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A Wessels

Publications and source records attributed to A Wessels.

50 records · Page 3Linked to original sources
PubMed1991

Spatial distribution of "tissue-specific" antigens in the developing human heart and skeletal muscle. II. An immunohistochemical analysis of myosin heavy chain isoform expression patterns in the embryonic heart.

The spatial distribution of alpha- and beta-myosin heavy chain isoforms (MHCs) was investigated immunohistochemically in the embryonic human heart between the 4th and the 8th week of development. The development of the overall MHC isoform expression pattern can be outlined as follows: (1) In all stages examined, beta-MHC is the predominant isoform in the ventricles and outflow tract (OFT), while alpha-MHC is the main isoform in the atria. In addition, alpha-MHC is also expressed in the ventricles at stage 14 and in the OFT from stage 14 to stage 19. This expression pattern is very reminiscent of that found in chicken and rat. (2) In the early embryonic stages the entire atrioventricular canal (AVC) wall expresses alpha-MHC whereas only the lower part expresses beta-MHC. The separation of atria and ventricles by the fibrous annulus takes place at the ventricular margin of the AVC wall. Hence, the beta-MHC expressing part of the AVC wall, including the right atrioventricular ring bundle, is eventually incorporated in the atria. (3) In the late embryonic stages (approx. 8 weeks of development) areas of alpha-MHC reappear in the ventricular myocardium, in particular in the subendocardial region at the top of the interventricular septum. These coexpressing cells are topographically related to the developing ventricular conduction system. (4) In the sinoatrial junction of all hearts examined alpha- and beta-MHC coexpressing cells are observed. In the older stages these cells are characteristically localized at the periphery of the SA node.

Adult↗
PubMed1991

Different localization of dystrophin in developing and adult human skeletal muscle.

Duchenne and Becker muscular dystrophy are caused by defects in dystrophin synthesis. Using affinity-purified polyclonal anti-dystrophin antibodies, we have studied immunohistochemically the subcellular localization of dystrophin in embryonic, fetal, and adult human skeletal muscle. In the embryonic stages dystrophin first appears in the sarcoplasm at the peripheral ends of the myotubes, immediately adjacent to the tendons, whereas in fetal stages dystrophin is found throughout the entire myofibers. In agreement with literature data, in adult muscle dystrophin expression was found to be restricted to the sarcolemma. The sarcoplasmic localization in embryonic and fetal tissue and the sarcolemmal localization of dystrophin in mature muscle suggests the accumulation of dystrophin in the cytoplasm prior to its integration into the membrane. These results increase our knowledge of the ontogenesis of dystrophin and may lead to a better understanding of the great diversity in pathological cases of Duchenne and Becker muscular dystrophy.

Animals↗
PubMed1991

Demonstration of 'cardiac-specific' myosin heavy chain in masticatory muscles of human and rabbit.

Human and rabbit masticatory muscles were analyzed immuno- and enzyme-histochemically using antibodies specific to 'cardiac' alpha, slow and fast myosin heavy chain isoforms. In human masseter, temporalis, and lateral pterygoid muscle 'cardiac' alpha myosin heavy chain is found in fibres that contain either fast, or fast and slow myosin heavy chain. In rabbit masseter, temporalis and digastric muscles, fibres are present that express 'cardiac' alpha myosin heavy chain either exclusively, or concomitantly with slow myosin heavy chain or fast myosin heavy chain. Our results demonstrate a much broader distribution of 'cardiac' alpha myosin heavy chain than hitherto recognized and these might explain in part the specific characteristics of masticatory muscles. The 'cardiac' alpha myosin heavy chain is only found in skeletal muscles originating from the cranial part of the embryo (including the heart muscle), suggesting that its expression might be determined by the developmental history of these muscles.

Adult↗
PubMed1991

Immunohistochemical studies show truncated dystrophins in the myotubes of three fetuses at risk for Duchenne muscular dystrophy.

We have performed immunohistochemical studies on muscle tissue of three 12 week old fetuses at risk for DMD, using antisera directed against regions located NH2-proximally and centrally in the rod shaped spectrin-like domain and against the COOH-terminus of dystrophin. All three fetuses had a family history of DMD. Truncated dystrophins were identified in all three cases by a positive reaction with the NH2-proximal antibody, different reactions with the central antibody, and a negative reaction with the COOH-terminal antibody. These data indicate that a panel of antibodies would, in principle, permit 'immunological' mapping of dystrophin mutations. This is diagnostically important in the 35% of families where no mutation is detectable at the DNA level. Secondly, by using this mapping technique it may also become possible to identify the at risk haplotype when DNA analysis is not informative. This may be of great value in DMD carrier detection.

Dystrophin↗
PubMed1990

Spatial distribution of "tissue-specific" antigens in the developing human heart and skeletal muscle. I. An immunohistochemical analysis of creatine kinase isoenzyme expression patterns.

Using monoclonal antibodies against the M and B subunit isoforms of creatine kinase (CK) we have investigated their distribution in developing human skeletal and cardiac muscle immunohistochemically. It is demonstrated that in skeletal muscle, a switch from CK-B to CK-M takes place around the week 8 of development, whereas in the developing heart, CK-M is the predominant isoform from the earliest stage examined onward (i.e., 4 1/2 weeks of development). In all hearts examined, local differences in concentration of the CK isoforms are observed. The CK-M expression in the developing outflow tract (OFT) and conduction system is described in detail. Between the weeks 5 and 7 of development, the distal portion of the OFT is characterized by low CK-M expression, whereas around the week 8-10 of development the myocardium around the developing semilunar valves in the OFT expresses a very high level of CK-M. At all stages examined, a relatively low CK-M level is observed in those regions in which the "slow" components of the conduction system do develop (e.g., the sinoatrial junction and atrioventricular junction), whereas a relatively high concentration of CK-M is observed in those areas that are destined to become the "fast" components, i.e., the subendocardial myocardium of the ventricles. The high expression of CK-M in the developing "fast components" of the conduction system contrasts with the relatively low expression of CK-M in the force-producing myocardium of the interventricular septum and free ventricular wall.

Creatine Kinase↗
PubMed1990

Detection of truncated dystrophin in fetal DMD myotubes.

An immunohistochemical study was carried out on a twelve-week old fetus, aborted for high risk of Duchenne muscular dystrophy. Southern and FIGE analysis showed an intragenic duplication in the DMD gene, which had previously resulted in a severe Duchenne phenotype in three relatives. Polyclonal antibodies directed against the NH2-terminal half of dystrophin showed a positive reaction an a similar distribution of dystrophin in the skeletal myotubes of a twelve-week old normal fetus and the affected fetus. In contrast, a polyclonal antibody directed against the COOH-terminus of dystrophin, i.e., distal to the mutation in this family, did only react with the myotubes of the normal fetus and not with those of the affected fetus. This indicates the presence of a truncated dystrophin in the affected fetus. Apparently at this stage, before binding of dystrophin to the sarcolemma, no distinction is made yet between normal and abnormal dystrophins. This implies that the potential to bind to the sarcolemma could be a major point of discrimination between normal and defective dystrophins. The truncated dystrophin will probably be degraded in a later stage during fetal development. So it appears that the use of dystrophin immunostaining to confirm high Duchenne risk abortions requires great caution. To prevent false-positive results, the combined use of NH2- and COOH-terminal antibodies is mandatory.

Dystrophin↗
PubMed1988

Medtronic Hall valve replacement in a third-world population group. A review of the performance of 1000 prostheses.

Between May 1980 and December 1984, 1000 Medtronic Hall prostheses (538 mitral and 462 aortic) were implanted in 852 patients (mean age 30 +/- 15 years) of a third-world type of population group. The most common valve lesions were aortic and mitral regurgitation, and 32% of the patients were in New York Heart Association class IV or greater. Double valve (aortic and mitral) operations were performed in 209 patients. The 782 operative survivors were followed up for 2 to 6.5 years (mean 3.5 years) for a cumulative 2676 patient-years. Valve performance was analyzed in each position separately for valve-related complications. Results for the whole group for the following events are expressed in both linearized (percent/patient-year) and actuarial (percent +/- standard error of the mean freedom at 5 years) terms, respectively: valve-related mortality, 2.9 and 92 +/- 2; reoperation, 1.9 and 90 +/- 2; systemic thromboembolism, 3.3 and 85 +/- 2; thrombotic obstruction, 1.2 and 95 +/- 1; prosthetic valve endocarditis, 0.7 and 97 +/- 1; anticoagulant-related hemorrhage, 0.7 and 98 +/- 1; and periprosthetic leak, 0.7 and 97 +/- 1. Corresponding composite figures for valve failure were 4.3 and 85 +/- 2, and for all valve-related morbidity and mortality were 6.7 and 75 +/- 3. Thrombotic obstruction (fatal in 71% of the cases), anticoagulant-related hemorrhage (61% fatal), and prosthetic endocarditis (44% fatal) were the most lethal complications. Although the differences did not reach statistical significance, aortic prostheses appeared to have a higher incidence of complications than the mitral prostheses. When analyzed against the background of an essentially noncompliant population group, the Medtronic Hall prosthesis proved to be reliable and remarkably free from structural failure. The high incidence of thromboembolism and thrombotic obstruction still mandates anticoagulation.

Adult↗
PubMed1986

Inverted Y chromosome polymorphism in the Gujerati Muslim Indian population of South Africa.

An inverted Y chromosome has been found at a very high frequency in a Muslim Indian community living in the Johannesburg-Witwatersrand area of the Transvaal Province of South Africa: 8 of 141 (5.7%) retrospectively identified Indian males had an inv(Y)(p11.2q11.23) and all were of the Muslim faith. The inversion was found in 22 of 72 (30.5%) prospectively studied normal Muslim Indian males. All the carriers of the inversion were Gujarati-speakers whose families migrated to the Transvaal from the Gujerat Province of India during the first half of this century. The origins of the ancestors of the individuals with inv(Y) were traced to a small village, Kholvad, near the city of Surat, and some neighbouring villages. The polymorphic frequency of the inv(Y) has probably been produced through random genetic drift in a reproductively isolated community, maintained by strict endogamous marriage customs based on religious and linguistic affiliations. There was no indication that the inverted Y was associated with any reproductive disadvantages.

Black People↗
PubMed1984

Pharyngoesophageal barotrauma in children: a report of six cases.

Pharyngeal and pharyngoesophageal penetrating injury occurred in six children following the explosive discharge of compressed carbon dioxide into their mouths. The gas was contained in plastic, screw-cap soft-drink containers overpressurized by the addition of dry ice. Three children were managed surgically and three conservatively. All recovered fully, and at follow-up of from 3 to 52 months, swallowing is normal.

Anti-Bacterial Agents↗
PubMedDate not supplied

[Effect of various criteria on the course and therapy result in Perthes disease].

The present treatise gives an account of the courses of illness as well as of the results of a follow-up examination of 116 patients, which have been treated in the period from 1965 to 1980 at the Orthopedic University Hospital Hamburg-Eppendorf because of a genuine Perthes' disease. Sufficient documented courses are going back to the year 1952. In the centre of interest is the question about the influence of the method of treatment, of the patients' age at the time of giving the diagnosis as well as of the radiological stage of illness at the moment of giving the diagnosis on the course and on the therapeutic result of Perthes' disease. Clinical parameters have been subdivided in the classifications of Renckhoff (1975) as well as of Howorth and Ferguson (1934). The assessment of the radiological results took place according to the classifications of Sundt (1949) as well as of Bauer und Jünger (1977). 4 therapeutic groups, 7 stage of disease and 5 age groups have been differentiated. According to the results of this long-term study at the moment the immediate intertrochanteric varus osteotomy, independent of the radiological stage of disease and of the patient's age, is being looked upon as the best method of treatment for Perthes' disease.

Bone Regeneration↗
PubMedDate not supplied

Myofibroblast induction and microvascular alteration in scleroderma lung fibrosis.

OBJECTIVE: Scleroderma (SSc) is an autoimmune connective tissue disorder characterized by progressive fibrosis of the skin and internal organs. The leading cause of death in SSc patients is pulmonary dysfunction as a result of interstitial fibrosis and pulmonary vasculopathy. Our objective was to evaluate histopathological abnormalities associated with the development of pulmonary fibrosis in SSc. METHODS: Postmortem SSc lung tissue from various stages of fibrosis and tissue from normal lung were analyzed by Masson's trichrome staining and immunohistochemistry. Monoclonal antibodies against smooth muscle-alpha actin (myofibroblast marker), von Willebrand Factor, platelet endothelial cell adhesion molecule-1 (endothelial cell markers), or caldesmon (smooth muscle cell marker) were employed. RESULTS: We found that in the early active stages of SSc lung fibrosis two major types of cellular abnormalities occur. One is the induction of a large number of smooth muscle alpha-actin-positive myofibroblasts in interstitia. The other is the excessive formation of alveolar capillaries (hypervascularity) accompanied by an increase in the number of microvascular endothelial cells. The vascular abnormality also involves the development of microvessels that are irregular in size and shape. However, the population of myofibroblasts and capillary endothelial cells decline as the fibrosis progresses to its most marked, later stages. CONCLUSION: We conclude that the induction of myofibroblasts and the overdevelopment of capillary microvessels characterize the progression of lung fibrosis in SSc. Using these histological alterations as criteria, therefore we have divided the fibrosis formed in the SSc lungs into four pathological stages. These results suggest that both fibroblast overproliferation and vascular abnormality play an important role in the pathogenesis of lung fibrosis in SSc.

Adult↗