: nine senescence-prone inbred strains (SAMP) including SAMP1, SAMP2, SAMP3, SAMP6, SAMP7, SAMP8, SAMP9, SAMP10, and SAMP11; and three senescence-resistant inbred strains (SAMR) including SAMR1, SAMR4, and SAMR5. Data from survival curves, Gompertzian function, and grading score of senescence, together with growth patterns of body weight of these SAMP and SAMR, revealed that the characteristic feature of aging common to all SAMP mice is "accelerated senescence;" early onset and irreversible advance of senescence manifested by several signs and gross lesions such as the loss of normal behavior, various skin lesions, increased lordokyphosis, etc., after a period of normal development. In the course of SAM development, it became evident that SAMP strains manifest various pathologic phenotypes that are characteristic enough to differentiate the SAM strains. The genetic background and significance of SAM development are discussed.

Aging↗