Successful plasmapheresis and immunoglobulin treatment for severe lipid storage myopathy: Doing the right thing for the wrong reason

Three consecutive skeletal muscle biopsies during a several months time-frame, showing different degrees of neutral lipid storage. This is highlighted by Oil-red-O stains (D, E, F) and electron microscopy (G, H, I). Note the impact on mitochondrial morphology with so called 'parking lots (K, L). Zooming 'in and out' into the ultrastructure, using the nanotomy platform provides interesting detailled information (http://nanotomy.org). ​

CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis

Studies on inflammatory disorders elucidated the pivotal role of the CX3CL1/CX3CR1 axis with respect to the pathophysiology and diseases progression. Coxsackievirus B3 (CVB3)-induced myocarditis is associated with severe cardiac inflammation, which may progress to heart failure. We therefore investigated the influence of CX3CR1 ablation in the model of acute myocarditis, which was induced by inoculation with 5x105 plaque forming units of CVB3 (Nancy strain) in either CX3CR1-/- or C57BL6/j (WT) mice. Seven days after infection, myocardial inflammation, remodeling, and titin expression and phosphorylation were examined by immunohistochemistry, real-time PCR and Pro-Q diamond stain. Cardiac function was assessed by tip catheter. Compared to WT CVB3 mice, CX3CR1-/- CVB3 mice exhibited enhanced left ventricular expression of inflammatory cytokines and chemokines, which was associated with an increase of immune cell infiltration/presence. This shift towards a pro- inflammatory immune response further resulted in increased cardiac fibrosis and cardiomyocyte apoptosis, which was reflected by an impaired cardiac function in CX3CR1-/- CVB3 compared to WT CVB3 mice. These findings demonstrate a cardioprotective role of CX3CR1 in CVB3-infected mice and indicate the relevance of the CX3CL1/CX3CR1 system in CVB3-induced myocarditis

Large Duodenal Hematoma Causing an Ileus after an Endoscopic Duodenal Biopsy in a 6-Year-Old Child: A Case Report

Intramural duodenal hematoma (IDH) in children is a rare complication after esophagogastroduodenoscopy. It is commonly described in patients with additional disorders or risk factors, such as coagulopathy. We present a case of a previously healthy 6-year-old boy with a large obstructing intramural duodenal hematoma and concomitant pancreatitis after an elective esophagogastroduodenoscopy. The patient presented with typical symptoms of an IDH, such as abdominal pain and distension, nausea and vomiting. IDH was diagnosed using ultrasound and magnetic resonance imaging examination. Conservative management with gastric decompression using a nasogastric feeding tube, bowel rest, total parenteral nutrition and analgesia was performed. After three weeks, the patient was discharged from the hospital without any complaints. Interventional management of IDH in pediatric patients with a lack of response to conservative therapy or complicating IDH should be discussed in an interdisciplinary team

Challenges and opportunities for Zimbabwean exports arising from environmental requirements in Europe

Umweltfragen spielen aus zwei Gruenden eine immer bedeutendere Rolle im internationalen Geschaeft: (1) In den Industrielaendern existiert eine staendig wachsende Anzahl von umweltfreundlichen bzw. -vertraeglichen Produktstandards, die sowohl von den heimischen Produzenten als auch von Importeuren zu beruecksichtigen sind; (2) Die Nachfrage der Verbraucher nach umweltvertraeglichen und gesunden Produkten steigt staendig. Die Studie untersucht diesen Trend und die daraus resultierenden Probleme am Beispiel Simbabwes und seinen Export von Textilien, Lederwaren, Holz und Nahrungsmitteln nach Europa. Die Ergebnisse der Studie zeigen, dass die Unternehmen dieser Branchen die Anforderungen und Vorstellungen der Europaeer noch weitgehend als koloniale Zumutungen erleben und sich ein Bewusstsein nur langsam entwickelt, dass hier ertragreiche Alternativen und Entwicklungsmoeglichkeiten liegen. (pre)German title: Herausforderungen und Gelegenheiten fuer den Export Zimbabwes durch Umweltanforderungen in EuropaAvailable from UuStB Koeln(38)-980106448 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEDEGerman

Using EM data to understand COVID-19 pathophysiology – Authors' reply

Peer Reviewe

За кадры. 1975. № 38 (1873)

Победы праздникПамять. Цветы. Клятва / Р. ГорскаяНародного доверия достоинКандидат томских физиковСобрание агитаторов / Г. ЕрмоленкоАудитория Дмитрия Староверова / И. ТрофимовСпасибо за память / Е. СтаровероваНакануне сессии. Под контролем отстающие группы / С. КошиковаИдет аттестация / Э. Н. Камышев, Р. Б. КвескоНа межзональной олимпиаде / Э. ПодскребкоПриобщение к науке / Г. ИвановаГоворят гости конференции - студенты Тюменского индустриального института / [беседа с] А. Курсов ; [беседа с] М. АндртенкоЮбилейная, военнизированная / А. АлчубаевВсе на кросс! / Б. ПлотниковНа приз героев / Д. В. МоравецкийВстреча с ветеранами / Г. ЕрмоленкоПриходите в дом дружбы / Л. ДороховаПутешествие в страну Диккенса / Л. Ильин

Truncation of Titin's Elastic PEVK Region Leads to Cardiomyopathy With Diastolic Dysfunction

RATIONALE: The giant protein titin plays key roles in myofilament assembly and determines the passive mechanical properties of the sarcomere. The cardiac titin molecule has two mayor elastic elements, the N2B and the PEVK region. Both have been suggested to determine the elastic properties of the heart with loss of function data only available for the N2B region. OBJECTIVE: Investigate the contribution of titin’s PEVK region to biomechanics and growth of the heart. METHODS AND RESULTS: We removed a portion of the PEVK segment (exons 219–225; 282aa) that corresponds to the PEVK element of N2B titin, the main cardiac titin isoform. Adult homozygous PEVK knockout (KO) mice developed diastolic dysfunction, as determined by pressure-volume loops, echocardiography, isolated heart experiments, and muscle mechanics. Immunoelectron microscopy revealed increased strain of the N2B element, a spring region retained in the PEVK-KO. Interestingly, the PEVK-KO mice had hypertrophied hearts with an induction of the hypertrophy and fetal gene response that includes upregulation of FHL proteins. This contrasts the cardiac atrophy phenotype with decreased FHL2 levels that result from the deletion of the N2B element. CONCLUSIONS: Titin’s PEVK region contributes to the elastic properties of the cardiac ventricle. Our findings are consistent with a model in which strain of the N2B spring element and expression of FHL proteins trigger cardiac hypertrophy. These novel findings provide a molecular basis for the future differential therapy of isolated diastolic dysfunction versus more complex cardiomyopathies