The Efficacies of Banana Stem Extract as a Candidate of Coccidiostat Against Rabbit Eimeria Stiedaio Ocysts: an in Vitro Analysis

The objective of this research was to investigatethe ability of banana stem (Musa paradisiaca) to inhibitsporulation of Eimeria stiedaioocystsderived fromrabbit by in vitroanalysis.Analyze the active substance proximate analysis and active substancesin this research were performed too. Banana stem extract were used in this experiment andsulfaquinoxalline(Coxy ®)was run as acontrol. The Eimeria stiedaioocystswere incubated prior the presence of different concentration from banana stem extract 0%, 1%, 2%, 4%, 8%for 1, 2 and 3 daysat 26°C. In addition,Factorial patterned Completely Randomized Design (CRD) with five replicates wasapplied on the experiment. Result analysis was performed by using Analysis of Variance and following by Honestly Significant Difference (HSD) post hoc test. Here, we identified that banana stem extract contain different type of active substance such as tannin, saponin, and alkaloid. Banana stem extract significantly affected the oocysts sporulation included the amount of sporulatedoocysts (P<0.01), unsporulatedoocysts (P<0.01), and transformed oocysts (P<0.01). In conclusion banana stem could inhibit the development of Eimeria stiedaioocysts on in vitroexperiment. HSD test showed that the optimum potential efficacy of banana stem toinhibit sporulation was at 4% and 8% concentration during three days incubation

A Hypomorphic Lsd1 Allele Results in Heart Development Defects in Mice

Article Authors Metrics Comments Related Content Abstract Introduction Results Discussion Materials and Methods Supporting Information Acknowledgments Author Contributions References Reader Comments (0) Media Coverage (0) Figures Abstract Lysine-specific demethylase 1 (Lsd1/Aof2/Kdm1a), the first enzyme with specific lysine demethylase activity to be described, demethylates histone and non-histone proteins and is essential for mouse embryogenesis. Lsd1 interacts with numerous proteins through several different domains, most notably the tower domain, an extended helical structure that protrudes from the core of the protein. While there is evidence that Lsd1-interacting proteins regulate the activity and specificity of Lsd1, the significance and roles of such interactions in developmental processes remain largely unknown. Here we describe a hypomorphic Lsd1 allele that contains two point mutations in the tower domain, resulting in a protein with reduced interaction with known binding partners and decreased enzymatic activity. Mice homozygous for this allele die perinatally due to heart defects, with the majority of animals suffering from ventricular septal defects. Molecular analyses revealed hyperphosphorylation of E-cadherin in the hearts of mutant animals. These results identify a previously unknown role for Lsd1 in heart development, perhaps partly through the control of E-cadherin phosphorylation

Murine GRPR and Stathmin Control in Opposite Directions both Cued Fear Extinction and Neural Activities of the Amygdala and Prefrontal Cortex

Extinction is an integral part of normal healthy fear responses, while it is compromised in several fear-related mental conditions in humans, such as post-traumatic stress disorder (PTSD). Although much research has recently been focused on fear extinction, its molecular and cellular underpinnings are still unclear. The development of animal models for extinction will greatly enhance our approaches to studying its neural circuits and the mechanisms involved. Here, we describe two gene-knockout mouse lines, one with impaired and another with enhanced extinction of learned fear. These mutant mice are based on fear memory-related genes, stathmin and gastrin-releasing peptide receptor (GRPR). Remarkably, both mutant lines showed changes in fear extinction to the cue but not to the context. We performed indirect imaging of neuronal activity on the second day of cued extinction, using immediate-early gene c-Fos. GRPR knockout mice extinguished slower (impaired extinction) than wildtype mice, which was accompanied by an increase in c-Fos activity in the basolateral amygdala and a decrease in the prefrontal cortex. By contrast, stathmin knockout mice extinguished faster (enhanced extinction) and showed a decrease in c-Fos activity in the basolateral amygdala and an increase in the prefrontal cortex. At the same time, c-Fos activity in the dentate gyrus was increased in both mutant lines. These experiments provide genetic evidence that the balance between neuronal activities of the amygdala and prefrontal cortex defines an impairment or facilitation of extinction to the cue while the hippocampus is involved in the context-specificity of extinction

The Histone H3K79 Methyltransferase Dot1L Is Essential for Mammalian Development and Heterochromatin Structure

Dot1 is an evolutionarily conserved histone methyltransferase specific for lysine 79 of histone H3 (H3K79). In Saccharomyces cerevisiae, Dot1-mediated H3K79 methylation is associated with telomere silencing, meiotic checkpoint control, and DNA damage response. The biological function of H3K79 methylation in mammals, however, remains poorly understood. Using gene targeting, we generated mice deficient for Dot1L, the murine Dot1 homologue. Dot1L-deficient embryos show multiple developmental abnormalities, including growth impairment, angiogenesis defects in the yolk sac, and cardiac dilation, and die between 9.5 and 10.5 days post coitum. To gain insights into the cellular function of Dot1L, we derived embryonic stem (ES) cells from Dot1L mutant blastocysts. Dot1L-deficient ES cells show global loss of H3K79 methylation as well as reduced levels of heterochromatic marks (H3K9 di-methylation and H4K20 tri-methylation) at centromeres and telomeres. These changes are accompanied by aneuploidy, telomere elongation, and proliferation defects. Taken together, these results indicate that Dot1L and H3K79 methylation play important roles in heterochromatin formation and in embryonic development

Analisis Pengaruh Gender, Senioritas dan Umur terhadap Penilaian Etika Akuntan Publik yang Ada di Kantor Akuntan Publik (Kap) di Kota Surakarta

In this study, the author aims to determine the effect of gender, seniority and age on the ethical assessment of public accountants in the Public Accounting Firm (KAP) in Surakarta City, either partially or simultaneously. The hypothesis in this study is: "It is suspected that gender, seniority and age have a significant effect on the ethical assessment of public accountants in the Public Accounting Firm (KAP) in Surakarta City, either partially or simultaneously". The data needed in this study is primary data obtained from questionnaires distributed to respondents. The population in this study are public accountants at KAP in Surakarta, which amounted to 53 people with a research sample of 53 respondents. The analysis technique used in this study uses multiple linear regression test, t test, F test and coefficient of determination test. The results of data analysis in this study can be concluded that gender, seniority and age have a significant effect on the ethical assessment of public accountants in the Public Accounting Firm (KAP) in Surakarta, either partially or simultaneously

CRTC1 Nuclear Translocation Following Learning Modulates Memory Strength via Exchange of Chromatin Remodeling Complexes on the Fgf1 Gene

Summary: Memory is formed by synapse-to-nucleus communication that leads to regulation of gene transcription, but the identity and organizational logic of signaling pathways involved in this communication remain unclear. Here we find that the transcription cofactor CRTC1 is a critical determinant of sustained gene transcription and memory strength in the hippocampus. Following associative learning, synaptically localized CRTC1 is translocated to the nucleus and regulates Fgf1b transcription in an activity-dependent manner. After both weak and strong training, the HDAC3-N-CoR corepressor complex leaves the Fgf1b promoter and a complex involving the translocated CRTC1, phosphorylated CREB, and histone acetyltransferase CBP induces transient transcription. Strong training later substitutes KAT5 for CBP, a process that is dependent on CRTC1, but not on CREB phosphorylation. This in turn leads to long-lasting Fgf1b transcription and memory enhancement. Thus, memory strength relies on activity-dependent changes in chromatin and temporal regulation of gene transcription on specific CREB/CRTC1 gene targets. : Uchida et al. link CRTC1 synapse-to-nucleus shuttling in memory. Weak and strong training induce CRTC1 nuclear transport and transient Fgf1b transcription by a complex including CRTC1, CREB, and histone acetyltransferase CBP, whereas strong training alone maintains Fgf1b transcription through CRTC1-dependent substitution of KAT5 for CBP, leading to memory enhancement. Keywords: memory enhancement, long-term potentiation, hippocampus, nuclear transport, epigenetics, FGF1, CRTC1, KAT5/Tip60, HDAC3, CRE