Influence of Slim Rod Material Properties to the Siemens Feed Rod and the Float Zone Process

AbstractThe identification and understanding of material properties influencing the float zone process is important to crystallize high purity silicon for high efficiency solar cells. Also the knowledge of minimal requirements to crystallize monocrystalline silicon with the float zone process is of interest from an economic point of view. In the present study, feed rods for the float zone process composed of a central slim rod and the deposited silicon from the Siemens process are investigated. Previous studies have shown that the slim rod has a significant impact on the purity and suitability for further crystallization processes. In particular, contaminations like substitutional carbon and the presence of precipitates as well as the formation of oxide layers play an important role and are investigated in detail. For this purpose different slim rod materials were used in deposition and float zone crystallization experiments. Samples were prepared by cross sectioning and core drilling of Siemens rods, which were recrystallized with the float zone process. Recrystallized drilled cores are analyzed with FT-IR spectrometry concerning the carbon and oxygen content. To estimate the grain growth behavior on the slim rod surface in dependence of the used slim rod material, EBSD mappings inside a SEM are performed on squared and circular slim rods. TEM analysis was used to investigate the presence of an oxide layer at the interface between slim rod and deposited polycrystalline silicon. Additionally the influence of a nitrogen-containing gas atmosphere during the slim rod pulling is investigated by IR microscopy and ToF-SIMS regarding Si3N4 precipitation

A retrospective study on disease management in children and adolescents with phenylketonuria during the Covid-19 pandemic lockdown in Austria

BACKGROUND In classical phenylketonuria (PKU) phenylalanine (Phe) accumulates due to functional impairment of the enzyme phenylalanine hydroxylase caused by pathogenic variants in the PAH gene. PKU treatment prevents severe cognitive impairment. Blood Phe concentration is the main biochemical monitoring parameter. Between appointments and venous blood sampling, Austrian PKU patients send dried blood spots (DBS) for Phe measurements to their centre. Coronavirus disease-19 (COVID-19), caused by the SARS CoV-2 virus, was classified as a pandemic by the World Health Organization in March 2020. In Austria, two nationwide lockdowns were installed during the first and second pandemic wave with variable regional and national restrictions in between. This retrospective questionnaire study compared the frequency of Phe measurements and Phe concentrations during lockdown with the respective period of the previous year in children and adolescents with PKU and explored potential influencing factors. RESULTS 77 patients (30 female, 47 male; mean age 12.4 [8-19] years in 2020) from five centres were included. The decline of venous samples taken on appointments in 2020 did not reach significance but the number of patients with none or only one DBS tripled from 4 (5.2%) in 2019 to 12 (15.6%) in 2020. Significantly more patients had a decline than a rise in the number of DBS sent in between 2019 and 2020 (p < 0.001; Chi$^{2}$ = 14.79). Especially patients ≥ 16 years sent significantly less DBS in 2020 (T = 156, p = 0.02, r = 0.49). In patients who adhered to DBS measurements, Phe concentrations remained stable. Male or female sex and dietary only versus dietary plus sapropterin treatment did not influence frequency of measurements and median Phe. CONCLUSION During the COVID pandemic, the number of PKU patients who stopped sending DBS to their metabolic centre increased significantly, especially among those older than 16 years. Those who kept up sending DBS maintained stable Phe concentrations. Our follow-up system, which is based on DBS sent in by patients to trigger communication with the metabolic team served adherent patients well. It failed, however, to actively retrieve patients who stopped or reduced Phe measurements

Dokaz i kvantificiranje ovčjeg herpesvirusa 2 u Hrvatskoj

Ovine herpesvirus-2 (OvHV-2), a gammaherpesvirus (genus Rhadinovirus) causes a severe disease known as sheep-associated malignant catarrhal fever (SA-MCF) in certain ruminants, such as cow, deer, bison and water buffalo. Suspected cases of SA-MCF in cows without identififi cation of the agent have been reported in Croatia in the past. In June 2005, on a farm in northwest Croatia, where 17 Simmental diary cows and 2 heifers shared stables and meadows with sheep, a 13 month-old heifer showed symptoms reminiscent of SA-MCF, including anorexia, high fever, nasal discharge, and neurological symptoms, such as ataxia, tremor, convulsions and hyperesthesia. The animal died within 14 days. Gross necropsy fifi ndings were sharply demarcated erosions on mucosal surfaces, including the tongue, oral mucosa, esophagus, abomasum, jejunum, colon, caecum and urinary bladder. Histopathology revealed extremely severe perivascular and intramural arterial infifi ltrations with mononuclear cells, mostly lymphocytes. These lesions were seen in almost every organ, especially the brain and lungs. Formaldehyde fixed samples from the brain, cerebellum, spleen and lymph nodes were obtained and subjected to DNA extraction procedures. Fluorogenic real-time PCR (Polymerase chain reaction) amplififi cation specific to OvHV-2 DNA was performed and OvHV-2 DNA was detected in the brain, cerebellum and spleen, as well as in the lymph nodes. These data indicate that the animal had been infected with OvHV-2, the agent of SA-MCF. For the first time, OvHV-2 was identified and quantified in a Croatian heifer as the causative agent of SA-MCF.Ovčji herpesvirus 2 (OvHV-2) iz roda Rhadinovirus, potporodice Gammaherpesvirinae uzročnik je zarazne korice goveda u nekih vrsta domaćih i divljih preživača. Dosad su u Republici Hrvatskoj zabilježeni mnogi slučajevi sumnje na pojavu zarazne korice u goveda temeljeni na kliničkoj metodi dijagnosticiranja, ali bez dokaza uzročnika bolesti. U lipnju 2005. godine na jednoj farmi u sjeverozapadnoj Hrvatskoj zabilježena je pojava zarazne korice goveda u jedne junice, simentalske pasmine, u dobi od 13 mjeseci, koja je bila smještena u istoj staji s još 17 mliječnih krava i jednom junicom simentalske pasmine te manjim stadom ovaca. Životinja je naglo oboljela uz znakove gubitka apetita, visoke vrućice, seroznog iscjetka iz nosa te pojavom znakova središnjega živčanoga sustava, ataksije, tremora, grčeva i hiperestezije. Životinja je uginula 14. dan od početka prvih znakova bolesti. Razudbom je utvrđena prisutnost oštro ograničenih erozija na sluznici jezika, usne šupljine, jednjaka, sirišta, tankoga, debeloga i slijepoga crijeva te mokraćnoga mjehura. Histopatološki je gotovo u svakom organu, a posebno u mozgu i plućima, utvrđena jaka perivaskularna i intramuralna infiltracija arterija mononuklearnim stanicama, većinom limfocitima. Iz formalinom fiksiranih uzoraka mozga, maloga mozga, slezene i limfnih čvorova izdvojena je DNK i podvrgnuta fluorogenoj real-time PCR amplifikaciji specifičnoj za OvHV-2. OvHV-2 dokazan je i kvantificiran u svim pretraživanim organima. Dobiveni rezultat upućuje na to da je uginula životinja bila zaražena s OvHV-2 što je ujedno i prvi dokaz uzročnika zarazne korice goveda u Hrvatskoj

A NUMB–EFA6B–ARF6 recycling route controls apically restricted cell protrusions and mesenchymal motility

International audienceThe endocytic protein NUMB has been implicated in the control of various polarized cellular processes, including the acquisition of mesenchymal migratory traits through molecular mechanisms that have only been partially defined. Here, we report that NUMB is a negative regulator of a specialized set of understudied, apically restricted, actin-based protrusions, the circular dorsal ruffles (CDRs), induced by either PDGF or HGF stimulation. Through its PTB domain, NUMB binds directly to an N-terminal NPLF motif of the ARF6 guanine nucleotide exchange factor, EFA6B, and promotes its exchange activity in vitro. In cells, a NUMB-EFA6B-ARF6 axis regulates the recycling of the actin regulatory cargo RAC1 and is critical for the formation of CDRs that mark the acquisition of a mesenchymal mode of motility. Consistently, loss of NUMB promotes HGF-induced cell migration and invasion. Thus, NUMB negatively controls membrane protrusions and the acquisition of mesenchymal migratory traits by modulating EFA6B-ARF6 activity

Metabolic implication of tigecycline as an efficacious second-line treatment for sorafenib-resistant hepatocellular carcinoma

Sorafenib represents the current standard of care for patients with advanced-stage hepatocellular carcinoma (HCC). However, acquired drug resistance occurs frequently during therapy and is accompanied by rapid tumor regrowth after sorafenib therapy termination. To identify the mechanism of this therapy-limiting growth resumption, we established robust sorafenib resistance HCC cell models that exhibited mitochondrial dysfunction and chemotherapeutic crossresistance. We found a rapid relapse of tumor cell proliferation after sorafenib withdrawal, which was caused by renewal of mitochondrial structures alongside a metabolic switch toward high electron transport system (ETS) activity. The translation-inhibiting antibiotic tigecycline impaired the biogenesis of mitochondrial DNA-encoded ETS subunits and limited the electron acceptor turnover required for glutamine oxidation. Thereby, tigecycline prevented the tumor relapse in vitro and in murine xenografts in vivo. These results offer a promising second-line therapeutic approach for advanced-stage HCC patients with progressive disease undergoing sorafenib therapy or treatment interruption due to severe adverse events

Identification of regulatory variants associated with genetic susceptibility to meningococcal disease.

Non-coding genetic variants play an important role in driving susceptibility to complex diseases but their characterization remains challenging. Here, we employed a novel approach to interrogate the genetic risk of such polymorphisms in a more systematic way by targeting specific regulatory regions relevant for the phenotype studied. We applied this method to meningococcal disease susceptibility, using the DNA binding pattern of RELA - a NF-kB subunit, master regulator of the response to infection - under bacterial stimuli in nasopharyngeal epithelial cells. We designed a custom panel to cover these RELA binding sites and used it for targeted sequencing in cases and controls. Variant calling and association analysis were performed followed by validation of candidate polymorphisms by genotyping in three independent cohorts. We identified two new polymorphisms, rs4823231 and rs11913168, showing signs of association with meningococcal disease susceptibility. In addition, using our genomic data as well as publicly available resources, we found evidences for these SNPs to have potential regulatory effects on ATXN10 and LIF genes respectively. The variants and related candidate genes are relevant for infectious diseases and may have important contribution for meningococcal disease pathology. Finally, we described a novel genetic association approach that could be applied to other phenotypes