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  1. Kumar SS, Alarfaj AA, Munusamy MA, Singh AJ, Peng IC, Priya SP, et al.
    Int J Mol Sci, 2014;15(12):23418-47.
    PMID: 25526563 DOI: 10.3390/ijms151223418
    Human pluripotent stem cells, including human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs), hold promise as novel therapeutic tools for diabetes treatment because of their self-renewal capacity and ability to differentiate into beta (β)-cells. Small and large molecules play important roles in each stage of β-cell differentiation from both hESCs and hiPSCs. The small and large molecules that are described in this review have significantly advanced efforts to cure diabetic disease. Lately, effective protocols have been implemented to induce hESCs and human mesenchymal stem cells (hMSCs) to differentiate into functional β-cells. Several small molecules, proteins, and growth factors promote pancreatic differentiation from hESCs and hMSCs. These small molecules (e.g., cyclopamine, wortmannin, retinoic acid, and sodium butyrate) and large molecules (e.g. activin A, betacellulin, bone morphogentic protein (BMP4), epidermal growth factor (EGF), fibroblast growth factor (FGF), keratinocyte growth factor (KGF), hepatocyte growth factor (HGF), noggin, transforming growth factor (TGF-α), and WNT3A) are thought to contribute from the initial stages of definitive endoderm formation to the final stages of maturation of functional endocrine cells. We discuss the importance of such small and large molecules in uniquely optimized protocols of β-cell differentiation from stem cells. A global understanding of various small and large molecules and their functions will help to establish an efficient protocol for β-cell differentiation.
  2. Priya SP, Sakinah S, Sharmilah K, Hamat RA, Sekawi Z, Higuchi A, et al.
    Acta Trop, 2017 Dec;176:206-223.
    PMID: 28823908 DOI: 10.1016/j.actatropica.2017.08.007
    Immuno-pathogenesis of leptospirosis can be recounted well by following its trail path from entry to exit, while inducing disastrous damages in various tissues of the host. Dysregulated, inappropriate and excessive immune responses are unanimously blamed in fatal leptospirosis. The inherent abilities of the pathogen and inabilities of the host were debated targeting the severity of the disease. Hemorrhagic manifestation through various mechanisms leading to a fatal end is observed when this disease is unattended. The similar vascular destructions and hemorrhage manifestations are noted in infections with different microbes in endemic areas. The simultaneous infection in a host with more than one pathogen or parasite is referred as the coinfection. Notably, common endemic infections such as leptospirosis, dengue, chikungunya, and malaria, harbor favorable environments to flourish in similar climates, which is aggregated with stagnated water and aggravated with the poor personal and environmental hygiene of the inhabitants. These factors aid the spread of pathogens and parasites to humans and potential vectors, eventually leading to outbreaks of public health relevance. Malaria, dengue and chikungunya need mosquitoes as vectors, in contrast with leptospirosis, which directly invades human, although the environmental bacterial load is maintained through other mammals, such as rodents. The more complicating issue is that infections by different pathogens exhibiting similar symptoms but require different treatment management. The current review explores different pathogens expressing specific surface proteins and their ability to bind with array of host proteins with or without immune response to enter into the host tissues and their ability to evade the host immune responses to invade and their affinity to certain tissues leading to the common squeal of hemorrhage. Furthermore, at the host level, the increased susceptibility and inability of the host to arrest the pathogens' and parasites' spread in different tissues, various cytokines accumulated to eradicate the microorganisms and their cellular interactions, the antibody dependent defense and the susceptibility of individual organs bringing the manifestation of the diseases were explored. Lastly, we provided a discussion on the immune trail path of pathogenesis from entry to exit to narrate the similarities and dissimilarities among various hemorrhagic fevers mentioned above, in order to outline future possibilities of prevention, diagnosis, and treatment of coinfections, with special reference to endemic areas.
  3. Priya SP, Sunil PM, Varma S, Brigi C, Isnadi MFAR, Jayalal JA, et al.
    Virusdisease, 2022 Dec;33(4):429-444.
    PMID: 36311173 DOI: 10.1007/s13337-022-00793-9
    BACKGROUND: Severe acute respiratory syndrome Coronavirus-2 invades the cells via ACE2 receptor and damages multiple organs of the human body. Understanding the pathological manifestation is mandatory to endure the rising post-infection sequel reported in patients with or without comorbidities.

    MATERIALS AND METHODS: Our descriptive review emphasises the direct, indirect and post-infection damages due to COVID-19. We have performed an electronic database search according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines with selective inclusion and exclusion criteria.

    RESULTS: The included studies substantiated the extensive damages in the multiple organs due to direct and indirect consequences of COVID-19. After an apparent recovery, the prolonged presentation of the symptoms manifests as post-COVID that can be related with persisting viral antigens and dysregulated immune response.

    CONCLUSION: A few of the symptoms of respiratory, cardiovascular, and neuropsychiatric systems that persist or reappear as post-COVID manifestations. Vaccination and preventive programs will effectively reduce the prevalence but, the post-COVID, a multisystem manifestation, will be a significant tribulation to the medical profession. However, the issue can be managed by implementing public health programs, rehabilitation services, and telemedicine virtual supports to raise awareness and reduce panic.

  4. Priya SP, Sakinah S, Ling MP, Chee HY, Higuchi A, Hamat RA, et al.
    Acta Trop, 2017 Jul;171:213-219.
    PMID: 28427958 DOI: 10.1016/j.actatropica.2017.04.010
    Dengue virus (DENV) has emerged as a major economic concern in developing countries, with 2.5 billion people believed to be at risk. Vascular endothelial cells (ECs) lining the circulatory system from heart to end vessels perform crucial functions in the human body, by aiding gas exchange in lungs, gaseous, nutritional and its waste exchange in all tissues, including the blood brain barrier, filtration of fluid in the glomeruli, neutrophil recruitment, hormone trafficking, as well as maintenance of blood vessel tone and hemostasis. These functions can be deregulated during DENV infection. In this study, BALB/c mice infected with DENV serotype 2 were analyzed histologically for changes in major blood vessels in response to DENV infection. In the uninfected mouse model, blood vessels showed normal architecture with intact endothelial monolayer, tunica media, and tunica adventitia. In the infected mouse model, DENV distorted the endothelium lining and disturbed the smooth muscle, elastic laminae and their supporting tissues causing vascular structural disarrangement. This may explain the severe pathological illness in DENV-infected individuals. The overall DENV-induced damages on the endothelial and it's supporting tissues and the dysregulated immune reactions initiated by the host were discussed.
  5. Sakinah S, Priya SP, Kumari S, Amira F, K P, Alsaeedy H, et al.
    Tissue Cell, 2017 Feb;49(1):86-94.
    PMID: 28034555 DOI: 10.1016/j.tice.2016.11.005
    In this research, we characterized the histopathological impact of dengue virus (serotype DENV-2) infection in livers of BALB/c mice. The mice were infected with different doses of DENV-2 via intraperitoneal injection and liver tissues were processed for histological analyses and variation was documented. In the BALB/c mouse model, typical liver tissues showed regular hepatocyte architecture, with normal endothelial cells surrounding sinusoid capillary. Based on histopathological observations, the liver sections of BALB/c mice infected by DENV-2 exhibited a loss of cell integrity, with a widening of the sinusoidal spaces. There were marked increases in the infiltration of mononuclear cells. The areas of hemorrhage and micro- and macrovesicular steatosis were noted. Necrosis and apoptosis were abundantly present. The hallmark of viral infection, i.e., cytopathic effects, included intracellular edema and vacuole formation, cumulatively led to sinusoidal and lobular collapse in the liver. The histopathological studies on autopsy specimens of fatal human DENV cases are important to shed light on tissue damage for preventive and treatment modalities, in order to manage future DENV infections. In this framework, the method present here on BALB/c mouse model may be used to study not only the effects of infections by other DENV serotypes, but also to investigate the effects of novel drugs, such as recently developed nano-formulations, and the relative recovery ability with intact immune functions of host.
  6. Sakinah S, Priya SP, Mok PL, Munisvaradass R, Teh SW, Sun Z, et al.
    Front Cell Dev Biol, 2021;9:637270.
    PMID: 34291043 DOI: 10.3389/fcell.2021.637270
    Extensive clinical efforts have been made to control the severity of dengue diseases; however, the dengue morbidity and mortality have not declined. Dengue virus (DENV) can infect and cause systemic damage in many organs, resulting in organ failure. Here, we present a novel report showing a tailored stem-cell-based therapy that can aid in viral clearance and rescue liver cells from further damage during dengue infection. We administered a combination of hematopoietic stem cells and endothelial progenitor cells in a DENV-infected BALB/c mouse model and found that delivery of this cell cocktail had improved their liver functions, confirmed by hematology, histopathology, and next-generation sequencing. These stem and progenitor cells can differentiate into target cells and repair the damaged tissues. In addition, the regime can regulate endothelial proliferation and permeability, modulate inflammatory reactions, enhance extracellular matrix production and angiogenesis, and secrete an array of growth factors to create an enhanced milieu for cell reparation. No previous study has been published on the treatment of dengue infection using stem cells combination. In conclusion, dengue-induced liver damage was rescued by administration of stem cell therapy, with less apoptosis and improved repair and regeneration in the dengue mouse model.
  7. Sakinah S, Priya SP, Mok PL, Munisvaradass R, Teh SW, Sun Z, et al.
    Front Cell Dev Biol, 2021;9:800659.
    PMID: 35178398 DOI: 10.3389/fcell.2021.800659
    [This corrects the article DOI: 10.3389/fcell.2021.637270.].
  8. Krishnan P, Rajan M, Kumari S, Sakinah S, Priya SP, Amira F, et al.
    Sci Rep, 2017 09 08;7(1):10962.
    PMID: 28887536 DOI: 10.1038/s41598-017-09140-1
    Camptothecin (CPT) is an anti-cancer drug that effectively treats various cancers, including colon cancer. However, poor solubility and other drawbacks have restricted its chemotherapeutic potential. To overcome these restrictions, CPT was encapsulated in CEF (cyclodextrin-EDTA-FE3O4), a composite nanoparticle of magnetic iron oxide (Fe3O4), and β-cyclodextrin was cross-linked with ethylenediaminetetraacetic acid (EDTA). This formulation improved CPT's solubility and bioavailability for cancer cells. The use of magnetically responsive anti-cancer formulation is highly advantageous in cancer chemotherapy. The chemical characterisation of CPT-CEF was studied here. The ability of this nano-compound to induce apoptosis in HT29 colon cancer cells and A549 lung cancer cells was evaluated. The dose-dependent cytotoxicity of CPT-CEF was shown using MTT. Propidium iodide and Annexin V staining, mitochondrial membrane depolarisation (JC-1 dye), and caspase-3 activity were assayed to detect apoptosis in CPT-CEF-treated cancer cells. Cell cycle analysis also showed G1 phase arrest, which indicated possible synergistic effects of the nano-carrier. These study results show that CPT-CEF causes a dose-dependent cell viability reduction in HT29 and A549 cells and induces apoptosis in colon cancer cells via caspase-3 activation. These data strongly suggest that CPT could be used as a major nanocarrier for CPT to effectively treat colon cancer.
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