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G Gradl

Publications and source records attributed to G Gradl.

31 records · Page 2Linked to original sources
PubMed1996

Subclavian carotid transposition: an analysis of a clinical series and a review of the literature.

OBJECTIVE: To analyse the clinical results and long-term patency rates of 108 patients with subclavian carotid transposition (SCT) and compare the outcomes to other clinical series using the same technique, as well as to those reported for other surgical procedures and PTA in the treatment of proximal subclavian artery disease. METHODS: The hospital records of 108 patients with carotid subclavian transposition were retrospectively reviewed for preoperative symptoms, Doppler examination, arteriography, blood pressure differentials and postoperative complications. Long-term patency and symptoms were determined during a follow-up examination including a history, physical examination, blood pressure differentials, Doppler examinations and arteriography in selected cases. RESULTS: The indication for SCT were subclavian steal (78%), upper extremity ischaemia (59%), rest pain or acral necrosis (5%), vertigo (6%). There was no mortality, blood pressure differentials were equalised in all patients without any early reocclusions. The complication rate was 15% with a permanent morbidity of 3%. Eighty-four patients (77%) could be re-examined during follow-up. For them the overall patency after a mean observation period of 70 months (1-144 months) was 100%. CONCLUSIONS: Subclavian carotid transposition is an excellent method for the treatment of proximal subclavian occlusive disease because of its exceptional long-term patency and low morbidity.

Anastomosis, Surgical↗
PubMed1995

Density-dependent regulation of cell growth by contactinhibin and the contactinhibin receptor.

BACKGROUND: The number of cells within mammalian tissues is maintained by growth-stimulating and growth-inhibiting mechanisms, with inhibitory signals being superimposed over growth stimuli. This is reflected, in the culture of normal adherent cells, by the phenomenon of density-dependent inhibition of growth: cells cease proliferation after becoming a confluent monolayer. We have shown previously that a plasma membrane glycoprotein, contactinhibin, is a major effector of negative growth regulation. Although transformed cells express contactinhibin in a functionally active form, they are not growth-inhibited, suggesting that the defects that lead to their aberrant growth are located 'downstream' of contactinhibin. RESULTS: Here, we provide evidence that a 92 kD plasma membrane protein, which we call CiR, binds specifically to contactinhibin and acts as a receptor mediating the contact-dependent inhibition of growth of cultured human fibroblasts. When polyclonal antibodies against CiR were introduced into cells using liposomes, confluent cells were released from density-dependent growth control. By contrast, cross-linking CiR that is localized to the plasma membrane, using anti-CiR antibodies, led to growth inhibition, suggesting that CiR is a signalling molecule and implicating CiR oligomerization in signal generation. This conclusion is supported by the finding that binding of contactinhibin by CiR is strongly dependent on the local concentration of both molecules and has a sharp threshold. When CiR was isolated by immuno-precipitation under conditions favouring phosphorylation, it was hyperphosphorylated on serine and threonine residues and had reduced contactinhibin-binding capacity; the binding capacity of CiR was restored after treatment with potato acid phosphatase. Fibroblasts transformed with simian virus 40 had reduced CiR expression, higher CiR phosphorylation levels, and a strongly reduced capacity of CiR to bind to contactinhibin. Phosphatase treatment of the CiR isolated from transformed cells only partially restored its contactinhibin-binding capacity. CONCLUSIONS: Homeostasis is the net result of a highly balanced network of growth-stimulating and growth-inhibitory signals. We have shown that density-dependent inhibition of growth in vitro is mediated by the interaction of contactinhibin with a 92 kD plasma membrane glycoprotein, CiR, the contactinhibin-binding capacity of which is regulated by phosphorylation.

Cell Count↗
PubMed1994

The Met/hepatocyte growth factor receptor (HGFR) gene is overexpressed in some cases of human leukemia and lymphoma.

The proto-oncogene c-met encodes a heterodimeric (alpha, beta) tyrosine kinase receptor which binds the hepatocyte growth factor (HGF). Recently, overexpression of the Met/HGF receptor gene has been detected in fresh samples of carcinomas and in epithelial tumor cell lines but not in cell lines derived from human leukemia and lymphoma. Our analysis of 50 primary samples of human leukemia and lymphoma and 23 hematopoietic cell lines revealed expression of mRNA and protein of the met/HGF receptor in 6 out of the 73 hematopoietic tumor samples analyzed. Four of the six samples positive for expression of the Met/HGF receptor gene were derived from patients with Hodgkin's disease. In addition, in one Burkitt's lymphoma cell line and in one acute myeloid leukemia (AML), expression of the Met/HGF receptor gene was detected. In normal unstimulated lymphocytes, granulocytes or monocytes we did not find expression of the Met/HGF receptor gene. Upon stimulation with the phorbol ester TPA we detected a weak expression of Met/HGF receptor specific transcripts of 9.0 kb in peripheral blood mononuclear cells of a healthy donor. Cytogenetic analyses of three of the four cell lines which express the Met/HGF receptor gene revealed structural or numerical abnormalities of the long arm of chromosome 7, where the Met/HGFR gene is located, in each of the three cell lines analyzed. In one of these cell lines (L540) the Met/HGFR gene is translocated to a marker chromosome. Southern blot and pulsed field gel electrophoresis experiments did not show any rearrangement in a region of 600 kb around the Met/HGF receptor gene excluding an activation of Met/HGFR by a TPR/Met oncogenic rearrangement as described for MNNG-HOS cells and for some gastric tumors. Our data indicate that the Met/HGFR gene is deregulated in a few cases of human leukemia, Burkitt's lymphoma and Hodgkin's disease possibly by chromosomal rearrangements resulting in an overexpression of the normal Met/HGF receptor mRNA and protein without formation of a hybrid gene.

Chromosome Aberrations↗
PubMed1990

Chromosomal in situ hybridization of a Hodgkin's disease-derived cell line (L540) using DNA probes for TCRA, TCRB, MET, and rRNA.

The Hodgkin's lymphoma-derived cell line L540, which exhibits multiple marker chromosomes and a genotype characteristic of T-cell origin, showed expression of MET oncogene. L540 was studied by in situ hybridization for chromosomal rearrangements concerning the regions where genes for TCRA and TCRB chains, for MET oncogene, and for rRNA are located. All four genes were demonstrated to be involved in the formation of marker chromosomes. Especially remarkable was the participation of rDNA-bearing regions in two different translocations.

Cell Line↗
PubMed1989

Translocation of c-abl oncogene and PDGFB (c-sis) gene in a case of CML with 46,XY, t(22;22).

In a case of CML with a variant Philadelphia translocation (Ph1 or Ph) t(22;22) (q11;q13) in bone marrow cells and unstimulated peripheral blood cells, no cytogenetically detectable involvement of chromosome 9 was observed. Southern blot experiments using probes specific for bcr and c-sis however revealed rearrangement of the bcr, but not of PDGFB (c-sis) gene. Northern blot analysis of bone marrow RNA showed a very weak signal with the c-sis probe, while in a lymph-node biopsy PDGFB m-RNA could not be detected. Chromosomal in situ hybridization gave evidence for translocation of c-abl from chromosome 9 to Ph and of PDGFB from chromosome 22 to chromosome 9, as the result of a threefold translocation t(9;22;22).

Bone Marrow↗
PubMed1989

Characterization of rearranged Y chromosomes in human testicular tumor cell lines.

Cytogenetic analysis of four cell lines established from two different human testicular tumors revealed rearranged or missing Y chromosomes. Southern blot analysis and in situ hybridization with different Y-derived human DNA sequences revealed the existence of Y chromosomal material even in a line without a cytogenetically visible Y chromosome and clarified the composition of Y marker chromosomes.

Base Sequence↗
PubMed1987

Assignment of the TCP1 locus to the long arm of human chromosome 6 by in situ hybridization.

TCP1, the human homolog of the Tcp-1 locus in the mouse, which is part of the murine t complex and codes for an abundant testicular germ-cell protein, has been mapped within the human genome by in situ hybridization. Using a cDNA probe for TCP1, pB1.4 hum, we assigned TCP1 to human chromosome region 6q23----qter, with the most likely localization being 6q25----q27.

Animals↗
PubMed1987

[Chromosome aberrations and malignant lymphomas].

Chromosomal findings in malignant lymphomas are correlated to the histopathology and the immunologic phenotype of lymphoma subgroups. The prognostic significance of a cytogenetic analysis and its value for therapy planning are discussed. With respect to tumorigenesis it is emphasized that a number of proto-oncogenes and genes for cell differentiation, such as immunoglobulin and T-cell receptor genes, have been localized at sites of recurring chromosomal rearrangements. One chapter deals with cytogenetic data in correlation to findings of DNA recombination studies in Hodgkin's disease.

Chromosome Aberrations↗
PubMedDate not supplied

[Experiences with calcitonin treatment of patients with type I complex regional pain syndrome (CRPS I--Sudeck disease)].

UNLABELLED: PURPOSE/METHODS/PATIENTS: Calcitonin is a common treatment in patients suffering from Complex Regional Pain Syndrome Type 1 (CRPS I), although its effects are being controversially discussed. In a prospective study of 24 patients with CRPS I of the upper limb, we examined the tolerance of daily doses of 0.5 mg human calcitonin administered subcutaneously over 8 weeks. To assess the benefit of this therapy, the patients were clinically examined every second week. The results were compared to a consecutive group of 25 CRPS 1 patients who received only analgetics and physiotherapy. RESULTS: With regard to all examined parameters (spontaneous pain, grip strength, edema, hand function, systematic temperature difference), the patients treated with calcitonin showed an improvement during the observation time. However, a statistically significant difference to the control group was calculated only for the reduction of the edema (P < 0.01). 83% (20/24 patients) of the calcitonin-treated patients suffered from severe, mostly gastroenterological side-effects. Hence therapy had to be discontinued in 3 cases (13%). CONCLUSION: The therapy with calcitonin has the burden of numerous unpleasant side-effects and causes only a slight therapeutic improvement. Thus, calcitonin must only be prescribed with reservations for patients suffering from CRPS I.

Aged↗
PubMedDate not supplied

Assessment of the peripheral microcirculation using computer-assisted venous congestion plethysmography in post-traumatic complex regional pain syndrome type I.

In complex regional pain syndrome type I (CRPS-I), edema of the affected limb is a common finding. Therefore, the changes in macro- and microcirculatory parameters were investigated to elucidate the underlying pathophysiology. Twenty-four patients with post-traumatic CRPS-I and 25 gender- and age-matched healthy subjects were examined by means of an advanced computer-assisted venous congestion strain-gauge plethysmograph. The recording of the volume response of the forearm to a stepwise inflation of an occlusion cuff placed at the upper arm enabled the calculation of the arterial blood flow into the arm (Q(a)), the vascular compliance (C), the peripheral venous pressure (P(v)), the isovolumetric venous pressure (P(vi); = hydrostatic pressure needed to achieve net fluid filtration) and the capillary filtration capacity (CFC)--an index of microvascular permeability. The study revealed no difference in any of the parameters between the right and left hand of healthy subjects. In CRPS-I patients, however Q(a), P(v), P(vi) and CFC were significantly (p < 0.01/0.001) elevated in the affected arm (Q(a) 11.2 +/- 7.0 ml x min(-1) x 100 ml(-1), P(v) 20.2 +/- 8.1 mm Hg, P(vi) 24.7 +/- 4.2 mm Hg, CFC 0.0058 +/- 0.0015 ml x min(-1) x 100 ml(-1) x mm Hg(-1)) compared to the unaffected arm (Q(a) 4.2 +/- 2.4 ml x min(-1) x 100 ml(-1), P(v) 10.0 +/- 5.1 mm Hg, P(vi) 13.2 +/- 3.7 mm Hg, CFC 0.0038 +/- 0.0005 ml x min(-1) x 100 ml(-1) x mm Hg(-1)) and the values obtained in healthy controls (Q(a) 5.1 +/- 1.3 ml x min(-1) x 100 ml(-1), P(v) 10.4 +/- 4.3 mm Hg, P(vi) 15.7 +/- 3.3 mm Hg, CFC 0.0048 +/- 0.0012 ml x min(-1) x 100 ml(-1) x mm Hg(-1)). Whereas the values in the unaffected arm of CRPS-I patients revealed no difference in Q(a), P(v) and P(vi) but a lower CFC (p < 0.01) compared to those from healthy controls. These results suggest profound changes in both macro- and microvascular perfusion in the affected arm of CRPS-I patients. The high CFC contributes to the edema formation, and combined with the elevated P(vi), they are in agreement with the hypothesis of an inflammatory origin of CRPS.

Adult↗