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At least 1,063 records · Page 59Linked to original sources
PubMed2001

Periodontal ligament cells secrete the factor that inhibits osteoclastic differentiation and function: the factor is osteoprotegerin/osteoclastogenesis inhibitory factor.

The periodontal ligament, a highly specialized connective tissue situated between the tooth and the alveolar bone of the tooth socket, has been thought to influence the remodeling of the alveolar bone. The effects of two human periodontal ligament fibroblastic cell populations (HPLFs) on osteoclast-like cell (OCL) formation and the function of authentic osteoclasts were examined. The addition of the conditioned media (CM) from both HPLF cultures (HPLF-CMs) to mouse bone marrow culture inhibited OCL formation in spite of the presence of 10(-8)M 1alpha, 25 dihydroxyvitamin D3 (1alpha,25(OH)2D3). This inhibitory effect was most remarkable when both CMs were added during day 6 to day 9 following bone marrow culture, just at the late stage of OCL differentiation. HPLF-CMs also induced a significant decrease in the pit area and the pit number formed by authentic osteoclasts on ivory slices. The administration of neutralizing monoclonal antibody (OI-1) against human osteoprotegerin (OPG)/osteoclastogenesis inhibitory factor (OCIF) with HPLF-CMs to mouse bone marrow culture almost completely blocked the inhibitory effect of these CMs on OCL formation. Immunofluorescent examination of HPLF with OI-1 revealed intense positive reactivity in the cytoplasm. Western blot analysis of HPLF-CM using anti-human OPG/OCIF polyclonal antibody resulted in the detection of bands of 60 kDa and 120 kDa which were consistent with those of OPG/OCIF. These results suggest that HPLF cells produce and secrete OPG/OCIF, and that this factor from HPLF prevents the differentiation of the late preosteoclast and the function of the mature osteoclasts.

Adolescent↗
PubMed1999

Human and mouse XAP-5 and XAP-5-like (X5L) genes: identification of an ancient functional retroposon differentially expressed in testis.

Although most retroposons that arose by reverse transcription of cellular mRNAs and by reintegration into the genome are nonfunctional, several examples exist in which the retroposon acquired a novel function and became fixed in the genome as a functional gene. We identified another such case: the ubiquitously expressed X-linked XAP-5 gene with unknown function gave rise to its retroposed counterpart, XAP-5-like (X5L), which has an intronless open reading frame and is autosomal in human. Phylogenetic analysis of the human and mouse XAP-5 and X5L genes shows that the retroposition most likely took place before the radiation of eutherian mammals. The XAP-5 and X5L genes are expressed in a wide range of tissues but are differentially expressed in testis. The ancient origin and broad expression of the X5L retroposon indicate that the XAP-5 and X5L genes may have assumed different functions in somatic cells. In addition to this, because of its autosomal location and its high level and particular pattern of expression in spermatogenic cells, the X5L expression in testis may compensate for the X-linked XAP-5 gene, which may be silenced during spermatogenesis.

Amino Acid Sequence↗
PubMed2000

Do executive function deficits differentiate between adolescents with ADHD and oppositional defiant/conduct disorder? A neuropsychological study using the Six Elements Test and Hayling Sentence Completion Test.

Two neuropsychological measures of executive functions--Six Elements Tests (SET) and Hayling Sentence Completion Test (HSCT)--were administered to 110 adolescents, aged 12-15 years. Participants comprised four groups: Attention Deficit Hyperactivity Disorder (ADHD) only (n = 35). ADHD and Oppositional Defiant Disorder/Conduct Disorder (ODD/CD) (n = 38), ODD/CD only (n = 11), and a normal community control group (n = 26). Results indicated that adolescents with ADHD performed significantly worse on both the SET and HSCT than those without ADHD, whether or not they also had ODD/CD. The adolescents with ADHD and with comorbid ADHD and ODD/CD were significantly more impaired in their ability to generate strategies and to monitor their ongoing behavior compared with age-matched controls and adolescents with ODD/CD only. It is argued that among adolescents with clinically significant levels of externalizing behavior problems, executive function deficits are specific to those with ADHD. The findings support the sensitivity of these two relatively new tests of executive functions and their ecological validity in tapping into everyday situations, which are potentially problematic for individuals with ADHD.

Adolescent↗
PubMed1994

Suppression of sodium channel function in differentiating C2 muscle cells stably overexpressing rat androgen receptors.

Differentiation of skeletal muscle and the formation of the neuromuscular junction are regulated by steroid hormones. The effects of androgens on ion channel proteins central to neuromuscular signalling have been investigated in differentiating mouse muscle C2 cells and in C2 cells that stably overexpress the rat androgen receptor (AR) cDNA. Neither the expression nor function of ACh receptors was regulated by androgenic actions in these cells. However, voltage-dependent sodium (Na) current density was decreased by androgen treatment of C2 cells and was abolished, even in the absence of androgens, in C2 cells that overexpress the AR. The decrease in functional Na current was not accompanied by concomitant decreases in Na channel mRNA, suggesting that AR influence posttranscriptional processing of Na channels in differentiating C2 cells.

Acetylcholine↗
PubMed2000

Myeloid specific human CD33 is an inhibitory receptor with differential ITIM function in recruiting the phosphatases SHP-1 and SHP-2.

CD33 is a myeloid specific member of the sialic acid-binding receptor family and is expressed highly on myeloid progenitor cells but at much lower levels in differentiated cells. Human CD33 has two tyrosine residues in its cytoplasmic domain (Y340 and Y358). When phosphorylated, these tyrosines could function as docking sites for the phosphatases, SHP-1 and/or SHP-2, enabling CD33 to function as an inhibitory receptor. Here we demonstrate that CD33 is tyrosine phosphorylated in the presence of the phosphatase inhibitor, pervanadate, and recruits SHP-1 and SHP-2. Co-expression studies suggest that the Src-family kinase Lck is effective at phosphorylating Y340, but not Y358, suggesting that these residues may function in the selective recruitment of adapter molecules and have distinct functions. Further support for overlapping, but nonredundant, roles for Y340 and Y358 comes from peptide-binding studies that revealed the recruitment of both SHP-1 and SHP-2 to Y340 but only SHP-2 to Y358. Analysis using mutants of SHP-1 demonstrated that binding Y340 of CD33 was primarily to the amino Src homology-2 domain of SHP-1. The potential of CD33 to function as an inhibitory receptor was demonstrated by its ability to down-regulate CD64-induced calcium mobilization in U937. The dependence of this inhibition on SHP-1 was demonstrated by blocking CD33-mediated effects with dominant negative SHP-1. This result implies that CD33 is an inhibitory receptor and also that SHP-1 phosphatase has a significant role in mediating CD33 function. Further studies are essential to identify the receptor(s) that CD33 inhibits in vivo and its function in myeloid lineage development. (Blood. 2000;96:483-490)

Amino Acid Sequence↗
PubMed2002

Differentiation of functional dendritic cells and macrophages from human peripheral blood monocyte precursors is dependent on expression of p21 (WAF1/CIP1) and requires iron.

Iron is required for monocyte/macrophage differentiation of HL-60 leukaemia cells. Differentiation requires induction of the cyclin-dependent kinase inhibitor p21 (WAF1/CIP1), and cell cycle arrest at the G1/S checkpoint. With iron depletion, p21 induction and differentiation are blocked. To establish the roles of iron and p21 in normal monocyte/macrophage differentiation, we examined generation of dendritic cells (DCs) and macrophages from peripheral monocytes. Monocytes were cultured with interleukin 4 and granulocyte-macrophage colony-stimulating factor (GM-CSF), then treated with lipopolysaccharide to produce DCs or with M-CSF to produce macrophages. Iron deprivation was induced by desferrioxamine (DF). Monocyte-derived DCs had characteristic phenotype and morphology, and stimulated proliferation of naïve allogeneic T lymphocytes. In contrast, DCs generated under iron deprivation were phenotypically undifferentiated and did not stimulate T cells. Similarly, macrophages expressed a characteristic phenotype and morphology, and phagocytosed latex beads, but macrophages generated under iron deprivation failed to develop a mature phenotype and had impaired phagocytosis. Iron deprivation blocked induction of p21 (WAF1/CIP1) expression in both DC and macrophage cultures. Furthermore, p21 antisense oligonucleotides, but not sense oligonucleotides, inhibited both DC and macrophage differentiation. These data indicate that a key role of iron in haematopoiesis is to support induction of p21 which, in turn, is required for DC and macrophage differentiation.

Cell Culture Techniques↗
PubMed1984

Differentiation specific functions in cultured and transplanted mouse keratinocytes: environmental influences on ultrastructure and keratin expression.

Keratinocytes from neonatal mouse back skin, growing in primary culture (PEC) under conventional conditions (immersed), exerted a reduced programme of differentiation as indicated by cell morphology and organisation, ultrastructure and keratin composition. Four major keratins were found in cytoskeletal extracts (mol.wt. 60K, 59K, 53K, 49K) of primary cultures, together with a minor 51K protein and some residual actin. This "culture-type" keratin profile remained stable and little variation was observed after repeated treatment with various agents, such as 12-0-tetradecanoylphorbol-13-acetate (TPA), retinoic acid (RA) or dimethylsulphoxide (DMSO). The profile was unaltered by long-term growth of primary cultures in low Ca2+ (0.1 mM) medium or on 3T3 feeder-layers. Nevertheless, TPA, RA and low Ca2+ did alter the morphology and filament architecture (as observed by indirect immunofluorescence microscopy with anti-keratin antibodies). Comparison of keratinocytes from primary culture with basal cells isolated from epidermis revealed similarities in electrophoretic profile, with the 60K and 53K keratins being common to both. The other in vivo keratins had a characteristic spatial distribution; 67K and 58K keratins were present in suprabasal cells (spinous and granular), while 64K, 62K, 58.5K and 57.5K keratins were present only in stratum corneum. None of these keratins were found in cultured cells grown under regular conditions. Several morphological features of epidermal differentiation could be restored by the growth of PEC on collagen gels exposed to the atmosphere ("organotypic" culture) without influencing the keratin profile. Almost complete restoration of epidermal function was achieved after transplantation of PEC onto adult syngeneic mice. In this in vivo environment, well-structured epithelia developed which resembled interfollicular epidermis. Restoration of both typical ultrastructure and in vivo type keratin expression occurred within 2 or 3 weeks. Thus, although keratinocytes in primary culture differ considerably from those in vivo, they have not irreversibly lost the capacity for complete differentiation.

Animals↗
PubMed1999

Developmental neuropathology and impact of perinatal brain damage. III: gray matter lesions of the neocortex.

The evolving neuropathology of primarily undamaged cortical regions adjacent to the injured site has been studied in 36 infants who survived a variety of perinatally acquired encephalopathies (microgyrias, ulegyrias, multicystic encephalopathies, porencephalies, and hydranencephalies) and later died of unrelated causes. Their survival times range from hours, days, weeks, or months, to several years. Ten of these children developed epilepsy, 2 developed cerebral palsy, and several were neurologically and mentally impaired. In all cases studied, the undamaged cortex adjacent to the injured site survives, retains its intrinsic vasculature, and is capable of continuing differentiation. However, its postinjury development is characterized by progressive alterations compatible with acquired cortical dysplasia that affects the structural and functional differentiation of its neurons, synaptic profiles, fiber distribution, glial elements, and vasculature. The synaptic profiles of many neurons are transformed by an increased number of intrinsic loci that replace extrinsic ones vacated by the destruction of afferent fibers. The intrinsic fibers of layer I and some Cajal-Retzius cells survive even in severe lesions and may be capable of interconnecting cortical regions that have lost other type of connections. Some intrinsic neurons undergo postinjury structural and functional hypertrophy, acquire new morphologic and functional features, and achieve a large size (meganeurons). Probably, these meganeurons acquire their structural and functional hypertrophy by partial endomitotic DNA and/or RNA reduplication (polyploidy). These postinjury alterations are not static but ongoing processes that continue to affect the structural and functional differentiation of the still developing cortex and may eventually influence the neurologic and cognitive maturation of affected children. This study proposes that, in acquired encephalopathies, the progressive postinjury reorganization of the undamaged cortex and its consequences (acquired cortical dysplasia), rather than the original lesion, represent the main underlying mechanism in the pathogenesis of ensuing neurological sequelae, such as, epilepsy, cerebral palsy, dyslexia, cognitive impairment, and/or poor school performance.

Acute Disease↗
PubMed1979

Differentiation of functionally active mouse T lymphocytes from functionally inactive bone marrow precursors. IV. Recovery of T-cell function from bone marrow precursors in a histo-incompatible environment.

Regeneration of T-cell activities in vivo or in vitro from mouse bone marrow precursors differentiating in the presence of an allogeneic thymus was investigated. The data indicated that T-depleted bone marrow cells fail to affect long-term reconstitution of allogeneic recipients unless a pool of rapidly maturing T-precursor cells is also removed (post-thymic pool). Animals reconstituted with pre-thymic bone marrow stem cells become stable chimaeras in which cells capable of generating an in vitro CML response to host antigens, as well as cells capable of suppressing that response, could be demonstrated. Similar data (CML directed against the H-2 antigens of the 'host' thymus feeder layer and cells capable of inhibiting that response) were obtained when pre-thymic bone marrow cells were grown in vitro on allogeneic thymus feeder cells. When cytotoxic T-lymphocyte precursor (CTLp) and helper (CTLh) cells were separately investigated, a restriction in their co-operation for an anti-host response was observed when precursor cells differentiated in an allogeneic environment. Only CTLp and CTLh differentiating in the presence of the same allogeneic thymus source (whether in vivo or in vitro) could co-operate to generate CTL directed to H-2 antigens of that thymus source.

Animals↗
PubMed2004

The interview mode effect on the Center for Epidemiological Studies Depression (CES-D) scale: an item response theory analysis.

BACKGROUND: Evidence of a mode effect has raised concerns about the comparability and validity of self- versus interviewer-administered versions of the Center for Epidemiological Studies Depression (CES-D) scale. Response anonymity has been proposed to explain this effect. However, the factors that contribute to this mode effect are not well understood. We used item response theory (IRT) to examine the nature of the CES-D mode effect. METHODS: A sample of depressed primary care patients from the Partners-in-Care Study were randomized to receive either a phone interview (N=139) or a mail survey (N=139) of the CES-D. We used likelihood ratio tests to identify differentially functioning items in the 2 groups. Category response curves are used to describe these effects. RESULTS: Twelve items manifested differential functioning. Category response curves consistently indicate that phone respondents had a lower probability of endorsing the third of 4 response categories than mail respondents, suggesting a possible cognitive effect. CONCLUSION: Although response anonymity could be important in mode effects observed in surveys of sensitive topics, cognitive factors appear more important to the mode effect in the CES-D.

Adult↗
PubMed1984

Ego ideal and ideal ego.

A genetic and functional differentiation between the ego ideal and the ideal ego is proposed. This differentiation allows for a more precise characterization and interpretation of ego libido in symptoms and transference. These genetic and functional differentiations of ego ideal and ideal ego can be used to clarify the differing severities of the types of narcissistic disorder: psychosis, borderline personality disorder, narcissistic personality disorder, from normal maturity. It can also be put to work in refining one's formulation of the narcissistic complications of the classical transference neurosis. This usefulness has been demonstrated in relation to clinical material. In neurosis the ideal ego is a source of symptoms and inappropriate transference demands; in culture it finds embodiment in aggrandized concepts of human nature; in mature adults it is the comforting memory of a vanished splendour.

Ego↗
PubMed2000

Regulation of the differentiation and function of osteoclasts.

The osteoclast is the cell that resorbs bone. It has been known for many years that its formation and function are regulated by cells of the osteoblastic lineage. Recently the molecular basis for this regulation was identified; osteoblastic cells induce osteoclastic differentiation and resorptive activity through expression of tumour necrosis factor (TNF) activation-induced cytokine (TRANCE) (also known as RANKL, ODF, OPGL, and TNFSF11), a novel membrane-inserted member of the TNF superfamily. Osteoclastic regulation is assisted through secretion of an inhibitor, osteoprotegerin (OPG) (OCIF, TNFRSF11B), a soluble (decoy) receptor for TRANCE. Osteoclast formation and survival also depend on and are substantially enhanced by transforming growth factor-beta (TGF-beta), which is abundant in bone matrix. Surprisingly, not only TRANCE but also TNF-alpha can induce osteoclast formation in vitro from bone marrow-derived mononuclear phagocytes, especially in the presence of TGF-beta. Whether or not TNF-alpha does the same in vivo, its ability to generate osteoclasts in vitro has significant implications regarding the nature of osteoclasts and their relationship to other mononuclear phagocytes, and a possible wider role for TRANCE in macrophage pathobiology. A hypothesis is presented in which the osteoclast is a mononuclear phagocyte directed towards a debriding function by TGF-beta, activated for this function by TRANCE, and induced to become specifically osteoclastic by the characteristics of the substrate or signals from bone cells that betoken such characteristics.

Bone Resorption↗