APPRAISAL ANALYSIS OF THE JAKARTA POST’S NEWS ARTICLE ON THE ENVIRONMENTAL ISSUE

This research discusses journalists' ideology and position in four selected news articles from the English-language newspaper, The Jakarta Post. The news articles report on the no-deforestation pledge of the 26th Conference of Parties (COP26), which commits to working collectively to halt and reverse forest loss and land degradation by 2030. This research aims to find the appraisal devices used by the journalist and explain the journalist's ideology and position toward the deforestation pledge. The revelation of ideology is analyzed through Appraisal System by Martin and White (2005). There are 90 sentences obtained in this thesis. The result shows that the three appraisal subsystems are applied in the texts. We found that the ideology of the journalists in two opposite sides. From four selected news articles, two news articles support the capitalist ideology, and the other supports the environmentally friendly ideology

Search in weighted complex networks

We study trade-offs presented by local search algorithms in complex networks which are heterogeneous in edge weights and node degree. We show that search based on a network measure, local betweenness centrality (LBC), utilizes the heterogeneity of both node degrees and edge weights to perform the best in scale-free weighted networks. The search based on LBC is universal and performs well in a large class of complex networks.Comment: 14 pages, 5 figures, 4 tables, minor changes, added a referenc

DIAGNOSTIK KESULITAN BELAJAR MAHASISWA BERDASARKAN SISTEM METAKOGNIF PADA TAKSONOMI MARZANO

Penelitian ini bertujuan untuk mendeskripsikan kesulitan belajar mahasiswa pada mata kuliah Kalkulus. Penelitian ini termasuk dalam penelitian studi kasus dengan menggunakan pendekatan deskriptif kuantitatif. Subjek dari penelitian ini adalah mahasiswa Program Studi Sistem Komputer dan Prodi Teknologi Informasi ITB STIKOM Bali yang mengikuti mata kuliah kalkulus pada semester genap 2022/2023. Pengumpulan data dilakukan menggunakan tes diagnostic berupa tes hasil belajar kalkulus dan kuesioner kesulitan belajar terhadap 31 mahasiswa. Kesulitan belajar dilihat dari sistem metakognitif pada Takzonmi Marzano yang teridiri dari level specifying goals process monitoring, monitoring clarity dan monitoring accuracy.  Hasil penelitian menunjukkan bahwa (1) Pada level specifying goals (penetuan berbagai tujuan belajar) diketahui bahwa mahasiswa memiliki kesulitan dalam menentukan tujuan belajar adalah sebesar 51,61%.  (2) Pada level process monitoring menunjukkan bahwa mahasiswa memiliki kesulitan belajar sebesar 64,52%. (3) Pada level monitoring clarity menunjukkan bahwa mahasiswa memiliki kesulitan belajar sebesar 51,61%. (4) Pada level Monitoring Accuracy menunjukkan bahwa mahasiswa memiliki kesulitan belajar sebesar 48,39%

Estandarización de hojas de Feronia limonia L. por HPLC, HPTLC, parámetros fisicoquímicos e histológicos

Feronia limonia (Familia Rutaceae, subfamilia Aurantioideae), comúnmente conocida como kaitha o manzana de madera, y es extensamente usada como una ethnomedicina en India. Sus hojas son indicadas para una amplia variedad de dolencias como diarrea, desórdenes urinarios, el tratamiento de hemorroides, acidez, úlceras, tiña y otras infecciones crónicas de la piel. Sin embargo, la información científica detallada no está disponible para identificar el material de la especie y averiguar su calidad y pureza. En la presente comunicación, un análisis cualitativo de extractos de Feronia limonia (FL), se realizó por HPTLC y HPLC, lo que proporcionó información cualitativa de los componentes bioactivos presentes en los extractos. También, los caracteres anatómicos, fisico- químicos y morfológicos, junto con un examen fitoquímico y análisis de fluorescencia de la planta en polvo fueron realizados para la identificación sistémica y autentificación de las hojas. Este estudio proporciona la información de referencia para identificación y caracterización de las hojas de FL y sus extractos

PELATIHAN KETERAMPILAN KOMPUTER BAGI ANAK-ANAK PANTI ASUHAN TAT TWAM ASI DENPASAR

Mitra dalam kegiatan pengabdian ini adalah Panti Asuhan Tat Twam Asi Denpasar. Permasalahan utama yang dihadapi mitra yaitu kurangnya keterampilan anak-anak panti dalam menggunakan teknologi komputer sebagai persiapan menuju dunia kerja. Tujuan kegiatan pengabdian adalah meningkatkan pemahaman dalam menggunakan internet sehat dan mengetahui dampak media social bagi remaja, meningkatkan kemampuan menggunakan microsoft office dan keterampilan dalam desain grafis menggunakan Canva. Peserta yang terlibat dalam kegiatan ini sebanyak 24 anak pada jenjang SMP dan SMA. Metode pelaksanaan Program Kemitraan Masyarakat (PKM) dibagi menjadi tiga tahap yaitu perencanaan, pelaksanaan, dan evaluasi. Peningkatan pemahaman dan keterampilan peserta diukur menggunakan kuesioner diakhir kegiatan pengabdian. Hasil pengabdian menunjukkan bahwa (1) pemahaman peserta terkait internet sehat dan dampak sosial media bagi remaja sebelum kegiatan pelatihan adalah sebesar 25% dan terjadi peningkatan sebesar 75% setelah kegiatan berlangsung menjadi 100% dengan kategori baik, (2) pemahaman peserta terkait penggunaan Microsoft Office sebagai aplikasi perkantoran sebelum kegiatan pelatihan adalah sebesar 20,83% dan terjadi peningkatan sebesar 79,17% setelah kegiatan berlangsung menjadi 100% dengan kategori baik. (3) pemahaman peserta dalm membuat desain grafis menggunakan Canva menunjukkan bahwa sebelum pelatihan, pemahamn peserta sebesar 12,50% dan terjadi peningkatan sebesar 87,50% setelah kegiatan berlangsung menjadi 100% dengan kategori baik. Seluruh peserta memberikan respon positif terhadap pelaksanaan kegiatan pengabdian masyarakat

The pathophysiology of fluid and electrolyte balance in the older adult surgical patient

Background & aims: Age-related physiological changes predispose even the healthy older adult to fluid and electrolyte abnormalities which can cause morbidity and mortality. The aim of this narrative review is to highlight key aspects of age-related pathophysiological changes that affect fluid and electrolyte balance in older adults and underpin their importance in the perioperative period. Methods: The Web of Science, MEDLINE, PubMed and Google Scholar databases were searched using key terms for relevant studies published in English on fluid balance in older adults during the 15 years preceding June 2013. Randomised controlled trials and large cohort studies were sought; other studieswere used when these were not available. The bibliographies of extracted papers were also searched for relevant articles. Results: Older adults are susceptible to dehydration and electrolyte abnormalities, with causes ranging from physical disability restricting access to fluid intake to iatrogenic causes including polypharmacy and unmonitored diuretic usage. Renal senescence, as well as physical and mental decline, increase this susceptibility. Older adults are also predisposed to water retention and related electrolyte abnormalities, exacerbated at times of physiological stress. Positive fluid balance has been shown to be an independent risk factor for morbidity and mortality in critically ill patients with acute kidney injury. Conclusions: Age-related pathophysiological changes in the handling of fluid and electrolytes make older adults undergoing surgery a high-risk group and an understanding of these changes will enable better management of fluid and electrolyte therapy in the older adult

GWAS and meta-analysis identifies 49 genetic variants underlying critical COVID-19

Critical illness in COVID-19 is an extreme and clinically homogeneous disease phenotype that we have previously shown1 to be highly efficient for discovery of genetic associations2. Despite the advanced stage of illness at presentation, we have shown that host genetics in patients who are critically ill with COVID-19 can identify immunomodulatory therapies with strong beneficial effects in this group3. Here we analyse 24,202 cases of COVID-19 with critical illness comprising a combination of microarray genotype and whole-genome sequencing data from cases of critical illness in the international GenOMICC (11,440 cases) study, combined with other studies recruiting hospitalized patients with a strong focus on severe and critical disease: ISARIC4C (676 cases) and the SCOURGE consortium (5,934 cases). To put these results in the context of existing work, we conduct a meta-analysis of the new GenOMICC genome-wide association study (GWAS) results with previously published data. We find 49 genome-wide significant associations, of which 16 have not been reported previously. To investigate the therapeutic implications of these findings, we infer the structural consequences of protein-coding variants, and combine our GWAS results with gene expression data using a monocyte transcriptome-wide association study (TWAS) model, as well as gene and protein expression using Mendelian randomization. We identify potentially druggable targets in multiple systems, including inflammatory signalling (JAK1), monocyte-macrophage activation and endothelial permeability (PDE4A), immunometabolism (SLC2A5 and AK5), and host factors required for viral entry and replication (TMPRSS2 and RAB2A)

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 hospitalisation2-4 following SARS-CoV-2 infection. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from critically-ill cases with population controls in order to find underlying disease mechanisms. Here, we use whole genome sequencing in 7,491 critically-ill cases 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 involved in interferon signalling (IL10RB, PLSCR1), leucocyte differentiation (BCL11A), and blood type antigen secretor status (FUT2). Using transcriptome-wide association and colocalisation to infer the effect of gene expression on disease severity, we find evidence implicating multiple genes, including reduced expression of a membrane flippase (ATP11A), and increased mucin expression (MUC1), in critical disease. Mendelian randomisation provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5, CD209) and 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 critically-ill cases and population controls is highly efficient for detection of therapeutically-relevant mechanisms of disease

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 care(1) or hospitalization(2-4) 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. © 2022, The Author(s)

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice