Modelling Hydrogen Induced Stress Corrosion Cracking in Austenitic Stainless Steel

The authors are thankful to the University of Aberdeen and Apache North Sea for their support for this project.Peer reviewedPostprin

Peningkatan Skil Presentasi Ilmiah Berbahasa Inggris Mahasiswa di Universitas Bumigora Berbasis Strategi Graphic Organizers (GOs)

The GOs (Graphic Organizers) strategy, which was used in reading comprehension and writing skills research, was then developed into a strategy that could be used as a medium for developing ppt materials. and as an effective and efficient presentation strategy to be used in scientific presentations. This GOs strategy is applied in guiding students in the computer science undergraduate study program in the form of community service (PkM) aimed at increasing student creativity as participants in developing GOs-based creative materials and developing communication skills in delivering scientific presentation materials in class. . This activity was carried out for level I students at Bumigora University with a total of 30 participants. The following are the solutions and steps involved in this PkM activity, namely the use of Graphic Organizers as an effective solution in providing guidance and improvement in conducting scientific presentations carried out by PkM partners. . There are two methods used in providing guidance on the use of the GOs strategy, namely the lecture method where they are given an understanding of the basic concepts of GOs and the simulation method or practice of implementing the Graphic Organizers strategy directly which is carried out by the facilitator/PKM implementation team and followed by the participants. in a participatory manner. The results of this activity show good results and the level of achievement of its use is high. Based on structured observations, it reached a score of 3.7 with a percentage of 73%. The second evaluation was carried out by measuring the perceptions of GOs users, which was a score of 3.8 with a percentage of 77%. Evaluation based on this perception value is high (3.01-4.0)

Kids Preneur (Kp), Solusi Pendidikan Karakter untuk Anak Jalanan Kampung Dayak, Purwokerto Selatan

Kampung Sri Rahayu (Dayak village) is a marginalized village in the town of Purwokerto with majority of the society bearing the social problems, such as prostitutes, transvestites, unemployed, beggars and street children. There are at least 200 street children in this village, and only 20 percent are able to receive education until graduated elementary school. The main factors causing educational process blocked in this village is the lack of parental support and absence of local government programs. This condition makes mental street children in Dayak village materialistic, self-sufficient and not depend on others. Therefore we need Kids Preneur (KP) as an alternative education so that street children in Dayak village still has a chance to grow up, standalone, creative based on religious character. The objectives of this program are: 1) Increase the knowledge, skills street children of Dayak village; 2) Increase environmental awareness and creative street children of Dayak village; 3) Grow the spirit of standalone and religious life street children of Dayak village. Method of implementation this program include: 1) Kids Prenuer Leadership that aims inculcate spirit of leadership and standalone on street children; 2) Kids Preneur Educative that aim to give education such as hardskill to street children; 3) Kids Preneur Innovative that aims to give softskill training, creative attitude to environmental conditions; 4) Kids Preneur Community, is a forum for the street children of Dayak village to learn the knowledge and entrepreneurship. The results and conclusions of the implementation of Kids Preneur's programs are to improve the knowledge, skills, spirit care for environment, creative, standalone, religious and entrepreneurial character to street children of Dayak village, South Purwokerto. So that the education of the marginalized society gradually be resolved

A simple method for generating full length cDNA from low abundance partial genomic clones

BACKGROUND: PCR amplification of target molecules involves sequence specific primers that flank the region to be amplified. While this technique is generally routine, its applicability may not be sufficient to generate a desired target molecule from two separate regions involving intron /exon boundaries. For these situations, the generation of full-length complementary DNAs from two partial genomic clones becomes necessary for the family of low abundance genes. RESULTS: The first approach we used for the isolation of full-length cDNA from two known genomic clones of Hox genes was based on fusion PCR. Here we describe a simple and efficient method of amplification for homeobox D13 (HOXD13) full length cDNA from two partial genomic clones. Specific 5' and 3' untranslated region (UTR) primer pairs and website program (primer3_www.cgv0.2) were key steps involved in this process. CONCLUSIONS: We have devised a simple, rapid and easy method for generating cDNA clone from genomic sequences. The full length HOXD13 clone (1.1 kb) generated with this technique was confirmed by sequence analysis. This simple approach can be utilized to generate full-length cDNA clones from available partial genomic sequences

Decreased STARD10 expression is associated with defective insulin secretion in humans and mice

Genetic variants near ARAP1 (CENTD2) and STARD10 influence type 2 diabetes (T2D) risk. The risk alleles impair glucose-induced insulin secretion and, paradoxically but characteristically, are associated with decreased proinsulin:insulin ratios, indicating improved proinsulin conversion. Neither the identity of the causal variants nor the gene(s) through which risk is conferred have been firmly established. Whereas ARAP1 encodes a GTPase activating protein, STARD10 is a member of the steroidogenic acute regulatory protein (StAR)-related lipid transfer protein family. By integrating genetic fine-mapping and epigenomic annotation data and performing promoter-reporter and chromatin conformational capture (3C) studies in β cell lines, we localize the causal variant(s) at this locus to a 5 kb region that overlaps a stretch-enhancer active in islets. This region contains several highly correlated T2D-risk variants, including the rs140130268 indel. Expression QTL analysis of islet transcriptomes from three independent subject groups demonstrated that T2D-risk allele carriers displayed reduced levels of STARD10 mRNA, with no concomitant change in ARAP1 mRNA levels. Correspondingly, β-cell-selective deletion of StarD10 in mice led to impaired glucose-stimulated Ca2+ dynamics and insulin secretion and recapitulated the pattern of improved proinsulin processing observed at the human GWAS signal. Conversely, overexpression of StarD10 in the adult β cell improved glucose tolerance in high fat-fed animals. In contrast, manipulation of Arap1 in β cells had no impact on insulin secretion or proinsulin conversion in mice. This convergence of human and murine data provides compelling evidence that the T2D risk associated with variation at this locus is mediated through reduction in STARD10 expression in the β cell

Musculoskeletal Manifestations of COVID-19: A Systematic Search and Review

Coronavirus disease (COVID-19) started its journey around the world from Wuhan, China and gradually became a pandemic. COVID-19 often affects the respiratory system, but symptoms may include fatigue, myalgia, arthralgia, arthritis, and spine and bone pain as presenting complaints. In the present systematic search and review, we aim to highlight the musculoskeletal manifestations during COVID-19. PubMed Central and Google Scholar search engines were searched for the key words “muscle pain”, “joint pain”, “body ache”, and “fatigue”, in Covid-19 patients. After screening, a total of 76 articles dated between January 1 and July 1, 2020 met the inclusion criteria and were included in the study. All articles were published in English comprising 36,558 COVID-19 cases. In cross-sectional studies, fatigue was found in 55%, myalgia in 26%, and arthralgia in 20% of cases, respectively. In cohort studies, fatigue was found in 35%, myalgia in 15%, and arthralgia in 5%, respectively. Sporadic case reports also mention back pain, bone pain, myositis, and arthritis as presenting symptoms of COVID-19. Fatigue was the most frequent musculoskeletal (MSK) manifestation of COVID-19 followed by myalgia and joint pain. The frequency of the different MSK manifestations in COVID-19 may vary widely among different geographic regions. MSK like fatigue, myalgia and arthralgia are frequent symptoms in COVID-19 patients and may vary in different countries

Tuftsin Promotes an Anti-Inflammatory Switch and Attenuates Symptoms in Experimental Autoimmune Encephalomyelitis

Multiple sclerosis (MS) is a demyelinating autoimmune disease mediated by infiltration of T cells into the central nervous system after compromise of the blood-brain barrier. We have previously shown that administration of tuftsin, a macrophage/microglial activator, dramatically improves the clinical course of experimental autoimmune encephalomyelitis (EAE), a well-established animal model for MS. Tuftsin administration correlates with upregulation of the immunosuppressive Helper-2 Tcell (Th2) cytokine transcription factor GATA-3. We now show that tuftsin-mediated microglial activation results in shifting microglia to an anti-inflammatory phenotype. Moreover, the T cell phenotype is shifted towards immunoprotection after exposure to tuftsin-treated activated microglia; specifically, downregulation of pro-inflammatory Th1 responses is triggered in conjunction with upregulation of Th2-specific responses and expansion of immunosuppressive regulatory T cells (Tregs). Finally, tuftsin-shifted T cells, delivered into animals via adoptive transfer, reverse the pathology observed in mice with established EAE. Taken together, our findings demonstrate that tuftsin decreases the proinflammatory environment of EAE and may represent a therapeutic opportunity for treatment of MS

1B/(−)IRE DMT1 Expression during Brain Ischemia Contributes to Cell Death Mediated by NF-κB/RelA Acetylation at Lys310

The molecular mechanisms responsible for increasing iron and neurodegeneration in brain ischemia are an interesting area of research which could open new therapeutic approaches. Previous evidence has shown that activation of nuclear factor kappa B (NF-κB) through RelA acetylation on Lys310 is the prerequisite for p50/RelA-mediated apoptosis in cellular and animal models of brain ischemia. We hypothesized that the increase of iron through a NF-κB-regulated 1B isoform of the divalent metal transporter-1 (1B/DMT1) might contribute to post-ischemic neuronal damage. Both in mice subjected to transient middle cerebral artery occlusion (MCAO) and in neuronally differentiated SK-N-SH cells exposed to oxygen-glucose-deprivation (OGD), 1A/DMT1 was only barely expressed while the 1B/DMT1 without iron-response-element (−IRE) protein and mRNA were early up-regulated. Either OGD or over-expression of 1B/(−)IRE DMT1 isoform significantly increased iron uptake, as detected by total reflection X-ray fluorescence, and iron-dependent cell death. Iron chelation by deferoxamine treatment or (−)IRE DMT1 RNA silencing displayed significant neuroprotection against OGD which concomitantly decreased intracellular iron levels. We found evidence that 1B/(−)IRE DMT1 was a target gene for RelA activation and acetylation on Lys310 residue during ischemia. Chromatin immunoprecipitation analysis of the 1B/DMT1 promoter showed there was increased interaction with RelA and acetylation of H3 histone during OGD exposure of cortical neurons. Over-expression of wild-type RelA increased 1B/DMT1 promoter-luciferase activity, the (−)IRE DMT1 protein, as well as neuronal death. Expression of the acetylation-resistant RelA-K310R construct, which carried a mutation from lysine 310 to arginine, but not the acetyl-mimic mutant RelA-K310Q, down-regulated the 1B/DMT1 promoter, consequently offering neuroprotection. Our data showed that 1B/(−)IRE DMT1 expression and intracellular iron influx are early downstream responses to NF-κB/RelA activation and acetylation during brain ischemia and contribute to the pathogenesis of stroke-induced neuronal damage

Laser capture microdissection of human pancreatic islets reveals novel eQTLs associated with type 2 diabetes.

Genome wide association studies (GWAS) for type 2 diabetes (T2D) have identified genetic loci that often localise in non-coding regions of the genome, suggesting gene regulation effects. We combined genetic and transcriptomic analysis from human islets obtained from brain-dead organ donors or surgical patients to detect expression quantitative trait loci (eQTLs) and shed light into the regulatory mechanisms of these genes. Pancreatic islets were isolated either by laser capture microdissection (LCM) from surgical specimens of 103 metabolically phenotyped pancreatectomized patients (PPP) or by collagenase digestion of pancreas from 100 brain-dead organ donors (OD). Genotyping (> 8.7 million single nucleotide polymorphisms) and expression (> 47,000 transcripts and splice variants) analyses were combined to generate cis-eQTLs. After applying genome-wide false discovery rate significance thresholds, we identified 1,173 and 1,021 eQTLs in samples of OD and PPP, respectively. Among the strongest eQTLs shared between OD and PPP were CHURC1 (OD p-value=1.71 × 10 <sup>-24</sup> ; PPP p-value = 3.64 × 10 <sup>-24</sup> ) and PSPH (OD p-value = 3.92 × 10 <sup>-26</sup> ; PPP p-value = 3.64 × 10 <sup>-24</sup> ). We identified eQTLs in linkage-disequilibrium with GWAS loci T2D and associated traits, including TTLL6, MLX and KIF9 loci, which do not implicate the nearest gene. We found in the PPP datasets 11 eQTL genes, which were differentially expressed in T2D and two genes (CYP4V2 and TSEN2) associated with HbA1c but none in the OD samples. eQTL analysis of LCM islets from PPP led us to identify novel genes which had not been previously linked to islet biology and T2D. The understanding gained from eQTL approaches, especially using surgical samples of living patients, provides a more accurate 3-dimensional representation than those from genetic studies alone