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Biomedical subjects

H Ebel

Publications and source records attributed to H Ebel.

At least 19 recordsLinked to original sources

Spinal epidural abscess: prognostic factors and comparison of different surgical treatment strategies.

BACKGROUND: Spinal epidural abscess (SEA) is a rare but potentially devastating disease requiring immediate surgical intervention and appropriate antibiotic treatment. The standard approach to decompress SEA is laminectomy. No report covers comprehensively the indications for the less invasive interlaminar approach, the usefulness of intra-operative ultrasonography and the suspected benefit of inserting a suction-irrigation drainage. METHOD: A retrospective evaluation of the medical and radiological data was undertaken in 27 consecutive patients with SEA operated on during a period of 10 years by a dorsal approach. Factors influencing outcome were evaluated with special regard to different surgical strategies concerning the invasiveness of the operative approach, the use of intra-operative ultrasound and the use of different drainage systems. FINDINGS: Outcome was mainly determined by the pre-operative neurological condition and the localization of the abscess. Recurrence rate was dependent on the longitudinal extent of the mass and the intra-operative finding of granulation tissue, but not on the administration of a postoperative suction-irrigation drainage. An interlaminar approach was equally matched to a decompression by laminectomy in lumbar SEA concerning the incidence of residual/recurrent abscess formation. In concomitant spondylodiscitis, laminectomy bore the risk of the formation of a postoperative kyphotic deformity. The use of intra-operative ultrasound allowed the visualization of hidden inflammatory masses and, thus, reduced the rate of residual abscess formation. CONCLUSION: An interlaminar approach should be considered instead of laminectomy in lumbar SEA and in impending anterior column instability due to spondylitis. Intra-operative ultrasound is a beneficial aid for the determination of the extent of decompression during surgery and is practicable even through a narrow interlaminar bony window. The insertion of postoperative suction-irrigation drainage had no beneficial effect on outcome but bore the risk of epidural fluid congestion.

Adolescent↗

Na+/Mg2+ antiport in erythrocytes of spontaneously hypertensive rats: role of Mg2+ in the pathogenesis of hypertension.

Total Mg2+ content in plasma and erythrocytes did not significantly differ between WKY and SHR. Mg2+ efflux via Na+/Mg2+ antiport was 10% lower in non Mg(2+)-loaded erythrocytes of SHR than in WKY, and 16% lower in Mg(2+)-loaded erythrocytes of SHR. The activation of Na+/Mg2+ antiport in erythrocytes by Cl-, as tested by substitution of Cl- with SCN-, and the regulation of Na+/Mg2+ antiport by protein kinases, as tested by PMA and staurosporine, showed no differences between WKY and SHR. The reduction of Na+/Mg2+ antiport was explained by a reduction in the number of Na+/Mg2+ antiporter molecules in SHR erythrocytes. Mg2+ efflux in KCl medium by K+/Mg2+ antiport via the unspecific choline exchanger was not significantly reduced in SHR and was equally affected by PMA and staurosporine in WKY and SHR. An explanation for some controversial results, unchanged or reduced concentration of Mg2+ in serum, total Mg2+ and free Mg2+ in erythrocytes of SHR and patients with essential hypertension was proposed. The role of Na+/Mg2+ antiport and [Mg2+]i in the pathogenesis of experimental and clinical hypertension was discussed.

Animals↗

Differential effect of imipramine and related compounds on Mg2+ efflux from rat erythrocytes.

The effect of imipramine on Mg2+ efflux in NaCl medium (Na+/Mg2+ antiport), on Mg2+ efflux in choline.Cl medium (choline/Mg2+ antiport) and on Mg2+ efflux in sucrose medium (Cl- -coupled Mg2+ efflux) was investigated in rat erythrocytes. In non-Mg2+-loaded rat erythrocytes, imipramine stimulated Na+/Mg2+ antiport but inhibited choline/Mg2+ antiport and Cl- -coupled Mg2+ efflux. The same effect could be obtained by several other compounds structurally related to imipramine. These drugs contain a cyclic hydrophobic ring structure to which a four-membered secondary or tertiary amine side chain is attached. At a physiological pH, the amine side chain expresses a cationic choline-like structure. The inhibitory effect on choline/Mg2+ antiport is lost when the amine side chain is modified or abandoned, pointing to competition of the choline-like side chain with choline or another cation at the unspecific choline antiporter or at the Cl- -coupled Mg2+ efflux. Other related drugs either stimulated Na+/Mg2+ antiport and choline/Mg2+ antiport, or they were ineffective. For stimulation of Na+/Mg2+ antiport and choline/Mg2+ antiport, there is no specific common structural motif of the drugs tested. The effects of imipramine on Na+/Mg2+ antiport and choline/Mg2+ antiport are not mediated by PKCalpha but are caused by a direct reaction of imipramine with these transporters. By increasing the intracellular Mg2+ concentration, the stimulation of Na+/Mg2+ antiport at a physiological intracellular Mg2+ concentration changed to an inhibition of Na+/Mg2+ antiport. This effect can be explained by the hypothesis that Mg2+ loading induced an allosteric transition of the Mg2+/Mg2+ exchanger with low Na+/Mg2+ antiport capacity to the Na+/Mg2+ antiporter with high Na+/Mg2+ antiport capacity. Both forms of the Mg2+ exchanger may be differently affected by imipramine.

Animals↗

Regulation of Na+/Mg2+ antiport in rat erythrocytes.

In rat erythrocytes, the regulation of Na+/Mg2+ antiport by protein kinases (PKs), protein phosphatases (PPs), intracellular Mg2+, ATP and Cl- was investigated. In untreated erythrocytes, Na+/Mg2+ antiport was slightly inhibited by the PK inhibitor staurosporine, slightly stimulated by the PP inhibitor calyculin A and strongly stimulated by vanadate. PMA stimulated Na+/Mg2+ antiport. This effect was completely inhibited by staurosporine and partially inhibited by the PKC inhibitors Ro-31-8425 and BIM I. Participation of other PKs such as PKA, the MAPK cascade, PTK, CK I, CK II, CAM II-K, PI 3-K, and MLCK was excluded by use of inhibitors. Na+/Mg2+ antiport in rat erythrocytes can thus be stimulated by PKCalpha. In non-Mg2+ -loaded erythrocytes, ATP depletion reduced Mg2+ efflux and PMA stimulation in NaCl medium. A drastic activation of Na+/Mg2+ antiport was induced by Mg2+ loading which was not further stimulated by PMA. Staurosporine, Ro-31-8425, BIM I and calyculin A did not inhibit Na+/Mg2+ antiport of Mg2+ -loaded cells. Obviously, at high [Mg2+]i Na+/Mg2+ antiport is maximally stimulated. PKCalpha or PPs are not involved in stimulation by intracellular Mg2+. ATP depletion of Mg2+ -loaded erythrocytes reduced Mg2+ efflux and the affinity of Mg2+ binding sites of the Na+/Mg2+ antiporter to Mg2+. In non-Mg2+ -loaded erythrocytes Na+/Mg2+ antiport essentially depends on Cl-. Mg2+ -loaded erythrocytes were less sensitive to the activation of Na+/Mg2+ antiport by [Cl-]i.

Animals↗

Effect of mycophenolate mofetil on kidney graft function and body weight in patients with chronic allograft nephropathy.

BACKGROUND: Chronic allograft nephropathy (CAN) is the most common cause of late graft loss. A beneficial effect of mycophenolate mofetil (MMF) on CAN was observed, although, due to the loss of body weight (BW) under MMF, serum creatinine (sCr) and reciprocal sCr may be unsuitable markers of graft function. METHODS: In 17 kidney transplant patients with CAN, azathioprine (Aza) was replaced by MMF. The remaining therapy was not changed; specifically, the cyclosporine (CsA) dose was not decreased. The mean values and regression coefficients of reciprocal sCr, CCr, urinary creatinine excretion (uCr x V), proteinuria, BW, blood pressure (BP), serum cholesterol (sChol), and serum triglycerides (sTG) versus time were analyzed 12 months before and after institution of MMF by a paired-comparison t test. RESULTS: The mean regression coefficient of reciprocal sCr differed significantly before and after conversion to MMF (mean -0.01 +/- 0.01 vs +0.012 +/- 0.029 mg/dL per month), suggesting improved graft function. However, the mean values of BW (74 +/- 15 vs 71 +/- 15 kg, P <.001) and uCr x V (1152 +/- 321 vs 1065 +/- 266 mg per 24 hours, P=.0897) decreased, making the increase in CCr less significant (mean -1.16 +/- 2.69 vs 0.40 +/- 1.79 mL/min per month, P <.05). BP, sChol, sTG, and proteinuria before and after conversion did not differ significantly. Among patients with long-term stable graft function at 36.5 +/- 16.9 months after conversion to MMF there was an almost significant improvement in renal protein excretion. CONCLUSIONS: MMF improved graft function, although this effect was overestimated using reciprocal sCr. Other risk factors, such as BP, sChol, and sTG, showed no significant differences, suggesting that MMF accounted for the improvement in CAN. The course of proteinuria under MMF seems to be of prognostic significance.

Albuminuria↗

Stimulation of Na+/Mg2+ antiport in rat erythrocytes by intracellular Cl-.

Mg(2+) efflux from rat erythrocytes was measured in NaCl, NaNO(3), NaSCN and Na gluconate medium. Substitution of extracellular and intracellular Cl(-) with the permeant anions NO(3)(-) and SCN(-) reduced Mg(2+) efflux via Na(+)/Mg(2+) antiport. After substitution of extracellular Cl(-) with the non-permeant anion gluconate, Mg(2+) efflux was not significantly reduced. In Na gluconate medium, an influence of the changed membrane potential and intracellular pH on Mg(2+) efflux could be excluded. The results indicate the existence of Cl(-)-independent Na(+)/Mg(2+) antiport and of Na(+)/Mg(2+) antiport stimulated by intracellular Cl(-). Intracellular Cl(-), as determined by means of (36)Cl(-), was found to stimulate Na(+)/Mg(2+) antiport through a cooperative effect according to a sigmoidal kinetics. The Hill coefficient for intracellular Cl(-) amounted to 1.4-1.8, indicating that two intracellular Cl(-) may be simultaneously active. With respect to specificity, Cl(-) was most effective, followed by Br(-), J(-), and F(-). Stimulation of Na(+)/Mg(2+) antiport by intracellular Cl(-) together with intracellular Mg(2+) may play a role during deoxygenation of erythrocytes and in essential hypertension.

Animals↗

[Organic schizophreniform disorder with pre-existing autoimmune thyroiditis].

We report the case of a 63-year-old patient with sudden onset of an acute syndrome of auditory hallucinations and delusions. Considering the anamnesis, course of the illness, and organopathologic results, we assumed an organic schizophreniform disorder within the scope of pre-existing autoimmune thyroiditis. Under treatment with high-potency neuroleptics, we observed partial regression and, after strumectomy, complete regression of the psychotic symptoms. Apparently, the acute organic schizophreniform disorder was caused by a changed metabolic situation with a transition to hyperthyroidism coinciding with beginning a small dose of antithyroid drugs.

Antipsychotic Agents↗

Acute demyelination: diagnostic difficulties and the need for brain biopsy.

BACKGROUND: Despite the rapid development in neuro-imaging over the past two decades, ring like contrast-enhancing lesions on CCT or MRI still may pose a diagnostic challenge. The main differential diagnoses of these lesions include metastatic carcinoma, high-grade glioma and brain abscess. Acute demyelination seldom turns out to be the underlying pathology. METHOD: Retrospective analysis was done on six patients with acute demyelination treated at our neurosurgical department between 1990 and 2001. Clinical, radiological, PET, intra-operative and histological findings were evaluated. FINDINGS: In five patients, the diagnosis of acute demyelination was established by histopathological evaluation of stereotactic biopsy specimen, in the sixth patient following microsurgical extirpation of the lesion. Neuropathology revealed demyelination with the presence of myelin-phagocytosing macrophages. In addition, lymphocytic infiltrates were present. Symptoms and signs improved significantly after high-dose steroid therapy. CONCLUSIONS: Despite CNS tissue destruction, necrosis and cyst formation are not usually found in demyelinating disease, being rather more common in young patients with ring-like contrast-enhancing lesions on CCT and MRI. Though an incorrect diagnosis can lead to a potentially fatal therapeutic intervention, histological diagnosis should be made in all cases. Due to minimum morbidity, stereotactic biopsy is the method of choice to obtain representative specimens for histological diagnosis. Open microsurgery of these lesions is not indicated since conservative medical treatment with steroids results in a favourable outcome in most cases.

Acute Disease↗

Are syndromes in environmental medicine variants of somatoform disorders?

To date, relatively little is known about the etiology, pathophysiology, diagnosis, therapy, prevention and prognosis of environment-related syndromes like multiple chemical sensitivity (MCS), idiopathic environmental intolerance (IEI), sick building syndrome (SBS), chronic fatigue syndrome (CFS), candida syndrome (CS) and burnout syndrome (BS). Part of the reason is that these syndromes have not been clearly defined and classified in scientific categories distinct from each other, and that they show clinical similarities to classified somatoform disorders. Furthermore, there are at least three possible explanations for the existence of these syndromes: (1) The syndromes may result from the interaction of environmental factors, individual susceptibility and psychological factors (i.e., how they are perceived and seen by the patient); (2) they may reflect socially and culturally accepted methods of expressing distress; and/or (3) they may be iatrogenic. Despite all the uncertainties in evaluation of environmental syndromes, physicians have the duty to take the affected person's problems seriously. A comprehensive systematic classification which better accounts for these complex clinical manifestations is long overdue. Until these syndromes are well defined, the terms used for them should definitely not be applied to connote a specific disease process.

Environment↗

Influence of TachoComb in comparison to local hemostyptic agents on epidural fibrosis in a rat laminectomy model.

This animal experimental study was designed to examine the effects of TachoComb, a fixed combination of collagen with tissue adhesive, as an interposition membrane on the development of spinal epidural fibrosis in comparison to other hemostyptic materials. In 10 Wistar rats, four laminectomies were performed at lumbar and sacral vertebrae. Alternately, a piece of TachoComb, Spongostan, or Tabotamp was placed into each laminectomy site. One laminectomy site served as an empty control (n = 10). 8 weeks later, the animals were sacrificed, and the spinal column including surrounding muscle tissue was removed en bloc from each rat and fixed in formaldehyde. After decalcification and staining the specimens were graded by a neuropathologist in a blindfold test for severity of epidural fibrosis as "light-moderate" or "marked". Epidural scarring of variable density was seen in all laminectomy sites. Light epidural fibrosis, without any adhesion to dura, as only noted in cases after application of TachoComb (n = 4/10) and Spongostan (n = 1/10). All other slices showed marked epidural fibrosis with dura adherence regardless of the implanted material. Statistical analysis revealed significantly lower epidural fibrosis after application of TachoComb compared to all other groups (p < 0.05). In this series, TachoComb is more effective in reducing the epidural fibrosis than Spongostan, and Tabotamp. However, complete prevention of scar tissue formation was not achieved.

Animals↗

Role of the choline exchanger in Na(+)-independent Mg(2+) efflux from rat erythrocytes.

Two types of Na(+)-independent Mg(2+) efflux exist in erythrocytes: (1) Mg(2+) efflux in sucrose medium and (2) Mg(2+) efflux in high Cl(-) media such as KCl-, LiCl- or choline Cl-medium. The mechanism of Na(+)-independent Mg(2+) efflux in choline Cl medium was investigated in this study. Non-selective transport by the following transport mechanisms has been excluded: K(+),Cl(-)- and Na(+),K(+),Cl(-)-symport, Na(+)/H(+)-, Na(+)/Mg(2+)-, Na(+)/Ca(2+)- and K(+)(Na(+))/H(+) antiport, Ca(2+)-activated K(+) channel and Mg(2+) leak flux. We suggest that, in choline Cl medium, Na(+)-independent Mg(2+) efflux can be performed by non-selective transport via the choline exchanger. This was supported through inhibition of Mg(2+) efflux by hemicholinum-3 (HC-3), dodecyltrimethylammonium bromide (DoTMA) and cinchona alkaloids, which are inhibitors of the choline exchanger. Increasing concentrations of HC-3 inhibited the efflux of choline and efflux of Mg(2+) to the same degree. The K(d) value for inhibition of [(14)C]choline efflux and for inhibition of Mg(2+) efflux by HC-3 were the same within the experimental error. Inhibition of choline efflux and of Mg(2+) efflux in choline medium occurred as follows: quinine>cinchonine>HC-3>DoTMA. Mg(2+) efflux was reduced to the same degree by these inhibitors as was the [(14)C]choline efflux.

Animals↗

[Subdural empyema and cerebritis as a sequela of dentogenous suppurative pansinusitis].

BACKGROUND: Complications and local extension of dentogenous and paranasal sinus infections most often involve the periorbit and frontal cranium. Because of the widespread use of antibiotics, intracranial extension of maxillofacial sinusitis is rarely seen today. Nevertheless, the clinician must be aware of the potential for these complications, because late recognition of this condition and delay in treatment can increase morbidity and mortality rates. CASE REPORT: A case report of sinogenic intracranial complications is presented, with sinogenic empyema, cerebritis, and subdural empyema. The mechanisms and potential for intracranial spread of infection from the frontal, sphenoid, and ethmoid sinuses are discussed. The management of complications is outlined, including the use of computed tomography and the role of surgical drainage.

Actinobacillus Infections↗

[Obligatory and facultative symptoms of the Alice in wonderland syndrome].

The Alice in Wonderland syndrome (AIWS), as described by Todd in 1955, denotes a variety of self-experienced paroxysmal body schema disturbances (obligatory core symptoms of the AIWS) which may co-occur with depersonalization, derealization, visual illusions and disorders of the time perception (facultative symptoms of the AIWS). The name comes, of course, from Lewis Carroll's 1865 novel "Alice's Adventures in Wonderland", which is believed to have been inspired by Carroll's own migraine experiences documented as early as 1856. Recent studies of the AIWS occurring as somesthetic migraine aura indicated that the body schema disturbance of macrosomatognosia most frequently affects the head and upper extremities, paralleling the extension of their representation in the human brain. As a misapprehension commonly encountered in the medical literature, it has been suggested to define the AIWS by the presence of visual rather than somesthetic perceptual disturbances, e.g. metamorphopsia and/or visual hallucinations, but this change and broadening of Todd's definition of the AIWS turns it to a both scientifically and clinically useless concept.

Hallucinations↗

World Wide Web scaling exponent from Simon's 1955 model.

The statistical properties of the World Wide Web have attracted considerable attention recently since self-similar regimes were first observed in the scaling of its link structure. One characteristic quantity is the number of (in-)links k that point to a particular web page. Its probability distribution P(k) shows a pronounced power-law scaling P(k) approximately k(-gamma) that is not readily explained by standard random graph theory. Here, we recall a simple and elegant model for scaling phenomena in general copy- and growth-processes as proposed by Simon in 1955. When combined with an experimental measurement of network growth in the World Wide Web, this classical model is able to model the in-link dynamics and predicts the scaling exponent gamma=2.1 in accordance with observation.

Journal Article↗

[Syndromes in environmental medicine: variants of somatoform disorders].

Concerning the syndromes in environmental medicine, like Multiple Chemical Sensitivities (MCS), Idiopathic Environmental Intolerances (IEI), Sick Building Syndrome (SBS), Chronic Fatigue Syndrome (CFS), Candida Syndrome (CS), and Burnout Syndrome (BS), scientific knowledge in etiology, pathology, pathophysiology, diagnosis, therapy, prevention and prognosis is still lacking until now. A critical comparison shows that it is still impossible to find a scientifically satisfying delimitation. Syndromes in environmental medicine show clinical similarities to somatoform disorders. Furthermore, there are the following possible explanations for the existence of these syndromes: Firstly, they may be a complex interaction of environmental impacts, individual predispositions, psychological influences, as well as processes of mental perception and interpretation. Secondly, they may be an effect of distress influenced by culture and social structures and/or thirdly, they may be an latrogenic determination. A more comprehensive characterisation which better considers the complex clinical manifestations is overdue. Although there are neither scientifically validated procedures for diagnosis or therapy nor prophylactic measures, a hardly comprehensible number of partly unvalidated methods is in practical use. Until the syndromes are not finally defined the terms for the syndromes should not be applied to a certain disease. Despite all uncertainities in the evaluation of syndromes in environmental medicine, physicians have the duty to take the affected persons' problems seriously.

Environmental Medicine↗

Effects of electrical stimulation of the Gasserian ganglion on regional cerebral blood flow after induced subarachnoid hemorrhage in pigs evaluated by 99mTc-HMPAO-SPECT.

It could be demonstrated that cervical spinal cord stimulation increases cerebral blood flow. The effects of electrical stimulation of the trigeminal ganglion in the acute phase of SAH in pigs were investigated. The experiments were carried out on 11 domestic pigs divided in two groups (group I: SAH [n = 5]; group II: SAH and trigeminal stimulation [n = 6]). In all animals a native SPECT was performed. The Gasserian ganglion was exposed for inserting the stimulation electrode. SAH was induced by injecting 10 ml autologous blood through a catheter placed in the suprasellar cistern. 30 minutes after SAH-induction electrical stimulation was started for two hours in group II (2.8-4.5 V, 50 Hz, 300 microseconds). 99mTc-HMPAO (400-540 MBq) was injected intravenously 110 minutes later. In group I 99mTc-HMPAO was applied after the same time interval. 80 minutes later SPECT was performed. Data were processed to calculate the uptake of radioactivity (%/kg tissue weight). The mean values were calculated for the different groups: native animal examination (%/kg tissue weight): 0.6343; group I: 0.468; group II: 0.6533. Comparing the mean values a highly significant difference between group I and group II (p < 0.01) and between native examination and group I (p < 0.01) could be found. No statistical significance could be detected on comparing the left/right-ratio in any ROI. The electrical stimulation of the Gasserian ganglion leads to a significantly increased uptake of 99mTc-HMPAO after induced SAH. Maybe the stimulation of the Gasserian ganglion constitutes a new therapeutic modality treating disturbed rCBF after SAH.

Animals↗