[Animal studies of the regeneration behavior of the inferior alveolar nerve following late microsurgical reconstruction. Histomorphometric results].
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Biomedical subjects
Publications and source records attributed to K Meier.
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To evaluate the persistence of antibody after Haemophilus influenzae type b polysaccharide vaccine (PRP) and H influenzae type b polysaccharide diphtheria toxoid conjugate vaccine (PRP-D), a group of 141 infants initially immunized between 15 and 24 months of age were studied 1 year later. One month after immunization with PRP, the man anti-PRP antibody level was 0.27 microgram/mL and 1 year later was 0.29 microgram/mL (not significant). In the group immunized with PRP-D, the levels were 1.34 micrograms/mL and 1.20 micrograms/mL (not significant), respectively. To evaluate immunogenicity and safety of a booster immunization 1 year after initial vaccination, subjects were randomly assigned to receive saline, PRP, or PRP-D. In addition, 73 age-matched previously unimmunized subjects were vaccinated with PRP or PRP-D. In all groups, adverse reactions were minor and resolved by 48 hours. Subjects receiving booster immunization with PRP or PRP-D had significantly greater antibody responses than children of the same age receiving their first dose of vaccine. The highest antibody levels were achieved in children initially immunized with PRP-D, regardless of whether the booster vaccine was PRP (112.8 micrograms/mL) or PRP-D (122.0 micrograms/mL) (not significant). Antibody levels after booster vaccine were significantly lower in those initially given PRP compared with those initially given PRP-D but significantly higher than in age-matched previously unimmunized control subjects (PRP booster 3.16 micrograms/mL vs control of 0.62 microgram/mL [P less than .05]; PRP-D booster 12.31 micrograms/mL vs control 2.31 micrograms/mL [P less than .01]).
The review of 7 autopsy cases shows, that the diagnosis of a sudden death due to mechanical irritation of the carotid sinus is possible, when an injury of this reflectogen zone is represented autoptically, when there are signs of acute cardio vascular failure and other causes of death are out of the question. Taking account of the ascerteinments at the scene as well as observations by witnesses of the death process is important for diagnostic reason. The proof of the carotid lesion depends on the preparation of neck organs in artificial lack of blood. The histological analysis of stepwise taken slides of the carotid arteries above the bifurcation is informative. The insurances consider a death due to carotid sinus reflex as an accident; in criminal law this kind of death is regularly linked to strangulation; diagnostic decision criteria are presented.
The purpose of the present study was to evaluate the effect of diltiazem on the left ventricular function in postinfarction patients. Twelve patients without cardiac decompensation at rest began diltiazem therapy beginning 3 months after an acute myocardial Q-wave infarction. Oral diltiazem was administered on the first day in a single dose (120 mg) and the following 2 weeks in a 60 mg three times a day (tid) regimen. The therapeutic effect was studied by isotope angiocardiography at rest using equilibrium measurements with technetium-99m. Acute as well as continuous treatment improved left ventricular function in terms of increased synergy of the contraction (decreased phase deviation from a median of 20.0 degrees to median of 12.4 degrees and 13.0 degrees, respectively, p less than 0.01) and increased ejection fraction from a median of 46% to a median of 50% and 51%, respectively, p less than 0.05. It is suggested that the improvement of left ventricular function may be due in part to decreased pressure rate product. This improved left ventricular function during diltiazem treatment may explain the improved prognosis induced by diltiazem in postinfarction patients.
Central hemodynamic parameters were registered by right-side heart catheterization before and after intravenous administration of 12 mmol magnesium chloride (MgCl) in 15 patients with chronic ischemic heart disease and heart failure, New York Heart Association classes II and III. Serum magnesium concentrations increased from 0.76 +/- 0.03 (mean +/- SD) to 1.54 +/- 0.05 mmol/l, which resulted in a reduction in mean arterial as well as pulmonary artery pressure by 10% (p less than 0.0001) and 7% (p less than 0.05), respectively. This reduction was caused by a marked decrease in systemic as well as pulmonary vascular resistance (from 1323 +/- 205 to 1132 +/- 158 dyn.s/cm5, p less than 0.001 and from 156 +/- 73 to 133 +/- 72 dyn.s/cm5 (p less than 0.05). Heart rate, cardiac index, stroke volume index, and stroke work index increased slightly, although these differences did not reach statistical significance. Right and left ventricular filling pressures were not influenced, which indicates that the dilatory effect of magnesium, at the dosages used in the present study, is pronounced only at the arterial side of the vascular bed. The observed hemodynamic effects of the magnesium infusions may be beneficial in the setting of an acute myocardial infarction by reducing left ventricular afterload, which, together with the antiarrhythmic effect of magnesium may contribute to the positive effect of magnesium infusions on mortality in patients with acute myocardial infarction.
Three different investigations do not demonstrate that treatment with certain antidepressants is combined with an increased risk of leucopenia/agranulocytosis as compared to other antidepressants. But prospective drug monitoring studies on large numbers of patients are necessary to find an answer to this question.
The incidence of fractures of the jaws and facial bones in children is less frequent than these same fractured bones in adults. The relative low incidence of facial fractures in children can be related to certain growth factors. Details of facial trauma and associated injuries were collected in 50 patients referred from the Medical School in Hannover. The age and sex distribution, anatomical types of fractures, associated nonmaxillofacial trauma and causes of the injuries are described. Fractures of the mandible occur in greater frequency than those of the middle third of the face in children. Emphasis is placed on paediatric mandibular and condylar fractures and their treatment difference from those in adults are noted. Facial bone fractures in children have the potential of deformity due to growth disturbances. Fractures of the facial skeleton are often accompanied by associated injuries, especially fractures of the skull and intracranial injuries. Of primary importance is an early assessment of the patient's general condition and associated injuries.
We report the cAMP-dependent phosphorylation of the chemotactic receptor of Dictyostelium discoideum in partially purified plasma membranes. The protein kinase responsible for receptor phosphorylation is associated with this fraction and preferentially phosphorylates the ligand-occupied form of the receptor. 8-Azido[32P]cAMP labeling of the cell surface has shown that the cAMP receptor exists in two forms. A 45-kDa protein is predominant on unstimulated cells. cAMP stimulation results in an increased receptor phosphorylation such that the receptor migrates on NaDodSO4/PAGE as a 47-kDa protein. Phosphorylation of the chemotactic receptor is not detected in membrane preparations unless cAMP is added to the incubation mixture. Only under those conditions is the phosphorylated 47-kDa form observed. The requirement for cAMP reflects the fact that the kinase involved preferentially uses the ligand-occupied receptor as a substrate. In vitro phosphorylation of the receptor does not involve tyrosine residues. The enzyme does not appear to be a cAMP- or cGMP-dependent protein kinase nor is it sensitive to guanine nucleotides, Ca2+/calmodulin, Ca2+/phospholipid, or EGTA. Similarities with the beta-adrenergic receptor protein kinase are discussed.
Changes in membrane potential may influence Ca2+-dependent functions through changes in cytosolic free calcium concentration [( Ca2+]i). This study characterized pharmacologically those voltage-dependent Ca2+ channels in normal rat anterior pituitary cells that are involved in the elevation of [Ca2+]i upon high potassium-induced membrane depolarization. The [Ca2+]i was monitored directly by means of the intracellularly trapped fluorescent indicator fura-2. The addition of K+ (6-100 mM) increased [Ca2+]i in a concentration-dependent manner. The fluorescent signal reached a peak within seconds and then decayed to form a new elevated plateau. K+ at the highest concentration used (100 mM) raised [Ca2+]i by about 450 nM. The K+-induced increase in [Ca2+]i was absent in a Ca2+-free medium. BAY K 8644, a 1,4-dihydropyridine Ca2+ channel agonist, also caused an increase in [Ca2+]i. The maximum response in [Ca2+]i upon stimulation with BAY K 8644 (100 nM) was about 40 nM. The half-maximally effective concentration of BAY K 8644 (100 nM) was about 20 nM. The response in [Ca2+]i upon BAY K 8644-stimulation was abolished in a Ca2+-free medium. Predepolarization with various K+ concentrations enhanced the effect of BAY K 8644 (1 microM) on [Ca2+]i. Pretreatment with BAY K 8644 (1 microM) enhanced the response in [Ca2+]i induced by K+ (25 mM). The addition of Mg2+ (30 mM) and nifedipine (1 microM) lowered the resting [Ca2+]i by about 40 and 20 nM, respectively. Mg2+, nifedipine, nimodipine, Gö 5438, verapamil, and diltiazem inhibited the K+ (25 mM)-induced increase in [Ca2+]i; the order of potency (and half-maximally inhibitory concentrations) were nimodipine = Gö 5438 = nifedipine (approximately 100 nM) greater than verapamil (900 nM) greater than diltiazem (greater than 10 microM) greater than Mg2+ (6 mM). Omega-Conotoxin (100 nM) did not inhibit the K+ (25 mM)-induced increase in [Ca2+]i. These data demonstrate that, over a wide range, membrane depolarization induced by high potassium concentration is indeed associated with increases in [Ca2+]i in normal rat anterior pituitary cells. This elevation of [Ca2+]i is mainly due to an influx of Ca2+ through 1,4-dihydropyridine-sensitive, omega-conotoxin-insensitive calcium channels (L-type).
To evaluate the safety and immunogenicity of the Haemophilus influenzae type b polysaccharide vaccine, PRP, and a new polysaccharide-diphtheria toxoid conjugate vaccine, PRP-D, a collaborative study was carried out in six centers in five states. Subjects were 585 infants 15 to 24 months of age. They were randomly assigned to receive a single dose of PRP or PRP-D vaccine. There were no significant differences in the rate of adverse reactions between the two vaccine groups. Minor local reactions occurred in 10.3% of PRP and 12.5% of PRP-D recipients, and fever in 27.4% of PRP and 23.8% of PRP-D recipients. All reactions resolved within 48 hours. Serum samples were obtained just before vaccination and after 1 month. Prevaccination antibody levels were similar for the PRP (0.035 micrograms/mL) and PRP-D (0.027 micrograms/mL) groups, with no differences in levels by age, sex, race, vaccine lot, or study site. Both groups had significant rises in geometric mean levels, but this difference was significantly greater for PRP-D (2.166 micrograms/mL) than for PRP (0.154 micrograms/mL). In addition, the percentage of responders as determined by three definitions (twofold titer rise, greater than 0.15 micrograms/mL, and greater than 1.0 micrograms/mL) was also significantly greater for PRP-D than PRP. In contrast to a marked age-related immunogenicity to PRP (P less than 0.001), there was no significant variation in immune response to PRP-D by age. PRP-D conjugate vaccine appears to be as safe and significantly more immunogenic than PRP vaccine for children vaccinated at 15 to 24 months of age.
Safety and immunogenicity of a Haemophilus influenzae type b polysaccharide-diphtheria toxoid conjugate vaccine (PRP-D) was evaluated in infants seven to 14 months of age. PRP-D (80% of subjects) or saline placebo (20%) was randomly and blindly administered (two doses separated by two months). Incidence of mild reactions lasting less than 48 hr did not differ significantly between the placebo and vaccine recipients. Preimmunization levels of antibody to PRP were less than or equal to 0.15 micrograms/ml in 97% of subjects. A twofold increase in antibody concentration occurred in 88% of subjects following the first dose and in 99% following the second dose of vaccine. No change occurred in placebo recipients. Mean level of antibody and percentage of subjects with levels of antibody greater than or equal to 1 microgram/ml after vaccination increased with increasing age. Responses were related to vaccine lot but not to sex, race, or geographic location. Two doses of PRP-D in infants seven months of age and older induced antibody levels equal to or greater than levels in infants 24 months of age given the polysaccharide alone.
We have modified the reduced silver procedure of Liesegang and added a gold treatment. The technique has been successfully and routinely used to impregnate both peripheral and central nervous tissues of mice of different ages, and central nervous tissue of man. It was applied on conventionally (formalin) fixed and cryostat-cut material. In the periphery, nerves, individual axons, and sensory and motor endings stained a dark purple. In the brain, both bundles of axons and individual fine axonal branches were stained. When counterstained by a Nissl method, an excellent overall image of CNS structure is obtained.
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Chronic administration of lithium (Li+) to human subjects results in reduction of Li+/Na+ countertransport in their erythrocytes (RBC). The time course of development of inhibition is much slower than one would expect for an immediate effect of Li+ on the RBC membrane. Possible explanations include pharmacokinetic delays, a mediating humoral agent, and a slow process in the RBC. To discriminate among these possibilities, we incubated human RBC in sterile culture by the method of Freedman (Freedman, J.C. 1983. J. Membrane Biol. 75:225--231), which permits much longer incubations than other methods. As gauged by eight measures, the incubated RBC remain viable for two weeks. Small changes in intracellular concentrations with time during incubation are in the same direction as the changes associated with natural aging of RBC in vivo, except for a rise in ATP and related cation shifts during the first few days of incubation. Treatment of incubated RBC with 2 mM Li+ inhibits countertransport by 48% without affecting Li+ leak efflux. The inhibition develops slowly: it is half-maximal after 1--2 days and maximal by 4--7 days. Differences between in vivo results and our incubated cells in the time course of inhibition are as expected from the pharmacokinetic delays operating in vivo. The inhibition is reversible on removing Li+. Li+ inhibits countertransport similarly slowly and to a similar degree from inside the RBC and from outside. Hence the slow time course of inhibition in vivo is not due to a humoral factor or to the time required for intracellular Li+ accumulation and is only partly due to pharmacokinetic delays. The delay must involve an unidentified slow process at the level of the RBC.
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Procedures have been developed for the preparation of pure myosin heavy chain (h-myosin) by preparative gel electrophoresis, and for the characterization of h-myosin by cyanogen bromide peptide mapping. Major sources of error are the oxidation of methionine and the proteolytic splitting of the chain during purification. These errors have been eliminated. A peculiar feature is the doubling or quadrupling of a peptide of molecular weight 17 000. The results show structural differences between isomyosins derived from myonal types within the same animal, as well as interspecies differences.