Biomedical subjects

M Berndt

Publications and source records attributed to M Berndt.

11 recordsLinked to original sources

PubMed2007

Carbon-11 labeling chemistry based upon [11C]methyl iodide.

Radiochemistry with the short-lived positron emitter 11C (half-life 20.38 min) represents special challenges in terms of synthesis time and labeling techniques. The recent developments in 11C radiochemistry have steadily expanded the number of 11C labeled compounds. This chapter addresses selected chemical and technical aspects of 11C chemistry based on the readily available labeling precursors [11 C]methyl iodide and, to a lesser extent, [11C]methyl triflate. Special emphasis is placed on heteroatom methylation reactions and 11C-C bond formations.

Alkylation↗

PubMed2002

[General medicine malpractice cases].

During the last five years legal proceedings about alleged treatment mistakes in Germany more than doubled. Using a standardized questionnaire about legal proceedings in general medicine, involving liability, an anonymous survey with the members of the workgroup law medicine of the Deutsche Anwaltsverein (DAV) was carried out. The questions included among other things the number and reasons of legal proceedings involving liability. Of 322 questioned lawyers who focused on medicine law 122 (38%) answered. 69.9% of the lawyers think poor information is the main reason for legal proceedings involving liability in general medicine. Three disease groups were mentioned more frequently: diseases of the digestive system (22 mentions), diseases of the circulatory system (21) and diseases of the muscles, skeleton and connective tissue (15). 40 mentions of injections as treatment mistakes build the most frequent therapeutic reason for legal proceedings involving liability. Most of the lawyers think that guidelines do not reduce legal proceedings involving liability. The most common reasons for legal proceedings involving liability such as poor information and insufficient medical examination may point out that the budgetary standards for consultation cannot guarantee enough time for firstly giving a sufficient individual information to the patient and secondly for developing a decision satisfactory for both sides.

Family Practice↗

PubMed1999

Concerning inorganic crystal structure types.

All representatives of an inorganic crystal structure type can be found systematically in the new database SICS (Standardized Inorganic Crystal Structures). It is derived from the Inorganic Crystal Structure Database (ICSD) by selecting the best determination of each phase. In addition, each entry is given in a standardized description and complemented by searchable descriptors Delta, which give the difference between all structures of an isopointal set. Because of the large number of structures the full information on relationships present can only be found by means of the new database itself. Some examples are given here in printed form. The limitations and the possibilities of expansion of SICS in terms of the concept of 'structure types' are demonstrated.

Journal Article↗

PubMed1999

[The DEGAM-concept--development, dissemination, implementation and evaluation of guidelines for general practice].

The German Society for General Practice/Family Medicine (DEGAM) has launched a project to develop and implement national guidelines for general practice accordingly to international models. Guidelines are seen as statements to assist practitioners and patients in deciding about appropriate, effective and efficient health care. They should be evidence-based, feasible for primary care practices, and purposefully addressing to physicians as well as practice staff and patients. The development follows a comprehensive and well-structured programme (10 stages) which requires the appraisal of medical evidence, the involvement of experienced general practitioners on various stages (primary review, feasibility testing), and comments of concerned specialists, before a guideline is promulgated. Implementation of each guideline is promoted by at least five tools (full text, quick reference guide, telephone card for practice staff; patient leaflet, and information-prescription--"infozept"). Methodological quality is checked for the first time in Germany according to the standards of the German Agency for Quality Assurance. Different targets and criteria for evaluation of guidelines in primary care are mandatory part of the DEGAM-concept.

Evaluation Studies as Topic↗

PubMed1998

[Congenital sternal cleft. Diagnosis and treatment].

The first known case of sternal cleft was described by Torres in 1740. Since then, many publications have appeared concerning sternal cleft, which have led to introduce a classification and some therapeutical procedures. This disease is a developmental anomaly of the sternum that usually shows vascular and cardiac malformations as well as diaphragmatic, abdominal wall, pericard and middle line organs anomalies. Two cases of sternal cleft are presented who have been treated in the neonatal period with different associated anomalies. Diagnostic procedures and therapeutical aspects are discussed.

Abnormalities, Multiple↗

PubMed1997

Novel cytokine-independent induction of endothelial adhesion molecules regulated by platelet/endothelial cell adhesion molecule (CD31).

Tumor necrosis factor-alpha, interleukin-1, and endotoxin stimulate the expression of vascular endothelial cell (EC) adhesion molecules. Here we describe a novel pathway of adhesion molecule induction that is independent of exogenous factors, but which is dependent on integrin signaling and cell-cell interactions. Cells plated onto gelatin, fibronectin, collagen or fibrinogen, or anti-integrin antibodies, expressed increased amounts of E-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1. In contrast, ECs failed to express E-selectin when plated on poly-L-lysine or when plated on fibrinogen in the presence of attachment-inhibiting, cyclic Arg-Gly-Asp peptides. The duration and magnitude of adhesion molecule expression was dependent on EC density. Induction of E-selectin on ECs plated at confluent density was transient and returned to basal levels by 15 h after plating when only 7 +/- 2% (n = 5) of cells were positive. In contrast, cells plated at low density displayed a 17-fold greater expression of E-selectin than did high density ECs with 57 +/- 4% (n = 5) positive for E-selectin expression 15 h after plating, and significant expression still evident 72 h after plating. The confluency-dependent inhibition of expression of E-selectin was at least partly mediated through the cell junctional protein, platelet/endothelial cell adhesion molecule-1 (PECAM-1). Antibodies against PECAM-1, but not against VE-cadherin, increased E-selectin expression on confluent ECs. Co- culture of subconfluent ECs with PECAM-1- coated beads or with L cells transfected with full-length PECAM-1 or with a cytoplasmic truncation PECAM-1 mutant, inhibited E-selectin expression. In contrast, untransfected L cells or L cells transfected with an adhesion-defective domain 2 deletion PECAM-1 mutant failed to regulate E-selectin expression. In an in vitro model of wounding the wound front displayed an increase in the number of E-selectin-expressing cells, and also an increase in the intensity of expression of E-selectin positive cells compared to the nonwounded monolayer. Thus we propose that the EC junction, and in particular, the junctional molecule PECAM-1, is a powerful regulator of endothelial adhesiveness.

Blood Platelets↗

PubMed1996

Clinical course of hypophosphatemic rickets in 23 adults.

Twenty-three adult patients (19 females, 4 males) with x-linked hypophosphatemic rickets (HPR) underwent a retrospective evaluation of the clinical course and a clinical examination by a nephrologist, orthopedic surgeon and dentist. Blood and urine analysis, bone density measurements with QCT and DEXA, ultrasonic examination of the kidneys were performed and the patients were asked to fill in a standardized questionnaire on pain and psychosocial rehabilitation. Mean final height was 152.4 cm +/- 8.5 SD in females and 157.3 cm +/- 8.9 SD in males. Decreased joint mobility was seen in all patients, deviations of the normal leg axis in 18/23 patients in spite of 69 correcting osteotomies in the past. Dental (n = 14) and psychosocial problems were associated with inability to work (n = 8). There was a trend that patients with a very low Tp/GFR had a more severe course of the disease. Early therapy with vitamin D metabolites and phosphate had a beneficial effect on growth, bone density and deformations. Eight patients had nephrocalcinosis due to vitamin D and phosphate therapy and had normal kidney function. Four patients had urinary tract abnormalities. We conclude that patients with HPR should receive continuous interdisciplinary care given by nephrologists, orthopedic surgeons, physiotherapists and dentists not only during childhood but also as adults.

Adult↗

PubMed1996

[Conformational changes of the platelet membrane glycoprotein IIb-IIIa complex stimulated by a monoclonal antibody to the N-terminal segment of glycoprotein IIIa].

During platelet activation, the glycoprotein (GP) complex IIb-IIIa (alpha 11b beta 3-integrin) changes its conformation, resulting in binding of adhesive proteins of RGD containing an amino acid sequence as well as in expression of new ligand-induced binding sites (LIBS) on the GPIIb-IIIa molecule. Like its F(ab)-fragments, the monoclonal antibody CRC54, whose epitope is located in the N-terminal part of the GPIIIa molecule, binds to no more than 10% of GPIIb-IIIa on the resting platelet surface. However, the binding of CRC54 increases considerably during activation of platelets by thrombin, platelet adhesion on plastic, GPIIb-IIIa interaction with RGDS-peptide as well as during dissociation of the complex in the presence of EDTA. These finding suggest that CRC54 is specifically directed against the LIBS epitope on the GPIIIa molecule. This epitope differs from those of other known conformation-dependent antibodies against GPIIb-IIIa (LIBS1, LIBS6, PMI-1, pl55 and p180), since those antibodies did not block the CRC54 binding to GPIIb-IIIa on the surface of adhering platelets. Unlike whole platelets, the binding of GPIIb-IIIa from lysates of platelets treated with Triton X-100 with immobilized CRC54 did not depend on the presence of the RGDS peptide. Under these conditions another anti-LIBS-antibody, p180 specifically directed against GPIIb, preserved its ability to discriminate the RGDS-occupied and resting conformations of GPIIb-IIIA. CRC54 and its F(ab) fragments induced platelet aggregation in both platelet-enriched plasma and in suspensions of washed platelets. CRC54 also stimulated the binding to platelets of GPIIb-IIIa ligand fibrinogen, labelled with 125I as well as adhesion of 51Cr-labelled platelets to immobilized ligands-fibrinogen and fibronectin. The CRC54-dependent aggregation was fully blocked by RGDS-peptide and antibody CRC64 inhibiting the GPIIb-IIIa binding to the ligands. However, the platelet activation inhibitor, prostaglandin EI, and the mixture of metabolic inhibitors, deoxyglucose-sodium azide, only party inhibited the CRC54-dependent aggregation. Incubation of platelets with CRC54 induced the binding to platelets of the anti-GPIIb LIBS antibody p180 and of the anti-GPIIb-IIIa activation-dependent antibody p155. The binding of GPIIb-IIIa from lysates of CRC54-treated platelets with immobilized p180 and p155 was also several times as high as that of GPIIb-IIIa from control platelet lysates. The data obtained indicate that the GPIIb-IIIa transition to the active state and its interaction with ligands induces conformational changes in the N-terminal part of GPIIIa and that the CRC54 binding to the N-terminal part of GPIIIa stimulates conformational changes in GPIIb-IIIa, complex interaction with ligands and platelet aggregation.

Amino Acid Sequence↗

PubMed1996

Pregnancy and delivery after liver transplantation.

The first case of pregnancy in a patient after an orthotopic liver transplantation (OLT) in Poland is presented. A 21-year-old woman was liver grafted 3 years prior to the pregnancy. Before having conceived the patient's graft function was stable. The woman was on immunosuppressive therapy with cyclosporine A and prednisolone. During pregnancy no significant changes in biochemical tests of liver function and liver blood flow were noted. Starting at the second trimester, a slight anemia occurred and the quantity of blood platelets continued to decrease, the latter having been observed immediately after the transplantation. The intrauterine growth of the fetus was monitored by ultrasound and the assessment of blood flow to the placenta was made. No abnormality was observed. In the second and third trimester the presence of HCV-RNA in the serum was found. In the 41-st week of pregnancy labor commenced. The threat of intrauterine infection indicated a cesarean delivery. The newborn weighed 4180 g and had an Apgar score of 10. The cesarean section, as well as puerperium, was normal. The immunosuppressive therapy was continued, and antibiotics were administered for prophylactic reasons. During the first month the infant was treated with antibiotics because of pneumonia and the suspicion of meningitis. Nine months after the delivery, the patient's health is satisfactory and the baby is making normal progress.

Adult↗

PubMed1993

von Willebrand's disease: laboratory investigation using an improved functional assay for von Willebrand factor.

This report details extensive studies investigating an improved screening procedure for the laboratory confirmation of clinically suspected von Willebrand's disease (vWD). Over the past two years, over 400 plasma samples, comprising samples derived from both normal individuals (n = 112) and from patients undergoing investigation on clinical grounds, underwent analysis in this screening procedure, comprising three distinct assays: a standard ELISA assay for von Willebrand Factor (vWF) antigen levels (vWF:Ag), a standard ristocetin cofactor (R Cof) assay, and a functional collagen based ELISA assay for vWF ('CBA'). Normal individual plasma samples yielded normal reference values (mean +/- 2SD) approximating 50-200% (vWF:Ag, R Cof) or 50-250% (CBA). In order to permit comparative analysis, and based upon derived assay values, and subsequent multimer analysis, patient samples were either deemed to derive from persons unlikely to suffer vWD ('non-vWD' patient group) or those potentially suffering vWD. The latter group was further separated into subgroups based upon the likelihood, and probable subtype of vWD. In conjunction with the vWF:Ag assay, the CBA provides the basis by which an effective predictor system (likelihood and probable subtype of vWD) can be offered on the basis of preliminary screening procedures. To date, there has been no overlap in vWF:Ag to CBA ratios (vWF:CBA) between patients yielding Type II vWD like multimer patterns and those yielding Type I vWD, or normal, multimer patterns. Thus, high vWF:CBA (i.e. > or = 3.0) would suggest a Type II, or pseudo, -vWD like defect, whereas low vWF:CBA (< or = 2.5) would likely derive from either normal individuals, or persons suffering from Type I vWD.(ABSTRACT TRUNCATED AT 250 WORDS)

Enzyme-Linked Immunosorbent Assay↗

PubMed1991

[Inhibition of Fc-receptor dependent platelet aggregation by monoclonal antibodies against the glycoprotein IIb-IIIa complex].

A murine monoclonal antibody (MoAb) VM16a specifically binding to human platelets has been produced. Approximately 56,000 molecules of VM16a bound per platelet at saturation (Kd = 7.9 nM) but no binding to platelets from Glanzmann's thrombasthenia patients was detected. VM16a precipitated two proteins with molecular masses corresponding to those of glycoproteins (GP) IIb and IIIa from solubilized surface-labelled platelets. However, after dissociation of the GPIIb--IIIa complex with EDTA VM16a did not bind to platelets and precipitated nothing from their lysate, thus evidencing that its determinant is complex-dependent. VM16a had no effect on ADP-, thrombin- and ristocetin-induced platelet aggregation but inhibited the aggregation induced by collagen. This inhibitory effect was more pronounced in the presence of plasma. VM16a completely blocked the Fc-receptor-mediated aggregation induced by aggregated human IgG, aggregated murine IgG1 and the previously described MoAb VM58. F(ab')2 fragments of VM16a were also able to inhibit this aggregation by decreasing the rate of aggregation induced by aggregated IgG and by extending the lag phase of VM58-induced aggregation. These results suggest that the platelet Fc-receptor may be topographically associated with the GPIIb-IIIa complex.

Adenosine Diphosphate↗