System Module for Student Idol

نویسندگان

  • M. S. Roslina
  • A. Noraziah
چکیده

Malaysia government had been trying hard in order to find the most efficient methods in learning. However, it is hard to actually access and evaluate students whom will then be called an excellent student. It is because in our realties student who excellent is only excel in academic. This evaluation becomes a problem because it not balances in our real life interm of to get an excellent student in whole area in their involvement of curiculum and cocuriculum. To overcome this scenario, we designed a module for Student Idol to evaluate student through three categories which are academic, co-curiculum and leadership. All the categories have their own merit point. Using this method, student will be evaluated more accurate compared to the previously. So, teacher can easily evaluate their student without having any emotion factor, relation factor and others. As conclusion this system module will helps the development of student evaluation more accurate and valid in Student Idol. Keywords—Evaluation, curiculum, co-curriculum, idol, system module.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

The IDOL-UBE2D complex mediates sterol-dependent degradation of the LDL receptor.

We previously identified the E3 ubiquitin ligase IDOL as a sterol-dependent regulator of the LDL receptor (LDLR). The molecular pathway underlying IDOL action, however, remains to be determined. Here we report the identification and biochemical and structural characterization of an E2-E3 ubiquitin ligase complex for LDLR degradation. We identified the UBE2D family (UBE2D1-4) as E2 partners for ...

متن کامل

The Deubiquitylase USP2 Regulates the LDLR Pathway by Counteracting the E3-Ubiquitin Ligase IDOL.

RATIONALE The low-density lipoprotein (LDL) receptor (LDLR) is a central determinant of circulating LDL-cholesterol and as such subject to tight regulation. Recent studies and genetic evidence implicate the inducible degrader of the LDLR (IDOL) as a regulator of LDLR abundance and of circulating levels of LDL-cholesterol in humans. Acting as an E3-ubiquitin ligase, IDOL promotes ubiquitylation ...

متن کامل

Post-transcriptional regulation of lipoprotein receptors by the E3-ubiquitin ligase inducible degrader of the low-density lipoprotein receptor.

PURPOSE OF REVIEW The hepatic low-density lipoprotein receptor (LDLR) pathway is essential for clearing circulating LDL and is an important therapeutic target for treating cardiovascular disease. Abundance of the LDLR is subject to both transcriptional and nontranscriptional control. Here, we highlight a new post-transcriptional mechanism for controlling LDLR function via ubiquitination of the ...

متن کامل

A Wireless Fingerprint Attendance System

In this paper we design a system which takes student attendance and the attendance records are maintained automatically in an academic institute. Taking the attendance manually and maintaining its record till end of year (or even beyond) is very difficult job as well as wastage of time and paper. This necessitates an efficient system that would be fully automatic. Top level design of the system...

متن کامل

Identification of a loss-of-function inducible degrader of the low-density lipoprotein receptor variant in individuals with low circulating low-density lipoprotein.

AIMS Recent genome-wide association studies suggest that IDOL (also known as MYLIP) contributes to variation in circulating levels of low-density lipoprotein cholesterol (LDL-C). IDOL, an E3-ubiquitin ligase, is a recently identified post-transcriptional regulator of LDLR abundance. Briefly, IDOL promotes degradation of the LDLR thereby limiting LDL uptake. Yet the exact role of IDOL in human l...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2010