Identifikasi Karakter Siswa Menggunakan Metode K-Means (Studi Kasus Sdn 156 Pekanbaru)

Good character education can have a characteristic impact on students. each student has a different character. Various ways done by the school in character education based on kemendiknas, including State Elementary School 156 Pekanbaru. Problems that arise in the field is there is no method that can determine the character of the students so that the school's special teachers can not understand precisely the characters in the students. The lack of understanding of the character of the students makes the vision of the school mission has not been seen so that character education in SDN 156 Pekanbaru has not been right target. Therefore, it needs to be done grouping student character in SDN 156 Pekanbaru with the aim of school know character owned by students in school. The K-Means algorithm is used to classify the character of the students with the number of clusters as much as 2 using the six attributes of characters studied: Honest, disciplined, confident, caring, creative and responsible with 130 student data. The results of K-Means manual calculation with sample data 10 data from 130 data that is weak character (C1) amounted to 1 student and weak character of 9 students, this result is same with calculation executed by RapidMiner application. Test results with 130 data using RapidMiner resulted in the number of students with weak character 26 students with the average centroid (0.665) with caring and creative characters. While students who have strong character 104 students with average value of centroid (0.900) with honest character, discipline, confidence, and responsibility. The result of character grouping based on class cluster position in RapidMiner is grade 3 which has weak character (C1) 8 students from 35 students, grade 4 is 8 out of 24 students, 5th grade is 1 of 17 students and grade 6 is 9 of 46 students. While clusters with strong characters (C2) class 3 amounted to 27 students, grade 4 amounted to 24 students, class 5 amounted to 16 students, and grade 6 amounted to 37 students. From the results of this study is expected Strong characters can be developed by school continue to perform habits which involves the students so that the characters in the students can be seen while for the caring and creative characters so as not to be weak then the school always provide guidance to the students and give examples of good habits and activities that can be followed by students in school

Sex Differences in Cardiovascular Impact of Early Metabolic Impairment: Interplay between Dysbiosis and Adipose Inflammation

The evolving view of gut microbiota has shifted toward describing the colonic flora as a dynamic organ in continuous interaction with systemic physiologic processes. Alterations of the normal gut bacterial profile, known as dysbiosis, has been linked to a wide array of pathologies. Of particular interest is the cardiovascular- metabolic disease continuum originating from positive energy intake and high-fat diets. Accumulating evidence suggests a role for sex hormones in modulating the gut microbiome community. Such a role provides an additional layer of modulation of the early inflammatory changes culminating in negative metabolic and cardiovascular outcomes. In this review, we will shed the light on the role of sex hormones in cardiovascular dysfunction mediated by high-fat diet-induced dysbiosis, together with the possible involvement of insulin resistance and adipose tissue inflammation. Insights into novel therapeutic interventions will be discussed as well.This work was supported by an American University of Beirut (AUB) Faculty of Medicine MPP grant to A.E.-Y. H.S.D. is supported by a Ph.D. Scholarship from the Faculty of Agriculture and Food Sciences at AUB and a l'Oreal-UNESCO for Women in Science Fellowship. I.A. is supported by a MasterCard Foundation Scholarship.Scopu

Enhanced activity of multiple TRIC‐B channels: an endoplasmic reticulum/sarcoplasmic reticulum mechanism to boost counterion currents

KEY POINTS:There are two subtypes of trimeric intracellular cation (TRIC) channels but their distinct single-channel properties and physiological regulation have not been characterized. We examined the differences in function between native skeletal muscle sarcoplasmic reticulum (SR) K+ -channels from wild-type (WT) mice (where TRIC-A is the principal subtype) and from Tric-a knockout (KO) mice that only express TRIC-B. We find that lone SR K+ -channels from Tric-a KO mice have a lower open probability and gate more frequently in subconducting states than channels from WT mice but, unlike channels from WT mice, multiple channels gate with high open probability with a more than six-fold increase in activity when four channels are present in the bilayer. No evidence was found for a direct gating interaction between ryanodine receptor and SR K+ -channels in Tric-a KO SR, suggesting that TRIC-B-TRIC-B interactions are highly specific and may be important for meeting counterion requirements during excitation-contraction coupling in tissues where TRIC-A is sparse or absent. ABSTRACT:The trimeric intracellular cation channels, TRIC-A and TRIC-B, represent two subtypes of sarcoplasmic reticulum (SR) K+ -channel but their individual functional roles are unknown. We therefore compared the biophysical properties of SR K+ -channels derived from the skeletal muscle of wild-type (WT) or Tric-a knockout (KO) mice. Because TRIC-A is the major TRIC-subtype in skeletal muscle, WT SR will predominantly contain TRIC-A channels, whereas Tric-a KO SR will only contain TRIC-B channels. When lone SR K+ -channels were incorporated into bilayers, the open probability (Po) of channels from Tric-a KO mice was markedly lower than that of channels from WT mice; gating was characterized by shorter opening bursts and more frequent brief subconductance openings. However, unlike channels from WT mice, the Po of SR K+ -channels from Tric-a KO mice increased as increasing channel numbers were present in the bilayer, driving the channels into long sojourns in the fully open state. When co-incorporated into bilayers, ryanodine receptor channels did not directly affect the gating of SR K+ -channels, nor did the presence or absence of SR K+ -channels influence ryanodine receptor activity. We suggest that because of high expression levels in striated muscle, TRIC-A produces most of the counterion flux required during excitation-contraction coupling. TRIC-B, in contrast, is sparsely expressed in most cells and, although lone TRIC-B channels exhibit low Po, the high Po levels reached by multiple TRIC-B channels may provide a compensatory mechanism to rapidly restore K+ gradients and charge differences across the SR of tissues containing few TRIC-A channels

Phosphorus Supplementation Mitigates Perivascular Adipose Inflammation–Induced Cardiovascular Consequences in Early Metabolic Impairment

Background The complexity of the interaction between metabolic dysfunction and cardiovascular complications has long been recognized to extend beyond simple perturbations of blood glucose levels. Yet, structured interventions targeting the root pathologies are not forthcoming. Growing evidence implicates the inflammatory changes occurring in perivascular adipose tissue (PVAT) as early instigators of cardiovascular deterioration. Methods and Results We used a nonobese prediabetic rat model with localized PVAT inflammation induced by hypercaloric diet feeding, which dilutes inorganic phosphorus (Pi) to energy ratio by 50%, to investigate whether Pi supplementation ameliorates the early metabolic impairment. A 12‐week Pi supplementation at concentrations equivalent to and twice as much as that in the control diet was performed. The localized PVAT inflammation was reversed in a dose‐dependent manner. The increased expression of UCP1 (uncoupling protein1), HIF‐1α (hypoxia inducible factor‐1α), and IL‐1β (interleukin‐1β), representing the hallmark of PVAT inflammation in this rat model, were reversed, with normalization of PVAT macrophage polarization. Pi supplementation restored the metabolic efficiency consistent with its putative role as an UCP1 inhibitor. Alongside, parasympathetic autonomic and cerebrovascular dysfunction function observed in the prediabetic model was reversed, together with the mitigation of multiple molecular and histological cardiovascular damage markers. Significantly, a Pi‐deficient control diet neither induced PVAT inflammation nor cardiovascular dysfunction, whereas Pi reinstatement in the diet after a 10‐week exposure to a hypercaloric low‐Pi diet ameliorated the dysfunction. Conclusions Our present results propose Pi supplementation as a simple intervention to reverse PVAT inflammation and its early cardiovascular consequences, possibly through the interference with hypercaloric‐induced increase in UCP1 expression/activity

Dampened activity of ryanodine receptor channels in mutant skeletal muscle lacking TRIC-A

TRIC-A is a major component of the nuclear and sarcoplasmic reticulum (SR) membranes of cardiac and skeletal muscle, and is localised closely with RyR channels in the SR terminal cisternae. The skeletal muscle of Tric-a KO mice is characterised by Ca2+ overloaded and swollen SR and by changes in the properties of SR Ca2+ release. We therefore investigated if RyR1 gating behaviour is modified in the SR from Tric-a KO mice by incorporating native RyR1 into planar phospholipid bilayers under voltage-clamp conditions. We find that RyR1 channels from Tric-a KO mice respond normally to cytosolic Ca2+, ATP, adenine, caffeine and to luminal Ca2+. However, the channels are more sensitive to the inactivating effects of divalent cations, thus, in the presence of Mg2+, ATP is inadequate as an activator. Additionally, channels are not characteristically activated by PKA even though phosphorylation levels of Ser2844 is similar to controls. Our results suggest that TRIC-A functions as an excitatory modulator of RyR1 channels within SR terminal cisternae. Importantly, this regulatory action of TRIC-A appears to be independent of, although it would be additive to, any indirect consequences to RyR1 activity that would arise due to K+ fluxes across the SR via TRIC-A

Structure of the polycystic kidney disease TRP channel Polycystin-2 (PC2)

Mutations in either polycystin-1 (PC1 or PKD1) or polycystin-2 (PC2, PKD2 or TRPP1) cause autosomal-dominant polycystic kidney disease (ADPKD) through unknown mechanisms. Here we present the structure of human PC2 in a closed conformation, solved by electron cryomicroscopy at 4.2-Å resolution. The structure reveals a novel polycystin-specific 'tetragonal opening for polycystins' (TOP) domain tightly bound to the top of a classic transient receptor potential (TRP) channel structure. The TOP domain is formed from two extensions to the voltage-sensor-like domain (VSLD); it covers the channel's endoplasmic reticulum lumen or extracellular surface and encloses an upper vestibule, above the pore filter, without blocking the ion-conduction pathway. The TOP-domain fold is conserved among the polycystins, including the homologous channel-like region of PC1, and is the site of a cluster of ADPKD-associated missense variants. Extensive contacts among the TOP-domain subunits, the pore and the VSLD provide ample scope for regulation through physical and chemical stimuli

Agonist binding evokes extensive conformational changes in the extracellular domain of the ATP-gated human P2X1 receptor ion channel

P2X receptors for ATP have a wide range of physiological roles and comprise a structurally distinct family of ligand-gated trimeric ion channels. The crystal structure of a P2X4 receptor, in combination with mutagenesis studies, has provided a model of the intersubunit ATP-binding sites and identified an extracellular lateral portal, adjacent to the membrane, that funnels ions to the channel pore. However, little is known about the extent of ATP-induced conformational changes in the extracellular domain of the receptor. To address this issue, we have used MTSEA-biotinylation (N-Biotinoylaminoethyl methanethiosulfonate) to show ATP-sensitive accessibility of cysteine mutants at the human P2X1 receptor. Mapping these data to a P2X1 receptor homology model identifies significant conformational rearrangement. Electron microscopy of purified P2X1 receptors showed marked changes in structure on ATP binding, and introducing disulphide bonds between adjacent subunits to restrict intersubunit movements inhibited channel function. These results are consistent with agonist-induced rotation of the propeller-head domain of the receptor, sliding of adjacent subunits leading to restricted access to the upper vestibule, movement in the ion conducting lateral portals, and gating of the channel pore