TRANSFER TEKNOLOGI BIOKONVERSI SAMPAH ORGANIK MENGGUNAKAN BLACK SOLDIER FLY PADA MASYARAKAT DUSUN GEDANGAN

Abstrak: Penanganan sampah merupakan salah satu masalah lingkungan yang sulit diatasi, termasuk di Dusun Gedangan, Bantul. Untuk mengatasi masalah ini, diperlukan adanya transfer teknologi tepat guna yang dapat digunakan oleh masyarakat setempat. Oleh karena itu, solusi yang ditawarkan adalah melalui transfer teknologi pengolahan sampah organik berkelanjutan melalui biokonversi menggunakan larva black soldier fly (BSF). Kegiatan transfer teknologi ini melibatkan 30 orang masyarakat Dusun Gedangan dan dilakukan melalui focus group discussion (FGD) dan pendampingan, mulai dari penetasan telur BSF, pemeliharaan dan pemberian pakan pada larva BSF, pemindahan pupa BSF untuk induksi imago dan telur. Evaluasi respon mitra dilakukan secara berkala di setiap kegiatan menggunakan pre-test dan post-test. Upaya transfer teknologi ini dinyatakan berhasil berdasarkan peningkatan kemampuan mitra (68,2%) dan minat mitra (90,9%) untuk mengadopsi teknologi biokonversi sampah ini. Mitra juga berhasil mempraktikkan metode biokonversi ini dan menghasilkan larva BSF yang memenuhi syarat dari segi ukuran dan tampilan. Keterlibatan masyarakat setempat dalam implementasi metode pengolahan sampah berbasis biokonversi ini diharapkan dapat membantu mengatasi permasalahan penanganan limbah secara holistik, khususnya limbah rumah tangga seperti sampah organik.Abstract: Waste management is one of hardly manageable environmental problems, including in Gedangan Sub District, Bantul. In order to solve this problem, transfer of applicable technology was recommended to be delivered for the local community. Therefore, the solution offered was through the transfer of a sustainable technology for organic waste management using black soldier fly (BSF) larvae-mediated bioconversion. This technology transfer involved 30 local people in Gedangan Sub District and carried out through focus group discussion (FGD) and supervision, starting from hatching of BSF eggs, cultivating and feeding the larvae, until transferring the pupae for imago and egg induction. Participants’ responses were evaluated periodically in each activity through pre- and post-test. This transfer technology was considered successful based on the increase on participants’ skill (68.2%) and interest (90.9%) to adopt this waste bioconversion technology. Participants also successfully demonstrated this bioconversion and produced BSF larvae with appropriate size and visual. This participation of local community in the implementation of bioconversion waste management might potentially helpful to manage the waste problem in a holistic way, particularly household waste such as organic waste

Opening the black box of artificial intelligence for clinical decision support: A study predicting stroke outcome

State-of-the-art machine learning (ML) artificial intelligence methods are increasingly leveraged in clinical predictive modeling to provide clinical decision support systems to physicians. Modern ML approaches such as artificial neural networks (ANNs) and tree boosting often perform better than more traditional methods like logistic regression. On the other hand, these modern methods yield a limited understanding of the resulting predictions. However, in the medical domain, understanding of applied models is essential, in particular, when informing clinical decision support. Thus, in recent years, interpretability methods for modern ML methods have emerged to potentially allow explainable predictions paired with high performance. To our knowledge, we present in this work the first explainability comparison of two modern ML methods, tree boosting and multilayer perceptrons (MLPs), to traditional logistic regression methods using a stroke outcome prediction paradigm. Here, we used clinical features to predict a dichotomized 90 days post-stroke modified Rankin Scale (mRS) score. For interpretability, we evaluated clinical features' importance with regard to predictions using deep Taylor decomposition for MLP, Shapley values for tree boosting and model coefficients for logistic regression. With regard to performance as measured by Area under the Curve (AUC) values on the test dataset, all models performed comparably: Logistic regression AUCs were 0.83, 0.83, 0.81 for three different regularization schemes; tree boosting AUC was 0.81; MLP AUC was 0.83. Importantly, the interpretability analysis demonstrated consistent results across models by rating age and stroke severity consecutively amongst the most important predictive features. For less important features, some differences were observed between the methods. Our analysis suggests that modern machine learning methods can provide explainability which is compatible with domain knowledge interpretation and traditional method rankings. Future work should focus on replication of these findings in other datasets and further testing of different explainability methods

Cortical contraction drives the 3D patterning of epithelial cell surfaces

Cellular protrusions create complex cell surface topographies, but biomechanical mechanisms regulating their formation and arrangement are largely unknown. To study how protrusions form, we focused on the morphogenesis of microridges, elongated actin-based structures that are arranged in maze-like patterns on the apical surfaces of zebrafish skin cells. Microridges form by accreting simple finger-like precursors. Live imaging demonstrated that microridge morphogenesis is linked to apical constriction. A nonmuscle myosin II (NMII) reporter revealed pulsatile contractions of the actomyosin cortex, and inhibiting NMII blocked apical constriction and microridge formation. A biomechanical model suggested that contraction reduces surface tension to permit the fusion of precursors into microridges. Indeed, reducing surface tension with hyperosmolar media promoted microridge formation. In anisotropically stretched cells, microridges formed by precursor fusion along the stretch axis, which computational modeling explained as a consequence of stretch-induced cortical flow. Collectively, our results demonstrate how contraction within the 2D plane of the cortex can pattern 3D cell surfaces

The Role of Purported Mucoprotectants in Dealing with Irritable Bowel Syndrome, Functional Diarrhea, and Other Chronic Diarrheal Disorders in Adults

Chronic diarrhea is a frequent presenting symptom, both in primary care medicine and in specialized gastroenterology units. It is estimated that more than 5% of the global population suffers from chronic diarrhea. and that about 40% of these subjects are older than 60 years. The clinician is frequently faced with the need to decide which is the best therapeutic approach for these patients. While the origin of chronic diarrhea is diverse, impairment of intestinal barrier function, dysbiosis. and mucosal micro-inflammation are being increasingly recognized as underlying phenomena characterizing a variety of chronic diarrheal diseases. In addition to current pharmacological therapies, there is growing interest in alternative products such as mucoprotectants, which form a mucoadhesive film over the epithelium to reduce and protect against the development of altered intestinal permeability, dysbiosis, and mucosal micro-inflammation. This manuscript focuses on chronic diarrhea in adults, and we will review recent evidence on the ability of these natural compounds to improve symptoms associated with chronic diarrhea and to exert protective effects for the intestinal barrier

A Role for Thrombospondin-1 Deficits in Astrocyte-Mediated Spine and Synaptic Pathology in Down's Syndrome

Down's syndrome (DS) is the most common genetic cause of mental retardation. Reduced number and aberrant architecture of dendritic spines are common features of DS neuropathology. However, the mechanisms involved in DS spine alterations are not known. In addition to a relevant role in synapse formation and maintenance, astrocytes can regulate spine dynamics by releasing soluble factors or by physical contact with neurons. We have previously shown impaired mitochondrial function in DS astrocytes leading to metabolic alterations in protein processing and secretion. In this study, we investigated whether deficits in astrocyte function contribute to DS spine pathology.Using a human astrocyte/rat hippocampal neuron coculture, we found that DS astrocytes are directly involved in the development of spine malformations and reduced synaptic density. We also show that thrombospondin 1 (TSP-1), an astrocyte-secreted protein, possesses a potent modulatory effect on spine number and morphology, and that both DS brains and DS astrocytes exhibit marked deficits in TSP-1 protein expression. Depletion of TSP-1 from normal astrocytes resulted in dramatic changes in spine morphology, while restoration of TSP-1 levels prevented DS astrocyte-mediated spine and synaptic alterations. Astrocyte cultures derived from TSP-1 KO mice exhibited similar deficits to support spine formation and structure than DS astrocytes.These results indicate that human astrocytes promote spine and synapse formation, identify astrocyte dysfunction as a significant factor of spine and synaptic pathology in the DS brain, and provide a mechanistic rationale for the exploration of TSP-1-based therapies to treat spine and synaptic pathology in DS and other neurological conditions

Tight junctions: from simple barriers to multifunctional molecular gates

Epithelia and endothelia separate different tissue compartments and protect multicellular organisms from the outside world. This requires the formation of tight junctions, selective gates that control paracellular diffusion of ions and solutes. Tight junctions also form the border between the apical and basolateral plasma-membrane domains and are linked to the machinery that controls apicobasal polarization. Additionally, signalling networks that guide diverse cell behaviours and functions are connected to tight junctions, transmitting information to and from the cytoskeleton, nucleus and different cell adhesion complexes. Recent advances have broadened our understanding of the molecular architecture and cellular functions of tight junctions

Low-dose acetaminophen induces early disruption of cell-cell tight junctions in human hepatic cells and mouse liver

Dysfunction of cell-cell tight junction (TJ) adhesions is a major feature in the pathogenesis of various diseases. Liver TJs preserve cellular polarity by delimiting functional bile-canalicular structures, forming the blood-biliary barrier. In acetaminophen-hepatotoxicity, the mechanism by which tissue cohesion and polarity are affected remains unclear. Here, we demonstrate that acetaminophen, even at low-dose, disrupts the integrity of TJ and cell-matrix adhesions, with indicators of cellular stress with liver injury in the human hepatic HepaRG cell line, and primary hepatocytes. In mouse liver, at human-equivalence (therapeutic) doses, dose-dependent loss of intercellular hepatic TJ-associated ZO-1 protein expression was evident with progressive clinical signs of liver injury. Temporal, dose-dependent and specific disruption of the TJ-associated ZO-1 and cytoskeletal-F-actin proteins, correlated with modulation of hepatic ultrastructure. Real-time impedance biosensing verified in vitro early, dose-dependent quantitative decreases in TJ and cell-substrate adhesions. Whereas treatment with NAPQI, the reactive metabolite of acetaminophen, or the PKCα-activator and TJ-disruptor phorbol-12-myristate-13-acetate, similarly reduced TJ integrity, which may implicate oxidative stress and the PKC pathway in TJ destabilization. These findings are relevant to the clinical presentation of acetaminophen-hepatotoxicity and may inform future mechanistic studies to identify specific molecular targets and pathways that may be altered in acetaminophen-induced hepatic depolarization

Biallelic Mutation of ARHGEF18, Involved in the Determination of Epithelial Apicobasal Polarity, Causes Adult-Onset Retinal Degeneration

Mutations in more than 250 genes are implicated in inherited retinal dystrophy; the encoded proteins are involved in a broad spectrum of pathways. The presence of unsolved families after highly parallel sequencing strategies suggests that further genes remain to be identified. Whole-exome and -genome sequencing studies employed here in large cohorts of affected individuals revealed biallelic mutations in ARHGEF18 in three such individuals. ARHGEF18 encodes ARHGEF18, a guanine nucleotide exchange factor that activates RHOA, a small GTPase protein that is a key component of tight junctions and adherens junctions. This biological pathway is known to be important for retinal development and function, as mutation of CRB1, encoding another component, causes retinal dystrophy. The retinal structure in individuals with ARHGEF18 mutations resembled that seen in subjects with CRB1 mutations. Five mutations were found on six alleles in the three individuals: c.808A>G (p.Thr270Ala), c.1617+5G>A (p.Asp540Glyfs∗63), c.1996C>T (p.Arg666∗), c.2632G>T (p.Glu878∗), and c.2738_2761del (p.Arg913_Glu920del). Functional tests suggest that each disease genotype might retain some ARHGEF18 activity, such that the phenotype described here is not the consequence of nullizygosity. In particular, the p.Thr270Ala missense variant affects a highly conserved residue in the DBL homology domain, which is required for the interaction and activation of RHOA. Previously, knock-out of Arhgef18 in the medaka fish has been shown to cause larval lethality which is preceded by retinal defects that resemble those seen in zebrafish Crumbs complex knock-outs. The findings described here emphasize the peculiar sensitivity of the retina to perturbations of this pathway, which is highlighted as a target for potential therapeutic strategies

Sergüzeştnâme

Nüshanın Baş Tarafı Eksiktir