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  1. Sulaiman ZH, Abdul Rahman KH, Ying TY, Taha HH, Muhd Taha NH
    Integr Zool, 2008 Sep;3(3):208-15.
    PMID: 21396070 DOI: 10.1111/j.1749-4877.2008.00098.x
    The genetic population structure of red snapper Lutjanus malabaricus and orange-spotted grouper Epinephelus coiodes in Brunei and Sabah was investigated using allozyme electrophoresis. Samples were collected from three sites in Brunei for E. coiodes and from three sites in Brunei and Sabah for L. malabaricus. A total of 22 loci and 16 loci were scored, respectively. The index of fixation (F(ST) ) for the E. coiodes population was 0.176 but, in general, it lacked within-population structuring. The F(ST) was particularly high between Brunei Bay/Jerudong and Brunei Bay/ Kuala Belait, suggesting genetic subdivision on a small spatial scale. Isolation of Brunei Bay from the South China Sea may constrain the movement of adult fishes and larval dispersal, thereby reducing homogeneity among subpopulations. All variable loci for E. coiodes were in Hardy-Weinberg equilibrium except for MDH* and GTDHP* (P < 0.01), in which two subpopulations showed an excess of heterozygotes (P < 0.01). The study on the L. malabaricus population showed a heterozygote deficit of approximately 60% in variable loci (F(ST) genetic variation within population = 0.45; P < 0.05); however, the mean observed heterozygosity for the population far exceeded L. malabaricus populations in Australia and Indonesia. A F(ST) value of 0.076 revealed moderate genetic differentiation among subpopulations of L. malabaricus. The genotypes were likely to be drawn from the same distribution in Jerudong and Kuala Belait. This study infers that sustainable management of snapper and grouper resources in Brunei waters must take into account the presence of a single stock and two stocks, respectively.
  2. Xin GLL, Khee YP, Ying TY, Chellian J, Gupta G, Kunnath AP, et al.
    Curr. Diab. Rep., 2019 03 23;19(5):22.
    PMID: 30905013 DOI: 10.1007/s11892-019-1144-3
    PURPOSE OF REVIEW: Type 1 diabetes (T1D) occurs when there is destruction of beta cells within the islets of Langerhans in the pancreas due to autoimmunity. It is considered a complex disease, and different complications can surface and worsen the condition if T1D is not managed well. Since it is an incurable disease, numerous treatments and therapies have been postulated in order to control T1D by balancing hyperglycemia control while minimizing hypoglycemic episodes. The purpose of this review is to primarily look into the current state of the available immunological therapies and their advantages for the treatment of T1D.

    RECENT FINDINGS: Over the years, immunological therapy has become the center of attraction to treat T1D. Immunomodulatory approaches on non-antigens involving agents such as cyclosporine A, mycophenolate mofetil, anti-CD20, cytotoxic T cells, anti-TNF, anti-CD3, and anti-thymocyte globulin as well as immunomodulative approaches on antigens such as insulin, glutamic acid decarboxylase, and heat shock protein 60 have been studied. Aside from these two approaches, studies and trials have also been conducted on regulatory T cells, dendritic cells, interleukin 2, interleukin 4, M2 macrophages, and rapamycin/interleukin 2 combination therapy to test their effects on patients with T1D. Many of these agents have successfully suppressed T1D in non-obese diabetic (NOD) mice and in human trials. However, some have shown negative results. To date, the insights into the management of the immune system have been increasing rapidly to search for potential therapies and treatments for T1D. Nevertheless, some of the challenges are still inevitable. A lot of work and effort need to be put into the investigation on T1D through immunological therapy, particularly to reduce complications to improve and enhance clinical outcomes.

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