Microclimate affects landscape level persistence in the British Lepidoptera

Microclimate has been known to drive variation in the distribution and abundance of insects for some time. Until recently however, quantification of microclimatic effects has been limited by computing constraints and the availability of fine-scale biological data. Here, we tested fine-scale patterns of persistence/extinction in butterflies and moths against two computed indices of microclimate derived from Digital Elevation Models: a summer solar index, representing fine-scale variation in temperature, and a topographic wetness index, representing fine-scale variation in moisture availability. We found evidence of microclimate effects on persistence in each of four 20 × 20 km British landscapes selected for study (the Brecks, the Broads, Dartmoor, and Exmoor). Broadly, local extinctions occurred more frequently in areas with higher minimum or maximum solar radiation input, while responses to wetness varied with landscape context. This negative response to solar radiation is consistent with a response to climatic warming, wherein grid squares with particularly high minimum or maximum insolation values provided an increasingly adverse microclimate as the climate warmed. The variable response to wetness in different landscapes may have reflected spatially variable trends in precipitation. We suggest that locations in the landscape featuring cooler minimum and/or maximum temperatures could act as refugia from climatic warming, and may therefore have a valuable role in adapting conservation to climatic change

PROFIL WISATAWAN MUSEUM RADYA PUSTAKA SURAKARTA

Anggit Margaret, C9407031 2011. Profil Wisatawan Museum Radya Pustaka Surakarta. Program Studi Diploma III Usaha Perjalanan Wisata Fakultas Sastra Dan Seni Rupa Universitas Sebelas Maret Surakarta. Penelitian tugas akhir ini mengkaji tentang Profil Wisatawan di Museum Radya Pustaka Surakarta. Tujuan dari penelitian ini adalah untuk mengetahui dari daerah mana saja wisatawan yang berkunjung ke Museum Radya Pustaka, bagaimana ciri-ciri wisatawan yang berkunjung ke Museum Radya Pustaka serta harapan-harapan yang diinginkan wisatawan terhadap Museum Radya Pustaka. Penelitian dilakukan dengan metode kualitatif. Pengumpulan data dilakukan melalui wawancara dengan narasumber wisatawan yang berkujung di Museum Radya Pustaka Surakarta tempat penulis melakukan penelitian, serta studi pustaka dan studi dokumen guna menambah sumber data. Hasil penelitian menunjukkan bahwa (1) Sebagian besar wisatawan yang datang berasal dari Semarang sebesar 32%. (2) Mayoritas wisatawan yang berkunjung ke Museum Radya Pustaka berusia antara 17-25 tahun dan kebanyakan dari mereka adalah pelajar atau mahasiswa dengan prosentase 52%. (3) Sebagian besar wisatawan yang datang ke Museum Radya Pustaka adalah bertujuan untuk melakukan penelitian yaitu sebesar 34%. (4) Harapan wisatawan yang berkunjung terhadap kelangsungan Museum Radya Pustaka sebagian besar adalah agar ditingkatkan lagi pengelolaan dan keamanan museum, agar kejadian hilangnya benda-benda koleksi museum tidak terulang lagi dikemudian hari. Kesimpulan dari hasil penelitian ini bahwa wisatawan yang berkujung ke Museum Radya Pustaka Surakarta mayoritas berasal dari Semarang, mayoritas berusia 17-25 tahun dan kebanyakan dari mereka adalah berprofesi sebagai pelajar dan mahasiswa. Kebanyakan wisatawan yang datang bertujuan untuk melakukan penelitian, serta harapan wisatawan terhadap Museum Radya Pustaka adalah supaya lebih ditingkatkan lagi pengelolaan dan keamanan museum

SARS-CoV-2 infects the human kidney and drives fibrosis in kidney organoids

Kidney failure is frequently observed during and after COVID-19, but it remains elusive whether this is a direct effect of the virus. Here, we report that SARS-CoV-2 directly infects kidney cells and is associated with increased tubule-interstitial kidney fibrosis in patient autopsy samples. To study direct effects of the virus on the kidney independent of systemic effects of COVID-19, we infected human-induced pluripotent stem-cell-derived kidney organoids with SARS-CoV-2. Single-cell RNA sequencing indicated injury and dedifferentiation of infected cells with activation of profibrotic signaling pathways. Importantly, SARS-CoV-2 infection also led to increased collagen 1 protein expression in organoids. A SARS-CoV-2 protease inhibitor was able to ameliorate the infection of kidney cells by SARS-CoV-2. Our results suggest that SARS-CoV-2 can directly infect kidney cells and induce cell injury with subsequent fibrosis. These data could explain both acute kidney injury in COVID-19 patients and the development of chronic kidney disease in long COVID

Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses

To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1–11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely

A História da Alimentação: balizas historiográficas

Os M. pretenderam traçar um quadro da História da Alimentação, não como um novo ramo epistemológico da disciplina, mas como um campo em desenvolvimento de práticas e atividades especializadas, incluindo pesquisa, formação, publicações, associações, encontros acadêmicos, etc. Um breve relato das condições em que tal campo se assentou faz-se preceder de um panorama dos estudos de alimentação e temas correia tos, em geral, segundo cinco abardagens Ia biológica, a econômica, a social, a cultural e a filosófica!, assim como da identificação das contribuições mais relevantes da Antropologia, Arqueologia, Sociologia e Geografia. A fim de comentar a multiforme e volumosa bibliografia histórica, foi ela organizada segundo critérios morfológicos. A seguir, alguns tópicos importantes mereceram tratamento à parte: a fome, o alimento e o domínio religioso, as descobertas européias e a difusão mundial de alimentos, gosto e gastronomia. O artigo se encerra com um rápido balanço crítico da historiografia brasileira sobre o tema

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Bilateral Ophthalmoplegia with Preservation of the Bell's Phenomenon in a 68-Year old Female with an Eosinophilic Adenoma of the Pituitary

Headache; DiplopiaA female patient initially evaluated in 1957 for symptoms and signs of a suprasellar mass with acromegaly. Radiation therapy was instituted with a diagnosis of eosinophilic adenoma of the pituitary, with prompt clearing of her partial field cut and motility disturbance on the right and lessening of her headache disorder.N/AN/ABell phenomenonSurgeryAttache

The product of the UL6 gene of herpes simplex virus type 1 is associated with virus capsids

We report on the analysis of the UL6 and UL7 open reading frames of the herpes simplex virus type 1 (HSV-1) genome. The UL6 and UL7 transcripts were identified in HSV-1-infected cells by Northern blotting and shown to be coterminal at their 3′ ends. Both transcripts were synthesized in the presence of phosphonoacetic acid, although in reduced amounts, indicating that UL6 and UL7 are expressed as delayed-early or γ-1 genes. The 5′ ends of the two transcripts were mapped by S1 nuclease and primer extension analysis. A polyclonal antiserum directed against an Escherichia coli-expressed 6X His-UL6 fusion protein identified a protein of approximate Mr 75,000 in cells infected with either HSV-1 or with a vaccinia virus recombinant expressing the HSV-1 UL6 protein. As with the transcript, the UL6 protein was synthesized at reduced levels in the absence of viral DNA replication. Western immunoblotting showed that the UL6 protein was present in purified virions but not in L-particles of HSV-1, and that it was located exclusively in the tegument/capsid fraction of virion. Further analysis of the UL6 protein revealed that this protein was associated with virus capsids

Suppression of amber nonsense mutations of herpes simplex virus type 1 in a tissue culture system

We have investigated the ability of monkey kidney cell lines (SupD3 and SupD12) inducibly expressing an amber suppressor tRNAser to suppress amber nonsense mutations in three genes of herpes simplex virus type 1 (HSV-1). HSV-1 mutant TK4, which contains a nonsense mutation in the non-essential viral thymidine kinase (TK) gene, synthesized a full-length TK polypeptide at about 30% of the wild-type (wt) level in induced SupD3 cells but not in the parental non-suppressor (Sup0) cells. Using complementing cells, we constructed HSV-1 mutants carrying nonsense mutations in an essential gene, UL8, encoding a protein essential for viral DNA replication (ambUL8) or in a partially dispensable gene, UL12, encoding alkaline nuclease (ambUL12). The growth of the mutants in Vero or Sup0 cells was either totally (ambUL8) or severely (ambUL12) impaired, whereas in cells expressing suppressor tRNA the mutants produced infectious virus. However, the yields were much lower than obtained with wt HSV-1. In Vero or Sup0 cells the mutants ambUL8 and ambUL12 failed to synthesize full-length UL8 and UL12 protein products, respectively. Western immuno-blotting showed that the virus ambUL12 produced full-length UL12 protein in SupD12 cells which yielded a level of 25.9% of the alkaline nuclease activity of the wt HSV-1 control. Our results show that the levels of suppression of the nonsense mutations in ambUL8 and ambUL12 are insufficient to allow their continuing propagation in the available Sup+ cells. Possible reasons are discussed