Analisis Penerapan Sistem Akuntansi Penjualan Kredit Dan Penerimaan Kas Dalam Mendukung Pengendalian Intern Perusahaan (Studi Kasus PT. Smart Tbk Refinery Surabaya)

System of selling credit accounting and system of cash receiving from account receivable is the source of life to achieving company goals. This research on the system of credit sales and cash receipts to support the company internal control. This research was conducted at PT. SMART Tbk Refinery Surabaya. PT. SMART Tbk Refinery Surabaya only selling cooking oil in the form of branded product and trading product on credit. PT. SMART Tbk Refinery Surabaya still has any weakness on system of selling credit accounting and system of cash receiving from account receivable, some of the sales transaction activity that occurred less supportive of the company\u27s internal control. This study aims to provide information to companies about the advantages and weakness of credit sales accounting system and cash receipts that have been applied by the company

The role of Ca²⁺ in PIP₂ and palmitoyl CoA regulation of TRPV1 currents.

<p>(A) Representative whole-cell recordings (n = 7) and (B) inside-out recording (n = 5) of currents elicited by 1 µM capsaicin in the absence of Ca²⁺. (C) Grouped data of the effect of Ca²⁺ on the desensitization of TRPV1 currents. (D) Representative inside-out recordings and histograms of the effect of 1 µM palmitoyl CoA (n = 7), 25 µM PIP₂ (n = 4) or 1 µM palmitoyl CoA combined with 25 µM PIP₂ (n = 9) on currents elicited by 1 µM capsaicin (n = 9) in the absence of Ca²⁺. (E) Representative inside-out recordings and grouped data of the application of 1 µM capsaicin (n = 6), 1 µM palmitoyl CoA (n = 8) or 25 µM PIP₂ (n = 8) in the presence of 2 mM Ca²⁺. (F) Representative inside-out recordings and grouped data of the effect of 1 µM capsaicin (n = 12), 1 µM palmitoyl CoA (n = 11) or 25 µM PIP₂ (n = 10) in the presence of 2 mMCa²⁺ and 2 µM U73122. *P<0.05. Dashed line denotes zero current level.</p

Chain-length, saturation and voltage-dependent effects of LC-CoA modulation of TRPV1 currents.

<p>(A) Representative inside-out recordings of the application various LC-CoAs (0.1 µM) in the presence, or (B) absence of 1 µM capsaicin. (C) Grouped data of the effect of 0.1 µM LC-CoAs in the presence or absence of 1 µM capsaicin. (D) I–V plot of currents elicited by 1 µM capsaicin in the presence of increasing concentration of palmitoyl CoA. (E) Concentration-effect curve of palmitoyl CoA modulation of currents elicited by 1 µM capsaicin. *P<0.05.</p

Kinetic parameters of WT TRPV1 and R702A mutant currents in the presence and absence of palmitoyl CoA.

<p>Currents were elicited by pH5.5. * Significantly different from values in the WT control (first pulse) (P<0.05). ** Significantly different from values in the WT control (second pulse) (P<0.05).</p

The effect of palmitoyl CoA on TRPV1 currents.

<p>(A) Representative whole-cell recordings elicited by 1 µM capsaicin (n = 5) in the presence of (B) 25 µM PIP₂ (n = 12) or (C) 1 µM palmitoyl CoA (n = 9). (D) Representative whole-cell recordings elicited by acidic pH (pH = 5.5, n = 5) in the presence of (E) 1 µM palmitoyl CoA (n = 5). (F) Grouped data of the effects of PIP₂ and palmitoyl CoA on TRPV1 currents. *P<0.05. Dashed line denotes zero current level.</p

The effect of LC-CoAs on [Ca²⁺]_i.

<p>(A) Representative intracellular paired pulse Ca²⁺ recordings and grouped data of the effect of intracellular LC-CoAs on capsaicin-elicited (1 µM) Ca²⁺ levels in tsA201 cells expressing recombinant TRPV1 channel following repeated exposure to capsaicin, Ad-Scramble (n = 5) and Ad-ACSL-1 (n = 6) or (B) Jurkat 6.1 T-cells expressing endogenous channels, Ad-Scramble (n = 8) and Ad-ACSL-1 (n = 9). (C) Representative intracellular Ca²⁺ recordings and grouped data of the effect of intracellular LC-CoAs on Jurkat 6.1 T-cells, Ad-Scramble (n = 8) and Ad-ACSL-1 (n = 9) following application of 20 µg/ml PHA. Grouped data showing the effect of 1 µM capsazepine on intracellular calcium levels in Jurkat 6.1 T-cells, Ad-ACSL-1 (n = 9) and Ad-ACSL-1+CPZ (n = 10) following application of 20 µg/ml PHA. *P<0.05, **P<0.01.</p

Kinetic parameters of WT TRPV1 and K711A mutant currents in the presence and absence of palmitoyl CoA.

<p>Currents were induced by 1 mmol/l capsaicin.</p><p>* Significantly different from values in the WT control (first pulse) (P<0.05).</p><p>** Significantly different from values in the WT control (second pulse) (P<0.05).</p

The role of R702 in LC-CoA modulation of TRPV1 channel function.

<p>(A) Representative current trace of WT TRPV1 during repeated exposure to 1 µM capsaicin. (B) Representative current traces of the R702A TRPV1 mutant in the presence or absence of 1 µM palmitoyl CoA following repeated exposure to acidic activating solution of pH 5.5. (C) Grouped data of the effect of the R702A mutation on TRPV1 channel kinetics in response to acidic solution of pH 5.5. (D) Grouped data of the effect of 1 µM palmitoyl CoA on WT and R702A TRPV1 channel kinetics in response to the pH 5.5 solution. *P<0.05, **P<0.01. Dashed line denotes zero current level.</p

The role of K711 in LC-CoA modulation of TRPV1 channel function.

<p>(A) Amino acid sequence alignment of TRPV1. (B) Representative current trace of WT TRPV1 during repeated exposure to 1 µM capsaicin. (C) Representative current traces of the K711A TRPV1 mutant in the presence or absence of 1 µM palmitoyl CoA following repeated exposure to 1 µM capsaicin. (B,C) inset: Overlay of WT and K711A current traces normalized to maximum current illustrate the similar kinetics. (D) Grouped data of the effect of the K711A mutation on TRPV1 channel kinetics in response to 1 µM capsaicin. (E) Grouped data of the effect of 1 µM palmitoyl CoA on WT and K711A TRPV1 channel kinetics in response 1 µM capsaicin. *P<0.05, **P<0.01. Dashed line denotes zero current level.</p

Inhibition of the Unfolded Protein Response Mechanism Prevents Cardiac Fibrosis

<div><p>Background</p><p>Cardiac fibrosis attributed to excessive deposition of extracellular matrix proteins is a major cause of heart failure and death. Cardiac fibrosis is extremely difficult and challenging to treat in a clinical setting due to lack of understanding of molecular mechanisms leading to cardiac fibrosis and effective anti-fibrotic therapies. The objective in this study was to examine whether unfolded protein response (UPR) pathway mediates cardiac fibrosis and whether a pharmacological intervention to modulate UPR can prevent cardiac fibrosis and preserve heart function.</p><p>Methodology/Principal Findings</p><p>We demonstrate here that the mechanism leading to development of fibrosis in a mouse with increased expression of calreticulin, a model of heart failure, stems from impairment of endoplasmic reticulum (ER) homeostasis, transient activation of the unfolded protein response (UPR) pathway and stimulation of the TGFβ1/Smad2/3 signaling pathway. Remarkably, sustained pharmacologic inhibition of the UPR pathway by tauroursodeoxycholic acid (TUDCA) is sufficient to prevent cardiac fibrosis, and improved exercise tolerance.</p><p>Conclusions</p><p>We show that the mechanism leading to development of fibrosis in a mouse model of heart failure stems from transient activation of UPR pathway leading to persistent remodelling of cardiac tissue. Blocking the activation of the transiently activated UPR pathway by TUDCA prevented cardiac fibrosis, and improved prognosis. These findings offer a window for additional interventions that can preserve heart function.</p></div