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PubMed1994

Postural control in sitting the SAM system: evaluation of use over three years.

The most appropriate posture in which to support the person with severe disability and diverse symptoms as a result of complex pathology remains more a matter of opinion than the result of research. This work reviews some of the studies which have attempted to identify definitive criteria for seating in such cases. Factors relating to measurement and conditions which threaten to invalidate the results of research in this field are highlighted. A description of the Seating and Mobility (SAM) system is given, together with a report of the monitoring of nine children with cerebral palsy using the system for a period of three years. The difficulties inherent in this work are noted and questions for future considerations are raised.

Activities of Daily Living↗
PubMed1998

A critical evaluation of several alcohol screening instruments using the CIDI-SAM as a criterion measure.

Four alcohol screening instruments (the AUDIT, CAGE, MAST, and Svanum's scale) were administered to a sample of 306 undergraduate students at a Midwestern university and were compared with regard to several test characteristics, using the alcohol section of the CIDI-SAM (DSM-IV version) as the criterion measure. The performance of these instruments was evaluated using two subsets of subjects: (1) students who currently met diagnostic criteria for alcohol dependence (n = 35); and (2) students who met diagnostic criteria for alcohol dependence in the past and/or at present (i.e., lifetime diagnosis; n = 50). The AUDIT performed significantly better than the other three instruments in identifying students who were currently alcohol dependent, providing a moderate degree of clinical utility with this group. The four instruments did not differ significantly in their ability to identify students with a lifetime diagnosis; each measure provided only a modest degree of clinical utility with this group.

Adolescent↗
PubMed1996

Age-related changes of the cementogenesis in the senescence-accelerated mouse (SAM).

Cementogenesis of the molars with aging was studied using senescence accelerated mouse (SAM) which included SAMP2/Iw and SAMP8@Iw as prone strains, and SAMR1/Iw as a resistant strain. Morphometric analysis was done for the cementum thickness at 2, 6, 12 and 16 months of age on 4 parts of the mice, i.e. at the mesial (M), the distal (D), the apical (A) and the furcational (F) cementum of the maxillary first molar. SAMR1/Iw was also studied at 20 months of age. Mean cementum thickness was statistically analyzed for age and strain differences. Mean thicknesses of the M and the D cementum in SAMP2/Iw and in SAMP8@Iw were usually higher than those in SAMR1/Iw. Furthermore, there were significant differences between SAMP2/Iw and SAMR1/Iw, and between SAMP8/Iw and SAMR1/Iw, both at 12 and 16 months of age. There was no difference in mean thickness in the F cementum in either strain and at any age. In the A cementum, SAMP2/Iw displayed significantly thicker cementum than SAMR1/Iw at 6, 12 and 16 months of age. The degree of molar eruption was thought to be more accelerated in SAMP2/Iw than in SAMR1/Iw. However, the thickness of the A cementum was not different for SAMP8@Iw and SAMR1/Iw in any age group. In this study, 2 conclusions were drawn as follows: first, that SAMP2/Iw and SAMP8@Iw exhibited more accelerated cementogenesis than SAMR1/Iw in the M and the D cementum. Secondly, several factors such as intrinsic factors, occlusal forces and degree of attrition affected the cementogenesis of the M and the D, the F and the A cementum, respectively.

Aging↗
PubMed2006

Inverse correlation between endogenous melatonin levels and oxidative damage in some tissues of SAM P8 mice.

To assess whether oxidative damage in some tissues was related to their melatonin concentration, endogenous melatonin levels and the age-linked protein and lipid damage in spleen, thymus and liver in 5-month-old SAM P8 mice were examined. The results show that high levels of melatonin in spleen and thymus correlate with lower protein and lipid damage. The liver, which had much lower melatonin concentrations than the other two tissues, had much higher levels of oxidatively damaged protein, as measured by carbonyl values. These results add new evidence concerning the protective role of endogenous melatonin as an antioxidant agent, and suggest that a treatment with this molecule might help to reduce age-associated functional deficits in many organs, including those of the immune system.

Aging↗
PubMed1990

Discrimination of modulation depth of sinusoidal amplitude modulation (SAM) noise.

The detection of sinusoidal amplitude modulation (SAM) provides a lower bound on the degree to which temporal information in the envelope of complex waveforms is encoded by the auditory system. The extent to which changes in the amount of modulation are discriminable provides additional information on the ability of the auditory system to utilize envelope fluctuations. Results from an experiment on the discrimination of modulation depth of broadband noise are presented. Discrimination thresholds, expressed as differences in modulation power, increase monotonically with the modulation depth of the standard, but do not obey Weber's law. The effects of carrier level and of modulation frequency are consistent with those observed in modulation detection: Changes in carrier level have little effect on modulation discrimination; changes in modulation frequency also have little effect except for standards near the modulation detection threshold. The discrimination of modulation depth is consistent with the leaky-integrator model of modulation detection for standards below--10 dB (20 log ms); for standards greater than--10 dB, the leaky integrator predicts better performance than that observed behaviorally.

Attention↗
PubMed2001

Localization, genomic organization, and alternative transcription of a novel human SAM-dependent methyltransferase gene on chromosome 2p22-->p21.

As part of our studies to identify the gene responsible for hereditary gingival fibromatosis, GINGF (OMIM 135300), we have identified and cloned a novel human gene that contains the highly conserved methyltransferase domain characteristic of S-adenosylmethionine-dependent methyltransferases. We localized this gene (C2orf8 encoding 288L6 SAM-methyltransferase) to chromosome 2p22-->p21 by FISH, and sublocalized it to BAC RP11 288L6 flanked by D2S2238 and D2S2331. Computational analysis of aligned ESTs identified ten exons in the hypothetical C2orf8 gene. Results of RACE analyses in placenta identified multiple transcripts of this gene with heterogeneity at the 5'-UTR. Alternative transcription and tissue specific expression of C2orf8 were detected by RT-PCR and Northern blot analyses. C2orf8 is expressed in a variety of tissues including brain, colon, gingiva, heart, kidney, liver, lung, placenta, small intestine, spleen, and thymus. Open reading frame analysis of the alternative transcripts identified a shared coding region spanning exons 6-10. This ORF consists of 732 nucleotides encoding a putative 244 amino acid protein. Bioinformational searches of both C2orf8 and the putative protein product identified three methyltransferase motifs conserved across many prokaryotic and eukaryotic species. Sequence analyses of C2orf8 excluded coding region mutations as causative of GINGF.

Chromosomes, Human, Pair 2↗
PubMed1997

Dementia three months after stroke. Baseline frequency and effect of different definitions of dementia in the Helsinki Stroke Aging Memory Study (SAM) cohort.

BACKGROUND AND PURPOSE: Vascular dementia is a common cause of dementia, and cerebrovascular disease is related to a higher risk of dementia. The frequency of dementia associated with ischemic stroke and the effects of different definitions of dementia in the diagnosis are still incompletely known. We evaluated the frequency of cognitive decline and dementia 3 months after ischemic stroke in a large stroke cohort. METHODS: Our cohort consisted of consecutively admitted ischemic stroke patients (n = 486) aged 55 to 85 years in the Helsinki (Finland) Stroke Aging Memory Study (SAM). Subjects were assessed by structured medical, neurological, and radiological examinations and interview with a close informant, as well as by the Mini-Mental State Examination and detailed clinical mental status examination of defined cognitive domains. The criteria for dementia were those of the Diagnostic and Statistical Manual of Mental Disorders (DSM) (DSM-III, DSM-III-R, and DSM-IV), the National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN), and the International Classification of Diseases, 10th Revision (ICD-10). RESULTS: We found that 451 (92.8%) of the patients were testable, 239 (49.2%) of the patients were women, and the mean age was 71.2 years. Any cognitive decline was present in 61.7%. In the groups aged 55 to 64, 65 to 74, and 75 to 85 years, the frequency of any cognitive decline was 45.7%, 53.8%, and 74.1% (P = .0008), respectively. The frequency of dementia was 25.5% by DSM-III, 20.0% by DSM-III-R, 18.4% by DSM-IV, 21.1% by NINDS-AIREN, and 6.0% by ICD-10 criteria. The frequency increased with increasing age: by the DSM-III definition, frequency in the aforementioned age groups was 19.3%, 23.7%, and 25.5%, respectively (P = .014). There was an overlap in the cases diagnosed as demented according to the different guidelines. Compared with standard diagnosis, the DSM-III was the most sensitive and ICD-10 the most specific. Concordance was moderate between the DSM criteria and NINDS-AIREN criteria but was poor between ICD-10 and the other criteria. CONCLUSIONS: Cognitive decline and dementia were frequent in the cohort of ischemic stroke patients, and the frequency increased with increasing age. Different definitions gave different frequency estimates, and overlap in the cases was observed. Our findings question the validity of current criteria for dementia in the setting of cerebrovascular disease and emphasize the need for further debate and studies to refine the categories of cognitive impairment related to cerebrovascular disease.

Aged↗
PubMed1990

Sam Shepard and the dysfunctional American family: therapeutic perspectives.

In depicting dysfunctional families Sam Shepard brought a greater intensity level to family portrayals than had previously been seen in modern American theater. In part, his plays appear to reflect the tumultuous tone of the late 1960s and early 1970s when American society was in flux and when the national uncertainty reached down to the basic unit of society, the family. Yet, despite addressing recently emerging social issues, Shepard's plays also depict universal family conflicts. There have been and always will be compelling forces that threaten domestic cohesiveness. While Shepard's families reflect extremely high levels of disorganization, they also demonstrate scenarios recognizable to all family therapists. They reassert the family's power and its influence on individual development. They also indirectly ask us to reflect on our current clinical practice and research. Family therapists need to continue to pay attention the content issues of family organization as well as therapeutic techniques. Shepard's plays remind therapists to look beyond internal dynamics in order to consider connections and affiliations that integrate families with outside communities. He underscores the importance of knowing the meaning and context of traditional rites of passage within families. Family therapists or other care providers may unwittingly undermine the significance of these family rituals by prescription of "expert" advice.

Cultural Characteristics↗
PubMed2003

Heterozygous mutation in the SAM domain of p63 underlies Rapp-Hodgkin ectodermal dysplasia.

Several ectodermal dysplasia syndromes, including Ectrodactyly-Ectodermal dysplasia-Clefting (EEC) and Ankyloblepharon-Ectodermal Dysplasia-Clefting (AEC) syndromes, are known to result from mutations in the p63 gene. We investigated whether Rapp-Hodgkin syndrome (RHS) is also caused by mutations in the p63 gene. We identified a heterozygous de novo germline missense mutation, S545P, in the sterile-alpha-motif (SAM) domain of p63, in a Thai patient affected with RHS. This is the first genetic abnormality to be described in RHS. The amino acid substitution is the most downstream missense mutation in p63 reported thus far. Histological assessment of a skin biopsy from the patient's palm showed hyperkeratosis and keratinocyte cell-cell detachment in the upper layers of the epidermis, along with numerous apoptotic keratinocytes. Collectively, these investigations demonstrate that RHS is also caused by mutations in p63 and that the clinical similarities to AEC syndrome are paralleled by the nature of the inherent mutation.

Adolescent↗
PubMed2006

Effect of dietary restriction on learning and memory impairment and histologic alterations of brain stem in senescence-accelerated mouse (SAM) P8 strain.

The age-associated spontaneous spongy degeneration in the brain stem of senescence-accelerated mouse (SAM) P8 strain has been suggested to be closely associated with the ability to learn and memorize. In this study, we investigated the effects of dietary restriction (DR) initiated from weaning on learning and memory and histologic changes of the brain stem in P8 and control R1 mice. Although no effect of DR was observed in the retention of the passive-avoidance response in both the P8 and R1 mice, the acquisition of the task was significantly improved by DR in P8 mice. On the other hand, the total area and number of vacuoles in the brain stem was significantly higher in ad libitum-fed (AD)-P8 mice than in AD-R1 mice. However, no significant effect was observed on the vacuole formation in the brain stem of P8 mice by DR. These observations suggest that the improvement of the acquisition of the task by DR in P8 mice is possibly due to changes in neuronal function rather than histologic alteration in brain stem.

Age Factors↗
PubMed2005

Alteration of leptin-induced STAT3 activation in the brain of senescence-accelerated mouse (SAM) P8.

We used senescence-accelerated mouse prone 8 (SAMP8), a useful model of accelerated aging, to investigate the responsiveness to leptin with aging. The state of leptin-induced STAT3 phosphorylation in the hypothalamus was found to be higher in SAMP8 than in SAMR1, a control mouse showing normal aging, at 14-18 months of age but not at 2 months of age. Moreover, leptin receptor Ob-Rb expression in the hypothalamus was up-regulated in SAMP8. The results indicate that leptin sensitivity increases with aging in the SAM mouse brain.

Aging↗
PubMed2005

The age-related degeneration of oligodendrocytes in the hippocampus of the senescence-accelerated mouse (SAM) P8: a quantitative immunohistochemical study.

The senescence-accelerated mouse (SAM) is known as a murine model for accelerated aging. The SAMP8 shows age-related deficits of learning and memory at an earlier age than control mice (SAMR1). We investigated the changes in oligodendrocytes in the brain of SAMP8, using immunohistochemistry for myelin basic protein (MBP) and 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP) as an oligodendrocyte marker. SAMP8 at 10 months old showed a decrease in MBP-immunoreactivity (IR) and CNP-IR in the hippocampal CA1 subfield, compared with SAMR1. There were no significant differences in MBP and CNP old in the cerebral cortex and the optic tract between SAMR1 and SAMP8 at 10 months. Furthermore, we measured the area of MBP-IR in the CA1 subfield of both strains and found that the area of MBP-IR in SAMP8 had decreased progressively with age, compared with SAMR1. These results suggest that age-related degeneration of oligodendrocytes had occurred in the hippocampus of SAMP8.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed2003

Abnormal structural luteolysis in ovaries of the senescence accelerated mouse (SAM): expression of Fas ligand/Fas-mediated apoptosis signaling molecules in luteal cells.

Senescence accelerated mouse-prone (SAMP) mice with a shortened life span show accelerated changes in many of the signs of aging and a shorter reproductive life span than SAM-resistant (SAMR) controls. We previously showed that functional regression (progesterone dissimilation) occurs in abnormally accumulated luteal bodies (aaLBs) of SAMP mice, but structural regression of luteal cells in aaLB is inhibited. A deficiency of luteal cell apoptosis causes the abnormal accumulation of LBs in SAMP ovaries. In the present study, to show the abnormality of Fas ligand (FasL)/Fas-mediated apoptosis signal transducing factors in the aaLBs of the SAMP ovaries, we assessed the changes in the expression of FasL, Fas, caspase-8 and caspase-3 mRNAs by reverse transcription-polymerase chain reaction, and in the expression and localization of FasL, Fas and activated caspase-3 proteins by Western blotting and immunohistochemistry, respectively, during the estrus cycle/luteolysis. These mRNAs and proteins were expressed in normal LBs of both SAMP and SAMR ovaries, but not at all or only in trace amounts in aaLBs of SAMP, indicating that structural regression is inhibited by blockage of the expression of these transducing factors in luteal cells of aaLBs in SAMP mice.

Aging↗
PubMedDate not supplied

Subcloning of the histone DNA sequences of phage lambda Sam 7 h 22 in plasmid pBR 322.

The histone DNA sequences of the Hind III cluster of the sea urchin Psammechinus miliaris which are carried by the chimeric phage DNA of lambda Sam 7 h 22 have been subcloned in plasmid p BR 322. Due to this procedure single segments of the cluster have been separated from each other and are available as gene specific hybridization probes.

Animals↗
PubMed2005

Management and visualization of whole genome shotgun assemblies using SAM.

We have designed and implemented a system to manage whole genome shotgun sequences and whole genome sequence assembly data flow. The Sequence Assembly Manager (SAM) consists primarily of a MySQL relational database and Perl applications designed to easily manipulate and coordinate the analysis of sequence information and to view and report genome assembly progress through its Common Gateway Interface (CGI) web interface. The application includes a tool to compare sequence assemblies to fingerprint maps that has been used successfully to improve and validate both maps and sequence assemblies of the Rhodococcus sp.RHAI and Cryptococcus neoformans WM276 genomes.

Algorithms↗
PubMed1998

Age-related changes in blood pressure in the senescence-accelerated mouse (SAM): aged SAMP1 mice manifest hypertensive vascular disease.

Age-related changes in systolic blood pressure were assessed, using the senescence-accelerated mouse (SAM) model for aging research with strains SAMR1, SAMP1, and SAMP8. Each of the strains manifested a characteristic change in blood pressure with age. The SAMR1 strain, with normal aging, did not have chronologic changes from 2 to 27 months of age. The SAMP1 strain, with accelerated senescence, had a significant increase in blood pressure with age, and some (8 of 39) mice manifested hypertensive vascular disease characterized by high blood pressure, cardiac hypertrophy, and arteriolar fibrinoid necrosis at 11 to 14 months of age. The gradual increase in blood pressure after 8 to 10 months was considered to be preceded by progressive renal changes, from glomerulonephritis to contraction of the kidney, suggesting that the high blood pressure in the SAMP1 strain was of renal origin. Blood pressure in the SAMP8 strain, with age-related deficits in learning and memory, gradually decreased after 5 to 7 months of age, and was suggested to be due to the astrogliotic changes in response to spongiform degeneration in the medulla oblongata at 11 to 14 and 15 to 18 months of age.

Aging↗
PubMedDate not supplied

[Proliferative senescence of embryo fibroblasts of Japanese senescence accelerated mice (SAM) is accompanied by parallel decreasing of response to various growth factors].

The Japanese senescence accelerated mice (SAM) are a group of the low-longevity mouse lines and represent a new convenient model for studying the senescence process. We studied the proliferation of embryo fibroblasts of SAMP1 and SAMR1 mouse lines. It was shown that fibroblasts of the shortest longevity line SAMP1 have a markedly decreased proliferative potential of the mean 8.7 population doublings, whereas fibroblasts of a relatively high-longevity line SAMR1 have an average proliferative potential of 12.3 doublings. The fibroblast senescence in both lines is accompanied by a simultaneous lowering of the cell proliferative response to the blood serum, epidermal, fibroblast, and platelet-derived growth factors. At initial stages of the cell culture growth, lines SAMP1 and SAMR1 exhibit the same reactions to growth factors, but already beginning from the fifth doubling, the SAMP1 cell response is sharply decreased as compared with SAMR1. Lowering the proliferative reaction is accompanied by a decreased phosphorylation of tyrosine in the cell proteins responsible for mitogenic reaction. Thus, the parallel decrease of proliferative response to different growth factors during fibroblast senescence is most likely due the emergence of a regulatory block at common stages of the mitogenic signal transduction.

Animals↗
PubMed2002

The Sam Bulkley Rocky Mountain Travelling Fellowship report.

The Sam Bulkley Rocky Mountain Travelling Fellowship afforded me a wonderful opportunity to study and to be involved at the cutting-edge of orthodontic treatment, especially in the treatment of aesthetically and functionally disadvantaged members of our community. I would like to thank everyone responsible for making this award possible, and also to thank all the clinicians, researchers and their staff who welcomed me and educated me during my visit. It has been most beneficial and rewarding.

Australia↗