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Biomedical subjects

C Sommer

Publications and source records attributed to C Sommer.

At least 73 records · Page 4Linked to original sources
PubMed2000

Improperly placed anterior cruciate ligament grafts: correlation between radiological parameters and clinical results.

Despite increasing knowledge on knee biomechanics and refined operative techniques, an increasing number of patients are being seen with failed anterior cruciate ligament (ACL) reconstruction. Failure of the reconstruction and further damage to the knee are correlated with improper placement of the graft, which interferes with graft biology and biomechanical demands. Between 1994 and 1995, 63 patients with improperly placed ACL grafts were referred to our institution because of persistent knee instability and pain. A method for analysis of the femoral drill hole on radiography was developed. Before reoperation the radiograph was evaluated by our method, noting the clinical aspects according to the recommendations of the International Knee Documentation Committee (IKDC). The femoral placement of the ACL graft could easily be defined on the lateral and anteroposterior tunnel radiography. The most common error was a femoral placement anterior to the anatomical insertion of the ACL. A significant correlation (P < 0.05) was found between femoral placement of the graft in the sagittal plane and clinical results: the IKDC score declined with increasing distance of the graft from the most isometric bundle of the ACL in the anteroposterior direction.

Activities of Daily Living↗
PubMed2000

Hyperparathyroidism in a patient with proximal myotonic myopathy (PROMM).

We describe a 60-year-old woman with progressive proximal leg weakness and dystrophic changes of the quadriceps and the adductor muscles on magnetic resonance imaging. She also suffered from primary hyperparathyroidism. A biopsy of the left deltoid muscle showed vacuoles as an unusual histopathological finding.

Adenosine Triphosphatases↗
PubMed2000

[A typical snowboarding injury--fracture of the processus lateralis tali].

Before the development of the snowboard sport, the fracture of the lateral process of the talus was a very rare injury. Since the increasing popularity of snowboarding, starting in Europe at about 1980, these fractures occurred more frequently. The largest epidemiological serie from Kirkpatrick in 1998 reports an incidence of 2.3% of all snowboarding injuries representing 15% of all snowboarding ankle injuries [1]. The common mechanism for fracture is dorsiflexion of the ankle and inversion of the hindfoot. Early diagnosis is emphasized in all series reviewed in the literature to prevent long-term complications [4]. Because routine radiographs failed to determine either the size or comminution of the fractured process, CT imaging was used to accurately assess the size, displacement, and comminution of the fractured process. CT scans also showed the extent of subtalar joint involvement, any associated tendon pathology, or additional fractures [5]. Many of these fractures are not visible on plain radiographs and require computed tomography imaging to be diagnosed. Diagnosis of this fracture pattern is paramount; the physician should be very suspicious of anterolateral ankle pain in the snowboarder, where subtle fractures that may require surgical intervention can be confused with anterior talofibular ligament sprains [1]. Most authors agree, that nondisplaced fractures are best treated with cast immobilization and that displaced fractures require a surgical treatment: Single large displaced fragments are reduced and internally fixed, small displaced or comminuted fragments may need surgical excision. After two to three days bedrest with elevated leg, ambulation is started under partial weight bearing of 10-15 kg for 6 weeks. Physicians caring for snowboarders should look specifically for fracture of the lateral process of the talus in a snowboarder with a lateral ankle or foot injury [3]. This fracture can mimic a lateral ankle sprain, yet the fracture is easily missed on plain radiographs of the ankle. Because displaced or comminuted fractures can cause long-term disability, primary care physicians and specialists alike need to be aware of the association of this fracture with snowboarding [3].

Athletic Injuries↗
PubMed2000

Size, flexibility, and scattering functions of semiflexible polyelectrolytes with excluded volume effects: monte carlo simulations and neutron scattering experiments

We present a systematic Monte Carlo study of the scattering function S(q) of semiflexible polyelectrolytes at infinite dilution, in solutions with different concentrations of added salt. In the spirit of a theoretical description of polyelectrolytes in terms of the equivalent parameters, namely, persistence length and excluded volume interactions, we used a modified wormlike chain model, in which the monomers are represented by charged hard spheres placed at distance a. The electrostatic interactions are approximated by a Debye-Huckel potential. We show that the scattering function is quantitatively described by that of uncharged wormlike chains with excluded volume effects provided that an electrostatic contribution is added to the persistence length. In addition we have studied the expansion of the radius of gyration and of the end-to-end distance. The results are in agreement with the picture outlined in the Odijk-Skolnick-Fixman theory, in which the behavior of charged polymers is described only in terms of increasing local rigidity and excluded volume effects. Moreover, the Monte Carlo data are found to be in very good agreement with experimental scattering measurements with equilibrium polyelectrolytes, i.e., giant wormlike micelles formed in mixtures of nonionic and ionic surfactants in dilute aqueous solution, with added salt.

Journal Article↗
PubMed2000

Intravenous brain-derived neurotrophic factor reduces infarct size and counterregulates Bax and Bcl-2 expression after temporary focal cerebral ischemia.

BACKGROUND AND PURPOSE: Pretreatment with intraventricular brain-derived neurotrophic factor (BDNF) reduces ischemic damage after focal cerebral ischemia. In this experiment we studied the effect of intravenous BDNF delivered after focal cerebral ischemia on neurological outcome, infarct size, and expression of proapoptotic and antiapoptotic proteins Bax and Bcl-2, respectively. METHODS: With the use of the suture occlusion technique, the right middle cerebral artery in rats was temporarily occluded for 2 hours. Thirty minutes after vessel occlusion, BDNF (300 microg/kg per hour in vehicle; n=12) or vehicle alone (n=13) was continuously infused intravenously for 3 hours. After 24 hours the animals were weighed and neurologically assessed on a 5-point scale. The animals were then killed, and brains underwent either 2,3,5-triphenyltetrazolium chloride staining for assessment of infarct volume or paraffin embedding for morphology and immunohistochemistry (Bax, Bcl-2). RESULTS: Physiological parameters (mean arterial blood pressure, PO(2), PCO(2), pH, body temperature, glucose) and weight revealed no difference between groups. Neurological deficit was improved in BDNF-treated animals versus controls (P:<0.05, unpaired, 2-tailed t test). Mean+/-SD infarct volume was 229.7+/-97.7 mm(3) in controls and 121.3+/-80.2 mm(3) in BDNF-treated animals (P:<0.05, unpaired, 2-tailed t test). Cortical infarct volume was 155.5+/-78.5 mm(3) in the placebo group and 69.9+/-50.2 mm(3) in the BDNF-treated group (P:<0.05, unpaired, 2-tailed t test). Subcortical infarct volume was 74.1+/-30.6 mm(3) in the placebo group and 51.1+/-26.8 mm(3) in the BDNF-treated group (P:=NS). Bax-positive neurons were significantly reduced in the ischemic penumbra in BDNF-treated animals (P:<0.05, unpaired, 2-tailed t test), whereas Bcl-2-positive neurons were significantly increased in this area (P:<0.001, unpaired, 2-tailed t test). CONCLUSIONS: This study demonstrates a neuroprotective effect of BDNF when delivered intravenously after onset of focal cerebral ischemia. As shown here, one possible mechanism of action of neuroprotection of BDNF after focal ischemia appears to be counterregulation of Bax/Bcl-2 proteins within the ischemic penumbra.

Animals↗
PubMed2000

Ammonia and 1-octen-3-ol as attractants for Haematopota pluvialis, Hybomitra expollicata (Diptera: Tabanidae), and Morellia spp. (Diptera: Muscidae).

1-Octen-3-ol with and without ammonia were evaluated as attractants in canopy traps for Haematopota pluvialis L., Hybomitra expollicata Pand., and Morellia spp. Baited traps collected significantly more Tabanidae and female Morellia spp. than unbaited traps. 1-Octen-3-ol or 1-octen-3-ol with ammonia, increased catch by 4.2- and 4.3-fold for H. pluvialis, 5.9- and 8.6-fold for H. expollicata, and 1.2- and 1.6-fold for female Morellia spp., respectively.

Ammonia↗
PubMed1999

[Animal studies on neuropathic pain: the role of cytokines and cytokine receptors in pathogenesis and therapy].

When pain becomes chronic this is a process that takes place at several levels of the peripheral and central nervous systems. In recent years, proinflammatory substances like bradykinin, prostaglandins and signal molecules like cytokines have been identified as allogenic factors. In the present paper we examined whether cytokines play a role also in non-inflammatory peripheral nerve lesions, i.e. whether they are of importance in the causation of pain in general and whether their antagonists can be used therapeutically. The development of pain after peripheral nerve lesion in animal models follows the process of Wallerian degeneration. During Wallerian degeneration the expression of proinflammatory cytokines in the nerve is upregulated. Here we studied the temporal course of cytokine expression with several different analytical methods, analyzing tumor necrosis factor-alpha (TNF) and interleukin-beta (IL-beta) in the mouse model of chronic constrictive injury (CCI) of the sciatic nerve. This model is associated with reproducible pain related behavior in the animals. We found an early increase of TNF 12 hours after injury. Neutralizing antibodies to TNF were able to reduce the hyperalgesia that evolved due to the nerve injury. As TNF exerts its effects via two receptors, TNF receptor 1 (TNF-R1) and TNF receptor 2 (TNF R2), we also investigated, which of the receptors is relevant to the causation of pain in this model. It turned out that antibodies to TNF-R1, but not to TNF-R2 reduced hyperalgesia, indicating that TNF-R1 is the receptor concerned. Neutralizing antibodies to IL-1 receptor and to IL-6 receptor also reduced pain related behavior. These results lead to the conclusion that proinflammatory cytokines are involved not only in inflammatory pain but also in neuropathic pain. Therapeutic strategies involving cytokine inhibition have been tested experimentally and are already being used in preliminary clinical studies in immune-mediated diseases. In the future, they might be a useful addition to the range of treatments for patients with neuropathic pain.

English Abstract↗
PubMed1999

Neutralizing antibodies to interleukin 1-receptor reduce pain associated behavior in mice with experimental neuropathy.

We investigated whether interleukin-1 (IL-1), a mediator of inflammatory pain, also plays a role in pain induced by nerve injury. Female C57BL/6-mice with a chronic constrictive injury of one sciatic nerve, an established model of neurogenic hyperalgesia and allodynia, were treated with different doses (10-80 microg) of a neutralizing monoclonal rat antibody to IL-1 receptor I (anti-IL-1RI). This antibody dose-dependently reduced thermal hyperalgesia and mechanical allodynia in the animals. Furthermore, immunoreactivity for the proinflammatory cytokine tumor necrosis factor-alpha (TNF) was reduced in mice treated with the highest dose of anti-IL-1RI. Degeneration of myelinated fibers was not altered by any of the treatment schedules. We conclude that IL-1 may be a mediator of hyperalgesia after nerve lesion.

Animals↗
PubMed1999

Temporo-spatial expression of bFGF and TGFbeta2 in embryonic dopaminergic grafts in a rat model of Parkinson's disease.

In the present study we analyzed the temporo-spatial expression pattern of basic fibroblast growth factor (bFGF) and transforming growth factor beta 2 (TGFbeta2) in embryonic dopaminergic transplants in the 6-hydroxydopamine rat model of Parkinson's disease. The grafts differentiated for 1, 2, 4 and 8 weeks, respectively and were then analyzed using antibodies directed against tyrosine hydroxylase, bFGF and TGFbeta2. At all time points investigated, grafts contained tyrosine hydroxylase immunoreactive neurons. One week after transplantation the grafts displayed no immunoreactivity for bFGF and TGFbeta2. In more mature grafts (starting at 2 weeks post transplantation) bFGF and TGFbeta2 immunoreactivity became detectable within the graft and at the graft-host interface but was restricted only to astrocytes. In the striatum surrounding the graft, a transient increase of TGFbeta2 immunoreactive astrocytic processes was observed between 1 and 2 weeks after transplantation. This temporo-spatial expression pattern of TGFbeta2 immunoreactive astrocytes suggests that the upregulation of TGFbeta2 is more likely due to the trauma imposed by the transplantation procedure than to an intrinsic differentiation program. Lack of both bFGF and TGFbeta2 expression in grafted dopaminergic neurons compared to their normal expression in the adult rat substantia nigra indicates that these transplanted neurons do not develop their complete physiological phenotype. Together with the observed deficiency in astrocytic bFGF early after grafting this may be responsible for the poor survival of grafted embryonic dopaminergic cells.

Age Factors↗
PubMed1999

[POEMS-Syndrome--unusual manifestation with bilateral Charcot's Joint].

HISTORY AND CLINICAL FINDINGS: A 45-year-old patient with no significant past medical history was admitted 8 weeks after minor foot trauma with injury of the left ankle joint with massive destructive arthropathy. On admission the arch of both feet was flattened and both feet showed massive painless soft tissue swelling. Due to loss of muscle strength elevation of feet and toes was reduced and there was a "stocking-like" loss of sensation of the lower extremity. The gait was ataxic. No other abnormalities were detected besides hepatomegaly and hyperhidrosis. INVESTIGATIONS: Advanced polyneuropathy was confirmed by nerve conduction study. Laboratory tests revealed paraproteinaemia type IgG-lambda. Bone marrow biopsy, bone scan and skeletal survey did not provide additional information. Sonography confirmed hepatosplenomegaly, endocrinological work up showed impaired glucose tolerance and lowered testosterone levels. Based on these findings the diagnosis of POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, M-protein and skin changes) was established. TREATMENT AND COURSE: Plasma exchange was unsuccessful and due to worsening of the symptoms long term treatment with cyclophosphamide was started. Furthermore the patient received NSAIDs for symptomatic relief and orthopedic shoes. One year after initial presentation the patient continues to walk. CONCLUSION: Usually neurogenic arthropathy is associated with diabetes mellitus, syringomyelia or with infections. Our report illustrates that POEMS syndrome might present with Charcot arthritis.

Ankle Injuries↗
PubMed1999

Epstein-Barr virus meningoencephalitis with a lymphoma-like response in an immunocompetent host.

We report the clinical and neuropathological findings in an immunocompetent 19-year-old patient with a fatal acute Epstein-Barr virus (EBV) meningoencephalitis and a lymphoma-like B-lymphocyte response. Our results suggest that an immunotoxic rather than direct viral neuronal invasion mediates brain damage in EBV encephalitis and rule out primary central nervous system lymphoma (PCNSL) in our patient. We discuss immunosuppression as a therapeutic option, because present strategies mainly consist of symptomatic therapy due to unclear pathogenesis and nonavailability of effective antiviral agents.

Adolescent↗
PubMed1999

Serial determination of tumor necrosis factor-alpha content in rat sciatic nerve after chronic constriction injury.

Wallerian degeneration, induced after injury to a peripheral nerve, is associated with upregulation of proinflammatory cytokines, which are suggested to contribute to the development of lesion-induced neuropathic pain. In chronic constrictive injury (CCI), an animal model of injury-induced painful mononeuropathy, inhibition of synthesis, release, or function of the cytokine tumor necrosis factor-alpha (TNF) results in reduced pain-associated behavior. Here, changes of TNF content in rat sciatic nerves after CCI (days 0, 0.5, 1, 3, 7 and 14) were investigated by enzyme-linked-immunoassay. Low levels of TNF were already detectable in control nerves. Concentrations increased rapidly after CCI, with a maximum (2.7-fold) at 12 h, and remained elevated on a lower level until day 3. Baseline levels were reached again at day 14. These results indicate that TNF is produced at an early time point in the cascade of events resulting in Wallerian degeneration and hyperalgesia following peripheral nerve injury. Given that only prophylactic treatment with TNF inhibitors efficiently reduces hyperalgesia in CCI, TNF seems to contribute to the initiation of neuropathic pain in this model.

Animals↗
PubMed1999

Increased lipocortin-1 (annexin-1) expression in the sciatic nerve of Lewis rats with experimental autoimmune neuritis.

Lipocortin-1 exerts a potent immunosuppressive effect on pathogenic T cells. In multiple sclerosis and experimental autoimmune encephalomyelitis levels of lipocortins are raised, suggesting their involvement in the recovery from an immunological insult or in neural regeneration. To further understand the role of lipocortins in the peripheral nervous system we have characterized lipocortin-1 levels and cellular distribution of lipocortin-1 immunoreactivity in sciatic nerves of rats with experimental autoimmune neuritis (EAN), a model of human Guillain-Barré syndrome. EAN was induced actively by immunization with bovine peripheral myelin (active EAN) or by adoptive-transfer (AT-EAN) of P2-specific T cells. Cellular infiltrates in serial and semithin cryosections were characterized by immunohistochemistry. In parallel, lipocortin-1 levels in tissue extracts were quantified by a sandwich-ELISA. Only weak lipocortin-1 immunoreactivity was found in nerves of control animals injected with non-pathogenic T cells. The majority of macrophages and lymphocytes in EAN lesions exhibited lipocortin-1 immunoreactivity. Some very heavily stained cells showed a distribution and morphology similar to ED-2-positive macrophages which were abundant during early stages of EAN. Lipocortin-1 expression in T cells and macrophages was proven by immunocytochemical studies in semithin serial sections. In tissue extracts, lipocortin-1 levels increased from 0.24 +/- 0.14 micrograms/mg protein in controls receiving non-pathogenic T cells to a maximum of 0.55 +/- 0.1 micrograms/mg protein in AT-EAN at the peak of disease, and then slowly decreased during clinical recovery but still remained elevated. In dose-response studies in AT-EAN, highest values of lipocortin-1 (0. 71 +/- 0.23 micrograms/mg protein) were recorded after transfer of 2 x 10(7) T cells. Increased levels of lipocortin-1 were also measured in active EAN but occurred during the recovery phase (0.65 +/- 0.27 micrograms/mg protein). By analogy with other immune-mediated disorders, increased lipocortin-1 expression in the inflamed sciatic nerve in EAN may exert immunoregulatory functions in-situ and contribute to the termination of the autoimmune response.

Adrenal Cortex Hormones↗
PubMed1999

Lymphocytic hypophysitis masking a suprasellar germinoma in a 12-year-old girl--a case report.

Case history, light and electron microscopic findings of a case of a lymphocytic hypophysitis in coincidence with a suprasellar germinoma in a 12-year-old girl are reported. The girl presented with a long time case history of diabetes insipidus and subsequent panhypopituitarism. Two years after the diagnosis of diabetes insipidus magnetic resonance imaging (MRI) showed a tumorous enlargement of the sellar content and pituitary stalk. A transnasal exploration was initially performed and revealed a lymphocytic hypophysitis. Light microscopy showed a dense infiltration of mature lymphocytes and plasma cells in the interstitium of the anterior pituitary gland. The stalk area could not be exposed to exclude a germinoma. One year later the lesion relapsed despite dexamethason therapy and a second operation by another neurosurgeon had to be performed. Light microscopy showed lymphocytic infiltrates, fibrosis and necrosis. The diagnosis was a lymphocytic hypophysitis again. Though transcranially exposed only pituitary tissue was removed. No infundibular mass became visible at surgery as shown by MRI. The girl developed five months later multiple cerebral lesions, which revealed to be a germinoma. Lymphocytic hypophysitis in children is very rare and a coincidence with a germinoma has not been described from histopathological aspect until now. The origin of the pituitary infiltration is discussed.

Child↗
PubMed1999

Extradural spinal hemangioblastomas: report of two cases.

Two cases of predominantly extraspinally extra- and intradural spinal cord hemangioblastomas in two patients each with and without von Hippel-Lindau-disease are reported. Preoperative MRI and angiographic findings are presented and the differential diagnosis is discussed. The surgical procedure is described and the literature of hemangioblastomas in this rare localization is reviewed. Improvements in both radiologic diagnosis and microsurgical techniques, and consequent screening programs will enhance life expectancy in patients afflicted with von Hippel-Lindau disease.

Adult↗