[Properties, effects, indications and contra-indications of toothpastes].
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Biomedical subjects
Publications and source records attributed to H Schmidt.
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An eleven-year-old boy with congenital paresis of the left superior rectus eye muscle developed symptoms of acute left orbital expansion: pain, ptosis, redness, extraocular muscle dysfunction. Computer assisted tomography of the orbit showed typical signs of inflammatory orbital pseudotumor and immunological screening cryoglobulinemia. Short-term treatment with prednisone (2 mg/kg bodyweight/day) rapidly improved symptoms. However several relapses occurred following discontinuation of therapy. Therefore a long-term treatment with corticosteroids was instituted. The simultaneous development of inflammatory orbital pseudotumor and cryoglobulinemia support the hypothesis that orbital pseudotumor is an autoimmune disease. The meaning of the congenital superior rectus muscle paresis in this case for the development of the inflammatory process remains uncertain.
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In 20 juvenile diabetic inpatients the relationship between nocturnal hypoglycemia and overnight urinary cortisol excretion was studied. Cortisol was expressed as absolute quantity per kg body weight because the cortisol/creatinine ratio does not always yield reliable results in diabetic patients. Comparison between different patients yielded no significant difference between posthypoglycemic and non-posthypoglycemic cortisol values. Testing the difference between urinary cortisol excretion in posthypoglycemic and non-posthypoglycemic urine samples for every one of the patients intraindividually, however, a significant posthypoglycemic elevation was found. Posthypoglycemic cortisol response was irregular and variable not only in different patients, but also within the same patient. If a high excretion of cortisol is found in an overnight urine sample, it is very likely to be caused by nocturnal hypoglycemia. On the other hand it is impossible to exclude nocturnal hypoglycemia by normal urinary cortisol findings. Reactive hyperglycemia as described by Somogyi was seen only rarely in this study. It is concluded that even if a distortion by falsely high creatinine measurements in diabetics is ruled out, cortisol measurement in overnight urine samples cannot be used as easy routine method for the detection of nocturnal hypoglycemia.
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1,3,7-Trimethylxanthine "caffeine" (CAF) is reported to induce a differential effect on the cytotoxicity of the DNA intercalators actinomycin-D versus Adriamycin (ADR). In the present study the effect of caffeine and/or trifluoperazine in modulating cell cycle traverse, drug accumulation, and cytotoxicity of anthracyclines was evaluated. The survival in soft agar of P388 mouse leukemia cells treated with ADR (0.05-0.25 micrograms/ml) alone for 1 h was 1.2- to 3-fold lower when the cells were incubated for 24 h in drug-free medium versus medium supplemented with 2 mM CAF. In contrast, for P388 cells treated with ADR in the presence of 2 mM CAF for 1 h and subsequently incubated for 24 h in the absence or presence of 2 mM CAF, cell killed based on colony formation in soft agar was 2- to 20-fold lower than in ADR-treated cells never exposed to 2 mM CAF. In cells treated continuously for 24 h with ADR (0.01-0.05 micrograms/ml) or the DNA nonbinding ADR analogue N-trifluoro-acetyladriamycin-14-valerate (AD32) (0.05 and 0.1 micrograms/ml) the survival in soft agar was 3- to 20-fold higher in the presence versus the absence of 2 mM CAF. The decreased cytotoxicity in cells treated with ADR or AD32 in the presence of CAF was accompanied by a significant reduction in the accumulation of cells in G2. However, in cells treated with ADR or AD32 in the presence of 2 mM CAF plus 5 microM trifluoperazine the decreased G2 accumulation was not accompanied by a reduction in anthracycline cytotoxicity. The modulation by CAF of ADR and AD32 cytotoxicity did not correlate with decreased cellular ADR and AD32 accumulation. Results from this study indicate that CAF markedly reduces the cytotoxicity of ADR or AD32 and trifluoperazine circumvents the effects of CAF.
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Doxorubicin-resistant P388 mouse leukemia cells are cross-resistant to anthracycline and non-anthracycline DNA intercalators as well as to natural and semisynthetic anthracyclines which bind weakly or not at all to DNA. In the presence of a non-lethal concentration of 5 microM trifluoperazine cytotoxic effects of the strong DNA binding drugs actinomycin-D, mitoxantrone and m-AMSA were enhanced less than 2 fold in doxorubicin-sensitive cells and up to 50 fold in doxorubicin-resistant cells. Additionally, trifluoperazine induced a greater than 2-fold enhancement in the cytotoxic effects (but not accumulation and retention) of the strong DNA binder N,N-dimethyladriamycin-14-valerate only in doxorubicin resistant cells. In contrast, cell kill, drug accumulation and retention in P388/S and P388/DOX cells treated with the weak DNA binders N-benzyl-adriamycin-14-valerate and 7(R)-O-methylnogarol, and DNA-nonbinding N,N-dibenzyldaunorubicin was similar with or without trifluoperazine treatment. The study demonstrates that the calmodulin inhibitor trifluoperazine induces a specific and marked enhancement in the cytotoxic effects of strong vs weak DNA binding antitumor drugs in doxorubicin-resistant cells.
It is reported of acute beta-blocker intoxications in 34 patients (16 with talinolol, 18 with propranolol ingestion). The mean ingestion dose was for talinolol 2.5 g, for propranolol 1.55 g, the mean time of latency up to the appearance of intoxication symptoms 116 min after intake of talinolol, 79 min after intake of propranolol. The picture of intoxication was characterized in the two substances by the antiadrenergic effects, there was no more a cardioselectivity in the high ingestion doses. In talinolol were in the first place dysrhythmias, hypotension and vomiting and nausea, respectively, in propranolol central-nervous symptoms and hypotension. Substance-specific intoxication symptoms are also possible. In mixed intoxications alcohol accelerated the beginning of the effect, sedatives prolonged the latency. Threatening of life is to be expected in ingestion doses over 2 g. In 6 patients the course was lethal after extreme doses of talinolol - according to the present experiences due to the too late beginning of therapy and/or insufficient intensity of therapy. Distinct intoxication symptoms need extremely high applications of antidotes of beta-stimulants, in their inffectiveness glucagon. Furthermore, treatment with cardiac pacemakers and 24-hour control in an intensive care unit proved necessary.
220 consecutive patients with acquired valvular defects were checked within the preoperative examination by means of heart catheter with regard to significant coronary stenoses. In these cases a relative frequency of typical and atypical angina pectoris troubles of 0.136 and 0.459, respectively, was the result. In contrast to this significant coronary stenoses could relatively infrequently made evident angiographically: 6/220 (= 0.027). In patients with valvular defects angina pectoris cannot be used as the leading symptom of an additionally existing coronary heart disease on account of bad sensitiveness.
Whipple's disease is a curious disorder with the involvement of many organ systems, primarily gut, synovium and the central nervous system, characterized by the presence of numerous proliferating bacteria in tissue macrophages and other cell types. While clinically this disease entity has previously been defined by the classical triad of diarrhoea, malabsorption and weight loss, some patients do not show these features. In this report, a clinically unusual case of Whipple's disease is described presenting with high persistent fever, severe arthralgias and headaches, but without malabsorption, diarrhoea or weight loss. Nevertheless, the histological and electron microscopical pictures demonstrated the typical findings of intracellular micro-organisms along with the presence of bacteria in Schwann nerve cells, which has only once been described previously. Immunological findings before treatment demonstrated a decrease of T cells with the helper/inducer phenotype, and a concomitant rise in cells with the suppressor/cytotoxic phenotype, an elevation of "activated" Ia positive T cells and a significant reduction of T cell mitogenic responsiveness. Of special interest, after a successful treatment these immunological abnormalities shifted to normal with the exception of a still elevated number of Ia+ T cells. The discussion of this unusual case of Whipple's disease includes - besides possible cellular immunological abnormalities - genetic factors, especially since this patient was HLA-B-27-positive as was his son who is suffering from ankylosing spondylitis.
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Iliofibularis muscles of Rana temporaria were minced and allowed to regenerate in the iliofibularis or the sartorius bed of the same frog. Regenerated muscles were examined for the presence of slow muscle fibers using electrophysiologic, histochemical, and contractile parameters. Muscle regeneration from sartorius mince was also studied. Regeneration was more successful from iliofibularis than from sartorius mince, and the iliofibularis bed was more favorable for regeneration than the sartorius bed for both types of muscle. Twitch fibers regenerated within a few months, but slow fibers could not be identified earlier than 14 months after muscle destruction. Slow muscle fibers regenerated only from iliofibularis mince, both orthotopically and heterotopically. All regenerates capable of maintaining a K-contracture contained histochemically identified slow fibers; the membrane properties of electrophysiologically identified slow fibers were normal. It is concluded that slow muscle fibers regenerate only from the remnants of a muscle that contains slow fibers. The results are discussed with respect to the role of innervating nerve fibers.
Seventeen measuring parameters were used to characterize 197 mandibles (109 males, 88 females) taken from the corpses of people 20-80 years of age from the Rhine-Main-Neckar area. The representative measuring parameters and discriminating functions of intact lower jaws and lower jaw fragments of most frequent fracture types were determined in this practice group by means of discriminating analysis. In the present research material it was possible to determine sex accurately from an intact lower jaw bone in 82.6% (m) and 79.5% (f) of the cases. Furthermore, our results show clearly that sex may even be determined from lower jaw fragments. The classification was correct, depending on the type of fragment, in 72.5%-81.7% (m) and 71.6%-79.5% (f) of the cases.
Small bundles of muscle fibres were isolated from diaphragm, extensor digitorum longus (EDL) and soleus (SOL) muscles of normal and dystrophic (C57 BL/6J dy2J/dy2J) mice, and their isometric tension developed in response to acetylcholine (ACh) was recorded. For each type of muscle the relationship between the maximum amplitude of the ACh-contracture and log [ACh] was similar in normal and dystrophic animals. However, this relationship was steeper for normal and dystrophic SOL than for EDL and diaphragm muscles. Dystrophy did not induce changes in the time course of the ACh-contractures, except a significant 'speeding' of dystrophic SOL that appeared in the time to peak of the contractile response. The amplitude of ACh-contractures of both normal and dystrophic diaphragm preparations increased by about 50% after perfusion for 80-90 min in physiological solution containing phospholipase C 5 mU/ml. ACh-sensitivity was measured in normal and dystrophic diaphragm preparations by iontophoretic application of ACh from high resistance pipettes. ACh-potentials were similar in time course in the two types of muscle fibres, and there was also no significant difference in the length of sensitive fibre segments and maximum sensitivity values. Extrajunctional ACh-sensitivity was absent in normal as well as in dystrophic fibres. It is concluded that the absence in dystrophic muscles of stronger ACh-contractures and of extrajunctional sensitivity can be considered as evidence against a primary neuronal involvement in murine dystrophy of the dy2J strain.
The used hormone prednisolone bisuccinate causes in the concentration range of 2-1,000 micrograms/ml visible changes of the cell morphology and enzymatic activity in all leukocytes. These alterations appear immediately after the application of the glucocorticoid and remain nearly constant during the time of investigation (1 h). The changes in the cell morphology and the loss of enzymatic activity increase with enhanced hormone concentration. The following reproducible morphological changes caused by the hormone comprise swelling, vacuolization and deformation of the nuclei with concomitant release of nuclei material. In addition, cloverleaf and fircone-like structures originate in connection with the formation of small bubbles.