Bibliothek

X
feed icon rss

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
  • 1
    Digitale Medien
    Digitale Medien
    Allele-specific and asymmetric polymerase chain reaction amplification in combination: A one step polymerase chain reaction protocol for rapid diagnosis of familial defective apolipoprotein B-100
    Amsterdam : Elsevier
    Analytical Biochemistry 204 (1992), S. 22-25 
    Details
    ISSN: 0003-2697
    Quelle: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Thema: Biologie , Chemie und Pharmazie
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1016/0003-2697(92)90133-R
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Artikel (Nationallizenzen)
    Volltext
  • 2
    Digitale Medien
    Digitale Medien
    Basic biochemical data on blood from antarctic Weddell seals (Leptonychotes weddelli): Ions, lipids, enzymes, serum proteins and thyroid hormones
    Amsterdam : Elsevier
    Comparative Biochemistry and Physiology -- Part A: Physiology 102 (1992), S. 449-451 
    Details
    ISSN: 0300-9629
    Quelle: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Thema: Biologie , Chemie und Pharmazie
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1016/0300-9629(92)90192-S
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Artikel (Nationallizenzen)
    Volltext
  • 3
    Digitale Medien
    Digitale Medien
    Lipoatrophic diabetes (1993)
    Springer
    Journal of molecular medicine 71 (1993), S. 264-269 
    Details
    ISSN: 1432-1440
    Schlagwort(e): Acanthosis nigricans ; Generalized lipodystrophy ; Hepatic ketogenesis ; Insulin receptor ; Insulin binding ; Insulin resistance ; Lipoatrophic diabetes ; Seip's syndrome
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00184724
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Artikel (Nationallizenzen)
    Volltext
  • 4
    Digitale Medien
    Digitale Medien
    Relapsing polychondritis presenting as cutaneous polyarteritis nodosa (1993)
    Springer
    Journal of molecular medicine 71 (1993), S. 305-309 
    Details
    ISSN: 1432-1440
    Schlagwort(e): Cutaneous polyarteritis nodosa ; Relapsing polychondritis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Relapsing polychondritis is an infrequently diagnosed, though not neccessarily uncommon, systemic disorder characterized by recurrent and potentially destructive inflammation of cartilaginous structures, the eye, and the audiovestibular and cardiovascular systems. Although dermal involvement occurs in approximately 25% of patients with relapsing polychondritis, in only few cases has a skin biopsy been obtained revealing lesions such as leukocytoclastic vasculitis, livedo reticularis, erythema nodosum or keratodermia blenorrhagicum. We describe a patient with relapsing polychondritis in whom a cutaneous polyarteritis nodosa preceded cartilage inflammation by 6 months. Cutaneous polyarteritis nodosa is a rare form of vasculitis that appears to be limited primarily to the skin, muscles, and joints. In contrast to the systemic form of the disease it is characterized by the absence of visceral lesions and a relapsing but benign course. The present case and the fact that vasculitis is a concomitant feature in approximately 30% of patients with relapsing polychondritis [21] demonstrates that this condition may not represent a distinct clinical entity.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00184732
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Artikel (Nationallizenzen)
    Volltext
  • 5
    Digitale Medien
    Digitale Medien
    Familial defective apolipoprotein B-100: a common cause of primary hypercholesterolemia (1992)
    Springer
    Journal of molecular medicine 70 (1992), S. 77-84 
    Details
    ISSN: 1432-1440
    Schlagwort(e): Apolipoprotein B-100 ; LDL ; atherosclerosis ; Hypercholesterolemia ; Haplotypes ; Mutation ; Review
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Familial defective apolipoprotein B-100 (FDB) is a recently identified dominantly inherited genetic disorder characterized by a decreased binding of low density lipoprotein (LDL) to the LDL receptor due to defective apo B-100. FD B is caused by a G to A mutation at nucleotide 10 708 in exon 26 of the apo B gene creating a substitution of glutamine for arginine in the codon for amino acid 3500. The arginine(3500) → glutamine mutation has been observed in several populations in North America and Europe with a similar frequency of approximately 1/500 to 1/700. Haplotype analysis has demonstrated that the arginine(3500) → glutamine mutation occurs on the same chromosomal background. The fact that all individuals with FDB are of Caucasian extraction implies that the mutation has its origin in this population. The arginine(3500) → glutamine mutation has a profound impact of varying strength on the plasma LDL cholesterol level, leading to heterogeneous clinical expression comparable to “classic” familial hypercholesterolemia (FH) caused by a defective LDL receptor: tendon xanthoma, premature atherosclerosis and arcus lipoides. The present data suggest that the combination of these clinical features is no longer appropriate for the diagnosis of LDL-receptor-defective FH, but may be a common feature of a defective LDL receptor pathway originating either from defective LDL receptors or from malfunctioning ligand apo B-100.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00422946
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Artikel (Nationallizenzen)
    Volltext
  • 6
    Digitale Medien
    Digitale Medien
    Similar frequency of autoantibodies against pneumocytes type II and Clara cells in patients with interstitial lung diseases and healthy persons (1991)
    Springer
    Journal of molecular medicine 69 (1991), S. 297-302 
    Details
    ISSN: 1432-1440
    Schlagwort(e): Autoantibodies ; Pneumocytes type II ; Clara cells ; Pulmonary surfactant ; Pulmonary fibrosis ; Sarcoidosis ; Rheumatoid arthritis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Several experimental findings suggest an association between interstitial lung diseases and autoantibodies. Antibodies against lung tissue including pneumocytes type II in patients suffering from idiopathic pulmonary fibrosis (IPF) were reported in recent years. In this investigation the serum of 103 persons (10 with IPF, 23 with M. Boeck, 18 with rheumatoid arthritis (RA) and 52 healthy controls) was examined for autoantibodies against pneumocytes type II and Clara cells by indirect immunofluorescence on human lung tissue. These antibodies against both cell types are an additional proof for common antigens in pneumocytes type II and Clara cells. The autoantibodies were present in similar frequency in the 4 groups (IPF: 20%, M. Boeck: 26.1%, RA: 22.2% and 23.1% of the healthy controls). So no significant association was found between the antibodies and the interstitial lung diseases. A role of the antibodies in the pathogenesis of the diseases, however, can not be excluded by this study. A possible role as parameter of development of interstitial lung diseases should be subject to further investigations in form of a prospective follow up study.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01644760
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Artikel (Nationallizenzen)
    Volltext
  • 7
    Digitale Medien
    Digitale Medien
    Identification of a heterozygous compound individual with familial hypercholesterolemia and familial defective apolipoprotein B-100 (1991)
    Springer
    Journal of molecular medicine 69 (1991), S. 320-324 
    Details
    ISSN: 1432-1440
    Schlagwort(e): Familial hypercholesterolemia ; Familial defective apolipoprotein B-100 ; LDL ; LDL receptor ; Atherosclerosis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Familial defective apolipoprotein B-100 (FDB) is a recently identified dominantly inherited genetic disorder, which leads to increased serum levels of low density lipoprotein (LDL) cholesterol with reduced affinity for the LDL receptor. This genetic disorder is characterized by defective binding of the apolipoprotein B-100 (apo B-100), which is virtually the sole protein constituent of LDL, to the LDL receptor. The defective binding results from a G to A mutation at amino acid 10708 in exon 26 of the apolipoprotein B (apo B) gene creating a substitution of glutamine for arginine in the codon for amino acid 3500. It is postulated that FDB can exhibit the same clinical features as familial hypercholesterolemia (FH) caused by a defective LDL receptor. The purpose of this paper is to report on an individual with a defective LDL and a defective LDL receptor. The clinical features of this individual were the same as in the family members with either defective LDL or a defective LDL receptor: premature arcus lipoides, tendon xanthomata, and premature atherosclerosis. Although the clinical features were present to the same degree as in individuals with either defect the prognosis and treatment of such an individual could be different.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01644767
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Artikel (Nationallizenzen)
    Volltext
  • 8
    Digitale Medien
    Digitale Medien
    First international workshop on familial defective apo B-100 (1992)
    Springer
    Journal of molecular medicine 70 (1992), S. 961-964 
    Details
    ISSN: 1432-1440
    Schlagwort(e): Apolipoprotein B-100 ; Familial defective apo B-100 ; Hypercholesterolemia
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00180448
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Artikel (Nationallizenzen)
    Volltext
  • 9
    Digitale Medien
    Digitale Medien
    Sweet-Syndrom bei chronisch myeloischer Leukämie (1989)
    Springer
    Journal of molecular medicine 67 (1989), S. 506-510 
    Details
    ISSN: 1432-1440
    Schlagwort(e): Chronic myeloid leukemia ; Sweet's syndrome ; Skin changes
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary A 31-year-old woman with chronic myeloid leukemia developed bullous skin changes not responding to antibiotic therapy. A biopsy showed a sterile predominantly neutrophilic infiltrate consistent with Sweet's syndrome. These skin changes responded well to methylprednisolon. Seven month later the patient died in a blast crisis.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01721678
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Artikel (Nationallizenzen)
    Volltext
  • 10
    Digitale Medien
    Digitale Medien
    Book review (1992)
    Springer
    Journal of molecular medicine 70 (1992), S. 21-21 
    Details
    ISSN: 1432-1440
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00422932
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Artikel (Nationallizenzen)
    Volltext
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...