Perforatationstrauma im Gesichtsschädel: Eine ungewöhnliche Verletzung beim Skifahren

Zusammenfassung: Pfählungsverletzungen am Kopf und im Gesicht sind selten. Wir berichten über den Fall eines 48-jährigen Patienten, der sich beim Skifahren eine Pfählungsverletzung des Gesichtschädels mit einem 11cm langen Ast zugezogen hatte. Der Patient präsentierte sich bei der Einlieferung in die Klinik neurologisch unauffällig und kreislaufstabil. In den CT-Untersuchungen des Kopfs konnten Frakturen im Gesichtschädel und ein 11cm langer Fremdkörper, ausgehend vom Sinus maxillaris durch den Gesichtschädel bis paravertebral reichend, ohne Verletzung von Gefäßen nachgewiesen werden. Zusätzlich zog sich der Patient Frakturen an der Hand und an den Rippen zu. Er wurde in ein Zentrum für Kiefer- und Gesichtschirurgie verlegt, mehrfach operiert und konnte 8Monate nach dem Unfall wieder in sein gewohntes privates und berufliches Leben zurückkehre

Focal neuromyotonia: do I love you?

We present a rare case of focal neuromyotonia in a 73-year-old woman with a follow up of 5years. The clinical picture showed a fixed contraction of the 3rd and 4th finger of the left hand. Similar to other published cases, our patient suffered from COPD and was treated with beta-2-sympathomimetics. This clinical picture shows a rare but rather salient differential diagnosis of Dupuytren's contracture. EMG of the affected muscles may yield a diagnosis and prevent the patient from a long and ineffective treatment "odyssey

Perforatationstrauma im Gesichtsschädel. Eine ungewöhnliche Verletzung beim Skifahren

Facial perforation injuries are very rare. We describe a case of a 48-year-old man who sustained a perforation trauma from an 11 cm long wooden tree branch in the middle of the face in a skiing accident. He suffered from additional injuries, such as fractures of the ribs and hand, but was neurologically without pathologic findings and was cardiopulmonary stable.The branch penetrated the head from the sinus maxillaris through the maxilla just missing the internal and external carotid arteries and ending just short of the cervical vertebra. The patient was transported to a center for oral and maxillofacial surgery and underwent several operations.He could return to his normal social and professional life 8 months after the accident

The calcar screw in angular stable plate fixation of proximal humeral fractures - a case study

Background: With new minimally-invasive approaches for angular stable plate fixation of proximal humeral fractures, the need for the placement of oblique inferomedial screws ('calcar screw') has increasingly been discussed. The purpose of this study was to investigate the influence of calcar screws on secondary loss of reduction and on the occurrence of complications. Methods: Patients with a proximal humeral fracture who underwent angular stable plate fixation between 01/2007 and 07/2009 were included. On AP views of the shoulder, the difference in height between humeral head and the proximal end of the plate were determined postoperatively and at follow-up. Additionally, the occurrence of complications was documented. Patients with calcar screws were assigned to group C+, patients without to group C-. Results: Follow-up was possible in 60 patients (C+ 6.7 ± 5.6 M/C- 5.0 ± 2.8 M). Humeral head necrosis occurred in 6 (C+, 15.4%) and 3 (C-, 14.3%) cases. Cut-out of the proximal screws was observed in 3 (C+, 7.7%) and 1 (C-, 4.8%) cases. In each group, 1 patient showed delayed union. Implant failure or lesions of the axillary nerve were not observed. In 44 patients, true AP and Neer views were available to measure the head-plate distance. There was a significant loss of reduction in group C- (2.56 ± 2.65 mm) compared to C+ (0.77 ± 1.44 mm; p = 0.01). Conclusions: The placement of calcar screws in the angular stable plate fixation of proximal humeral fractures is associated with less secondary loss of reduction by providing inferomedial support. An increased risk for complications could not be shown

Ear, nose and throat manifestations of Lyme disease

The manifestations of Lyme disease as they may present to the ENT surgeon are discussed. The most important ENT symptom is facial palsy. Particularly when combined with other cranial palsies, systemic illness or signs of meningeal irritation, the diagnosis must be considered. Three case reports are used to illustrate the presentation and diagnosis and treatment of Lyme disease. The characteristics of the disease are reviewed and the limitations of serological testing outlined. The literature has concentrated on bilateral or relapsing facial palsy. A review of palsies in Zurich that presented to the ENT clinic found only unilateral and partial palsies. The diagnosis should be considered in every case of facial palsy of unknown aetiology especially in childre

Nephrotoxicity, high frequency ototoxicity, efficacy and serum kinetics of once versus thrice daily dosing of netilmicin in patients with serious infections

The effect of dosing regimen on nephrotoxicity, high frequency ototoxicity, efficacy and serum kinetics was studied in a prospective, randomised clinical study. Therapy was started with total daily doses of 6 mg/kg given once (od) or thrice (tid) daily to 56 and 57 patients, respectively. Subsequent doses were adjusted according to serum levels. No major differences in toxicity or efficacy were noticed between od and tid regimens: clinical failures occurred in two and two patients, four and five patients suffered from a decrease of ≥20 dB at least unilaterally at one frequency between 8 and 18 kHz, six and seven patients had a >25 μmol/L or >25% increase in serum creatinine, respectively. Serum creatinine or creatinine clearance did not change significantly during either therapy. Major differences between the two study groups were limited to pharmacokinetic parameters. Od dosing resulted in higher peak (mean of 21.6 vs 7.2 mg/L) and lower trough levels (0.5 vs 1.4mg/L). Half-lives of netilmicin determined between 1 and 8 h increased significantly during therapy with tid (from a mean of 2.75 to a mean of 3.33 h, P<0.01) but not significantly with od (rise from 2.8 to 3.03 h). Much longer half-lives were determined between 8 and 24 h in the od group (mean of 5.7 h, P<0.01). In conclusion, only minimal differences in toxicity and efficacy were observed. Their clinical relevance appears to be minima

Redox signals at the ER-mitochondria interface control melanoma progression.

Reactive oxygen species (ROS) are emerging as important regulators of cancer growth and metastatic spread. However, how cells integrate redox signals to affect cancer progression is not fully understood. Mitochondria are cellular redox hubs, which are highly regulated by interactions with neighboring organelles. Here, we investigated how ROS at the endoplasmic reticulum (ER)-mitochondria interface are generated and translated to affect melanoma outcome. We show that TMX1 and TMX3 oxidoreductases, which promote ER-mitochondria communication, are upregulated in melanoma cells and patient samples. TMX knockdown altered mitochondrial organization, enhanced bioenergetics, and elevated mitochondrial- and NOX4-derived ROS. The TMX-knockdown-induced oxidative stress suppressed melanoma proliferation, migration, and xenograft tumor growth by inhibiting NFAT1. Furthermore, we identified NFAT1-positive and NFAT1-negative melanoma subgroups, wherein NFAT1 expression correlates with melanoma stage and metastatic potential. Integrative bioinformatics revealed that genes coding for mitochondrial- and redox-related proteins are under NFAT1 control and indicated that TMX1, TMX3, and NFAT1 are associated with poor disease outcome. Our study unravels a novel redox-controlled ER-mitochondria-NFAT1 signaling loop that regulates melanoma pathobiology and provides biomarkers indicative of aggressive disease

The endogenous caspase-8 inhibitor c-FLIPL regulates ER morphology and crosstalk with mitochondria

Components of the death receptors-mediated pathways like caspase-8 have been identified in complexes at intracellular membranes to spatially restrict the processing of local targets. In this study, we report that the long isoform of the cellular FLICE-inhibitory protein (c-FLIPL), a well- known inhibitor of the extrinsic cell death initiator caspase-8, localizes at the endoplasmic reticulum (ER) and mitochondria-associated membranes (MAMs). ER morphology was disrupted and ER Ca2+-release as well as ER-mitochondria tethering were decreased in c-FLIP-/- mouse embryonic fibroblasts (MEFs). Mechanistically, c-FLIP ablation resulted in enhanced basal caspase-8 activation and in caspase-mediated processing of the ER-shaping protein reticulon-4 (RTN4) that was corrected by re-introduction of c-FLIPL and caspase inhibition, resulting in the recovery of a normal ER morphology and ER-mitochondria juxtaposition. Thus, the caspase-8 inhibitor c-FLIPL emerges as a component of the MAMs signaling platforms, where caspases appear to regulate ER morphology and ER-mitochondria crosstalk by impinging on ER-shaping proteins like the RTN4

The Krüppel-like factor 9 (KLF9) network in HEC-1-A endometrial carcinoma cells suggests the carcinogenic potential of dys-regulated KLF9 expression

<p>Abstract</p> <p>Background</p> <p>Krüppel-like factor 9 (KLF9) is a transcriptional regulator of uterine endometrial cell proliferation, adhesion and differentiation; processes essential for pregnancy success and which are subverted during tumorigenesis. The network of endometrial genes controlled by KLF9 is largely unknown. Over-expression of KLF9 in the human endometrial cancer cell line HEC-1-A alters cell morphology, proliferative indices, and differentiation, when compared to KLF9 under-expressing HEC-1-A cells. This cell line provides a unique model for identifying KLF9 downstream gene targets and signaling pathways.</p> <p>Methods</p> <p>HEC-1-A sub-lines differing in relative levels of KLF9 were subjected to microarray analysis to identify differentially-regulated RNAs.</p> <p>Results</p> <p>KLF9 under-expression induced twenty four genes. The KLF9-suppressed mRNAs encode protein participants in: aldehyde metabolism (AKR7A2, ALDH1A1); regulation of the actin cytoskeleton and cell motility (e.g., ANK3, ITGB8); cellular detoxification (SULT1A1, ABCC4); cellular signaling (e.g., ACBD3, FZD5, RAB25, CALB1); and transcriptional regulation (PAX2, STAT1). Sixty mRNAs were more abundant in KLF9 over-expressing sub-lines. The KLF9-induced mRNAs encode proteins which participate in: regulation and function of the actin cytoskeleton (COTL1, FSCN1, FXYD5, MYO10); cell adhesion, extracellular matrix and basement membrane formation (e.g., AMIGO2, COL4A1, COL4A2, LAMC2, NID2); transport (CLIC4); cellular signaling (e.g., BCAR3, MAPKAPK3); transcriptional regulation [e.g., KLF4, NR3C1 (glucocorticoid receptor), RXRα], growth factor/cytokine actions (SLPI, BDNF); and membrane-associated proteins and receptors (e.g., CXCR4, PTCH1). In addition, the abundance of mRNAs that encode hypothetical proteins (KLF9-inhibited: C12orf29 and C1orf186; KLF9-induced: C10orf38 and C9orf167) were altered by KLF9 expression. Human endometrial tumors of high tumor grade had decreased KLF9 mRNA abundance.</p> <p>Conclusion</p> <p>KLF9 influences the expression of uterine epithelial genes through mechanisms likely involving its transcriptional activator and repressor functions and which may underlie altered tumor biology with aberrant KLF9 expression.</p