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Biomedical subjects

H Walter

Publications and source records attributed to H Walter.

At least 73 records · Page 4Linked to original sources
PubMed1998

Genital pathology: its impact on the interpretation of signs of genital trauma (SEAL development training).

A seminar was held in October 1997 at Wood Street Police Station by courtesy of the City of London Police to explore the diagnostic difficulties posed by pathological conditions affecting the vulva and penis, which may cause problems when assessing the nature and degree of genital injury in allegations of sexual assault. While a lot of the presentations were visual, in the form of slides of the discussed conditions, a synopsis of each speaker's contribution is given below.

Journal Article↗
PubMed1998

Lack of involvement of basic fibroblast growth factor (FGF-2) in capillary growth in skeletal muscles exposed to long-term contractile activity.

Fibroblast growth factors (FGFs) are involved in stimulation of angiogenesis in tumors and other pathological circumstances. Increased activity of normal skeletal muscles resulting from chronic electrical stimulation is a very potent stimulus for capillary growth but a relationship between the initiation of this angiogenesis and the involvement of autocrine growth factors has yet to be established. Although FGF expression has been reported in muscles stimulated for 3 weeks, capillary growth is underway significantly earlier, beginning around 3 days. The present experiments have therefore studied the possible involvement of basic fibroblast growth factor (FGF-2) in stimulated rat fast skeletal muscles prior to, and coincident with, capillary growth. Muscle contractions were induced via electrodes implanted in the vicinity of the peroneal nerve and maintained for 8h/day for 2, 4 or 7 days. Capillary/fiber ratio (C/F), based on staining of capillary endothelium for alkaline phosphatase, was not changed in either extensor digitorum longus (EDL) or tibialis anterior (TA) after 2 days stimulation, but increased in TA stimulated for 4 days and in both muscles after 7 days. The expression of mRNA for FGF-2, detected by ribonuclease protection assay, was decreased in all stimulated muscles compared with control or contralateral muscles; immunohistochemistry showed FGF-2 gene product in nerves and larger blood vessels but not in capillaries. There was no evidence from immunohistochemistry for up-regulation of receptors flg and bek for FGF-2. The presence of FGF-2, flg and bek in arterioles may indicate a possible role for FGF-2 in the regulation of blood flow since we have previously shown it to be a dilator of small arterioles. However, based on the lack of correlation between changes in capillary density and the expression of mRNA and protein for FGF-2 and its receptors, it is unlikely that it is directly linked with the initiation of angiogenesis resulting from chronic activity in skeletal muscles.

Journal Article↗
PubMed1998

Coronary artery stent placement with postprocedural antiplatelet therapy in acute myocardial infarction.

BACKGROUND: We have shown that coronary artery stent implantation in acute myocardial infarction (AMI) is feasible and safe when combined with effective postprocedural antiplatelet therapy. However, the concept of coronary stenting in AMI has not been validated in large cohorts. In this observational study, we investigated the outcome in 318 consecutive patients. METHODS AND RESULTS: From January 1995 until December 1996, 420 of 455 (92.3%) patients admitted to our institutions with AMI underwent infarct artery stent placement. This report describes the 318 patients treated with combined antiplatelet therapy whose AMI was not complicated by cardiogenic shock or mechanical ventilation before the intervention. Postinterventional therapy consisted of 100 mg aspirin and 250 mg ticlopidine twice daily. There were 21 (6.6%) cardiac events during 30-day follow-up: five cardiac deaths (1.6%), four nonfatal re-infarctions (1.3%) and 13 target vessel revascularizations (4.1%). Six months of clinical follow-up yielded a 94.7% survival rate free of repeat AMI. The rate of repeat interventions was 11%. Quantitative computerized angiography at 6 months, performed in 79.4% of the eligible patients, revealed a binary restenosis rate of 25%. CONCLUSIONS: With postprocedural antiplatelet therapy, coronary stenting in AMI yields favorable short- and long-term outcomes.

Angioplasty, Balloon, Coronary↗
PubMed1998

Capillary growth in relation to blood flow and performance in overloaded rat skeletal muscle.

Rat extensor digitorum longus muscles were overloaded by stretch after removal of the synergist tibialis anterior muscle to determine the relationship between capillary growth, muscle blood flow, and presence of growth factors. After 2 wk, sarcomere length increased from 2.4 to 2.9 micrometers. Capillary-to-fiber ratio, estimated from alkaline phosphatase-stained frozen sections, was increased by 33% (P < 0.0001) and 60% (P < 0.01), compared with control muscles (1.44 +/- 0.06) after 2 and 8 wk, respectively. At 2 wk, the increased capillary-to-fiber ratio was not associated with any changes in mRNA for basic fibroblast growth factor (FGF-2) or its protein distribution. FGF-2 immunoreactivity was present in nerves and large blood vessels but was negative in capillaries, whereas the activity of low-molecular endothelial-cell-stimulating angiogenic factor (ESAF) was 50% higher in stretched muscles. Muscle blood flows measured by radiolabeled microspheres during contractions were not significantly different after 2 or 8 wk (132 +/- 37 and 177 +/- 22 ml. min-1. 100 g-1, respectively) from weight-matched controls (156 +/- 12 and 150 +/- 10 ml. min-1. 100 g-1, respectively). Resistance to fatigue during 5-min isometric contractions (final/peak tension x 100) was similar in 2-wk overloaded and contralateral muscles (85 vs. 80%) and enhanced after 8 wk to 92%, compared with 77% in contralateral muscles and 67% in controls. We conclude that increased blood flow cannot be responsible for initiating expansion of the capillary bed, nor does it explain the reduced fatigue within overloaded muscles. However, stretch can present a mechanical stimulus to capillary growth, acting either directly on the capillary abluminal surface or by upregulating ESAF, but not FGF-2, in the extracellular matrix.

Animals↗
PubMed1998

Domiciliary liquid oxygen versus concentrator treatment in chronic hypoxaemia: a cost-utility analysis.

Whether long-term oxygen therapy (LTOT) improves quality of life in chronic hypoxaemia has been questioned. LTOT with an oxygen concentrator (C/C) and gas cylinders for ambulation is considered cumbersome compared to mobile liquid oxygen equipment (L). The hypothesis for this study was that LTOT with liquid oxygen treatment (L) improves patients' health-related quality of life, but that it is also more expensive compared to concentrator (C/C) treatment. A prospective, randomized multicentre trial comparing C/C with L for LTOT was conducted during a six-month period. Fifty-one patients (29 on L and 22 on C/C) with chronic hypoxaemia, regularly active outside the home, participated in the study initially. Costs for oxygen were obtained from the pharmacies. Patient diaries and telephone contacts with members of the healthcare sector were used to estimate costs. Health-related quality of life was measured by the Sickness Impact Profile (SIP) and the EuroQol, instruments at the start and after 6 months. The average total cost per patient for group C/C for the six-month period was US$1,310, and for group L it was US$4,950. Health-related quality of life measured by the SIP instrument showed significant differences in favour of group L in the categories/dimensions of physical function, body care, ambulation, social interaction and total SIP score. In conclusion, liquid-oxygen treatment was more expensive compared to concentrator treatment. However, treatment effects showed that liquid oxygen had a better impact on quality of life.

Chronic Disease↗
PubMed1998

Gene alterations at the CDKN2A (p16/MTS1) locus in soft tissue tumors.

The CDKN2A gene (p16/MTS1) is a tumor suppressor that is frequently deleted, mutated, or inactivated by transcriptional silencing in certain tumor types and many tumor cell lines. We analyzed CDKN2A gene mutations and the frequency of loss of heterozygosity (LOH) at the CDKN2A locus in 135 soft tissue sarcomas. PCR-SSCP analysis of exons 1 and 2 of CDKN2A gene revealed only one missense mutation in codon 15 in a rhabdomyosarcoma. LOH-analysis was performed with two polymorphic markers in the surrounding regions of the CDKN2A gene (D9S171, D9S162) and the sequence-tagged-site marker c5.1. An allelic loss was found in 7/135 cases (5.1%) and was a characteristic of poorly differentiated sarcomas. We observed a high frequency of microsatellite instability expressed as allelic imbalances (25%). Presumably, alterations of the CDKN2A gene do not contribute to the oncogenesis in the majority of soft tissue tumors.

Alleles↗
PubMed1998

[Telomere lengths and telomerase activity in liposarcomas].

We measured telomerase activity in 36 malignant and seven benign lipomatous neoplasias from 34 patients to assess the role of telomerase in the development of liposarcoma. The sensitive PCR-based telomerase assay (telomeric repeat amplification protocol-TRAP) was applied. We correlated telomerase activity with the shortening or elongation of telomeric repeat fragment length (TRF), measured by using hybridization with a telomere specific oligonucleotide probe. Telomerase activity was demonstrated in 69% of malignant tumors. This information may be helpful in distinguishing benign tumors from malignant neoplasias. Telomerase expression, however, seems to be characteristic of poorly differentiated liposarcomas. Telomerase activity was not correlated with age at the time of diagnosis or with sex. We observed that telomerase expressing tumors had higher proliferation indices than neoplasias lacking telomerase. Telomerase activity was observed in all eight recurrences, suggesting a close association of telomerase with the biologic behavior of liposarcomas. Therefore, we assume that telomerase plays a key role in the establishment and progression of lipomatous tumors.

Humans↗
PubMed1998

Transferrin receptor assay and zinc protoporphyrin as markers of iron-deficient erythropoiesis in end-stage renal disease patients.

To evaluate storage iron deficiency and iron-deficient erythropoiesis we determined, in a cross-sectional study of 95 patients mainly including end-stage renal disease patients (ESRD) with (32) and without rh-EPO therapy (55), the following parameters: hemoglobin, mean corpuscular red cell volume, ferritin, transferrin saturation (TS), zinc protoporphyrin (ZPP) and soluble transferrin receptor (TfR). In the dialysis group the percentage of positive samples with each marker of tissue iron supply defined as TS < 20%, ZPP > 40 mumol/mol Heme and TfR > 3.05 microgram/ml was as follows: TS 43.7% and 32.2% at a diagnostic threshold level of < 16%, ZPP 33.3% and TfR 17.2%. Manifest storage iron deficiency defined as ferritin < 30 ng/ml was observed in 5.7% of the samples while the mean ferritin concentration of the rh-Epo treated dialysis patients was 509.3 ng/ml compared to 262.5 ng/ml in the group without rh-EPO therapy. These data reflect a generous iron substitution in our series taking a TS < 20% as an intervention criterion. Looking at the different results of the three markers the best correspondence was found between ZPP and TfR resulting in a weak positive correlation (+0.64). In conclusion, we found quite different results with different assays when evaluating endogenous iron availability in our series of mainly ESRD patients in a cross-sectional study. Because a gold-standard is not defined further firm conclusions cannot be drawn from this type of study. The adequacy of the different parameters of iron metabolism including threshold levels and, consequently, the decision and route of iron substitution deserve an evaluation in a longitudinal study to characterize the best marker or marker combination in this setting.

Adult↗
PubMed1998

Genetic history of the population of Sicily.

We investigated the genetic heterogeneity of 2354 individuals from the 9 provinces of Sicily. The genetic markers we used were HP, GC, TF, PI, and AK1 plus other previously tested polymorphisms, for a total of 24 independent markers. Distinct multivariate statistics were applied to verify the claimed genetic distinctiveness between extant eastern and western Sicilian populations. Our hypothesis stated that any diversity found between the two subpopulations would represent the signature of early colonization of the island by Greek and Phoenician peoples. Correspondence analysis showed that there was no clear geographic clustering within Sicily. The genetic distance matrix used for identifying the main genetic barriers revealed no east-west differences within the island's population, at least at the provincial level. FST estimates proved that the population subdivision did not affect the pattern of gene frequency variation; this implies that Sicily is effectively one panmictic unit. The bulk of our results confirm the absence of genetic differentiation between eastern and western Sicilians, and thus we reject the hypothesis of the subdivision of an ancient population in two areas.

Acute-Phase Proteins↗
PubMed1998

Detection of HHV-8 DNA in a German patient with classical Kaposi's sarcoma may allow an estimation of the incubation period.

DNA of HHV-8 (Kaposi's sarcoma-associated Herpes virus [KSHV]) was detected in a biopsy of a Kaposi's sarcoma in an elderly male patient from Saxony (East Germany). The diagnosis of classical Kaposi's sarcoma was first made in 1986. During World War II, the patient had been on active service on the Greek Islands of Crete and Rhodes only, he did not travel outside East Germany after the war. It is assumed that the patient was infected during his stay on the islands of Crete or Rhodes, where classical Kaposi's sarcoma is endemic. If so, the incubation period of classical Kaposi's sarcoma could be as long as 40 years.

Aged↗
PubMed1998

Genetic variability of apolipoprotein E in a Polish population.

Apolipoprotein E (apoE, protein; APOE, gene) is a component of very low density lipoprotein and high-density lipoprotein and plays an important role in lipoprotein metabolism. There are three common alleles of APOE (*2, *3, and *4), which encode the E2, E3, and E4 isoforms of the protein. Distribution of apoE isoforms shows marked variation among various ethnic groups. Direct phenotyping of human APOE in plasma was used to estimate APOE allele frequencies in 137 unrelated blood donors from 3 regions of Poland. The relative frequencies observed for the APOE*2, APOE*3, and APOE*4 alleles were 0.055, 0.839, and 0.106, respectively. The data have been compared with data found in other population groups. The frequency of the APOE*2 allele in Poles was among the lowest in Europe.

Adult↗
PubMed1997

Predictive factors of restenosis after coronary stent placement.

OBJECTIVES: The objective of this study was to identify clinical, lesional and procedural factors that can predict restenosis after coronary stent placement. BACKGROUND: Coronary stent placement reduces the restenosis rate compared with that after percutaneous transluminal coronary angioplasty (PTCA). However, restenosis remains an unresolved issue, and identification of its predictive factors may allow further insight into the underlying process. METHODS: All patients with successful coronary stent placement were eligible for this study unless they had had a major adverse cardiac event during the 1st 30 days after the procedure. Of the 1,349 eligible patients (1,753 lesions), follow-up angiography at 6 months was performed in 80.4% (1,084 patients, 1,399 lesions). Demographic, clinical, lesional and procedural data were prospectively recorded and analyzed for any predictive power for the occurrence of late restenosis after stenting. Restenosis was evaluated by using three outcomes at follow-up: binary restenosis as a diameter stenosis > or =50%, late lumen loss as lumen diameter reduction and target lesion revascularization (TLR) as any repeat PTCA or coronary artery bypass surgery involving the stented lesion. RESULTS: Multivariate analysis demonstrated that diabetes mellitus, placement of multiple stents and minimal lumen diameter (MLD) immediately after stenting were the strongest predictors of restenosis. Diabetes increased the risk of binary restenosis with an odds ratio (OR) [95% confidence interval] of 1.86 [1.56 to 2.16] and the risk of TLR with an OR of 1.45 [1.11 to 1.80]. Multiple stents increased the risk of binary restenosis with an OR of 1.81 [1.55 to 2.06] and that of TLR with an OR of 1.94 [1.66 to 2.22]. An MLD <3 mm at the end of the procedure augmented the risk of binary restenosis with an OR of 1.81 [1.55 to 2.06] and that of TLR with an OR of 2.05 [1.77 to 2.34]. Classification and regression tree analysis demonstrated that the incidence of restenosis may be as low as 16% for a lesion without any of these risk factors and as high as 59% for a lesion with a combination of these risk factors. CONCLUSIONS: Diabetes, multiple stents and smaller final MLD are strong predictors of restenosis after coronary stent placement. Achieving an optimal result with a minimal number of stents during the procedure may significantly reduce this risk even in patients with adverse clinical characteristics such as diabetes.

Aged↗
PubMed1997

Restenosis after coronary stent placement and randomization to a 4-week combined antiplatelet or anticoagulant therapy: six-month angiographic follow-up of the Intracoronary Stenting and Antithrombotic Regimen (ISAR) Trial.

BACKGROUND: Platelets and mural thrombus at the lesion site may play a key role in initiating the restenosis process after coronary interventions. The ISAR Trial provides a comparison of the outcomes of patients randomized to two different antithrombotic regimens administered for 4 weeks after successful coronary stent placement: combined antiplatelet therapy (aspirin plus ticlopidine) or a conventional anticoagulant regimen (phenprocoumon with initial overlapping heparin plus aspirin). Within the first 4 weeks after stent placement, combined antiplatelet therapy has been associated with a significant reduction of ischemic complications. In the present study, we examined whether combined antiplatelet therapy administered for 4 weeks after stent placement is able to reduce the process of restenosis at 6 months. METHODS AND RESULTS: Of 517 patients initially randomized, 496 were eligible for 6-month angiographic follow-up. Scheduled angiography was performed in 432 of the eligible patients (87.1%), 216 in each group. In a comparison of the two groups, there were no significant differences in clinical and procedural variables or in qualitative and quantitative lesion characteristics before and after stenting. At 6 months, minimal luminal diameter was 1.95+/-0.86 mm in the group with initial combined antiplatelet therapy and 1.90+/-0.87 mm in the group with initial anticoagulant therapy (P=.55). Late lumen loss was 1.10+/-0.81 and 1.15+/-0.75 mm (P=.54), and the restenosis rate was 26.8% and 28.9%, respectively (P=.70). Target lesion revascularization rate was 14.6% in the antiplatelet therapy group and 15.6% in the anticoagulant therapy group (P=.85). CONCLUSIONS: This study shows that combined antiplatelet therapy (aspirin plus ticlopidine) administered for 4 weeks after coronary Palmaz-Schatz stent placement does not result in a detectable benefit for the prevention of restenosis compared with conventional anticoagulant therapy (phenprocoumon with initial overlapping heparin plus aspirin).

Administration, Oral↗
PubMed1997

Major benefit from antiplatelet therapy for patients at high risk for adverse cardiac events after coronary Palmaz-Schatz stent placement: analysis of a prospective risk stratification protocol in the Intracoronary Stenting and Antithrombotic Regimen (ISAR) trial.

BACKGROUND: The Intracoronary Stenting and Antithrombotic Regimen (ISAR) Trial is a randomized study in which antiplatelet therapy is compared with anticoagulant therapy after coronary stent placement, showing a significantly lower rate of noncardiac and cardiac events with antiplatelet therapy. The present study is a report of the analysis of a prospective risk stratification protocol in the ISAR Trial and the association with the incidence of adverse cardiac events and stent vessel occlusion. METHODS AND RESULTS: In all 517 patients randomized in the ISAR Trial, risk stratification was done with a list of 18 clinical, procedural, and angiographic variables: 165 patients with two or fewer criteria were classified as low risk, 148 patients with three criteria were classified as intermediate risk, and 204 patients with four or more criteria were classified as high risk. Within a 30-day follow-up, cardiac event rate (death, myocardial infarction, repeat intervention) was 6.4% for high-risk, 3.4% for intermediate-risk, and 0% for low-risk patients (P<.01). Stent vessel occlusion occurred in 5.9%, 2.7%, and 0%, respectively (P<.01). There was no significant difference between anticoagulant and antiplatelet therapy in the low- and intermediate-risk groups. In high-risk patients, however, the cardiac event rate was 12.6% with anticoagulant therapy and 2.0% with antiplatelet therapy (P=.007), and the rate of stent vessel occlusion was 11.5% and 0%, respectively (P<.001). CONCLUSIONS: This risk stratification protocol can help to identify patients at risk for adverse cardiac events and stent vessel occlusion. Patients in the high-risk group had the most benefit from antiplatelet therapy. These data suggest that antiplatelet therapy is the therapy of choice after coronary stenting specifically for patients with acute ischemic syndromes, difficult procedures, or suboptimal final results.

Angioplasty, Balloon, Coronary↗
PubMed1997

GM and KM allotypes in eight tribal populations of Madyha Pradesh and Orissa, India.

Serum samples from eight endogamous Indian tribal populations of Madhya Pradesh (Dhurwa, Halba, Bhatra, Muria, Maria) and Orissa (Deshia Khond, Binjhal, Kisan) with a total of n = 731 unrelated individuals were typed for G1M (1,2,3,17), G3M (5,10,11,13,14,15,16,21, 26), and KM (1). In seven of these populations five different GM haplotypes were found: GM* 1,17;21,26; GM* 1,17;10,11,13,15,16; GM* 1,2, 17;21,26; GM* 1,3;5,10,11,13,14,26; and GM* 3;5,10,11,13,14,26. In the Kisan sample the haplotype GM* 1,2,17;21,26 is absent. The intergroup variability in the distribution of these haplotypes is considerable and statistically highly significant. The reasons for that can be attributed to the ethnohistory and to the genetic isolation of these eight endogamous tribal populations. The GM haplotype distribution pattern of all these groups is quite different from that of the non-tribal populations of India, whereas it is in good agreement with that of the so far tested other tribal populations from India. This can be explained by different origin and history of the Indian tribal and non-tribal populations. In the KM system, too, remarkable variability is seen in the distribution of phenotype and allele frequencies among the eight tribal populations under study.

Ethnicity↗
PubMed1997

Coronary stent placement in patients with acute myocardial infarction: comparison of clinical and angiographic outcome after randomization to antiplatelet or anticoagulant therapy.

OBJECTIVES: The Intracoronary Stenting and Antithrombotic Regimen (ISAR) trial is a randomized comparison of combined antiplatelet with anticoagulant therapy after coronary Palmaz-Schatz stent placement. The objective of this study was to compare early and late clinical and angiographic outcome in a subgroup of patients with stent placement for acute myocardial infarction. BACKGROUND: Stenting has become a treatment option for acute myocardial infarction, but it is not known which antithrombotic regimen is more adequate after stent implantation. METHODS: One hundred twenty-three patients with successful stenting after acute myocardial infarction were randomized to receive aspirin plus ticlopidine (n = 61) or intense anticoagulant therapy (n = 62). Six-month repeat angiography was performed in 101 (86.3%) eligible patients. RESULTS: During the first 30 days after stenting, patients with antiplatelet therapy had a significantly lower clinical event rate (3.3% vs. 21.0%, p = 0.005) and stent vessel occlusion rate (0% vs. 9.7%, p = 0.03) and a trend to fewer cardiac events (1.6% vs. 9.7%, p = 0.12). After 6 months, the survival rate free of recurrent myocardial infarction was higher in patients with antiplatelet therapy (100% vs. 90.3%, p = 0.03), and the rate of stent vessel occlusion was lower (1.6% vs. 14.5%, p = 0.02). Both groups had comparable restenosis rates (26.5% vs. 26.9%, p = 0.87). CONCLUSIONS: This study demonstrates that combined antiplatelet therapy after stent placement in patients with acute myocardial infarction is associated with an overall better clinical and angiographic outcome than anticoagulant therapy.

Anticoagulants↗
PubMed1997

Antiplatelet effect of ticlopidine after coronary stenting.

OBJECTIVES: This study sought to investigate the contribution of ticlopidine to the inhibition of platelet activation after coronary stent placement. BACKGROUND: After coronary stenting, antiplatelet therapy with aspirin and ticlopidine improves stent patency compared with anticoagulation. However, the specific role of ticlopidine has not been elucidated. METHODS: After successful coronary stent placement, we randomized 22 patients to receive ticlopidine and aspirin (ticlopidine group) and 25 to receive aspirin alone (aspirin group). Surface expression on platelets of the activated fibrinogen receptor and of P-selectin was assessed by flow cytometry. RESULTS: In the aspirin group the percent of platelets with activated fibrinogen receptors increased between days 1 and 5 (p = 0.001), whereas there were no substantial changes in the ticlopidine group. The percent of P-selectin-positive platelets did not change significantly in the aspirin group but decreased in the ticlopidine group (p = 0.019). At day 5 after the intervention, the percent of platelets with activated fibrinogen receptors in the ticlopidine group was significantly lower (median [interquartile range]: 8.5 [3.1 to 17.8] vs. 18.1 [8.5 to 35.5], p = 0.025), and there was a trend to fewer P-selectin-positive platelets than in the aspirin group (5.8 [3.4 to 9.5] vs. 8.8 [4.0 to 15.8], p = 0.073). CONCLUSIONS: Combined antiplatelet therapy with ticlopidine plus aspirin is superior to treatment with aspirin alone in suppressing platelet activation after coronary stenting.

Aged↗