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Biomedical subjects

E S Kalter

Publications and source records attributed to E S Kalter.

13 recordsLinked to original sources
PubMed1997

Tissue banking programmes in Europe.

In Europe, organ centres such as Bio Implant Services (BIS) in cooperation with Eurotransplant, play an intermediary role from donation of tissue and organs to allocation and transplantation. They take responsibility for donor medical/safety screening and organize procurement. Tissue banks are autonomous and are responsible for tissue processing and preservation. Allocation of scarce tissues is performed according to rules set by committees of renowned experts in the field. Most frequently donated types of tissues are corneas, heart valves, bone and soft tissue and skin. In this article, optimal serological screening of the donor, and the banking of these tissues in Europe is reviewed in relation to clinical need and volume of transplantable tissues available, number of banks and their organisational level, methods of explantation, processing and preservation, quality standards and new developments.

Bone Banks↗
PubMed1985

Activation and inhibition of Hageman factor-dependent pathways and the complement system in uncomplicated bacteremia or bacterial shock.

Levels of components of the contact activation, coagulation, and complement systems and their main inhibitors were measured in 45 critically ill patients during 61 episodes of uncomplicated bacteremia or bacterial shock. Levels of Hageman factor (factor XII), prekallikrein, high-molecular-weight kininogen, factor XI, factor VII, total hemolytic complement, alternative pathway activity, and C3 were within the normal range during uncomplicated bacteremia (n = 29), but during fatal bacterial shock (n = 13) a significant decrease by 40%-50% was observed in all measurements. During nonfatal bacterial shock (n = 19) a moderate decrease was observed in most of these measurements. The capacity of plasma to inactivate kallikrein was significantly higher during bacteremia than during bacterial shock because of a significant increase in the level of C1 esterase inhibitor. Levels of antithrombin III and alpha 2-macroglobulin were below normal in all groups. Thus increased inhibition of the contact activation and complement systems is beneficial during bacteremia.

Angiotensin III↗
PubMed1985

Induction of the early hypotensive phase by Escherichia coli: role of bacterial surface structures and inflammatory mediators.

An early hypotensive phase was induced in rats by different strains of Escherichia coli and cell wall fractions to study the role of the bacterial surface structure, the complement system, histamine, and serotonin in induction of hypotension. E. coli strains with only core glycolipid (E. coli strain J5) or with intact lipopolysaccharide O antigens on their surface induced hypotension and thrombopenia within 5 min after intravenous administration. This response was reduced by prior decomplementation of the rats and by methysergide, a serotonin antagonist. Two K antigen-positive strains induced no hypotension except after removal of K antigen. The isolated lipopolysaccharide fractions and the lipid A subfractions, but not the polysaccharide subfractions, were also able to induce hypotension. Thus the core glycolipid structure, by interactions that involve platelets and the complement system, is mainly responsible for induction of an early hypotensive phase in rats, and K antigens interfere with this response.

Animals↗
PubMed1984

Host-parasite interaction in serious infections due to gram-negative bacteria.

Gram-negative rods such as Enterobacteriaceae and Pseudomonadaceae are normal habitants of the digestive tract. However, if defense mechanisms of the host are compromised by underlying diseases such as malignant neoplasms, renal insufficiency, extensive traumata, or immunosuppressive therapy, invasion of the blood-stream can occur. Gram-negative septicaemia is associated with high morbidity and mortality, despite intensive care and administration of potent antibiotics. A central role in the pathophysiology of life-threatening bacteriaemia is attributed to endotoxin, a constituent of the gram-negative cell wall. This paper reviews current concepts of septic shock, the acquisition of gram-negative bacteraemia and the role of endotoxin. It also deals with a new approach to prevention and control of severe gram-negative infections using serotherapy based on the structure of endotoxin.

Animals↗
PubMed1984

Inflammatory mediators and acute infections.

In this paper some important mediation systems of inflammation are reviewed; special emphasis is laid on basic aspects of these systems, their interrelationships, and on clinically relevant effects with regard to the circulatory and pulmonary complications of sepsis. The references cited are selected on the basis of their review aspects.

Arachidonic Acid↗
PubMed1983

Activation of purified human plasma prekallikrein triggered by cell wall fractions of Escherichia coli and Staphylococcus aureus.

Whether Escherichia coli and Staphylococcus aureus cell wall fractions can trigger the activation of prekallikrein was investigated in a mixture of purified human factor XII, prekallikrein, and high-relative-molecular-weight (Mr) kininogen. After exposure for 30 min to bacterial preparations (0.02-5 mg/ml) at 0 C, lallikrein amidolytic activity was expressed as a percentage of the optimal activation of prekallikrein induced by dextran sulfate. Lipopolysaccharide (LPS) fractions of five E coli strains and lipid A of E coli O111B4 induced 50%-90% optimal activity. However, the polysaccharide fraction induced less than 5% activity. Peptidoglycan and teichoic acid of S aureus induced 70%-100% optimal activity at 5 mg/ml, but protein A did not generate activity. No activation of prekallikrein occurred in the absence of factor XII. Thus, LPS and lipid A of E coli and peptidoglycan and teichoic acid of S aureus can generate kallikrein amidolytic activity in a mixture of purified factor XII, prekallikrein, and high-Mr kininogen.

Cell Wall↗
PubMed1980

Effects of methylprednisolone on P50, 2,3 diphosphoglycerate and arteriovenous oxygen difference in acute myocardial infarction.

In a double-blind randomized study, 30 mg/kg of methylprednisolone sodium succinate (MPN) or 15 mg/kg of mannitol placebo (PL) were infused in 28 patients after acute myocardial infarction. Measurements were obtained immediately before and after for 24 hours after the initial infusion. The partial pressure of oxygen at 50% saturation of hemoglobin (P50) did not change significantly in vitro or in vivo after MPN, whereas 2,3 diphosphoglycerate (2,3 DPG) increased from 13.2 to 14.2 mumol/g Hb (p < 0.05) in the group receiving PL. The arteriovenous oxygen difference (Ca-VO2) remained constant after MPN or PL. The cardiac index (CI) increased after MPN (p < 0.02) associated with an increase in the oxygen consumption index (CI X A-V O2) from 146 to 170 ml/min/m2 (p < 0.05). These data show that MPN increases CI after acute myocardial infarction, but has no specific effects on P50, 2,3 DPG or Ca-VO2.

Adult↗