Biomedical subjects

M Schönermark

Publications and source records attributed to M Schönermark.

17 recordsLinked to original sources

PubMed1996

[Accidental dirt tattooing. Removal with Q-switched ruby laser].

The Q-switched ruby laser (wave length 694 nm; pulse durations 25 ns or 40 ns) cause selective damage to natural and artificial skin pigments. Treatable lesions include benign pigmented growths (benign, lentigo, ephelides, caféau-lait spots and Becker's nevi), as well as amateur and professional tattoos. The Q-switched ruby laser is also very effective in the treatment of traumatic tattoos. We report our experiences with two patients whose traumatic tattoos resolved completely without any scarring after ruby laser therapy. Our findings show that Q-switched ruby laser treatment may represent the therapy of choice for these tattoos.

Adult↗

PubMed1996

[Reconstructive surgery in the head-neck area with regional and free tissue transfer].

BACKGROUND: Operative treatment of head and neck cancer requires radical resection of the tumor with not only severe impairment of important functions like swallowing speech, and respiration but also aesthetic mutilation because of the exposed character of the head and neck region. Therefore the rehabilitation from a functional and cosmetic standpoint is an essential goal of treatment in addition to control of the malignant disease. Fortunately regional plastic surgery offers a variety of options for reconstruction of the defects to receive a solution tailored to each individual patient. PATIENTS: Between the years 1986 and 1996, 107 patients with advanced head and neck cancer were treated surgically by radical resection of the tumor and plastic reconstruction. In this study we made a retrospective analysis of the functional and aesthetic outcome of the techniques of reconstructive surgery we used for rehabilitation. The sex ratio was 79 males to 28 females. Average age was 59.4 years (ranging from 39 to 78 years). Most of the patients suffered from squamous cell carcinoma of the upper digestive tract (97 cases). The others included an adenocarcinoma of the paranasal sinuses (three cases), adenoid cystic cancer of the palate (two cases), squamous cell carcinoma of the temporal bone (two cases), two deep infiltrating basaliomas in the area of the nose and forehead and one chondrosarcoma of the neck. Our oncological concept includes a radical resection of the tumor and a onestep reconstruction of the defect, if the patient's general condition enables this approach. The surgical techniques we used include the approved pedicled myocutaneous flaps like the pectoralis major flap, latissimus dorsi flap (which can be also applied as a free microvascular tissue graft), temporalis muscle flap, and the free radial forearm flap. RESULTS: In previous years, the pedicled myocutaneous pectoralis-major- and latissimus-dorsi-flaps were used for reconstruction (n = 67), but the arc of rotation and the huge bulk of the graft are limiting factors for the indication of these techniques. The free forearm flap has increasingly been used to provide an excellent closure of large pharyngeal defects (n = 16), whereas the temporalis flap is useful for restoration after limited resection of the palate (n = 18). Beside these rather invasive procedures, aesthetic rehabilitation may be achieved with bone-anchored epithesis especially after exenteration of the orbit and ablation of the external ear in case of elderly patients with multiple morbidities (n = 5). In most cases, sufficient rehabilitation from the anatomical and functional point of view was possible even after large tumor resections. A main problem can be longstanding aspiration after resection of large areas of the pharyngeal mucosa (n = 8). Complications included eight cases of necrosis of the flaps and seven patients who developed significant seromas at the donor site. CONCLUSIONS: The potential of modern regional reconstructive surgery enables the surgeon to achieve anatomically and functionally rehabilitation in a one-step procedure in most cases, even after extended resection for head and neck cancer. One should be aware of the fact that these techniques do not offer a significant improvement of prognosis. As such, the aggressiveness of surgical therapy should remain in reasonable relation to the prognosis of the malignant disease.

Adenocarcinoma↗

PubMed1996

[Indications for middle ear obliteration within the scope of cochlear implant management].

BACKGROUND: Cochlear implants have gained worldwide acceptance as a reliable method of rehabilitation of profoundly hearing-impaired patients. Due to thorough patient selection major postoperative complications rarely occur and are flap related in most cases. Deafness can develop during chronic suppurative otitis media, either coincidentally or secondary to the medical treatment; normally this condition is regarded as a contraindication for cochlear implantation. In cases with a mastoid cavity after surgical treatment for cholesteatoma, the electrode covered only by the epithelial lining will likely become exposed or extruded. Therefore we suggest the obliteration of the middle ear cleft with abdominal fat and the blindsac closure of the external ear canal before cochlear implantation in these conditions. PATIENTS: The average age of our 12 patients was 48 years, whereas the youngest was 2 1/2 years of age. Due to chronic inflammatory ear disease. 11 patients had a mastoid cavity on both ears. Eight patients had a cholesteatoma, the chronic bone destroying process in the temporal bone of two female patients was considered as a fibroinflammatory pseudotumor. The child had a congenital deafness in both ears with a Mondini dysplasia in CT scan. She had already developed two episodes of pneumococcal meningitis which was caused by a defect in the stapes footplate through which a liquor-filled cystic sac herniated in the middle ear. Because of a massive liquorrhoea after opening of the sac, we decided to obliterate the middle ear cleft after successful insertion of the electrode array. RESULTS: All active electrodes of 10 Nucleus implants (Cochlear) and two Clarion devices (Advanced Bionics Corp.) were successfully inserted in the cochlea of the 12 patients. After an average follow-up of 15 months, a temporary facial palsy in one patient and an insufficient closure of a retroauricular fistula over the mastoid cavity in two cases were observed as postoperative complications. One patient with a fibroinflammatory pseudotumor developed a massive inflammatory reaction in the implanted ear two months after cochlear implantation, which could not be controlled by conservative treatment. The implant had to be removed and local conditions settled after administration of immunosuppressive treatment with cyclophosphamide. The patient received a new implant seven months ago. CONCLUSIONS: Implantation of a foreign body in a potentially infected space which communicates intracranially means a surgical challenge which can be managed by obliteration of the middle ear after subtotal petrosectomy with abdominal wall fat combined with a reliable closure of the external ear canal. In case of massive inflammation we would prefer a two-stage procedure.

Adipose Tissue↗

PubMed1996

Expression of matrix-metalloproteinases and their inhibitors in human cholesteatomas.

The proteolytic erosion of the temporal bone is the key event in the pathognomonic course of cholesteatoma progression. The molecular mechanisms of bone resorption, endangering the ossicles, the inner ear, the facial nerve, large vessels or the brain, are not understood. Recently, a new family of proteolytic enzymes, the matrix-metalloproteinases (MMP's) has been described and identified, which seems to play a pivotal role in matrix- and bone homeostasis and inflammatory osteolytic diseases, e.g. osteoarthritis and periodontitis. These enzymes are sophisticatedly controlled by specific inhibitors and activation cascades. We investigated whether human cholesteatoma tissue expresses MMP's and MMP-inhibitors. By immunocytochemistry of cholesteatoma-cryosections, the expression of MMP-2 (72 kD collagenase), MMP-9 (92 kD collagenase), and MMP-3 (stromelysin-1) could be seen to be strictly confined to the basal and suprabasal cell layer of the cholesteatoma epithelium. The neutrophil collagenase (MMP-8) showed a more disseminated expression in the epithelium and the granulation tissue as well. The tissue inhibitor of metalloproteases, TIMP-1, could be detected only in very limited areas of the granulation tissue in a quite randomized manner. Therefore, a derailment in favor of proteolysis of the normally tightly controlled MMP-system might be postulated. The results indicate that members of the MMP-family could play an active role in the molecular mechanisms of cholesteatoma invasion into the temporal bone. This offers new insights into the pathophysiology of the disease and of potential therapeutic approaches.

Adolescent↗

PubMed1995

[Progressive hearing loss--pathophysiology, differential diagnosis, therapy].

Progressive sensorineural hearing loss (SNHL) is still a challenge to the otorhinolaryngologist. It can be solved only by a systematic and interdisciplinary approach to the patient and his disease. Most often an acute onset is observed with a non-linear, sometimes dramatic progress to chronicity and complete deafness. Cardiovascular and rheologic diseases, hereditary disorders, immunological phenomena, hormonal and metabolic derailments, infections, environmental causes like noise, ototoxic drugs and industrial substances and systemic maladies must be included in the diagnostic reflections. Otopathy is an idiopathic hearing loss which cannot be classed with the above mentioned disorders. Wherever possible a causal therapy should be carried out. Symptomatic therapeutic concepts include rheologic medications, corticosteroids or, with all reservation, cytotoxic drugs. Hearing aids should be prescribed in close relation to the dynamic deterioration of the hearing. The timely cochlear implant operation stands at the end of the therapeutic scale.

Cochlear Implants↗

PubMed1995

[Treatment of vascular malformations and pigment disorders of the face and neck by pulsed dye laser, Photoderm VL and Q-switched ruby laser].

BACKGROUND: Two new types of lasers, the pulsed dye laser and the Q-switched ruby laser, have shown good to excellent results in the treatment of vascular malformations and benign pigmented lesions of the skin. A new and very effective alternative to pulsed dye laser is the recently introduced Photoderm VL. This device is based on the use of a wide-band non-coherent intense pulsed light source which emits a continuous spectrum in the range of 515 nm to 1200 nm. PATIENTS AND METHODS: More than a 1000 patients with a variety of lesions of the skin were treated by these new laser systems and the Photoderm VL. The Q-switched ruby laser (wavelength 694 nm, pulse duration 25 ns) is suitable for the treatment of benign lentigines, café-au-lait macules, seborrhoic ceratosis, tattoos, and traumatic tattoos. The pulsed dye laser (585 nm, 0,3-0,45 ms) treats nevi flammei, capillary hemangiomas, telangiectasias, xanthelasma, hypertrophic scarring, and adenoma sebaceum. In addition we present the facilities of the new Photoderm VL (515 nm-1200 nm, 0,5-20 ms) for the treatment of nevi flammei, benign hemangiomatous malformations, telangiectasias, erythrosis interfollicularis colli, hypertrophic scarring, and hypertrichosis. RESULTS AND CONCLUSIONS: the Q-switched ruby laser, the pulsed dye laser, and the Photoderm VL show excellent results in the treatment of lesions of the skin, which otherwise would have been difficult to treat of untreatable. The efficiency of the laser types presented is based on the theory of selective photothermolysis. Scarring is almost never seen and hypo- or hyperpigmentation is in most cases transient.

Adolescent↗

PubMed1995

[Carcinoma of the temporal bone--current diagnostic and therapeutic aspects].

BACKGROUND: Carcinoma of the external ear canal and the middle ear is a rather rare event and is especially seen in patients with chronic inflammatory ear disease. PATIENTS: Between 1993 and 1994, we treated seven patients with such a tumor, of which six proved to be a squamous cell carcinoma and one presumably adenocarcinoma. In three patients, the malignoma developed in a radical cavity of the ear and caused a facial palsy. Only two patients were without any discharge of the ear. Beside facial palsy, hemorrhagic otorrhea and otalgia were the leading symptoms. One patient presented with a bilateral painless swelling of the neck due to lymph node metastasis. Diagnosis was made by means of biopsy in only three patients and on the basis of a resected specimen after mastoidectomy in four patients. Angiography and computed tomography and magnetic resonance imaging studies were performed prior to treatment to determine the extent of the tumor. RESULTS: The tumor was resected by petrosectomy, parotidectomy, and neck dissection in 5 patients. Three times the margins of the histological specimen were free of tumor. Lymph node metastasis in the neck were seen in 5 cases, while distant metastasis did not occur. Two patients underwent primary irradiation, but a postoperative radiation therapy was performed five times. To date, three patients died after one year follow-up. CONCLUSIONS: Carcinoma of the temporal bone is a rare tumor, which can be treated only in case of early diagnosis.

Adenocarcinoma↗

PubMed1995

[Jugular vein thrombosis as incidental ultrasound finding in tumor patients].

At present thrombosis of the internal jugular vein is an uncommon event that is now more frequently associated with diagnostic or therapeutic catheterization. If an apparent spontaneous thrombosis occurs, malignancy should be considered in the differential diagnosis. Two cases of clinically asymptomatic thrombosis of the internal jugular vein are presented. A 69-year-old female patient with metastasizing renal cell carcinoma had bilateral thrombosis and a 73-year-old male with a small laryngeal carcinoma had a unilateral thrombosis. Increased blood coagulability as part of a paraneoplastic syndrome was considered to be the possible etiology. The role of sonography in the diagnosis is emphasized.

Aged↗

PubMed1994

Human glomerular mesangial cells express CD16 and may be stimulated via this receptor.

CD16, a low affinity receptor for IgG, was found on cultured human glomerular mesangial cells (GMC) by Western blot analysis, cell ELISA and in situ hybridization. To characterize the molecule in more detail, reverse polymerase chain reaction was performed and the PCR products were analyzed. From sequence analysis and from hybridization experiments with oligonucleotides specific for either the transmembrane form or the glycosylphosphatidylinositol anchored form it was found that GMC-CD16 was similar to NK-CD16. This indicates that GMC express the transmembrane form of CD16. Comparison between nonstimulated GMC and GMC stimulated by aggregated gammaglobulin revealed no qualitative or quantitative difference in the expression of CD16. Incubation of GMC with aggregated gammaglobulin or with monoclonal antibodies to CD16 was followed by a time and dose dependent release of interleukin-6, suggesting that signals were transmitted by CD16. The occupancy of CD16 by immune complexes that may be deposited in various forms of glomerulonephritis might contribute to the perpetuation of inflammatory processes in the kidney.

Amino Acid Sequence↗

PubMed1992

Immune damage to the mesangium: antibody- and complement-mediated stimulation and destruction of mesangial cells.

The deposition of immune complexes in the tissue results in complement activation leading to the formation of the lytic C5b-9 complex. Tissue cells are relatively resistant to complement attack due to cellular mechanisms such as removing C5b-9 from the surface and the expression of membrane proteins, which regulate complement activation and attack on the cell surface. Hence, cell killing is not an important consequence of complement activation on nucleated cells. On the other hand, the sublethal C5b-9-membrane interaction leads to various cellular responses, among them the synthesis of eicosanoids, cytokines, matrix-degrading proteases, and extracellular matrix, resulting in the modification of cell proliferation, leukocyte function, matrix degradation, and the formation of scar tissue. Thus, the complement-dependent immune damage is caused by secondary mediators, either derived from leukocytes or mesangial cells, rather than by a direct C5b-9-mediated killing.

Animals↗

PubMed1991

Actions of 1,25-dihydroxyvitamin D3 on human mesangial cells.

In the present study, we examined specific binding of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] by an effects of 1,25(OH)2D3 on human mesangial cells (hMC), obtained from healthy portions of tumor-bearing kidneys. Receptors for 1,25(OH)2D3 were characterized by (1) sucrose density gradient analysis, (2) Scatchard analysis, and (3) DNA affinity of the receptor molecule. Specific binding occurred by a single class of macromolecules, sedimenting with 3.5 S in sucrose density gradients (5% to 20%). Receptors showed high affinity (Kd, 1.39 x 10(-10)), and specific binding capacity (Nmax) of 821 binding sites per cell. 1,25(OH)2D3 (10(-6) to 10(-10)) reduced both DNA synthesis (by [3H]thymidine incorporation) and cell growth (by cell counting) throughout the log-phase and confluence. Further evidence of functional effects of 1,25(OH)2D3 on hMC is provided by ultrastructural studies, which showed rapid increase of electron-dense lysosomal particles in hMC exposed to 1,25(OH)2D3. The data identify actions of 1,25(OH)2D3, a molecule with recently recognized immunoregulatory roles, on hMC. The results are consistent with a role of 1,25(OH)2D3 in control of mesangial cell function.

Calcitriol↗

PubMed1991

Induction of mediator release from human glomerular mesangial cells by the terminal complement components C5b-9.

Exposure of cultured human glomerular mesangial cells (GMC) to normal human serum and an activator of the complement system results in rapid uptake of the terminal complement proteins C5b-9 by the cells. This 'innocent bystander' complement attack, however, does not result in cell killing, but in the stimulation of the GMC to release prostaglandin E (PGE), interleukin 1 (Il-1) and tumor necrosis factor (TNF). Endogenously synthesized Il-1 in turn activates PGE release, indicating that the C5b-9 attack initiates an autocrine feedback stimulation. Together with the fact that C5b-9 is found in many forms of glomerulonephritis, the data point to a role of the terminal complement proteins in the initiation and perpetuation of an inflammatory response.

Complement Membrane Attack Complex↗

PubMed1990

Intermediate filaments vimentin and desmin share epitopes with M 1 protein of group A streptococci.

The cross reactivity of the murine monoclonal antibody PM II 40 against human glomeruli with streptococcal type 1 M protein was investigated. The antibody PM II 40 recognized a protective epitope on a glomerulonephritis-associated M type 1 strain. A 23 kD streptococcal surface protein extracted by limited pepsin digestion reacted with PM II 40 in the Western immunoblot. The aminoterminal sequence of this peptide was identical to the known aminoterminal amino acid sequence of type 1 M protein. Human renal podocytes carry the cross-reactive antigen of the antibody PM II 40 as could be shown by electron microscopy. The podocytes cultured from isolated human glomeruli showed a fibrillar pattern with the antibody in the immunofluorescence test. An anti-vimentin antibody and the antibody PM II 40 recognized the same proteins with molecular weights of 54, 52 and 43 kD of SDS-extracted isolated human glomeruli suggesting that vimentin is the glomerular antigen. The antibody PM II 40 not only react with vimentin but also with desmin suggesting that the recognized epitopes are distinct from that described by Kraus et al. for vimentin and type 1 M protein.

Amino Acid Sequence↗

PubMed1990

C5b-8 and C5b-9 modulate the collagen release of human glomerular epithelial cells.

Aside from their lytic function the late complement components C5b-9 stimulate release of prostanoids, interleukin 1 and oxygen radicals from a number of cells. Since C5b-9 has also been connected to the development of sclerosis in animal models of glomerulonephritis, we addressed the question whether C5b-9 would affect the collagen synthesis. We used human glomerular epithelial cells (GEC) obtained as primary outgrowth cultures. The cells were cultivated in the presence of 14C-proline. Collagen synthesis was quantitated by counting the radioactivity associated with collagenase digestible material. Furthermore, collagen was analyzed by SDS-PAGE. GEC in culture produce spontaneously some collagen type IV. Addition of sublytic doses of highly purified C5b-9 increased the collagen synthesis considerably within 12 to 24 hours. In the absence of C9, C5b-8 stimulated collagen synthesis to a similar extent, whereas in the absence of C7 or C8, the collagen synthesis was not enhanced. Furthermore, fluid-phase-formed C5b-9 complexes did not stimulate the collagen synthesis, indicating that assembly of the complex on the target membrane was required. Since C5b-9 deposits are found in sclerotic areas, our data support the hypothesis that C5b-9, by stimulating collagen synthesis as well as release, might contribute to the development of chronic nephritis.

Animals↗

PubMed1989

Effect of the late complement components C5b-9 and of platelet-derived growth factor on the prostaglandin release of human synovial fibroblast-like cells.

We examined the prostaglandin E (PGE) synthesis of cultured adherent synovial fibroblast-like cells (SFC) from patients with osteoarthritis (OA) in the noninflammatory state as well as with rheumatoid arthritis (RA). In cells from RA patients the spontaneous PGE release was generally higher compared to that of OA patients, but decreased fast with time in culture. After cell passage, similar PGE baseline levels were seen in cells of the two patient groups. The cells could then be stimulated by the terminal complement components C5b-9 or C5b-8. PGE synthesis was also stimulated by the platelet-derived growth factor (PDGF), interleukin-1 (IL-1), or lipopolysaccharide (LPS). The amount of PGE synthesis after incubation with PDGF, LPS and IL-1 was comparable to that released after C5b-9. Thus, like other inflammatory mediators C5b-9 and PDGF trigger the increased PGE production by SFC and thus may participate in the development of synovial inflammation and contribute to the pathogenesis of RA.

Arthritis, Rheumatoid↗

PubMed1989

Modulation of collagen synthesis in human glomerular epithelial cells by interleukin 1.

Human glomerular epithelial cells produce matrix material e.g. collagen type IV. In vitro, the synthesis of collagen can be monitored by the incorporation of 3H-proline, a precursor molecule of the collagens. We report on the enhancement of collagen synthesis by glomerular epithelial cells with highly purified or recombinant I1-1. Since I1-1 is released from monocytes or glomerular mesangial cells by inflammatory mediators, our results point to a participation of I1-1 in the development of sclerosis, which is seen in many forms of chronic inflammatory diseases.

Cells, Cultured↗

PubMedDate not supplied

Expression of the complement regulator factor C8 binding protein on human glomerular cells protects them from complement-mediated killing.

The complement-regulatory factor C8 binding protein (C8bp) was first identified on human erythrocyte membranes by its affinity for the complement component C8 and its ability to inhibit lysis by homologous complement. Cultured human glomerular mesangial or epithelial cells (GEC) expressed C8bp on the cell surface and in the cytoplasm. Following stimulation of the glomerular cells with interleukin 1 beta, C5b-9 or with endotoxin, a transient, protein synthesis-independent increase in C8bp surface expression was seen. Blocking of C8bp function with F(ab)2 fragment of an antibody to C8bp rendered GEC susceptible to complement-mediated killing, indicating that C8bp contributes to the cellular defense against complement attack.

Blood Proteins↗