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Biomedical subjects

B Zelle

Publications and source records attributed to B Zelle.

At least 19 recordsLinked to original sources
PubMed2006

Evaluation and outcome of patients after polytrauma--can patients be recruited for long-term follow-up?

INTRODUCTION: There is limited information available about the long-term follow-up of polytrauma patients. In this study, the social and medical sequelae of trauma were reinvestigated at 10 years after the injury. METHODS: Patients were selected out of a population of polytraumatised patients treated at Hannover Medical School between 1973 and 1990. INCLUSION CRITERIA: multiple injuries treated at one institution, age between 3 and 60 years of age at the time of injury. Patients were recruited by gathering their residences from the charts. If patients had moved, up to three different registration offices were contacted by mail. The patient was contacted by mail (maximum three times) and by telephone. A patient was documented as lost to follow-up if none of these attempts was successful, or if he did not fulfil three subsequent appointments. All patients were examined by a physician, using a patient questionnaire and a standardized physical exam. RESULTS: Six hundred thirty-seven patients (67.8% of the potential enrollees) were evaluated on an outpatient basis by a trauma surgeon using a self-administered patient questionnaire and a standardized physical exam. In these, the average follow-up was 17.5 (range 10-28) years; the average Injury Severity Score (ISS) was 20.7 (range 4-54). Head injuries were the third most frequent injuries, but represented the most frequent cause of permanent disability (40%). The overall rehabilitation status graded by the patients was very good in 14.1%, good in 33.0%, satisfactory in 29.3%, sufficient in 16.0% and poor or insufficient in 7.5%. CONCLUSIONS: This study suggests that a high percentage of patients can be recruited for follow-up even after 10 years post trauma with the use of a meticulous reinvitation strategy. Head injuries accounted for the most frequent cause of disability, suggesting that more research should be provided to minimise the degree of injury and improve the outcome for head injured patients. Subjective grading of the outcome was better than expected in patients who had regained complete social rehabilitation.

Adolescent↗
PubMed2004

[Osteotomy of the iliac fossa in the treatment of a hip dislocation associated with a two-column acetabular fracture. Modification of the ilioinguinal approach to avoid an extended surgical approach].

Open reduction and internal fixation is the treatment of choice for displaced acetabular fractures. The surgical approach depends on the fracture type, concomitant injuries, and general condition of the patient. The ilioinguinal approach provides a good exposure to the medial wall and is associated with an acceptable degree of surgical trauma. Exposure of the joint surface, however, is difficult when using the ilioinguinal approach. We report a case of a polytraumatized 39-year-old patient who sustained a posterior hip displacement and a two-column acetabular fracture. An osteotomy of the iliac ala was performed via an ilioinguinal approach to fragments of the acetabular surface that were displaced distally. Thereby, reposition of a craniolateral fragment was achieved without the need to extend the surgical approach or to perform a second incision.

Acetabulum↗
PubMed2003

[Validation of the Hannover Score for Polytrauma Outcome (HASPOC) in a sample of 170 polytrauma patients and a comparison with the 12-Item Short-Form Health Survey].

Improved survival rates of patients with multiple injuries have increased general interest in the quality of rehabilitation status after polytrauma. Due to the complex nature of multiple injuries, a special score is needed to evaluate the outcome after polytrauma. The aim of this study was to validate the Hannover Score for Polytrauma Outcome (HASPOC). One hundred seventy patients who had sustained multiple injuries were re-examined using the HASPOC 2 years after trauma. Results were correlated with the 12-Item Short Form Health Survey (SF-12), a validated and established scoring system. The HASPOC was also correlated with clinical parameters predictive of poor outcome. Two control groups consisting of either patients after single injuries or healthy controls were also evaluated using the HASPOC. In the group of patients after multiple injuries, the HASPOC correlated with the SF-12 in injury severity and polytrauma scores, intubation period, hospital stay, and occurrence of injuries below the knee. Differences between healthy controls,patients after single injuries, and patients after multiple injuries were statistically significant when evaluated with the HASPOC. This statistical significance was not achieved using the SF-12. The HASPOC is a valid scoring system and useful for evaluating the rehabilitation status after polytrauma.

Adolescent↗
PubMed1999

Health care policy reform: a microanalytic model for comparing hospitals in the United States and Germany.

Microcomparison, or single-component analysis, of health care systems offers a potentially better basis for reform than traditional macrocomparison analysis of aggregate elements. Using macroanalysis, available evidence shows that Germany provides cheaper but more effective hospital care than the United States. To find the causes for this outcome, we developed a microanalytic model of hospital administrators' perceptions, financial ratios, medical outcomes, and pharmaceutical costs. However, only data on pharmaceutical costs were available, and these were similar in both countries. Our significant outcome was development of a microcomparative model that gives world medical care providers new criteria for analyzing and improving cost to care ratios.

Delivery of Health Care↗
PubMed1989

Family and population studies on the human pepsinogen A multigene family.

Human pepsinogen A (PGA) displays highly polymorphic isozymogen patterns after polyacrylamide gel electrophoresis and activity staining. The patterns differ with respect to the presence and the relative intensity of the individual fractions. Family studies strongly suggest that these isozymogen patterns are encoded by allelic haplotypes, encompassing different numbers and types of PGA genes. In this paper, we confirm the essential features of this multigene model. We establish the relationship between the haplotypes and the corresponding isozymogen patterns by determination of the PGA polymorphism at both the DNA and the protein level in 117 Dutch individuals, 60 of whom were unrelated. The combination of HindIII and EcoRI restriction fragment length polymorphisms (RFLPs) has enabled us to define different haplotypes, which are shown to segregate within families. Most genes are characterized by their specific EcoRI fragments. The HindIII RFLP is in strong linkage disequilibrium with PGA genes showing strong expression of the relevant isozymogen. Although a general picture of the relationship between genotypes and phenotypes is emerging, there are exceptions, suggesting that rare haplotypes evolve by unique crossover events.

DNA↗
PubMed1989

Nucleotide sequence comparison of five human pepsinogen A (PGA) genes: evolution of the PGA multigene family.

To unravel the genetic basis for the pepsinogen A (PGA) protein polymorphism, we have isolated and characterized a number of PGA genes, distinguishable by polymorphic EcoRI fragments of 12.0, 15.0, and 16.6 kb. Using a HindIII or AvaII polymorphism, we can discriminate between different 15.0 (15.0 and 15.0*) and 12.0 (12.0s and 12.0l) genes, respectively. The coding sequences of a 15.0 and a 16.6 gene were determined, together with considerable stretches of the 5'- and 3'-flanking regions and introns. The genes were demonstrated to encode Pg5 and Pg4, respectively. Because substitutions in codons 43 and 207 appeared to be critical in the determination of the encoded proteins, we sequenced only these regions in the two 12.0 genes and the 15.0* gene. On the basis of these partial sequences, we assume that these genes encode Pg3. In the evolutionary model of the PGA gene cluster presented here, the 12.0 genes arose by an unequal, but homologous crossover. The results of sequence analysis of the second intron of the 12.0s, 12.0l, 15.0, and 16.6 genes suggest that the two 12.0 genes have arisen from two different crossover events.

Amino Acid Sequence↗
PubMed1988

Cloning and sequencing of rhesus monkey pepsinogen A cDNA.

The complete nucleotide sequence of Rhesus monkey (Macaca mulatta) pepsinogen A (PGA) cDNA was determined from two partially overlapping cDNA clones, covering the whole coding sequence and part of the flanking sequences. The nucleotide and deduced amino acid sequences were compared to known PGA sequences from other species. The degree of similarity with human PGA appeared to be 96% at the nucleotide sequence level and 94% at the amino acid sequence level. In the coding region the divergence was highest in the activation peptide. The amino acid sequence similarity between Japanese monkey (Macaca fuscata) PGA and Rhesus monkey PGA was shown to be 99%. Using the cDNA as probe in Southern hybridization of EcoRI-digested human and Rhesus monkey genomic DNAs, PGA patterns with inter-individual differences were observed. The hybridization patterns are compatible with the existence of a PGA multigene family in both species.

Amino Acid Sequence↗
PubMed1988

Genomic structure and evolution of the human pepsinogen A multigene family.

A human cosmid library was screened with a pepsinogen A (PGA) cDNA probe, yielding 18 clones with (parts of) one, two or three PGA genes. By aligning these cosmids a restriction map of a PGA gene quadruplet was obtained in which the four genes are arranged in a highly ordered fashion in a head-to-tail orientation. Using the length in kilobases of the large polymorphic EcoRI fragment of the PGA genes, this quadruplet can be described as 15.0-12.0-12.0-16.6. An AvaII polymorphism allowed us to identify the two PGA haplotypes of the individual whose DNA had been cloned in the cosmid library to be a gene triplet and a gene quadruplet. By comparing the restriction maps of the central 12.0 genes in these multiplets to those of the flanking 15.0 and 16.6 genes, we postulate that these central genes arose from unequal but homologous crossing over between two 15.0-16.6 gene pairs. This hypothesis provides for the creation of a variety of haplotypes by additional cross overs and mutations. Southern blots of family and population material supports the existance of at least five common PGA haplotypes, including a single-gene haplotype, giving rise to a large number of different EcoRI patterns. The single PGA gene is probably the reciprocal crossing over product. Comparison between the DNA and protein polymorphisms suggests further micro-heterogeneity in the different PGA haplotypes.

Biological Evolution↗
PubMed1987

Molecular cloning of a pair of human pepsinogen A genes which differ by a Glu----Lys mutation in the activation peptide.

Three human cosmid clones containing pepsinogen A (PGA) encoding sequences were isolated from a genomic bank derived from a single individual. One cosmid contains two PGA genes in tandem in a head-to-tail orientation, while the other two cosmids each contain a single PGA gene. The three cosmids were characterized by restriction mapping and sequence analysis (exons 1 and 2 and flanking regions). As judged from these data, three of the four PGA genes isolated appear to be nearly identical, but one of the tandem genes is clearly different from the other genes. The first exon of all four genes codes for the same amino acid sequence. However, in the second exon of one of the tandem genes we found a nucleotide substitution giving rise to a Glu----Lys substitution of the 43rd amino acid residue of the activation peptide, leading to a charge difference of the corresponding isozymogens. The presence of two distinct PGA genes in the isolated gene pair conclusively proves the multigene structure of the PGA system. These genes might be responsible for at least part of the electrophoretic polymorphism at the protein level.

Amino Acid Sequence↗
PubMed1985

Assignment of human pepsinogen A locus to the q12-pter region of chromosome 11.

A 0.9kb cDNA fragment, corresponding to a large part of Rhesus monkey pepsinogen A mRNA, was used as probe for the chromosomal localization of the human pepsinogen A gene(s) using human-rodent somatic cell hybrids. Southern blot analysis of 14 human-Chinese hamster and three human-mouse cell hybrids, strongly indicates that the human PGA locus is on chromosome 11. The human-mouse hybrids, containing a translocation involving chromosome 11, allow sublocalization to the region q12-pter.

Animals↗
PubMed1985

Transformation of human 143 tk- cells with plasmids containing the gene encoding the adenovirus DNA-binding protein.

Human cell lines that contain and express the gene encoding the adenovirus type 5 DNA-binding protein (Ad5 DBP) are very useful for the isolation of adenovirus mutants with an altered DBP. In order to obtain these cells, human 143 tk- cells were transfected, using the calcium phosphate technique, with plasmids containing the Ad5 DBP gene and the herpes simplex virus thymidine kinase (HSV tk) gene as a selectable marker. Characterization of several tk+ transformants revealed that these cells did contain the HSV tk gene, but in none of these cells could Ad5 DBP DNA sequences be detected. However, when 143 tk- cells were co-transfected with a plasmid containing the Ad5 DBP gene and another plasmid carrying early region E1, integration of the Ad5 DBP gene in chromosomal DNA could be detected. Integration of Ad5 DNA sequences was also observed when transfection was performed with plasmids containing the Ad5 DBP gene and the long terminal repeat of Moloney murine leukaemia virus. By employing a radioimmunoassay it could be shown that DBP-related proteins were synthesized in two of the cell lines containing the Ad5 DBP gene. Since both cell lines support the growth of the temperature-sensitive viral DBP mutant, H5ts125, at the non-permissive temperature, the DBP-related proteins expressed in these cells must be functional.

Adenoviruses, Human↗
PubMed1983

Differences in the regulation by poly(ADP-ribose) of repair of DNA damage from alkylating agents and ultraviolet light according to cell type.

Inhibition of poly(ADP-ribose) synthesis by 3-aminobenzamide in various human and hamster cells influenced the responses to DNA damage from methyl methanesulfonate, but not from ultraviolet light. After exposure to methyl methanesulfonate, 3-aminobenzamide increased the strand break frequency in all cell types studied, but only stimulated repair replication in lymphoid and HeLa cells, suggesting these are independent effects. 3-Aminobenzamide also inhibited the pathway for de novo synthesis of DNA purines, suggesting that some of its effects may be due to disturbance of precursor pathways and irrelevant to the role of poly(ADP-ribose) in repair. Previous claims that 3-aminobenzamide stimulates repair synthesis after exposure to UV light are probably artifacts, because the stimulations are only observed in lymphocytes in the presence of a high concentration of hydroxyurea that itself inhibits repair. The initial inhibition of semiconservative DNA synthesis and the excision of the major alkylation products and pyrimidine dimers were unaffected by 3-aminobenzamide. In general poly(ADP-ribose) synthesis appears to be uniquely involved in regulating the ligation stage of repair of alkylation damage but not ultraviolet damage. By regulating the ligation efficiency, poly(ADP-ribosylation) modulates the dynamic balance between incision and ligation, so as to minimize the frequency of DNA breaks. The ligation stage of repair of UV damage appears different and is not regulated by poly(ADP-ribosylation).

Animals↗
PubMed1981

Xeroderma pigmentosum patients from Egypt: II. Preliminary correlations of epidemiology, clinical symptoms and molecular biology.

Xeroderma pigmentosum (XP) occurs with high frequency in Egypt and a continuation of our field studies has identified representatives of the 3 major complementation groups A, C, and variant. Group A patients, with one exception, showed very early onset of sun sensitivity and development of skin cancers, and microcephaly and mental retardation. The exceptional group A patient was 35 yr old, with normal stature and intelligence who had 2 normal children. DNA repair was as low in his cells as in other group A cases. Group C patients showed a slightly slower onset of sun sensitivity and had no central nervous system disorders. The variants showed later onset of sun sensitivity and no skin cancers evident at the time of observation (about 20 yr of age). No sun sensitivity was present in the 25 heterozygotes we observed, nor reportedly in the additional 60 not yet observed. This indicates that only homozygosity for XP genes increases risk of skin cancer. Cell cultures from both normal persons and these XP patients reached in vitro "senescence" at similar passage levels. Groups A and C appear to have lost different major gene products that are involved in the excision of UV damage from DNA, but the residual repair in XP-C cells facilitates more recovery of DNA synthesis than in other groups. This may contribute to the higher in vitro survival in culture and milder clinical symptoms in group C as compared to group A. XP variants appear to have lost a gene product that permits normal cells to replicate, uninterrupted by DNA damage, and consequently synthesize DNA in smaller pieces than normal.

Adult↗
PubMed1980

Repair of DNA damage after exposure to 4-nitroquinoline-1-oxide in heterokaryons derived from xeroderma pigmentosum cells.

Xeroderma pigmentosum (XP) cells are deficient in the repair of damage induced by ultraviolet irradiation. Excision-repair-deficient XP cell strains have been classified into 7 distinct complementation groups, according to results of studies on cell fusion and UV irradiation. XP cells are not only abnormally sensitive to UV, but also to a variety of chemical carcinogens, including 4-nitro-quinoline-1-oxide (4NQO). Complementation analysis with XP strains from 4 different complementation groups with respect to the repair of 4NQO-induced DNA damage revealed that the classification of the strains into complementation groups with respect to 4NQO-induced repair coincides with the classification based on the repair of UV damage.

4-Nitroquinoline-1-oxide↗
PubMed1980

Repair of damage by ultraviolet radiation in xeroderma pigmentosum cell strains of complementation groups E and F.

The xeroderma pigmentosum fibroblast strains XP2RO, complementation group E, and XP23OS, group F, were compared with normal human primary fibroblasts with regard to repair of damage induced by 254-nm UV. In XP2RO cells, repair DNA synthesis, measured by autoradiography (unscheduled DNA synthesis = UDS), was about 50% of the value found in normal human cells. In these cells also the removal of UV-induced sites recognized by a specific UV-endonuclease proceeds at a reduced rate. By having BUdR incorporated into the repaired regions, followed by the induction of breaks in these patches by 313-nm UV, it was shown that the reduced repair synthesis is not caused by a shorter length of the repair regions in XP2RO, but is solely due to a reduction in the number of sites removed by excision repair. In XP23OS a discrepancy was observed between the level of UDS, which was about 10% of the normal value, and other repair-dependent properties such as UV survival, host-cell reactivation and removal of UV-endonuclease-susceptible sites, which were less reduced than could be expected from the UDS level. However, when UDS was followed over a longer period than the 2 or 3 h normally used in UDS analysis, it appeared that in XP23OS cells, the rate of UDS remained constant whereas the rate decreased in normal control cells. Consequently, the residual level of UDS varies with the period over which it is studied.

Bromodeoxyuridine↗
PubMed1979

Repair of UV-endonuclease-susceptible sites in the 7 complementation groups of xeroderma pigmentosum A through G.

7 strains of human primary fibroblasts were chosen from the complementation groups A through G of xeroderma pigmentosum; these strains are UV-sensitive and deficient in excision repair of UV damage on the criterion of unscheduled DNA synthesis (UDS). They were compared with normal human fibroblasts and one xeroderma pigmentosum variant with regard to their capacity to remove pyrimidine dimers, induced in their DNA by UV at 253.7 nm. The XP variant showed a normal level of dimer removal, whereas 6 of the other XP strains had a greatly reduced capacity to remove this DNA damage, in agreement with their individual levels of UDS. Strain XP230S (complementation group F), however, only showed a 20% reduction in the removal of dimers, which is much less than expected from the low level of UDS in this strain.

Cell Line↗