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Biomedical subjects

M Richter

Publications and source records attributed to M Richter.

At least 289 records · Page 16Linked to original sources
PubMed1989

[Sleep obstructive apnea syndrome and temporomandibular ankylosis. Maxillofacial correction for adults and children].

Juvenile temporomandibular bony ankylosis may generate micro- and retroposition of the mandible. Collapse of the upper airway during sleep due to muscle atonia awakens the patient, leading to compensative diurnal hypersomnia. In severe cases, alveolar hypoventilation may result in anoxic seizure, sudden death or development of life threatening cor pulmonale. The corrective surgical procedure for adult is an anterior sagittal osteotomy and in the growing child, costochondral grafting is proposed. Pre- and post-operative polysomnograms with recording of oxygen saturation are objective measures of good surgical results.

Ankylosis↗
PubMed1989

[Difficult intubation in maxillofacial surgery. Tracheotomy or fibroscopy?].

Prior to general anesthesia, some maxillofacial conditions may require tracheostomy or, in recent years, fiberoptic endotracheal intubation. This technic is efficient but delicate and therefore needs a skilled qualified operator. However, fiberoptic endoscope may avoid the inconvenience of tracheostomy. This article presents our method of fiberoptic endotracheal intubation with the specific indications and results.

Adolescent↗
PubMed1988

[Orthodontics--timing and possibilities].

Orthodontic therapy is available to children and adults as well and can achieve excellent results in every age group, whereas dentofacial orthopedics is restricted to childhood and adolescence. New technologies broke loose the range of therapeutic possibilities of former years.

Child↗
PubMed1988

Cells involved in the immune response. XXXV. The antigen-specific antibody response in the rabbit is suppressed by thymocytes of allogeneic immunized rabbits (ITSC) and by the non-toxic suppressor factor (ITSF) secreted by these thymocytes.

The antigen-specific suppressor cells (ITSC) detected in the thymus of the rabbit 7 days post-iv immunization with sheep or horse erythrocytes (SRBC and HRBC, respectively), and the antigen-specific suppressor factor (ITSF) which the ITSC secrete in culture, inhibit the antigen-specific primary immune response in vivo when injected iv into SRBC and/or HRBC immunized rabbits on Days 0, 3, and 5 (ITSC) or daily on Days 0 to 5 (ITSF) post-primary immunization. The rabbits recover the ability to synthesize the specific antibodies following reimmunization by day 80 post-primary immunization. The primary immune response toward a non-cross-reacting antigen is not inhibited by the antigen-specific ITSC or ITSF. Neither the thymocytes of unimmunized rabbits nor the secretions of these cells in culture can suppress the primary immune response in vivo to either SRBC or HRBC. It must be emphasized that the suppression of the immune response by ITSC and ITSF in the rabbit is antigen-specific. ITSC and ITSF are not cytotoxic to rabbit lymphocytes in vitro. No gross or microscopic changes were detected in any of the lymphoid and nonlymphoid organs of rabbits sacrificed 2 days following 5 daily iv injections of large doses (10 ml) of ITSF. ITSF causes no adverse reaction in vivo since it did not induce morbidity in the rabbits during the 80 days observation period following its injection iv daily for 5 days commencing with the primary immunization.

Animals↗
PubMed1988

Critical periods associated with stressor effects on antibody titers and on the plaque-forming cell response to sheep red blood cells.

A series of experiments assessed the effects of stressors on the antibody response in mice. A critical period existed (72 h following antigen administration; sheep red blood cells 10(6) cells, ip) at which footshock reduced the plaque-forming cell (PFC) response in CD-1 mice. When shock was applied at other intervals following immunization (0, 24, 48, or 95 h) the PFC response was unaffected. The immunosuppression was unrelated to the time between stressor application and sacrifice, in that the reduced PFC response was evident both 24 and 48 h after stressor application, and reduced serum antibody titers (IgG) were evident 1 week after stressor exposure. The reduction of the PFC response was dependent on the severity of the stressor, but was not related to stressor controllability, being evident after both escapable and inescapable shock. It appears that stressful events may profoundly influence the immune response but the time between antigen administration and subsequent exposure to a stressor is critical in determining whether such an effect will be evident.

Animals↗
PubMed1988

Cells involved in the immune response. XXXVI. The thymic antigen-specific suppressor cell in the immunized rabbit is a T cell with receptors for FcG and the antigen and it acts, via a secreted suppressor factor, directly on the immune splenic AFC B cell to inhibit antibody secretion.

Following i.v. immunization of the normal outbred rabbit with sheep (SRBC) or horse (HRBC) erythrocytes, antigen-specific suppressor cells are generated in the thymus capable of inhibiting the generation of haemolytic plaques by the autologous or allogeneic splenic antibody-forming cells (AFC) in the plaque-forming cell (PFC) assay. These suppressor cells secrete an antigen-specific suppressor factor in short-term (4-24 hr) culture in vitro. The suppressor cells are not detected in the thymus prior to Day 4, exhibit peak activity between Days 5 and 11 post-immunization, and decline slowly thereafter. Suppressor cells can no longer be detected in the thymus by Day 60 postimmunization. Suppressor cells are not detected in any of the other lymphoid organs of the immunized rabbit nor in any lymphoid organ in the unimmunized rabbit. The thymic suppressor cell is a T cell with surface receptors for the antigen (SRBC or HRBC) and for FcG. On the other hand, the AFC B cells generated in the spleen of the immunized rabbit possess cell-surface receptors for only the antigen and not for FcG. Both the suppressor cells and the secreted suppressor factor act directly on the AFC B lymphocytes to inhibit the generation of antigen-specific haemolytic plaques in the PFC assay.

Animals↗
PubMed1988

Defibrinogenation by batroxobin and acylated batroxobin in rats.

The thrombin-like snake venom enzyme, batroxobin, was acylated by 4-amidinophenyl benzoate at the active site serine hydroxyl. From the enzymatically inactive benzoyl-batroxobin, batroxobin is generated with a half-life of deacylation of about 1 hour. The clotting activity of benzoyl-batroxobin in plasma is recovered with deacylation. The effect of batroxobin and benzoyl-batroxobin were studied following intravenous injection in rats. Compared to defibrinogenation with batroxobin, that obtained with benzoyl-batroxobin was much retarded. Batroxobin caused microthrombosis initially, which did not develop upon injection of benzoyl-batroxobin in equivalent doses.

Acylation↗
PubMed1988

Quality control of 125I-labelled fibrinogen of various species.

The modified chloramine-T method used for radioiodination of human, rat, and bovine fibrinogen guaranteed mild labelling conditions and a satisfactory labelling efficiency. The quality of the 125I-human, rat, and bovine fibrinogen preparations obtained met the requirements with respect to clottability, low content of 125Iodide as well as in vitro and in vivo stability.

Animals↗
PubMed1988

Pharmacokinetics of 125I-hirudin in rats and dogs.

Hirudin was 125I-labelled using a modified chloramine-T method. 125I-hirudin proved to be a suitable marker in pharmacokinetic studies, if unchanged 125I-hirudin in body fluids was determined by means of a binding assay using immobilized thrombin. In rats and dogs a study was performed on the pharmacokinetic behaviour of hirudin following intravenous and subcutaneous injection, resp., or one-hour infusion and pharmacokinetic parameters were calculated.

Animals↗
PubMed1988

[Effect of ultraviolet irradiation of autologous blood on cell volumes, cell adhesion and phagocytosis in normal probands and patients with multiple sclerosis].

UVB induced changes of blood cell properties were investigated in 12 MS patients and in 10 healthy volunteers serving as normal controls. The mean cell volume (MCV) was determined by electronic sizing, the granulocyte and lymphocyte adherence was estimated in a capillary assay, and the phagocytic activity of granulocytes was measured in a test system based on the incorporation of opsonized baker's yeast (Saccharomyces cerevisiae). In MS patients the MCV of red cells and lymphocytes decreased rapidly within 6 UVB treatments. In contrast, the reduction of the granulocyte volume was delayed (between the 6th and 12th UVB). In the control group the mean value of the red cell and lymphocyte MCV remained rather unaffected. There was a slight rise of the granulocyte volume after the 6th UVB. The only significant change of adherence was an increase of granulocyte adherence in MS patients. Untreated patients had a significantly enhanced phagocytic activity in comparison to the control group. 6 UVB treatments included a significant reduction of the phagocytic activity in MS patients. However, subsequently the percentage of phagocytizing cells increased again, whereas the particle uptake per cell continued to decrease. In the control group only minor UVB induced changes of phagocytosis were observed. The in vitro UV irradiation caused an enhanced phagocytosis in the majority of cases in both controls and MS patients. In general, under the UVB treatment all parameters examined changed in the sense of a normalisation, in that the measured values reached a new level lying between the extreme pretreatment values accompanied by a reduced standard deviation. The effect of UVB was more pronounced in MS patients when compared with normal controls. This could result from an enhanced sensitivity to the influence of UVB of pathologically altered cells in MS patients. The monitoring of the MCV of red cells and lymphocytes as well as the repeated testing of granulocyte phagocytosis are recommended for supportion of therapy planning and follow-up of MS patients.

Blood↗
PubMed1988

[The problem and value of therapy in multiple sclerosis].

Some fundamental problems of therapy in multiple sclerosis (MS) and the difficulties in assessing the results of treatment are represented. Basing on a survey of several principles of therapy, the findings of own therapeutic trials using corticosteroids, immunosuppressive agents (azathioprine, cyclophosphamide, antihumanlymphocyte globulin) are pointed out; in particular, the analysis of a longer period of the course of disease produced few favourable effects. In further therapeutic studies, i.e. plasmapheresis and immunoadsorption, a long lasting observation of the course is lacking; this likewise concerns the study on ultraviolet irradiation of blood. As to the aspects of a multi-stage pathogenesis of MS an appraisal of therapeutic conceptions and procedures is given; in critical evaluation their efficacy is little convincing.

Adult↗