COVID-19 cases in spectators returning to Finland from UEFA Euro 2020 matches in Saint Petersburg

UEFA Euro 2020 tournament was scheduled to take place in 2020, but due to the coronavirus disease 2019 (COVID-19) pandemic was rescheduled to start on 11 June 2021. Approximately 4500 Finnish spectators participated, travelling between Finland and Russia during the period of 16 to 30 June to attend matches played on 16 and 21 June. A total of 419 persons returning from Russia or with a connection to Russia were detected positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Of the 321 sequenced samples 303 turned out to be of the Delta variant. None of these cases was hospitalised. In the following weeks findings of the Delta variant increased rapidly. Thus, EURO 2020 travel-related imported cases likely facilitated this rapid surge of Delta variant, but this impact would likely have been seen with the typical increase in the number of travellers entering Finland later in the summer.Peer reviewe

CLRN1 Is Nonessential in the Mouse Retina but Is Required for Cochlear Hair Cell Development

Mutations in the CLRN1 gene cause Usher syndrome type 3 (USH3), a human disease characterized by progressive blindness and deafness. Clarin 1, the protein product of CLRN1, is a four-transmembrane protein predicted to be associated with ribbon synapses of photoreceptors and cochlear hair cells, and recently demonstrated to be associated with the cytoskeleton. To study Clrn1, we created a Clrn1 knockout (KO) mouse and characterized the histological and functional consequences of Clrn1 deletion in the retina and cochlea. Clrn1 KO mice do not develop a retinal degeneration phenotype, but exhibit progressive loss of sensory hair cells in the cochlea and deterioration of the organ of Corti by 4 months. Hair cell stereocilia in KO animals were longer and disorganized by 4 months, and some Clrn1 KO mice exhibited circling behavior by 5–6 months of age. Clrn1 mRNA expression was localized in the retina using in situ hybridization (ISH), laser capture microdissection (LCM), and RT–PCR. Retinal Clrn1 transcripts were found throughout development and adulthood by RT–PCR, although expression peaked at P7 and declined to undetectable levels in adult retina by ISH. LCM localized Clrn1 transcripts to the retinas inner nuclear layer, and WT levels of retinal Clrn1 expression were observed in photoreceptor-less retinas. Examination of Clrn1 KO mice suggests that CLRN1 is unnecessary in the murine retina but essential for normal cochlear development and function. This may reflect a redundancy in the mouse retina not present in human retina. In contrast to mouse KO models of USH1 and USH2, our data indicate that Clrn1 expression in the retina is restricted to the Müller glia. This is a novel finding, as most retinal degeneration associated proteins are expressed in photoreceptors, not in glia. If CLRN1 expression in humans is comparable to the expression pattern observed in mice, this is the first report of an inner retinal protein that, when mutated, causes retinal degeneration

The Batten Disease Palmitoyl Protein Thioesterase 1 Gene Regulates Neural Specification and Axon Connectivity during Drosophila Embryonic Development

Palmitoyl Protein Thioesterase 1 (PPT1) is an essential lysosomal protein in the mammalian nervous system whereby defects result in a fatal pediatric disease called Infantile Neuronal Ceroids Lipofuscinosis (INCL). Flies bearing mutations in the Drosophila ortholog Ppt1 exhibit phenotypes similar to the human disease: accumulation of autofluorescence deposits and shortened adult lifespan. Since INCL patients die as young children, early developmental neural defects due to the loss of PPT1 are postulated but have yet to be elucidated. Here we show that Drosophila Ppt1 is required during embryonic neural development. Ppt1 embryos display numerous neural defects ranging from abnormal cell fate specification in a number of identified precursor lineages in the CNS, missing and disorganized neurons, faulty motoneuronal axon trajectory, and discontinuous, misaligned, and incorrect midline crossings of the longitudinal axon bundles of the ventral nerve cord. Defects in the PNS include a decreased number of sensory neurons, disorganized chordotonal neural clusters, and abnormally shaped neurons with aberrant dendritic projections. These results indicate that Ppt1 is essential for proper neuronal cell fates and organization; and to establish the local environment for proper axon guidance and fasciculation. Ppt1 function is well conserved from humans to flies; thus the INCL pathologies may be due, in part, to the accumulation of various embryonic neural defects similar to that of Drosophila. These findings may be relevant for understanding the developmental origin of neural deficiencies in INCL

Terveydenhuollon kansalliset laaturekisteripilotit loppusuoralla

Pilottiprojektin tulokset laaturekisterien toiminnan organisoimisesta kannustavat ­jatkamaan työtä moniammatillisesti ja pitkäjänteisesti. Kansallinen koordinaatio on välttämätöntä laatu- ja vaikuttavuustiedon vertailukelpoisuuden ja hyödyntämisen varmistamiseksi

ミナミ タイヘイヨウ ヒカク チタイ ジョウヤク ケイセイ カテイ ニ オケル オーストタリア ノ カクグンシュク ガイコウ セイサク

Alternate bilayer structures of N,N'-bis(2,5-di-tert-butylphenyl)-3,4,9,10- perylene dicarboximide (PDI), freebase phthalocyanines (Pc), and double-linked free-base phthalocyanine-fullerene dyad (Pc-C 60) were prepared by the Langmuir-Schäfer method and studied using a range of optical spectroscopy methods including femtosecond pump-probe and up-conversion. An efficient quenching of the PDI fluorescence by Pc and Pc-C 60 dyad was observed in both steady-state and time-resolved fluorescence measurements. The quenching takes place in less than a few picoseconds, and is due to energy transfer from perylene dicarboximide to phthalocyanine chromophore in PDI|Pc and PDI|Pc-C 60 films. In the PDI|Pc-C 60 bilayer structure the energy transfer is followed by a charge separation in the Pc-C 60 layer, yielding a long-lived (a few microseconds) intermolecular charge separated state similar to that reported recently for Pc-C 60 Langmuir-Blodgett films (Lehtivuori, H.; et al. J. Phys. Chem. C 2008, 112, 9896-9902)

CLRN1 is nonessential in the mouse retina but is required for cochlear hair cell development.

Mutations in the CLRN1 gene cause Usher syndrome type 3 (USH3), a human disease characterized by progressive blindness and deafness. Clarin 1, the protein product of CLRN1, is a four-transmembrane protein predicted to be associated with ribbon synapses of photoreceptors and cochlear hair cells, and recently demonstrated to be associated with the cytoskeleton. To study Clrn1, we created a Clrn1 knockout (KO) mouse and characterized the histological and functional consequences of Clrn1 deletion in the retina and cochlea. Clrn1 KO mice do not develop a retinal degeneration phenotype, but exhibit progressive loss of sensory hair cells in the cochlea and deterioration of the organ of Corti by 4 months. Hair cell stereocilia in KO animals were longer and disorganized by 4 months, and some Clrn1 KO mice exhibited circling behavior by 5-6 months of age. Clrn1 mRNA expression was localized in the retina using in situ hybridization (ISH), laser capture microdissection (LCM), and RT-PCR. Retinal Clrn1 transcripts were found throughout development and adulthood by RT-PCR, although expression peaked at P7 and declined to undetectable levels in adult retina by ISH. LCM localized Clrn1 transcripts to the retinas inner nuclear layer, and WT levels of retinal Clrn1 expression were observed in photoreceptor-less retinas. Examination of Clrn1 KO mice suggests that CLRN1 is unnecessary in the murine retina but essential for normal cochlear development and function. This may reflect a redundancy in the mouse retina not present in human retina. In contrast to mouse KO models of USH1 and USH2, our data indicate that Clrn1 expression in the retina is restricted to the Müller glia. This is a novel finding, as most retinal degeneration associated proteins are expressed in photoreceptors, not in glia. If CLRN1 expression in humans is comparable to the expression pattern observed in mice, this is the first report of an inner retinal protein that, when mutated, causes retinal degeneration