Displaying all 3 publications

Abstract:
Sort:
  1. Fulltext Regulatory Non-coding RNAs Network in Non-alcoholic Fatty Liver Disease
    Sulaiman SA, Muhsin NIA, Jamal R
    Front Physiol, 2019;10:279.
    PMID: 30941061 DOI: 10.3389/fphys.2019.00279
    Non-alcoholic fatty liver disease (NAFLD) spectrum comprises simple steatosis and non-alcoholic steatohepatitis (NASH) that can lead to fibrosis and cirrhosis. The patients usually have no history of excessive alcohol consumption and other etiologies that can cause fatty liver. Understanding of the pathophysiology of NAFLD has revealed that non-coding RNAs (ncRNAs) play significant roles in modulating the disease susceptibility, pathogenesis and progression. Currently, the ncRNAs are grouped according to their sizes and their regulatory or housekeeping functions. Each of these ncRNAs has a wide range of involvement in the regulation of the genes and biological pathways. Here, we briefly review the current literature the regulatory ncRNAs in NAFLD pathogenesis and progression, mainly the microRNAs, long non-coding RNAs and circular RNAs. We also discuss the co-regulatory functions and interactions between these ncRNAs in modulating the disease pathogenesis. Elucidation of ncRNAs in NAFLD may facilitate the identification of early diagnostic biomarkers and development of therapeutic strategies for NAFLD.
  2. A novel mutation in the mouse Pcsk1 gene showing obesity and diabetes
    Muhsin NIA, Bentley L, Bai Y, Goldsworthy M, Cox RD
    Mamm. Genome, 2020 Feb;31(1-2):17-29.
    PMID: 31974728 DOI: 10.1007/s00335-020-09826-4
    The proprotein convertase subtilisin/Kexin type 1 (PCSK1/PC1) protein processes inactive pro-hormone precursors into biologically active hormones in a number of neuroendocrine and endocrine cell types. Patients with recessive mutations in PCSK1 exhibit a complex spectrum of traits including obesity, diarrhoea and endocrine disorders. We describe here a new mouse model with a point mutation in the Pcsk1 gene that exhibits obesity, hyperphagia, transient diarrhoea and hyperproinsulinaemia, phenotypes consistent with human patient traits. The mutation results in a pV96L amino acid substitution and changes the first nucleotide of mouse exon 3 leading to skipping of that exon and in homozygotes very little full-length transcript. Overexpression of the exon 3 deleted protein or the 96L protein results in ER retention in Neuro2a cells. This is the second Pcsk1 mouse model to display obesity phenotypes, contrasting knockout mouse alleles. This model will be useful in investigating the basis of endocrine disease resulting from prohormone processing defects.
  3. Determining the Willingness to Pay for Innovative Oncology Medicines in Malaysia
    Dzulkipli MR, Shafie AA, Maon SN, Ramli A, Yahaya AHM, Ho SW, et al.
    Value Health Reg Issues, 2024 Mar;40:19-26.
    PMID: 37972430 DOI: 10.1016/j.vhri.2023.10.003
    OBJECTIVES: Early access to innovative oncology medicine is crucial to provide better treatment alternatives to patients with cancer. However, innovative oncology medicines often come at higher prices, thus limiting the government's ability for its universal coverage. Hence an alternative paying mechanism is needed. This study is intended to determine the willingness to pay (WTP) for innovative oncology medicines among Malaysians.

    METHODS: A cross-sectional contingent valuation study on 571 Malaysians was conducted to elicit respondents' WTP value via bidding game approach. A double-bounded dichotomous choice was used in 3 hypothetical scenarios: innovative diabetes medicine, innovative oncology medicine one-off (IOMO), and innovative oncology medicine insurance. Univariate logistic regression was used to determine the factors affecting respondent's WTP, whereas the mean WTP value and the factors affecting amount to WTP was determined using a parametric 2-part model.

    RESULTS: This study received 95% response rate. The mean age of the respondents is 48 years (SD 17) with majority of the respondents female (60.3%) and from ethnic Malay (62%). About 343 (64.7%) of the respondents expressed WTP for IOMO. Those in higher income bracket were willing to pay more for the access of IOMO than the overall WTP mean value (P = .046, coefficient 351.57).

    CONCLUSIONS: More than half of Malaysian are willing to pay for IOMO at mean value of Malaysian Ringgit 279.10 (US dollar 66.77). Collaborative funding mechanisms and appropriate financial screening among the stakeholders could be introduced as methods to expedite the access of innovative oncology medicine among patients with cancer in Malaysia.

Related Terms
    Try searching for something
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links