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PubMed1993

Signaling of programmed cell death induction in WEHI-231 B lymphoma cells.

The murine WEHI-231 B lymphoma is highly sensitive to membrane immunoglobulin ligation which leads to programmed cell death (PCD) in this cell line. To study the molecular pathways involved in PCD induction in these cells, we derived two variants of WEHI-231 resistant to anti-Ig treatment. The level of bcl-2 mRNA was identical in the wild type and the variants, either untreated or anti-Ig treated, suggesting that PCD is not under the control of bcl-2 in WEHI-231 cells. In contrast, c-myc gene expression was markedly different in the wild type and the variants, both in the unstimulated and anti-Ig-stimulated state. Our findings are interpreted in the context of the dual capacity of c-myc to promote cell growth or cell death, in conjunction with other growth regulatory signals.

Animals↗

PubMed1992

Tumor-associated karyotypic lesions coselected with in vitro macrophage differentiation.

Several cytogenetic lesions in chromosomes 2, 5, 12, and 16 have been repeatedly coselected with in vitro macrophage differentiation in a clonal murine thymic tumor cell line. Parental-type subclones, which show an extremely immature hemopoietic phenotype, do not carry the aberrations. The frequency of the stable differentiated variants is elevated by 5-azacytidine and bromodeoxyuridine, consistent with chromosome breakage being responsible for the phenotype. The frequency is also raised by dexamethasone. Since variants are 300-3,000-fold more resistant to dexamethasone than parental clones, we interpret this to be largely due to selection. Three of the lesions, on chromosome 2, match those previously described as associated specifically with in vivo-generated murine myeloid tumors, induced by X irradiation and corticosteroid treatment. Several implications follow from these observations. (1) In vitro differentiation in clonal tumor cell lines can be used to select for tumor-associated lesions. This should allow genetic and molecular analysis of the chromosome 2 lesions and of others that may pinpoint genes critical to macrophage differentiation and transformation. (2) Myeloid and lymphoid tumors that occur in response to X irradiation may diverge from a common initiating tumor. (3) The hemopoietic lineage switch phenomenon, previously described by several authors, may be caused by similar or identical chromosome aberrations.

Abelson murine leukemia virus↗

PubMed1983

6-Phosphogluconate dehydrogenase activity variants in Musca domestica L.: A further allele at the Pgd locus as proved by densitometric assay.

A new electrophoretic variant of 6-phosphogluconate dehydrogenase (6PGD) has been detected in flies of a laboratory Musca domestica strain. This variant is to be added to the two already described, PGD-A and PGD-B, identified by a fast-weak and a slow-thick electrophoretic band, respectively. The new variant, PGD-C, has the same mobility as PGD-A but provides a more intensely stained band; therefore it can be described as a fast-thick phenotype. The staining intensity of PGD-C is slightly lower than that of PGD-B. Genetic and densitometric tests have shown that the different levels of enzymatic activity of the two fast variants A and C are inherited as alternative genetic units, and they have been interpreted as one aspect of the phenotypic expression of two Pgd alleles, namely, PgdA and PgdC. These alleles determine both the rates of electrophoretic mobility (fast in both cases) and the levels of activity (low for A, strong for C; shown by weak or thick stained electrophoretic bands). Similarly, the two distinctive features of PGD-B, namely, slow mobility and high activity level, are always jointly inherited and appear as two pleiotropic aspects of the phenotype coded for by the PgdB allele. The PgdB/PgdC heterozygous flies provide a slightly asymmetrical three-banded zymogram, while the PgdA/PgdC combination leads to a single-banded pattern, showing the same mobility as the parents and an intermediate staining intensity. The quantitative analysis of enzyme activity of 6PGD zymograms, performed through densitometric methods, has led to the recognition of three different activity levels coded for by Pgd alleles, one of which, namely, PgdC, would not have been detected using electrophoretic methods alone.

Alleles↗

PubMed2004

[Common disorders and diseases of the nails. Anatomy, physiology, disorders, clarification and therapy].

Disorders of anatomical variants of the nails are often seen in clinical practice. Their correction identification and interpretation are essential dermatological skills. The increasing emphasis on aesthetic considerations in dermatology means that even the slightest nail changes may assume significance for their patients. In order to skillfully evaluate nails, one must be familiar with the terminology and classification of nail disorders. The nail plate, nail bed and periungual tissue may also be affected. Longitudinal melanonychia is especially important as a possible clue to subungual melanoma.

Diagnosis, Differential↗

PubMed1978

Isolation and preliminary characterization of rat liver cells resistant to 7-ketocholesterol.

Two clones of the rat liver cell line, GAI, were selected and propagated in 4 microgram/ml of the cholesterol analogue, 7-ketocholesterol. One of the variants was also found to be resistant to another toxic analogue, 25-hydroxycholesterol. 3-hydroxy-3-methylglutaryl coenzyme A reductase (EC 1.1.1.34) activity was elevated in both variant clones, but was not increased substantially upon incubation of the cells in lipid-depleted medium. The reductase activity was increased 3-fold in the wild type cells under the same conditions. Incubation of the cells in lipid-depleted medium resulted in a 3-fold increase in the rate of sterol synthesis from [14C]acetate in all three types. In the presence of 2 microgram/ml 7-ketocholesterol, the reductase activity in all three cell lines decreased at an equal rate, but activity of the enzyme was still measurable after 48 h in the presence of the analogue. Sterol synthesis was reduced almost to zero in the wild type cells under these conditions, while the variant cells retained 12--15% of their capacity for sterol synthesis. These results are interpreted to indicate that 7-ketocholesterol, besides affecting sterol synthesis at the level to 3-hydroxy-3-methylglutaryl coenzyme A reductase, must also affect sterol synthesis at another step further along the synthetic pathway.

Acetates↗

PubMed1987

On comprehension of active/passive sentences and language processing in a Polish agrammatic aphasic.

This paper presents the results of a study of active/passive sentence comprehension by a Polish-speaking agrammatic aphasic. The patient showed good performance on canonically ordered active and passive structures, but performed poorly on inverted variants. The systematically normal and deviant comprehension patterns observed are accounted for by normal interpretative strategies applied to syntactic structures built around verbs with reduced inflectional morphology. The differences between our Polish data and the English data discussed in the literature are explained by the fact that Polish possesses a richer derivational verb morphology. The interpretation of inverted sentences demonstrates the importance of S-V-O word order preference. Our analysis draws upon the notion of grammatical functions to explain the data.

Adult↗

PubMed1994

Origin and significance of the heterogeneity of protein hormones.

The heterogeneity of circulating protein hormone is the result of multiple steps including gene expression, mRNA maturation, post-translational processing and peripheral catabolism. As a consequence of these cumulative events, it seems difficult to evaluate the endocrine function by using specific radioimmunoassays for each circulating variant of a protein hormone. Moreover, the discovery of new molecular variants of protein hormones with unknown biological significance complicates the standardization and the clinical interpretation of immunoassays.

Blood Proteins↗

PubMed2000

Identification of target antigen for SLA/LP autoantibodies in autoimmune hepatitis.

BACKGROUND: Autoantibodies are a hallmark of autoimmune hepatitis, but most are not disease specific. Autoantibodies to soluble liver antigen (SLA) and to liver and pancreas antigen (LP) have been described as disease specific, occurring in about 30% of all patients with autoimmune hepatitis, but no standardised assays are available. Methods We tested 2000 serum samples from patients with various liver diseases and controls for SLA autoantibodies by inhibition ELISA. Serum samples positive for SLA antibodies were used for immunoscreening of cDNA expression libraries. Identified clones were tested against a panel of serum samples positive for SLA and LP autoantibodies and control serum samples, and the epitope mapped by deletion mutants and exonuclease digestion. FINDINGS: SLA and LP autoantibodies were identical. Of 2000 serum samples screened, 35 were positive for SLA autoantibodies. These positive samples came from patients with autoimmune hepatitis; three from patients with an overlap syndrome (primary biliary cirrhosis and secondary autoimmune hepatitis). Expression cloning and absorption experiments identified a 422 aminoacid protein present in two splice variants as the sole target antigen. Aminoacids 371-409 were critical for immune recognition. INTERPRETATION: The identified cDNA encodes the primary target antigen of SLA/LP autoantibodies. The SLA/LP antigen has a previously unknown aminoacid sequence, and presumably codes for an unindentified enzyme, suggested to be UGA-suppressor tRNA-associated protein. SLA/LP autoantibodies are disease specific and recognise a dominant epitope, suggesting a specific antigen-driven immune response. Identification of the SLA/LP target antigen will allow establishment of a reliable, widely available diagnostic assay. Furthermore, its role in the pathogenesis of autoimmune hepatitis can now be studied.

Autoantibodies↗

PubMed2006

Reduction in infectivity of endogenous transmissible spongiform encephalopathies present in blood by adsorption to selective affinity resins.

BACKGROUND: Transmissible spongiform encephalopathies (TSE) can be contracted through blood transfusion. Selective adsorption of the causative agent from donated blood might be one of the best ways of managing this risk. In our study, affinity resin L13, which reduces brain-derived infectivity spiked into human red blood cell concentrate by around 4 log(10)ID(50), and its equivalent, L13A, produced on a manufacturing scale, were assessed for their ability to remove TSE infectivity endogenously present in blood. METHODS: 500 mL of scrapie-infected hamster whole blood was leucoreduced at full scale before passage through the affinity resins. Infectivity of whole blood, leucoreduced whole blood (challenge), and the recovered blood from each flow-through was measured by limiting dilution titration. FINDINGS: Leucoreduction removed 72% of input infectivity. 15 of 99 animals were infected by the challenge, whereas none of the 96 or 100 animals inoculated with the final flow-throughs from either resin developed the disease after 540 days. The limit of detection of the bioassay was 0.2 infectious doses per mL. The overall reduction of the challenge infectivity was more than 1.22 log10ID. The results showed removal of endogenous TSE infectivity from leucoreduced whole blood by affinity ligands. The same resins adsorb normal and abnormal prion protein from human infections with variant, sporadic, and familial Creutzfeldt-Jakob disease, in the presence of blood components. INTERPRETATION: TSE affinity ligands, when incorporated into appropriate devices, can be used to mitigate the risks from TSE-infected blood, blood products, and other materials exposed to TSE infectivity.

Adsorption↗

PubMed1999

Transmission of antiretroviral-drug-resistant HIV-1 variants.

BACKGROUND: Resistance of HIV-1 to antiretroviral drugs is the main cause of antiretroviral-treatment failure. We assessed the transmission of drug-resistant variants among individuals with primary HIV-1 infection. METHODS: Population-based sequencing of the viral reverse-transcriptase and protease genes derived from plasma viral RNA was done in 82 consecutive individuals with documented primary HIV-1 infection from January, 1996, to July, 1998. Phenotypic resistance to protease inhibitors was assessed by recombinant virus assay in individuals with two or more mutations associated with resistance to protease inhibitors. FINDINGS: Zidovudine-resistance mutations were detected in seven (9%) of 82 individuals. Mutations associated with resistance to other reverse-transcriptase inhibitors (RTIs) were detected in two individuals. Primary-resistance mutations associated with protease inhibitors (V82A, L90M) were detected in three (4%) of 70 individuals; two of these had also RTI-resistance mutations. Decreased sensitivity to three or four protease inhibitors was seen in three individuals, one of whom was infected with HIV-1 variants that harboured 12 mutations associated with resistance to multiple RTI and protease inhibitors. INTERPRETATION: To introduce the best antiretroviral treatment, resistance testing should be done in recently HIV-1-infected individuals.

Adolescent↗

PubMed2026

Long-read proteogenomic atlas of human neuronal differentiation reveals isoform diversity informing neurodevelopmental risk mechanisms.

RNA splicing shapes neuronal identity and disease risk, yet current maps lack the developmental resolution and depth to resolve this complexity. Here, we integrate deep long-read RNA sequencing and proteomics in induced pluripotent stem cell-derived cortical neurons to generate a high-resolution proteogenomic atlas of human neuron development. We identify 182,371 mRNA isoforms (over half previously unknown) and provide direct peptide evidence for the translation of hundreds of novel protein-coding sequences. Population genetics demonstrates that variants affecting novel exons and splice sites are under negative selection, underscoring the potential significance of these isoforms. During neuronal maturation, we observe that autism risk genes undergo dynamic isoform switching, including microexon inclusion and intron retention, that remodel key protein domains and regulatory regions. Furthermore, we uncover widespread, long-range coordination between alternative transcript processing events, including transcription start sites, exon splicing, and polyadenylation. Finally, our atlas enables variant reinterpretation in autism, highlighting the value of an isoform-centric view for interpreting pathogenic variation in neurodevelopment.

Humans↗

PubMed2006

Association of the organic cation transporter OCTN genes with Crohn's disease in the Spanish population.

The SLC22A4 and SLC22A5 genes within the IBD5 risk locus encode the organic cation transporters OCTN1 and OCTN2. Two variants, 1672C>T in SLC22A4 and -207G>C in SLC22A5, were shown to alter these genes' functions and were identified as genetic susceptibility factors for Crohn's disease (CD). We pursued to check both putative etiologic variants in an independent population through a case-control study with 309 Spanish CD patients and 408 ethnically matched healthy subjects. Both polymorphisms were found in partial linkage disequilibrium (D'=0.86). The separate analysis of each OCTN variant evidenced no association. However, when the simultaneous presence of mutant variants in both genes was analyzed, an effect on CD susceptibility was observed (P=0.026, odds ratio (OR) (95% confidence interval (CI))=1.59 (1.03-2.45)). The previously described predisposition conferred by the 5q31-risk haplotype increased in the absence of the etiologic 1672T and -207C alleles (P=0.0006, OR (95% CI)=10.14 (1.97-98.04)). Moreover, the risk contributed by these polymorphisms was higher in the IBD5 wild-type population (P=0.003, OR (95% CI)=2.65 (1.32-5.35)), arguing against the exclusive etiological role of the OCTN variants. The haplotype pattern inferred led to the consideration of these variants as susceptibility markers only in a defined genetic context. Our data support the interpretation of the 1672C>T SLC22A4 and -207G>C SLC22A5 polymorphisms as genetic markers of susceptibility/protection haplotypes.

Case-Control Studies↗

PubMed1999

Laboratory assessment as a critical component of the appropriate diagnosis and sub-classification of von Willebrand's disease.

von Willebrand's disease (VWD) is now recognized to be most common inherited bleeding disorder. It arises from defects or deficiencies in a protein called von Willebrand factor (VWF). VWD is a heterogeneous disorder, and patients are typed according to pathophysiology. The correct diagnosis and sub-classification of a patient's VWD is crucial because the presenting biological activity of VWF determines the haemorrhagic risk, and since subsequent clinical management will differ accordingly. Although clinical assessment of the propositus will provide the initial clue to, or an index of clinical suspicion for, a diagnosis of VWD, it is the laboratory process that will confirm or discount the diagnosis. A variety of assays may be employed by the laboratory undertaking the investigation, and these will not necessarily be restricted to an assessment of VWF. Due to the limitations of each potential laboratory assay, and because of VWD heterogeneity, no single test procedure is sufficiently 'robust' to permit detection of all VWD variants. This situation often leads to some clinical confusion in the process of laboratory interpretation regarding the likelihood of VWD, and the subtype of VWD. Classically, the test panel might include any combination of the following: (i) determination of (skin) bleeding times, (ii) VWF antigen (VWF:Ag) levels, (iii) 'functional' activity of Factor VIII (i.e. FVIII:coagulant or FVIII:C), (iv) 'functional' activity of VWF (e.g. Ristocetin Cofactor [VWF:RCof] assay), and/or Ristocetin induced platelet aggregation [RIPA] analysis), and (v) assessment of the VWF molecular weight or structural profile (i.e. VWF multimeric analysis or VWF:Multimers). There have also been a number of new diagnostic developments, and these are beginning to significantly influence the overall clinical VWD-diagnostic process. These include automation of existing assay procedures, a relatively new functional VWF assay called the Collagen Binding Assay (VWF:CBA), new automated platelet function analysers such as the PFA-100 and the Xylum Clot Signature Analyser, and specific VWF:FVIII binding assays. The current report focuses on the recommended laboratory process for investigation of VWD. An analysis of this process shows that selection of an appropriate test panel is a critical component for the proper diagnosis and classification. This review also outlines those new and emerging technologies that will help streamline the diagnostic process. Because VWD is just one manifestation of a 'bleeding' disorder (albeit the most common), the review also briefly mentions other related diagnostic processes and general approaches to the investigation of 'bleeding disorders'. The review also provides two algorithms to assist clinicians in making appropriate diagnostic choices in response to the clinical findings. A number of summary tables describing each laboratory assay in detail, and summarising the likely diagnostic findings for each Type of VWD, are also provided. This review should be of value to both haemostasis scientists and clinical specialists involved in VWD diagnosis.

Clinical Laboratory Techniques↗

PubMed2006

Role of Hirudin-like factor Va heavy chain sequences in prothrombinase function.

Proexosite I on prothrombin has been implicated in providing a recognition site for factor Va within prothrombinase. To examine whether hirudin-like sequences (659-698) on the cofactor contribute to this interaction, we expressed and purified two-chain FVa derivatives that were intracellularly truncated at the C terminus of the heavy chain: FVa709 (des710-1545), FVa699 (des700-1545), FVa(692 (des693-1545), FVa678 (des679-1545), and FVa658 (des659-1545). We found that FVa709, FVa699, FVa692, and FVa678 exhibited specific clotting activities that were comparable with plasma-derived and recombinant FVa. Additionally, kinetic studies using prothrombin revealed that the Km and kcat values for these derivatives were unaltered. Fluorescent measurements and chromatography studies indicated that FVa709, FVa699, FVa692, and FVa678 bound to FXa membranes and thrombin-agarose in a manner that was comparable with the wild-type cofactors. In contrast, FVa658 had an approximately 1% clotting activity and reduced affinity for FXa membranes (approximately 20-fold) and did not bind to thrombin-agarose. Surprisingly, however, FVa(658) exhibited essentially normal kinetic parameters for prothrombin when the variant was fully saturated with FXa membranes. Overall our results are consistent with the interpretation that any possible binding interactions between prothrombin and the C-terminal region of the FVa heavy chain do not contribute in a detectable way to the enhanced function of prothrombinase.

Amino Acid Sequence↗

PubMed1997

Laboratory assays for von Willebrand factor: relative contribution to the diagnosis of von Willebrand's disease.

Appropriate investigation of a patient with suspected von Willebrand's disease (VWD) involves a clinical assessment of the patient followed by laboratory testing. A variety of laboratory assays may be performed, not necessarily restricted to an assessment of von Willebrand factor (VWF). Due to the limitations of each assay, and because of VWD heterogeneity, no single test procedure is sufficiently robust to permit detection of all VWD variants. Indeed, these factors often lead to considerable confusion in the process of laboratory interpretation regarding the likelihood of VWD, and the subtype of VWD. This paper attempts to clarify some of the issues that lead to this confusion. It analyses the relative contribution of four separate assays for VWF [VWF:Multimer analysis, VWF:Antigen (VWF:Ag), VWF:Ristocetin Cofactor (VWF:RCof), and VWF:Collagen Binding Activity assay (VWF:CBA)] to the diagnosis and classification of VWD. Although each assay detects VWF, it is important to recognise that each assay provides different information on the VWF so detected. For example, while the VWF:Ag assay is a quantitative assay and provides a very good measure of the overall level of VWF present in a patient's plasma, it is not a functional assay and yields no information concerning the quality of the VWF present. Thus, the VWF:Ag on its own will not permit detection of many qualitative defects (consequently, use of this assay alone will lead to many Type 2 VWD patients being missed by the laboratory). In contrast, the VWF:CBA is a functional assay which provides very useful information on the quality of VWF present. Although the VWF:CBA is also a quantitative assay, it is less sensitive than the VWF:Ag assay in terms of its ability to measure the overall level of VWF (i.e.; the VWF:CBA detects only highly adhesive VWF, and therefore only a proportion of overall VWF). In essence, the VWF:Ag and VWF:CBA assays are complementary assays and should be used in combination. The VWF:Multimer assay is a qualitative procedure, but at best is only semi-quantitative. The VWF:Multimer assay essentially provides a snap-shot of the VWF present. Unfortunately considerable technical and interpretive problems limits its overall applicability and usefulness. The VWF:RCof assay is both a quantitative and qualitative assay that provides information about the presence of VWF that lies between that provided individually by the VWF:Ag and VWF:CBA assays. Unfortunately, the VWF:RCof suffers considerable technical problems, including considerable assay variability, that also limits its overall usefulness. Laboratories performing assays for VWF need to develop diagnostic strategies which include the use of appropriate multiple test combinations so as to ensure that VWD is properly detected.

Clinical Laboratory Techniques↗

PubMed2002

Random energy model for dynamics in supercooled liquids: N dependence.

The random energy model (REM) for the critical points (saddles and minima) of the potential energy landscape of liquids is further developed. While thermodynamic properties may be calculated from the unconditional distribution of states G(E), dynamics requires the distribution G(c)(E';E) of energies E' of neighbors connected to a state with energy E. Previously it was shown [T. Keyes, Phys. Rev. E 62, 7905 (2000)] that an uncorrelated REM, G(c)(E';E)=G(E'), is badly behaved in the thermodynamic limit N--> infinity. In the following, a simple expression is obtained for G(c)(E';E), which leads to reasonable N dependences. Results are obtained for the fraction f(u) of imaginary-frequency instantaneous normal modes, the configuration entropy S(c), the distributions of the different-order critical points, and the rate R of escape from a state. Simulation data on f(u)(T) and the density of minima rho(0)(E) in Lennard-Jones and CS2 are fit with the theory, allowing a determination of some model parameters. A universal scaling form for f(u), and a consequent scheme for calculating the mode-coupling temperature T(c) consistently among different materials, is demonstrated. The dependence of the self-diffusion constant D upon R and f(u) is discussed, with the conclusion that D proportional, variant f(u) in deeply supercooled states. The phenomenology of fragile supercooled liquids is interpreted. It is shown that the REM need not have a Kauzmann transition in the relevant temperature range, i.e., above the glass transition.

Journal Article↗

PubMed1990

[Viral myocarditis and classical virology. Clinico-virologic and experimental data].

A viral etiology of myocarditis has been proven stringently only in a few cases and mostly enteroviruses have been shown to be involved. In fact, a virological diagnosis of viral myocarditis is still rarely possible today. Virus isolation from heart-tissue is hard to achieve and biopsies, if at all, are often performed too late. Successful virus isolation from other materials (e.g. faeces, throat swab) or a serological diagnosis of acute virus infection cannot easily be correlated etiologically with cardial symptoms, depending of course also on the kind of virus infection diagnosed. To prove an acute infection serologically a fourfold rise in antibody titer or for some viruses specific IgM has to be detected. A group specific diagnosis of "acute enterovirus infection" is not reliably possible at the moment. The neutralization test is the only relatively type specific test in enterovirus serology. Intraserotypic virus variants cannot be detected by normal serology. Even when determining neutralizing IgM-antibodies, interpretation of results raises problems due to long persistence and possible cross reactivity. In case of suspected viral myocarditis clinicians should institute early and broad virological diagnostic measures. Virologists have to establish methods for virus or antigen determinations by molecular biological means. Furthermore, a fast and easy serological method for the diagnosis of an "acute enterovirus infection' would be very helpful. For research on the pathogenesis established animal models have to be used.

Animals↗

PubMed1993

Human T-lymphotropic virus type I (HTLV-I) provirus-related DNA sequences in peripheral blood mononuclear cells of a patient, in the absence of a definite serological positivity.

The true extent of human T-lymphotropic virus type I and II (HTLV-I/II) infection in European countries and its pathogenetic potential are still unknown. To find out more about HTLV-I/II incidence in our area we studied a group of 160 outpatients attending a sexually transmitted disease clinic over a six-month period. All patients were screened for the presence of specific antibody by means of enzyme-linked immunosorbent assay (ELISA) and immunoblotting (IB) analysis, using commercially available reagents. A surprisingly high percentage of patients showed an antibody reactivity to HTLV-I/II antigens by ELISA (9.3%) and IB (6.8%), although none of the samples satisfied the internationally accepted criteria of serological positivity. All subjects, irrespective of doubtful and inconclusive serological results, were further analyzed for the presence of proviral DNA in peripheral blood mononuclear cells by polymerase chain reaction using different pairs of primers and probes. A clear cut positive result for the presence of HTLV-I provirus-related DNA sequences was obtained in peripheral blood mononuclear cells of only one patient, a 26 years old female presenting genital condylomatosis, with no history of blood transfusion and/or intravenous drug abuse. Her serum showed a borderline result at ELISA and an IB reactivity only against p21. These data are open to various possible interpretations and, among others, may represent a hint for the presence of divergent antigenic variants of HTLV-I in the geographical area investigated.

Adolescent↗