JDDG: Journal der Deutschen Dermatologischen GesellschaftVolume 7, Issue 11 p. 987-989 Entzündliche Auftreibungen der Fingerendglieder mit Nageldystrophie Peter Schulz, Peter Schulz Fachgebiet Dermatologie, Umweltmedizin, Gesundheitstheorie der Universität OsnabrückSearch for more papers by this authorChristoph Skudlik, Christoph Skudlik Fachgebiet Dermatologie, Umweltmedizin, Gesundheitstheorie der Universität Osnabrück Institut für interdisziplinäre dermatologische Prävention und Rehabilitation (iDerm) an der Universität Osnabrück, Standort Osnabrück und Dermatologisches Zentrum, Berufsgenossenschaftliches Unfallkrankenhaus HamburgSearch for more papers by this authorElmar Meyer, Elmar Meyer Fachgebiet Dermatologie, Umweltmedizin, Gesundheitstheorie der Universität Osnabrück Institut für interdisziplinäre dermatologische Prävention und Rehabilitation (iDerm) an der Universität Osnabrück, Standort Osnabrück und Dermatologisches Zentrum, Berufsgenossenschaftliches Unfallkrankenhaus HamburgSearch for more papers by this authorSwen Malte John, Swen Malte John Fachgebiet Dermatologie, Umweltmedizin, Gesundheitstheorie der Universität Osnabrück Institut für interdisziplinäre dermatologische Prävention und Rehabilitation (iDerm) an der Universität Osnabrück, Standort Osnabrück und Dermatologisches Zentrum, Berufsgenossenschaftliches Unfallkrankenhaus HamburgSearch for more papers by this author Peter Schulz, Peter Schulz Fachgebiet Dermatologie, Umweltmedizin, Gesundheitstheorie der Universität OsnabrückSearch for more papers by this authorChristoph Skudlik, Christoph Skudlik Fachgebiet Dermatologie, Umweltmedizin, Gesundheitstheorie der Universität Osnabrück Institut für interdisziplinäre dermatologische Prävention und Rehabilitation (iDerm) an der Universität Osnabrück, Standort Osnabrück und Dermatologisches Zentrum, Berufsgenossenschaftliches Unfallkrankenhaus HamburgSearch for more papers by this authorElmar Meyer, Elmar Meyer Fachgebiet Dermatologie, Umweltmedizin, Gesundheitstheorie der Universität Osnabrück Institut für interdisziplinäre dermatologische Prävention und Rehabilitation (iDerm) an der Universität Osnabrück, Standort Osnabrück und Dermatologisches Zentrum, Berufsgenossenschaftliches Unfallkrankenhaus HamburgSearch for more papers by this authorSwen Malte John, Swen Malte John Fachgebiet Dermatologie, Umweltmedizin, Gesundheitstheorie der Universität Osnabrück Institut für interdisziplinäre dermatologische Prävention und Rehabilitation (iDerm) an der Universität Osnabrück, Standort Osnabrück und Dermatologisches Zentrum, Berufsgenossenschaftliches Unfallkrankenhaus HamburgSearch for more papers by this author First published: 22 October 2009 https://doi.org/10.1111/j.1610-0387.2009.07152.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume7, Issue11November 2009Pages 987-989 RelatedInformation

The synthetic androgen mibolerone elicits a set of distinct changes in the behaviour of an androgen responsive human prostatic carcinoma cell line (LNCaP). Inhibition of cell proliferation, induction of morphological change and of a prostate specific mRNA, and inhibition of colony formation in soft agar are induced by very low concentrations of mibolerone. The natural androgen dihydrotestosterone is much less effective. The changes in growth characteristics and morphology are reverted by excess antiandrogen, i.e. cyproterone acetate or hydroxyflutamide. Cell lines lacking androgen receptors (PC-3, DU 145 and MRC-5) are completely unresponsive to mibolerone. Taken together, our results indicate androgen receptor mediated suppression of the transformed phenotype in LNCaP cells.

Stress and negative affective states are associated with cortisol in everyday life. However, it remains unclear what types of stressors and which affective states yield these associations, and the effect of trait anxiety is unknown. This study investigates the associations of specific task-related stressors and negative affective states in everyday lif e with salivary cortisol, and explores the mediating and moderating rote of state negative affect and trait anxiety, respectively.Salivary cortisol, subjective stress, and state negative affect were measured three times a day on 2 days in 71 participants in everyday life, using a handheld computer to collect self-reports and time stamps and an electronic device to monitor saliva sampling compliance. Stress measures comprised the experience of performance pressure and failure during daily tasks; measures of negative affect comprised worn-out, tense, unhappy, and angry. Effects were tested using multilevel fixed-occasion models.Momentary performance under pressure was related to higher momentary cortisol measures, white mean task failure was related to lower daily cortisol concentrations. The association of performance pressure with cortisol varied between subjects, and this variation was explained by trait anxiety, yielding stronger associations in participants scoring high on trait anxiety. No evidence was found for a mediating rote of state negative affect.These results describe the well-documented associations of everyday stressors and affect with salivary cortisol more precisely, suggesting that performance pressure is a significant condition related to short-term changes in cortisol. Subjects scoring high on trait anxiety seem to process stress-relevant information in a way that amplifies the association of performance pressure with reactions of the hypothalamus-pituitary-adrenal axis. (C) 2006 Elsevier Ltd. All rights reserved.

Objective: The cortisol increase after awakening has been shown to be associated with work-related stress. Several studies demonstrated a moderate stability of cortisol awakening responses on subsequent days, suggesting situation-dependent variance. This study tests whether cortisol awakening responses are different on weekdays compared with weekend days and whether such differences may be explained by chronic work overload and worrying. Methods: Two hundred nineteen participants took saliva samples immediately after awakening and 30, 45, and 60 minutes later on 6 consecutive days starting on Saturday. Perceived chronic work overload and worrying were assessed by a standardized questionnaire. Results: There is a clear weekend-weekday difference in the cortisol response to awakening. This difference is associated with chronic work overload and worry. Independent of sex and weekend-weekday differences in time of awakening and sleep duration, participants who report higher levels of chronic work overload and worrying show a stronger increase and higher mean levels of cortisol after awakening on weekdays, but not on weekend days. Conclusions: The weekend-weekday differences in the cortisol awakening response and their association with chronic stress clearly demonstrate that the day of cortisol assessment is crucial in psychoendocrinological stress studies.

The present study deals with the value determination of the TNM-classification of the carcinoma of the buccal cavity according to the UICC definitions. It is based on a joint comparison whereby the total number of cases were classified according to both the UICC-propositions and those by Spiessl /Fries. The lethal curve calculated according to the minimum survival rate was used as a parameter to assess which definitions would prove to be most useful in practice.

Annals of the New York Academy of SciencesVolume 1004, Issue 1 p. 409-413 Article Distribution of HSV-1 in Human Geniculate and Vestibular Ganglia: Implications for Vestibular Neuritis V. ARBUSOW, Corresponding Author V. ARBUSOW Department of Neurology, Klinikum Grosshadern, University of Munich, D-80337 Munich, GermanyAddress for correspondence: Dr. V. Arbusow, Department of Neurology, University of Munich, Klinikum Grosshadern, Marchioninistrasse 15, D-81377 Munich, Germany. Voice: +49-89-7095-2571; fax: +49-89-7095-8883. varbusow@nro.med.uni-muenchen.deSearch for more papers by this authorD. THEIL, D. THEIL Department of Neurology, Klinikum Grosshadern, University of Munich, D-80337 Munich, GermanySearch for more papers by this authorP. SCHULZ, P. SCHULZ Department of Neurology, Klinikum Grosshadern, University of Munich, D-80337 Munich, GermanySearch for more papers by this authorM. STRUPP, M. STRUPP Department of Neurology, Klinikum Grosshadern, University of Munich, D-80337 Munich, GermanySearch for more papers by this authorM. DIETERICH, M. DIETERICH Department of Neurology, University of Mainz, Mainz, GermanySearch for more papers by this authorE. RAUCH, E. RAUCH Institute of Forensic Medicine, University of Munich, D-80337 Munich, GermanySearch for more papers by this authorT. BRANDT, T. BRANDT Department of Neurology, Klinikum Grosshadern, University of Munich, D-80337 Munich, GermanySearch for more papers by this author V. ARBUSOW, Corresponding Author V. ARBUSOW Department of Neurology, Klinikum Grosshadern, University of Munich, D-80337 Munich, GermanyAddress for correspondence: Dr. V. Arbusow, Department of Neurology, University of Munich, Klinikum Grosshadern, Marchioninistrasse 15, D-81377 Munich, Germany. Voice: +49-89-7095-2571; fax: +49-89-7095-8883. varbusow@nro.med.uni-muenchen.deSearch for more papers by this authorD. THEIL, D. THEIL Department of Neurology, Klinikum Grosshadern, University of Munich, D-80337 Munich, GermanySearch for more papers by this authorP. SCHULZ, P. SCHULZ Department of Neurology, Klinikum Grosshadern, University of Munich, D-80337 Munich, GermanySearch for more papers by this authorM. STRUPP, M. STRUPP Department of Neurology, Klinikum Grosshadern, University of Munich, D-80337 Munich, GermanySearch for more papers by this authorM. DIETERICH, M. DIETERICH Department of Neurology, University of Mainz, Mainz, GermanySearch for more papers by this authorE. RAUCH, E. RAUCH Institute of Forensic Medicine, University of Munich, D-80337 Munich, GermanySearch for more papers by this authorT. BRANDT, T. BRANDT Department of Neurology, Klinikum Grosshadern, University of Munich, D-80337 Munich, GermanySearch for more papers by this author First published: 24 January 2006 https://doi.org/10.1111/j.1749-6632.2003.tb00249.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Volume1004, Issue1THE OCULOMOTOR AND VESTIBULAR SYSTEMS: THEIR FUNCTION AND DISORDERSOctober 2003Pages 409-413 RelatedInformation

The distribution of herpes simplex virus type 1 (HSV-1) in human geniculate, vestibular ganglia, and vestibular nuclei was determined in 10 human temporal bones and brainstems of five individuals by PCR. HSV-1 was found in 3 of 10 of each ganglia and vestibular nuclei. The various patterns of HSV-1 infection of vestibular structures are compatible with virus migration from the vestibular ganglia to the vestibular nuclei and from the ipsilateral to the contralateral vestibular nucleus via commissural fibers.

A unique case of initially right sided varicella zoster induced Ramsay-Hunt syndrome with complete vestibular loss is reported. The patient subsequently developed deficits of the left vestibule 5 months later. An autoimmune pathogenesis of the left vestibular failure rather than bilateral varicella zoster infection was suggested by the following data: (1) no evidence of vesicular eruptions on the left auricle and the virtual absence of antiviral antibodies after onset of bilateral vestibulopathy; (2) prompt response of the left vestibule to immunosuppressive therapy with corticosteroids; and (3) presence of atypical nervous tissue specific autoantibodies against a 45 kDa protein.

The aim of this study was to evaluate the pathological significance of antibodies against cornea and inner ear tissue in the development of audiovestibular and ocular symptoms in patients with Cogan's syndrome (CS). We analysed the serum of 5 CS patients for binding of IgM and IgG to fresh cryosections of rat labyrinth (semicircular canals, ampulla, utricle, saccule) and cornea by indirect immunofluorescence (IF). The predominant pattern of anti-corneal IgM was staining of the superficial cell layer of the non-keratinizing squamous epithelium. IgM against cornea was found in 3 patients, all of whom had bilateral inflammatory eye signs at the start of the disease. However, IgM was also detected in the chronic stage of the disease when no clinical signs of eye involvement were apparent. The study includes the first follow-up examination of anti-corneal IgM and IgG antibodies during a complete episode of active CS. During the first episode of CS in 1 patient, anti-corneal IgM became detectable 1 week after the onset of interstitial keratitis and 3 weeks after the onset of audiovestibular symptoms. It increased over several weeks and then fell to very low levels. However, at no time was anti-corneal IgG found. In the course of follow-up examinations, the serum of 4 patients intermittently contained low titre IgG antibodies against inner ear labyrinthine tissue, but without any clear correlation with the active stages of CS. In addition, high-resolution MRI (HR-MRI) of the inner ear was performed in the acute and chronic stages of CS to evaluate the activity of CS. In the acute stage, HR-MRI revealed abnormal MRI signals in the vestibule, semicircular canals, vestibular nerve, or cochlea. In the chronic stage, patients showed narrowing or occlusion of semicircular canals and the cochlea on the 3D-CISS images, but no high signal lesions (T1) and no enhancement. Antibodies against cornea or labyrinthine tissue were not consistently detected in CS and the level of organ-specific antibodies did not correlate with the activity of the disease.

Vestibular neuritis is a common cause of partial unilateral vestibular paralysis, which usually spares posterior semicircular canal function. The cause is assumed to be a viral reactivation of latent herpes simplex virus type 1 (HSV-1) in human vestibular ganglia. The existence of an anastomosis between the intermediate nerve and the superior vestibular nerve suggests the question of whether selective affliction of the superior vestibular nerve is the result of migration of HSV-1 from the geniculate ganglion along this faciovestibular anastomosis. We determined the distribution of HSV-1 among geniculate ganglia, vestibular ganglia, and within Scarpa's ganglion by examining 35 human temporal bones by polymerase chain reaction. HSV-1 was found in 66% of geniculate ganglia and 60% of vestibular ganglia; all examined parts of vestibular ganglia were almost equally HSV-1 infected. Our data provided no support for viral migration along this anastomosis or for a preferential latency of HSV-1 in the superior vestibular nerve. We suggest that the common double innervation of the posterior ampulla by two nerves running in two separate bony canals could offer an alternative explanation for the regular sparing of posterior canal function in vestibular neuritis.

Viral reactivation in temporal ganglia is the suspected cause of Bell's palsy, vestibular neuritis and sudden hearing loss. Since the distribution of latent herpes simplex type 1 (HSV-1) in geniculate, vestibular and spiral ganglia of individual human temporal bones could have implications for the explanation of isolated as well as combined disorders of these three cranial nerves, we examined these ganglia in 18 human temporal bones of adults by nested polymerase chain reaction. In all of the temporal bones HSV-1 specific DNA was detected: 10/18 (56%) of the geniculate, 11/18 (61%) of the vestibular and 9/18 (50%) of the spiral ganglia samples were positive. All combinations of positive and negative ganglia were found in individual temporal bones at roughly equal frequencies. These data support a viral etiology of all three conditions, especially their occasional combinations. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved

To investigate the possibility of an autoimmune mechanism in idiopathic bilateral vestibulopathy (IBV), we screened patients’ sera for antibodies against inner ear structures. IgG antibodies against membranous labyrinth (ampulla, semicircular canals, saccule and utricle) were detected in 8 of 12 patients by immunofluorescence on rat inner ear cryosections. All but one serum of 22 healthy controls and the sera of 6 patients with known autoimmune disorders showed only background staining. Low-titre anti-nuclear IgM antibodies were present in three control sera and one IBV serum. High-titre anti-nuclear IgM was found in a patient with lupus erythematosus and in one with scleroderma. Anti-nuclear IgM was not organ-specific. No human serum used contained detectable anti-vascular preformed antibodies. Cross-reactivity to sections of liver, kidney, cornea, brain and skeletal muscle was absent. Double-staining for IgG and F-actin, the primary constituent of hair cell cilia, did not show predominant Ig-coating of sensory hair cells. Immunosuppressive therapy in 3 IBV patients did not improve the disorder, probably owing to irreversible loss of sensory and neural structures. These data suggest that the bulk of anti-labyrinthine autoantibodies may be an epiphenomenon, yet a small subgroup of organ-specific autoantibodies may synergize with a cellular response in the development of vestibular lesions.

SUMMARY The present study investigated the association between chronic stress and cortisol changes during the first hour after awakening in the morning. According to results of a pilot study, it was hypothesized that chronically stressed subjects would show a more enhanced and prolonged increase of cortisol level after awakening compared to non-stressed subjects. In 100 subjects, chronic stress was assessed twice with a 1-week interval between measures and cortisol was repeatedly measured during the first hour of awakening on 3 consecutive days. Results showed that chronically stressed subjects had a significantly larger increase in cortisol (a15.5 nmol/l) compared to unstressed subjects (a9.1 nmol/l). Further analysis indicated a significant sex diAerence with larger increases in chronically stressed women (a16.5 nmol/l) compared to stressed men (a11.8 nmol/l). From these data we conclude that a repeated measurement of free cortisol in response to awakening should be considered a possible biological correlate of chronic stress. Possible causes, consequences and clinical relevance of this hypercortisolism in chronically stressed subjects are briefly discussed. #1998 John Wiley & Sons, Ltd. Stress Med., 14: 91‐97, 1998.

Recurrent episodes of oscillopsia, rotational vertigo, and postural imbalance were elicited and modulated by changing the horizontal head positions of a patient with an arachnoid cyst in the right cerebellopontine angle that distorted the vestibulocochlear nerve. Oculomotor analysis revealed two different types of attacks depending on the particular head position: 1) episodes of vestibular hypofunction (minutes to several hours) with normal head position and 2) paroxysmal vestibular excitation (seconds) with head rotation to the left. The most likely cause is a transition from conduction block to ectopic discharges, which occurs when various peripheral nerves are compressed. One week after resection of the cyst and decompression of the eighth cranial nerve the patient was symptom free, and the electronystagmogram was normal.

Immune mediated paraneoplastic neurological syndromes often become manifest before the underlying malignancy is detected. As a rule, these syndromes do not improve with antineoplastic treatment.1 We report on a case of a patient with small cell cancer with peripheral neurological syndromes that responded favourably to combination chemotherapy. At the time of admission the patient, a 66 year old woman, had had a combination of peripheral neurological symptoms for 3 months: ( a ) muscle weakness and muscle pain of the legs so that she could not walk unattended; ( b ) a numbness of both legs from the foot to the middle of the thigh; ( c ) dryness of the eyes and mouth; and ( d ) severe constipation. Clinical examination showed a load dependent, proximally accentuated symmetric muscle weakness and hypoaesthesia of the legs. The patient was unable to stand or walk without support. The deep tendon reflexes of the arms were decreased on both sides and leg reflexes could not be elicited. No pathological reflexes were detectable. Analysis of CSF yielded normal values for protein content, cell number, and glucose. Besides a slightly increased erythrocyte sedimentation rate (35 mm in the first hour), standard laboratory values showed no abnormalities. Abdominal auscultation and CT were unrevealing. Electrophysiological investigation (somatosensory evoked potentials of the tibial and median nerves, EMG, and …

PURPOSE:Because abundant fibronectin deposition is a hallmark of healing cutaneous wounds and provides a matrix for hyperproliferative and migratory epidermal cells, the distribution of fibronectin in aural cholesteatoma was investigated immunohistochemically. MATERIALS AND METHODS:A monoclonal antibody against the major cell binding domain of human fibronectin was used to stain 4-micron cryosections of cholesteatoma tissue by the alkaline phospatase-antialkaline phosphatase method. Section of normal retroauricular skin served as control. RESULTS:When processed in parallel, fibronectin staining was much stronger in the stroma of cholesteatoma than in normal dermis. The squamous epithelium of both tissues did not show any staining for fibronectin. CONCLUSIONS:These observations lend support to the view that the growth of cholesteatoma epithelium reflects an aberrant regenerative process.

Transforming growth factor alpha (TGF-α) wirkt auf den epidermal growth factor receptor (EGF-R) ein und ist ein wichtiger Regulator für die Proliferation von Keratinozyten. TGF-α wird in primären Zellkulturen humaner Keratinozyten produziert. Des weiteren ist TGF-α in der Lage, seine eigene Synthese in dieser Zellart zu stimulieren. In der vorliegenden immunhistochemischen Studie untersuchten wir die Verteilung und die Expressionsstärke von TGF-α und seinem Rezeptor in Gefrierschnitten von Cholesteatomgewebe, um die Faktoren herauszufinden, die in die Deregulation des Wachstumsverhaltens eingeschaltet sind.