SEKOLAH SEPAKBOLA USIA MUDA DI BANDA ACEH

Sepakbola merupakan olahraga yang sangat populer dan digemari di dunia, begitu juga di Indonesia. Tak heran jika hampir semua negara di dunia berlomba-lomba menggalang prestasi membanggakan di cabang olahraga ini. Indonesia belum mampu meraih prestasi yang membanggakan di cabang olahraga sepakbola, bahkan Indonesia sulit bersaing di kancah Internasional. Klub-klub sepakbola Aceh juga tidak dapat berbuat banyak di kompetisi internal, sedangkan Aceh merupakan salah satu provinsi yang banyak memunculkan pemain muda berbakat.Kualitas persepakbolaan di Indonesia yang rendah dan minim prestasi ini dikarenakan kurang pembinaan dan pelatihan pemain mulai dari usia dini untuk didik menjadi pemain profesional. Sarana pelatihan yang ada di Indonesia belum serius ke arah profesional seperti akademi sepakbola di Eropa. Di negara-negara maju dalam sepakbola, prestasi tim nasional pada umumnya dilatarbelakangi oleh sistem dan proses pembinaan klub yang sudah mapan.Sekolah sepakbola usia muda di Banda Aceh merupakan sebuah sarana pelatihan dan pembinaan sepakbola pemain usia dini di Banda Aceh. Pemain tersebut akan dididik, dilatih dan dibina sejak dini sebagai usaha pembibitan pemain sepakbola Aceh yang potensial. Sekolah sepakbola ini berlokasi di Lhong Raya, sesuai dengan rencana pengembangan kawasan pusat olahraga di Banda Aceh. Dengan mengusung tema arsitektur metafora, diharapkan bangunan sekolah sepakbola ini dapat menjadi objek arsitektur yang melekat di masyarakat.Tahap awal dalam proses perancangan Sekolah Sepakbola Usia Muda di Banda Aceh ini adalah studi literatur data dan studi banding. Selanjutnya permasalahan yang ada diidentifikasi dan dianalisis sesuai dengan batasan perancangan. Dalam lingkup batasan tema arsitektur metafora dan kondisi iklim setempat selanjutnya melahirkan konsep perancangan sesuai dengan hasil analisis.Kata kunci: olahraga, sekolah, sepakbolaBanda Ace

The change of non-alcoholic fatty liver disease is associated with risk of incident diabetes

Background & aimsThe effect of change in non-alcoholic fatty liver disease (NAFLD) status on incident diabetes has not been well studied. We aimed to investigate the association of NAFLD development and remission with the risk of incident diabetes during a median of 3.5-year follow-up.MethodsA total of 2690 participants without diabetes were recruited in 2011-2012 and assessed for incident diabetes in 2014. Abdominal ultrasonography was used to determine the change of NAFLD. 75 g oral glucose tolerance test (OGTT) was performed to determine diabetes. NAFLD severity was assessed using Gholam’s model. The odds ratios (ORs) for incident diabetes were estimated by logistic regression models.ResultsNAFLD was developed in 580 (33.2%) participants and NAFLD remission occurred in 150 (15.9%) participants during a median of 3.5-year follow-up. A total of 484 participants developed diabetes during follow-up, including 170 (14.6%) in consistent non-NAFLD group, 111 (19.1%) in NAFLD developed group, 19 (12.7%) in NAFLD remission group, and 184 (23.2%) in sustained NAFLD group. The development of NAFLD increased the risk of incident diabetes by 43% (OR, 1.43; 95%CI, 1.10-1.86) after adjustment for multiple confounders. Compared with sustained NAFLD group, remission of NAFLD reduced the risk of incident diabetes by 52% (OR, 0.48; 95%CI, 0.29-0.80). The effect of NAFLD alteration on incident diabetes was not changed after adjustment for body mass index or waist circumference, change of body mass index or waist circumference. In NAFLD remission group, participants with non-alcoholic steatohepatitis (NASH) at baseline were more likely to develop diabetes (OR, 3.03; 95%CI, 1.01-9.12).ConclusionsNAFLD development increases the risk of incident diabetes, whereas NAFLD remission reduces the risk of incident diabetes. Moreover, presence of NASH at baseline could attenuate the protective effect of NAFLD remission on incident diabetes. Our study suggests that early intervention of NAFLD and maintenance of non-NAFLD are important for prevention of diabetes

Human brain organoid-on-a-chip to model prenatal nicotine exposure

Nicotine has been recognized to trigger various neuronal disabilities in the fetal brain and long-lasting behavioral deficits in offspring. However, further understanding of fetal brain development under nicotine exposure is challenging due to the limitations of existing animal models. Here, we create a new brain organoid-on-a-chip system derived from human induced pluripotent stem cells (hiPSCs) that allows us to model neurodevelopmental disorders under prenatal nicotine exposure (PNE) at early stages. The brain organoid-on-a-chip system facilitates 3D culture, in situ neural differentiation, and self-organization of brain organoids under continuous perfused cultures in a controlled manner. The generated brain organoids displayed well-defined neural differentiation, regionalization, and cortical organization, which recapitulates the key features of the early stages of human brain development. The brain organoids exposed to nicotine exhibited premature neuronal differentiation with enhanced expression of the neuron marker TUJ1. Brain regionalization and cortical development were disrupted in the nicotine-treated organoids identified by the expressions of forebrain (PAX6 and FOXG1), hindbrain (PAX2 and KROX20) and cortical neural layer (preplate TBR1 and deep-layer CTIP2) markers. Moreover, the neurite outgrowth showed abnormal neuronal differentiation and migration in nicotine-treated brain organoids. These results suggest that nicotine exposure elicits impaired neurogenesis in early fetal brain development during gestation. The established brain organoid-on-a-chip system provides a promising platform to model neurodevelopmental disorders under environmental exposure, which can be extended for applications in brain disease studies and drug testing

Washability and Distribution Behaviors of Trace Elements of a High-Sulfur Coal, SW Guizhou, China

The float-sink test is a commonly used technology for the study of coal washability, which determines optimal separation density for coal washing based on the desired sulfur and ash yield of the cleaned coal. In this study, the float-sink test is adopted for a high-sulfur Late Permian coal from Hongfa coalmine (No.26), southwestern Guizhou, China, to investigate its washability, and to analyze the organic affinities and distribution behaviors of some toxic and valuable trace elements. Results show that the coal is difficult to separate in terms of desulfurization. A cleaned coal could theoretically be obtained with a yield of 75.50%, sulfur 2.50%, and ash yield 11.33% when the separation density is 1.57 g/cm3. Trace elements’ distribution behaviors during the gravity separation were evaluated by correlation analysis and calculation. It was found that Cs, Ga, Ta, Th, Rb, Sb, Nb, Hf, Ba, Pb, In, Cu, and Zr are of significant inorganic affinity; while Sn, Co, Re, U, Mo, V, Cr, Ni, and Be are of relatively strong organic affinity. LREE (Light rare earth elements), however, seem to have weaker organic affinity than HREE (Heavy rare earth elements), which can probably be attributed to lanthanide contraction. When the separation density is 1.60 g/cm3, a large proportion of Sn, Be, Cr, U, V, Mo, Ni, Cd, Pb, and Cu migrate to the cleaned coal, but most of Mn, Sb and Th stay in the gangue. Coal preparation provides alternativity for either toxic elements removal or valuable elements preconcentration in addition to desulfurization and deashing. The enrichment of trace elements in the cleaned coal depends on the predetermined separation density which will influence the yields and ash yields of the cleaned coal

Placental Barrier-on-a-Chip: Modeling Placental Inflammatory Responses to Bacterial Infection

Placental inflammation, as a recognized cause of preterm birth and neonatal mortality, displays extensive placental involvement or damage with the presence of organisms. The inflammatory processes are complicated and tightly associated with increased inflammatory cytokine levels and innate immune activation. However, the deep study of the underlying mechanisms was limited by conventional cell and animal models because of great variations in the architecture and function of placenta. Here, we established a micro engineered model of human placental barrier on the chip and investigated the associated inflammatory responses to bacterial infection. The multilayered design of the microdevice mimicked the microscopic structure in the fetal-maternal interfaces of human placenta, and the flow resembled the dynamic environment in the mother's body. Escherichia coli (E. coli), one of the predominant organisms found in fetal organs, were applied to the maternal side, modeling acute placental inflammation. The data demonstrated the complex responses including the increased secretion of inflammatory cytokines by trophoblasts and the adhesion of maternal macrophages following bacterial infection. Particularly, transplacental communication was observed between two placental cells, and implied the potential role of trophoblast in fetal inflammatory response syndrome in clinic. These complex responses are of potential significance to placental dysfunctions, even abnormal fetal development and preterm birth. Collectively, placental barrier-on-a-chip microdevice presents a simple platform to explore the complicated inflammatory responses in human placenta, and might help our understanding of the mechanisms underlying reproductive diseases

Engineering placenta‐like organoids containing endogenous vascular cells from human‐induced pluripotent stem cells

Abstract The placenta is an essential organ that maintains the health of both the fetus and its mother. Understanding the development of human placenta has been hindered by the limitations of existing animal models and monolayer cell cultures. Models that can recapitulate the essential aspects of human placental multicellular components and vasculature are still lacking. Herein, we presented a new strategy to establish placenta‐like organoids with vascular‐like structures from human‐induced pluripotent stem cells in a defined three‐dimensional (3D) culture system. The resulting placenta‐like tissue resembles first‐trimester human placental development in terms of complex placental components and secretory function. The multicellular tissue was characterized by the inclusion of trophoblasts (cytotrophoblasts, syncytiotrophoblasts, extravillous trophoblasts, and other endogenous vascular cells), which were identified by immunofluorescence, flow cytometry analyses, real‐time quantitative reverse transcription polymerase chain reaction and single‐cell RNA‐seq. Moreover, the 3D tissue was able to secrete the placenta‐specific hormone human chorionic gonadotropin β (hCG‐β) and vascular endothelial growth factor A (VEGFA). The tissue responded to the inflammatory factor tumor necrosis factor‐α (TNF‐α) and VEGF receptor inhibitors. This new model system can represent the major features of placental cellular components, and function, which have not been realized in 2D monolayer cultures. The developed tissue system might open new avenues for studying normal early human placental development and its disease states

Understanding SCLC heterogeneity and plasticity in cancer metastasis and chemotherapy resistance

Small cell lung cancer (SCLC) accounts for approximately 15% of all lung cancer cases and features a strong predilection for early metastasis and extremely poor prognosis. Despite being highly sensitive to chemotherapy and/or radiotherapy initially, most SCLC patients develop therapeutic resistance within one year and die of distant metastases. Multiple studies have revealed the high heterogeneity and strong plasticity of SCLC associated with frequent metastases and early development of therapeutic resistance as well as poor clinical outcome. Importantly, different SCLC subtypes are associated with different therapeutic vulnerabilities, and the inflamed subtype tends to have the best response to immunotherapy, which highlights the importance of precision medicine in the clinic. Here, we review recent advances in SCLC heterogeneity and plasticity and their link to distant metastases and chemotherapy resistance. We hope that a better understanding of the molecular mechanisms underlying SCLC malignant progression will help to develop better intervention strategies for this deadly disease

Structural Determination and Genetic Identification of the O-Antigen from an Escherichia coli Strain, LL004, Representing a Novel Serogroup

The O-antigen is the outermost component of the lipopolysaccharide layer in Gram-negative bacteria, and the variation of O-antigen structure provides the basis for bacterial serological diversity. Here, we determined the O-antigen structure of an Escherichia coli strain, LL004, which is totally different from all of the E. coli serogroups. The tetrasaccharide repeating unit was determined as →4)-β-d-Galp-(1→3)-β-d-GlcpNAc6OAc(~70%)-(1→3)-β-d-GalpA-(1→3)-β-d-GalpNAc-(1→ with monosaccharide analysis and NMR spectra. We also characterized the O-antigen gene cluster of LL004, and sequence analysis showed that it correlated well with the O-antigen structure. Deletion and complementation testing further confirmed its role in O-antigen biosynthesis, and indicated that the O-antigen of LL004 is assembled via the Wzx/Wzy dependent pathway. Our findings, in combination, suggest that LL004 should represent a novel serogroup of E. coli

Development and validation of a predictive model for febrile seizures

Abstract Febrile seizures (FS) are the most prevalent type of seizures in children. Existing predictive models for FS exhibit limited predictive ability. To build a better-performing predictive model, a retrospective analysis study was conducted on febrile children who visited the Children's Hospital of Shanghai from July 2020 to March 2021. These children were divided into training set (n = 1453), internal validation set (n = 623) and external validation set (n = 778). The variables included demographic data and complete blood counts (CBCs). The least absolute shrinkage and selection operator (LASSO) method was used to select the predictors of FS. Multivariate logistic regression analysis was used to develop a predictive model. The coefficients derived from the multivariate logistic regression were used to construct a nomogram that predicts the probability of FS. The calibration plot, area under the receiver operating characteristic curve (AUC), and decision curve analysis (DCA) were used to evaluate model performance. Results showed that the AUC of the predictive model in the training set was 0.884 (95% CI 0.861 to 0.908, p < 0.001) and C-statistic of the nomogram was 0.884. The AUC of internal validation set was 0.883 (95% CI 0.844 to 0.922, p < 0.001), and the AUC of external validation set was 0.858 (95% CI 0.820 to 0.896, p < 0.001). In conclusion, the FS predictive model constructed based on CBCs in this study exhibits good predictive ability and has clinical application value