Displaying publications 61 - 80 of 97 in total

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  1. Sio YY, Gan WL, Ng WS, Matta SA, Say YH, Teh KF, et al.
    Int Arch Allergy Immunol, 2023;184(10):1010-1021.
    PMID: 37336194 DOI: 10.1159/000530960
    INTRODUCTION: Previous studies have indicated the ERBB2 genetic variants in the 17q12 locus might be associated with asthma; however, the functional effects of these variants on asthma risk remain inconclusive. This study aimed to characterize the functional roles of asthma-associated ERBB2 single nucleotide polymorphisms (SNPs) in asthma pathogenesis by performing genetic association and functional analysis studies.

    METHODS: This study belongs to a part of an ongoing Singapore/Malaysia cross-sectional genetics and epidemiological study (SMCSGES). Genotype-phenotype associations were assessed by performing a genotyping assay on n = 4,348 ethnic Chinese individuals from the SMCSGES cohort. The phosphorylation levels of receptors and signaling proteins in the MAPK signaling cascades, including ErbB2, EGFR, and ERK1/2, were compared across the genotypes of asthma-associated SNPs through in vitro and ex vivo approaches.

    RESULTS: The ERBB2 tag-SNP rs1058808 was significantly associated with allergic asthma, with the allele "G" identified as protective against the disease (adjusted logistic p = 6.56 × 10-9, OR = 0.625, 95% CI: 0.544-0.718). The allele "G" of rs1058808 resulted in a Pro1170Ala mutation that results in lower phosphorylation levels of ErbB2 in HaCat cells (p < 0.001), whereas the overall ERBB2 mRNA expression and the phosphorylation levels of EGFR remained unaffected. In the SMCSGES cohort, individuals carrying the genotype "GG" of rs1058808 had lower phosphorylated ERK1/2 proteins in the MAPK signaling cascade. A lower phosphorylation level of ERK1/2 was also associated with reduced asthma risk.

    CONCLUSIONS: The present findings highlighted the involvement of a functional exonic variant of ERBB2 in asthma development via modulating the MAPK signaling cascade.

  2. Sio YY, Victoria Nanong GA, Lim JA, Matta SA, Say YH, Teh KF, et al.
    World Allergy Organ J, 2024 Jan;17(1):100853.
    PMID: 38235258 DOI: 10.1016/j.waojou.2023.100853
    BACKGROUND: Elaeis guineensis (Ela g, oil palm) pollen is one of the most predominant species of inhalant allergens in the tropical Southeast Asia region; however, its association with the manifestation of allergic diseases remains largely unexplored. This study aimed to determine the sensitization pattern of oil palm pollen and associate this with the risk and severity of allergic diseases.

    METHODS: Participants were recruited as a part of the Singapore and Malaysia cross-sectional genetic and epidemiological study (SMCSGES). Two independent cohorts were recruited: n = 564 serum samples were collected and serological assessment was performed against a panel of 16 crude inhalant allergens including house dust mite, pet, insect, pollen, and fungal allergens; n = 13 652 Singapore/Malaysia Chinese young adults were recruited and skin prick test was used to assess oil palm sensitization, which was tested for its association with the risk and severity of asthma, allergic rhinitis (AR), and atopic dermatitis (AD).

    RESULTS: The sensitization rate of oil palm pollen is 9.6% in the n = 564 Singapore/Malaysia cohort. In the n = 13 652 Singapore/Malaysia Chinese cohort, oil palm sensitization significantly associates with increased risks of asthma (p = 1.34x10-4), AR (p = 2.91x10-13), and AD (p = 6.95x10-7). Asthmatic patients with oil palm sensitization have increased risks of wheezing (p = 0.00995), nocturnal cough (p = 0.0122), and exacerbations (p = 0.00139) in the past 12 months. AR patients with oil palm sensitization also have an increased risk of developing moderate-to-severe symptoms (p = 0.00113).

    CONCLUSIONS: We have identified significant associations of oil palm sensitization with increased risks, exacerbations, and the severity of symptoms of allergic diseases in the tropical Southeast Asian region (Singapore/Malaysia).

  3. Bhat AA, Altamimi ASA, Goyal A, Goyal K, Kaur I, Kumar S, et al.
    Int Immunopharmacol, 2025 Jan 10;144:113675.
    PMID: 39608172 DOI: 10.1016/j.intimp.2024.113675
    CAR T cell therapy has revolutionized how we deliver cancer treatment, most notably for hematologic cancers, by compelling T cells to recognize and kill tumor cells. Nevertheless, current obstacles to utilizing this therapy in solid tumors and overcoming cancer resistance include radicalization. This review discusses how CD95 modulation can boost CAR T cell efficacy. Traditionally, CD95 was known to execute apoptosis induction, but it plays a dual role in induced cell death or in supporting cancer cell survival. Recent data have demonstrated that cancer cells escape CD95-mediated apoptosis via the downregulation of CD95, caspase 8 mutation, or the expression of the inhibition protein cFLIP. Additionally, the immunosuppressive tumor microenvironment, containing CD95L expressing immune cells, explains CAR T cell therapy resistance. Furthermore, we characterize the therapeutic potential of CD95 targeted approaches, including CD95L inhibition (APG101) and alterations in CAR T cell manufacturing (tyrosine kinase inhibitors to mitigate fratricide). In this review, we highlight the importance of multi-path way strategies combining CD95 modulation with CAR T cell engineering to overcome resistance, specifically to target tumor cells better and sustain CAR T cell persistence to enhance treatment efficacy in solid tumors.
  4. Balaraman AK, Moglad E, Afzal M, Babu MA, Goyal K, Roopashree R, et al.
    Clin Chim Acta, 2025 Feb 01;567:120105.
    PMID: 39706249 DOI: 10.1016/j.cca.2024.120105
    Pancreatic cancer is a highly fatal malignancy due to poor early detection rate and resistance to conventional therapies. This review examines the potential for liquid biopsy as a transformative technology to identify diagnostic and therapeutic targets in pancreatic cancer. Specifically, we explore emerging biomarkers such as exosomal non-coding RNAs (ncRNAs), circulating tumor DNA (ctDNA), and circulating tumor cells (CTCs). Tumor-derived exosomes contain nucleic acid and protein that reflect the unique molecular landscape of the malignancy and can serve as an alternative diagnostic approach vs traditional biomarkers like CA19-9. Herein we highlight exosomal miRNAs, lncRNAs, and other ncRNAs alongside ctDNA and CTC-based strategies, evaluating their combined ability to improve early detection, disease monitoring and treatment response. Furthermore, the therapeutic implications of ncRNAs such as lncRNA UCA1 and miR-3960 in chemoresistance and progression are also discussed via suppression of EZH2 and PTEN/AKT pathways. Emerging therapeutic strategies that target the immune response, epithelial-mesenchymal transition (EMT) and drug resistance are explored. This review demonstrates a paradigm shift in pancreatic cancer management toward personalized, less invasive and more effective approaches.
  5. Hussain MS, Mujwar S, Babu MA, Goyal K, Chellappan DK, Negi P, et al.
    PMID: 39862263 DOI: 10.1007/s00210-025-03809-5
    As a promising candidate for tackling drug-resistant cancers, triptolide, a diterpenoid derived from the Chinese medicinal plant Tripterygium wilfordii, has been developed. This review summarizes potential antitumor activities, including the suppression of RNA polymerase II, the suppression of heat shock proteins (HSP70 and HSP90), and the blockade of NF-kB signalling. Triptolide is the first known compound to target cancer cells specifically but spare normal cells, and it has success in treating cancers that are difficult to treat, including pancreatic, breast, and lung cancers. It acts against the tolerance mechanisms, including efflux pump upregulation, epithelial-mesenchymal transition, and cancer stem cells. Triptolide modulates important cascades, including PI3K/AKT/mTOR, enhancing the efficacy of conventional therapies. Nonetheless, its clinical application is constrained by toxicity and bioavailability challenges. Emerging drug delivery systems, such as nanoparticles and micellar formulations, are being developed to address these limitations. It has strong interactions with key anticancer targets, like PARP, as determined in preclinical and computational studies consistent with its mechanism of action. Early-phase clinical trials of Minnelide, a water-soluble derivative of triptolide, are promising, but additional work is necessary to optimize dosing, delivery, and safety. This comprehensive analysis demonstrates that triptolide may constitute a repurposed precision medicine tool to overcome tolerance in cancer therapy.
  6. Garegnani L, Franco JVA, Escobar Liquitay CM, Brant LCC, Lim HM, de Jesus Jessen NP, et al.
    Prev Med, 2023 Jul;172:107534.
    PMID: 37146731 DOI: 10.1016/j.ypmed.2023.107534
    BACKGROUND: In 2010 the American Heart Association defined the concept of ideal cardiovascular health to renew the focus on primordial prevention for cardiovascular disease. Evidence primarily from high-income countries suggests ideal CVH prevalence is low and decreases with age, with vulnerable populations differentially affected. We aimed to identify and characterize the evidence relevant to CVH metrics in low- and middle-income countries (LMICs).

    METHODS: We followed the Joanna Briggs Institute guideline for the conduct of this scoping review. We searched MEDLINE, Embase, LILACS and study registers from inception to 14 March 2022. We included cross-sectional and cohort studies in populations representing a geographically-defined unit (urban or rural) in LMICs, and with data on CVH metrics i.e. all health or clinical factors (cholesterol, blood pressure, glycemia and body mass index) and at least one health behavior (smoking, diet or physical activity). We report findings following the PRISMA-Scr extension for scoping reviews.

    RESULTS: We included 251 studies; 85% were cross-sectional. Most studies (70.9%) came from just ten countries. Only 6.8% included children younger than 12 years old. Only 34.7% reported seven metrics; 25.1%, six. Health behaviors were mostly self-reported; 45.0% of studies assessed diet, 58.6% physical activity, and 90.0% smoking status.

    CONCLUSIONS: We identified a substantial and heterogeneous body of research presenting CVH metrics in LMICs. Few studies assessed all components of CVH, especially in children and in low-income settings. This review will facilitate the design of future studies to bridge the evidence gap. This scoping review protocol was previously registered on OSF: https://osf.io/sajnh.

  7. Balaraman AK, Afzal M, Moglad E, Babu MA, Priya GP, Bansal P, et al.
    Biogerontology, 2025 Feb 05;26(2):50.
    PMID: 39907830 DOI: 10.1007/s10522-025-10194-2
    p16INK4a is a crucial tumor suppressor and regulator of cellular senescence, forming a molecular bridge between aging and cancer. Dysregulated p16INK4a expression is linked to both premature aging and cancer progression, where non-coding RNAs (ncRNAs) such as long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and small interfering RNAs (siRNAs) play key roles in modulating its function. These ncRNAs interact with p16INK4a through complex post-transcriptional and epigenetic mechanisms, influencing pathways critical to senescence and tumor suppression. In this review, we explore ncRNAs, including ANRIL, MIR31HG, UCA1, MALAT1, miR-24, miR-30, and miR-141, which collectively regulate p16INK4a expression, promoting or inhibiting pathways associated with cancer and aging. ANRIL and MIR31HG modulate p16INK4a silencing via interactions with polycomb repressive complexes (PRC), while miRNAs such as miR-24 and miR-30 target p16INK4a to influence cellular proliferation and senescence. This regulatory interplay underscores the therapeutic potential of ncRNA-targeted strategies to restore p16INK4a function. We summarize recent studies supporting that ncRNAs that control p16INK4a may be diagnostic biomarkers and therapeutic targets for age-related diseases and cancer.
  8. Ng JY, Wong QYA, Lim JJ, Cen D, Wong JYK, Lim YYE, et al.
    J Physiol Anthropol, 2025 Feb 08;44(1):3.
    PMID: 39923103 DOI: 10.1186/s40101-024-00383-2
    BACKGROUND: Skin ageing takes on many different forms. Despite this diversity in skin ageing phenotypes, literature published to date is limited in scope, as many research studies either focus on one single phenotype or just a few specific phenotypes. Presently, phenotypes such as wrinkles, pigment spots, and photo-ageing are receiving most of the research attention. We therefore wonder whether the current discourse on skin ageing places a disproportionate amount of focus on a few selected phenotypes, leaving other skin ageing phenotypes underexplored.

    METHODS: In this cross-sectional study, we performed a broad assessment of forty-one signs of skin ageing and characterised the phenotypes that constituted key components of skin ageing. We also explored the interrelationship among forty-one skin ageing phenotypes using Spearman's Correlation and Principal Component Analysis.

    RESULTS: We analysed our study population, which is composed of 3281 ethnic Chinese participants from the Singapore/Malaysia Cross-sectional Genetics Epidemiology Study (SMCGES). The first ten principal components cumulatively explain 46.88% of the variance of skin ageing phenotypes in our study population. We discovered that the commonly discussed forms of skin ageing (i.e., wrinkles, pigmentation, and photo-ageing) only accounted for a small portion (24.39%) of the variance of all skin ageing phenotypes in our study population. Telangiectasia, a poor lip fullness, a lighter skin colour, xerosis, ephelides (freckles), ptosis of eyelids (droopy eyelids), eyebags, and a low eyebrow positioning were other key components of skin ageing, accounting for a further 22.49% of the variance of skin ageing phenotypes in our study population. We found that each of these ten skin ageing phenotypes characterises a key and important aspect of skin ageing. In this broad assessment of skin ageing, we first described the prevalence of forty-one signs of skin ageing and then characterised in detail both the prevalence and severity distribution of ten key skin ageing phenotypes.

    CONCLUSIONS: We presented clear evidence that skin ageing is much more than just wrinkles, pigmentation and photo-ageing. The addition of telangiectasia, poor lip fullness, a lighter skin colour, xerosis, ephelides, ptosis of eyelids, eyebags, and a low eyebrow positioning added more dimensions to skin ageing phenotype presentations.

  9. Balaraman AK, Altamimi ASA, Babu MA, Goyal K, PadmaPriya G, Bansal P, et al.
    Biogerontology, 2025 Jan 20;26(1):46.
    PMID: 39832057 DOI: 10.1007/s10522-025-10190-6
    Aging is associated with a marked increase in cardiovascular diseases, such as myocardial infarction (MI). Cellular senescence is also a crucial factor in the development of age-related MI. Matrix metalloproteinases (MMPs) interaction with cellular senescence is a critical determinant of MI development and outcomes, most notably in the aged heart. After experiencing a heart attack, senescent cells exhibit a Senescence-Associated Secretory Phenotype (SASP) and are involved in tissue regeneration and chronic inflammation. MMPs are necessary for extracellular matrix proteolysis and have a biphasic effect, promoting early heart healing and detrimental change if overexpressed shortly. This review analyses the complex connection between senescence and MMPs in MI and how it influences elderly cardiac performance. Critical findings suggest that increasing cellular senescence in aged hearts elevates MMP activity and aggravates extended ventricular remodeling and dysfunction. Additionally, we explore potential therapeutics that address MMPs and senescence to enhance old MI patient myocardial performance and regeneration.
  10. Balaraman AK, Babu MA, Moglad E, Mandaliya V, Rekha MM, Gupta S, et al.
    Pathol Res Pract, 2025 Feb;266:155785.
    PMID: 39708520 DOI: 10.1016/j.prp.2024.155785
    Several molecular strategies based on targeted gene delivery systems have been developed in recent years; however, the CRISPR-Cas9 technology introduced a new era of targeted gene editing, precisely modifying oncogenes, tumor suppressor genes, and other regulatory genes involved in carcinogenesis. However, efficiently and safely delivering CRISPR-Cas9 to cancer cells across the cell membrane and the nucleus is still challenging. Using viral vectors and nanoparticles presents issues of immunogenicity, off-target effects, and low targeting affinity. Naturally, extracellular vesicles called exosomes have garnered the most attention as delivery vehicles in oncology-related CRISPR-Cas9 calls due to their biocompatibility, loading capacity, and inherent targeting features. The following review discusses the current progress in using exosomes to deliver CRISPR-Cas9 components, the approaches to load the CRISPR components into exosomes, and the modification of exosomes to increase stability and tumor-targeted delivery. We discuss the latest strategies in targeting recently accomplished in the exosome field, including modifying the surface of exosomes to enhance their internalization by cancer cells, as well as the measures taken to overcome the impacts of TME on delivery efficiency. Focusing on in vitro and in vivo experimentation, this review shows that exosome-mediated CRISPR-Cas9 can potentially treat cancer types, including pancreatic, lymphoma, and leukemia, for given gene targets. This paper compares exosome-mediated delivery and conventional vectors regarding safety, immune response, and targeting ability. Last but not least, we present the major drawbacks and potential development of the seemingly promising field of exosome engineering in gene editing, with references to CRISPR technologies and applications that may help make the target exosomes therapeutic in oncology.
  11. Menon S, Anand D, Kavita, Verma S, Kaur M, Jhanjhi NZ, et al.
    Sensors (Basel), 2023 Jul 04;23(13).
    PMID: 37447981 DOI: 10.3390/s23136132
    With the increasing growth rate of smart home devices and their interconnectivity via the Internet of Things (IoT), security threats to the communication network have become a concern. This paper proposes a learning engine for a smart home communication network that utilizes blockchain-based secure communication and a cloud-based data evaluation layer to segregate and rank data on the basis of three broad categories of Transactions (T), namely Smart T, Mod T, and Avoid T. The learning engine utilizes a neural network for the training and classification of the categories that helps the blockchain layer with improvisation in the decision-making process. The contributions of this paper include the application of a secure blockchain layer for user authentication and the generation of a ledger for the communication network; the utilization of the cloud-based data evaluation layer; the enhancement of an SI-based algorithm for training; and the utilization of a neural engine for the precise training and classification of categories. The proposed algorithm outperformed the Fused Real-Time Sequential Deep Extreme Learning Machine (RTS-DELM) system, the data fusion technique, and artificial intelligence Internet of Things technology in providing electronic information engineering and analyzing optimization schemes in terms of the computation complexity, false authentication rate, and qualitative parameters with a lower average computation complexity; in addition, it ensures a secure, efficient smart home communication network to enhance the lifestyle of human beings.
  12. Parvaresh Rizi E, Teo Y, Leow MK, Venkataraman K, Khoo EY, Yeo CR, et al.
    J Clin Endocrinol Metab, 2015 11;100(11):4249-56.
    PMID: 26308293 DOI: 10.1210/jc.2015-2639
    CONTEXT: Among Asian ethnic groups, Chinese or Malays are more insulin sensitive than South Asians, in particular in lean individuals. We have further reported that body fat partitioning did not explain this ethnic difference in insulin sensitivity.

    OBJECTIVE: We examined whether adipocytokines might explain the ethnic differences in the relationship between obesity and insulin resistance among the three major ethnic groups in Singapore.

    DESIGN AND PARTICIPANTS: This was a cross-sectional study of 101 Chinese, 82 Malays, and 81 South Asian men. Insulin sensitivity index (ISI) was measured using hyperinsulinemic euglycemic clamp. Visceral (VAT) and subcutaneous adipose tissue (SAT) volumes were quantified using magnetic resonance imaging.

    MAIN OUTCOME MEASURES: Plasma total and high-molecular-weight adiponectin, leptin, visfatin, apelin, IL-6, fibroblast growth factor 21 (FGF21), retinol binding protein-4 (RBP 4), and resistin were measured using enzyme-linked immunoassays.

    RESULTS: Principle component (PC) analysis on the adipocytokines identified three PCs, which explained 49.5% of the total variance. Adiponectin loaded negatively, and leptin and FGF21 loaded positively onto PC1. Visfatin, resistin, and apelin all loaded positively onto PC2. IL-6 loaded positively and RBP-4 negatively onto PC3. Only PC1 was negatively associated with ISI in all ethnic groups. In the path analysis, SAT and VAT were negatively associated with ISI in Chinese and Malays without significant mediatory role of PC1. In South Asians, the relationship between VAT and ISI was mediated partly through PC1, whereas the relationship between SAT and ISI was mediated mainly through PC1.

    CONCLUSIONS: The relationships between abdominal obesity, adipocytokines and insulin sensitivity differ between ethnic groups. Adiponectin, leptin, and FGF21 play a mediating role in the relationship between abdominal adiposity and insulin resistance in South Asians, but not in Malays or Chinese.

  13. Bakshi HA, Mishra V, Satija S, Mehta M, Hakkim FL, Kesharwani P, et al.
    Inflammation, 2019 Dec;42(6):2032-2036.
    PMID: 31377947 DOI: 10.1007/s10753-019-01065-3
    Hypoxia inducible factor (HIF)-prolyl hydroxylase (PHD) inhibitors are shown to be protective in several models of inflammatory bowel disease (IBD). However, these non-selective inhibitors are known to inhibit all the three isoforms of PHD, i.e. PHD-1, PHD-2 and PHD-3. In the present report, we investigated the associated changes in levels of PHDs during the development and recovery of chemically induced colitis in mice. The results indicated that in the experimental model of murine colitis, levels of both, PHD-1 and PHD-2 were found to be increased with the progression of the disease; however, the level of PHD-3 remained the same in group of healthy controls and mice with colitis. Thus, the findings advocated that inhibitors, which inhibited all three isoforms of PHD could not be ideal therapeutics for IBD since PHD-3 is required for normal gut function. Hence, this necessitates the development of new compounds capable of selectively inhibiting PHD-1 and PHD-2 for effective treatment of IBD.
  14. Yong VW, Tan YJ, Ng YD, Choo XY, Sugumaran K, Chinna K, et al.
    Parkinsonism Relat Disord, 2020 08;77:28-35.
    PMID: 32615497 DOI: 10.1016/j.parkreldis.2020.06.015
    INTRODUCTION: Although weight loss is common in Parkinson's disease (PD), longitudinal studies assessing weight and body composition changes are limited.

    METHODS: In this three-year longitudinal study, 125 subjects (77 PD patients and 48 spousal/sibling controls) underwent clinical, biochemical and body composition assessments using dual-energy X-ray absorptiometry.

    RESULTS: Patients were older than controls (65.6 ± 8.9 vs. 62.6 ± 7.1, P = 0.049), with no significant differences in gender, comorbidities, dietary intake and physical activity. Clinically significant weight loss (≥5% from baseline weight) was recorded in 41.6% of patients, with a doubling of cases (6.5 to 13.0%) classified as underweight at study end. Over three years, patients demonstrated greater reductions in BMI (mean -1.2 kg/m2, 95%CI-2.0 to -0.4), whole-body fat percentage (-2.5% points, 95%CI-3.9 to -1.0), fat mass index (FMI) (-0.9 kg/m2, 95%CI-1.4 to -0.4), visceral fat mass (-0.1 kg, 95%CI-0.2 to 0.0), and subcutaneous fat mass (-1.9 kg, 95%CI-3.4 to -0.5) than in controls, with significant group-by-time interactions after adjusting for age and gender. Notably, 31.2% and 53.3% of patients had FMI<3rd (severe fat deficit) and <10th centiles, respectively. Muscle mass indices decreased over time in both groups, without significant group-by-time interactions. Multiple linear regression models showed that loss of body weight and fat mass in patients were associated with age, dyskinesia, psychosis and constipation.

    CONCLUSIONS: We found progressive loss of weight in PD patients, with greater loss of both visceral and subcutaneous fat, but not muscle, compared to controls. Several associated factors (motor and non-motor disease features) were identified for these changes, providing insights on possible mechanisms and therapeutic targets.

  15. Lim JJ, Lim YYE, Ng JY, Malipeddi P, Ng YT, Teo WY, et al.
    World Allergy Organ J, 2022 Dec;15(12):100722.
    PMID: 36438192 DOI: 10.1016/j.waojou.2022.100722
    BACKGROUND: Atopic Dermatitis (AD) is a highly pruritic, chronic-recurrent inflammatory skin condition associated with erythematous lesions that affect a significant proportion of the population. Although AD is a non-communicable disease, it can cause pain, unbearable itchiness, sleep disturbance, loss of work productivity, and reduced quality of life. As a heterogeneous disease, AD is influenced by multiple genes and environmental triggers. As such, it is imperative to gain a deeper insight into the intricate gene-environment relationship that results in the manifestation of AD.

    METHODS: There are 3 objectives in our study. We first aim to update the epidemiological status of AD amongst young adults in Singapore and Malaysia, in particular amongst the Chinese ethnic background. Next, we re-evaluated the possible associated risk factors, identified in our previous meta-analysis and review studies, on the current cohort. Finally, we described here a detailed disease presentation and symptoms profile of our Singapore and Malaysia Cross-Sectional Genetics Epidemiology Study (SMCGES) cohort, which forms the base population for the discovery of associated genetic factors in relation to asthma, allergic diseases and skin conditions. Based on a skin prick test (SPT) and investigator-administered medical history responses, we assessed the AD profiles of 11 494 participants and the significant modifiable and non-modifiable factors associated with disease presentation.

    RESULTS: The prevalence of AD in the combined population was 13.5%. Chronic and moderate/severe AD were observed in 35.5% and 40.5% of the individuals with AD, respectively. Family history of atopic diseases, prior history of drug allergies, a history of acne, increased household family monthly income, higher number of individuals in the shared household, parental education, sedentary lifestyle, physical activities, alcoholic consumption, and even quality of diet was significantly associated with AD presentation, chronicity, and severity. Among all the factors evaluated, family and personal history of atopic diseases imposed the strongest associated risk.

    CONCLUSIONS: These findings supported our previous review studies and affirmed that familial history or genetic factors critically influence the development of AD in our population and environment. Environmental and other modifiable factors can also trigger AD throughout the lifetime of individuals who have especially inherited the atopic disease disposition. A better understanding of how these risk factors affect AD individuals in our population can facilitate disease surveillance, monitor disease control, and serve as a description for our future genetic epidemiology studies.

  16. Lim JJ, Lim YYE, Ng JY, Malipeddi P, Ng YT, Teo WY, et al.
    Dermatology, 2024;240(1):77-84.
    PMID: 37666213 DOI: 10.1159/000533942
    BACKGROUND: We see increasing evidence that dietary and nutrients factors play a pivotal role in allergic diseases and recent global findings suggest that dietary habits influence the pathogenesis of atopic dermatitis (AD). Frequent consumption of fast food diets is associated with AD development. Despite the rising prevalence of AD in Asia, efforts in investigating the role of dietary habits and AD in adults are still lacking.

    METHODS: We evaluated the association between the dietary intake of 16 food types and AD manifestations using our Singapore/Malaysia Cross-sectional Genetics Epidemiology Study (SMCGES) population. Dietary habits profiles of 11,494 young Chinese adults (1,550 AD cases/2,978 non-atopic controls/6,386 atopic controls) were assessed by an investigator-administered questionnaire. AD cases were further evaluated for their chronicity (550 chronic) and severity (628 moderate-to-severe). Additionally, we derived a novel food index, Quality of Diet based on Glycaemic Index Score (QDGIS), to examine the association between dietary intake of glycaemic index (GI) and various AD phenotypes.

    RESULTS: The majority of AD subjects are distributed in the good (37.1%) and moderate (36.2%) QDGIS classes. From the multivariable analyses for age and gender, a moderate QDGIS class was significantly associated with a lower odds of AD (adjusted odds ratio (AOR): 0.844; 95% confidence interval (CI): 0.719-0.991; p < 0.05) and moderate-to-severe AD (AOR: 0.839; 95% CI: 0.714-0.985; p < 0.05). A good QDGIS class was only significantly associated with a lower odds of chronic AD (AOR: 0.769; 95% CI: 0.606-0.976; p < 0.05). Among high GI foods, frequent consumption of burgers/fast food was strongly associated with an increased risk of chronic and moderate-to-severe AD. Among low GI foods, increased intake frequencies of fruits, vegetables, and pulses decreased the odds of AD. Finally, we identified significant associations between frequent seafood, margarine, butter, and pasta consumption with an increased odds of AD despite them having little GI values.

    CONCLUSION: While genetic components are well-established in their risks associated with increased AD prevalence, there is still a lack of a focus epidemiology study associating dietary influence with AD. Based on the first allergic epidemiology study conducted here in Singapore and Malaysia, it laid the groundwork to guide potential dietary interventions from changing personal dietary habits.

  17. Wong QYA, Lim JJ, Ng JY, Malipeddi P, Teo WY, Lim YYE, et al.
    World Allergy Organ J, 2022 Oct;15(10):100704.
    PMID: 36267097 DOI: 10.1016/j.waojou.2022.100704
    BACKGROUND: Allergic rhinitis (AR) is characterized by the occurrence of at least 2 symptoms of nasal itching, nasal blockage, rhinorrhea, and sneezing, when not afflicted with a cold or flu, with defined atopic sensitization demonstrated by skin prick test or specific IgE responses. Besides the detriment to standard of living and economic burden of AR, both multicentre and single-cohort studies have observed an increase in AR prevalence in Asia over time.

    METHODS: In total, 12 872 individuals, with mean age 22.1 years (SD = 4.8), were recruited from universities in Singapore and Malaysia. Each participant provided epidemiological data based on an investigator-administered questionnaire adapted from the validated International Study of Allergies and Asthma in Childhood (ISAAC) protocol, and atopy status was determined using a skin prick test (SPT) performed by qualified staff. AR was diagnosed according to Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines and a positive SPT result.

    RESULTS: Sensitization (determined by SPT) to either Blomia tropicalis or Dermatophagoides pteronyssinus was prevalent in 66.5% of the cohort. Current rhinitis (manifesting ≥2 rhinitis symptoms, within the past 12 months) was observed in 48.9% of our population, while AR, which included atopy status, was estimated at 39.4%. Sneezing and rhinorrhea were the most common symptoms among AR cases. AR prevalence decreased with increasing age (OR: 0.979; 95% CI: 0.969-0.989), while male gender (OR: 2.053; 95% CI: 1.839-2.294), and a parental history of allergic diseases (OR: 2.750; 95% CI: 2.284-3.316) were significant risk factors for AR. Upon adjustment for age, gender, and parental history, housing type (OR: 0.632; 95% CI: 0.543-0.736) and income level (>$6000 vs

  18. Boruah AP, Thakur KT, Gadani SP, Kothari KU, Chomba M, Guekht A, et al.
    J Neurol Sci, 2023 Dec 15;455:120858.
    PMID: 37948972 DOI: 10.1016/j.jns.2023.120858
    BACKGROUND: Pre-existing neurological diseases have been identified as risk factors for severe COVID-19 infection and death. There is a lack of comprehensive literature review assessing the relationship between pre-existing neurological conditions and COVID-19 outcomes. Identification of high risk groups is critical for optimal treatment and care.

    METHODS: A literature review was conducted for systematic reviews, meta-analyses, and scoping reviews published between January 1, 2020 and January 1, 2023. Literature assessing individuals with pre-existing neurological diseases and COVID-19 infection was included. Information regarding infection severity was extracted, and potential limitations were identified.

    RESULTS: Thirty-nine articles met inclusion criteria, with data assessing >3 million patients from 51 countries. 26/51 (50.9%) of countries analyzed were classified as high income, while the remaining represented middle-low income countries (25/51; 49.0%). A majority of evidence focused on the impact of cerebrovascular disease (17/39; 43.5%) and dementia (5/39; 12.8%) on COVID-19 severity and mortality. 92.3% of the articles (36/39) suggested a significant association between neurological conditions and increased risk of severe COVID-19 and mortality. Cerebrovascular disease, dementia, Parkinson's disease, and epilepsy were associated with increased COVID severity and mortality.

    CONCLUSION: Pre-existing neurological diseases including cerebrovascular disease, Alzheimer's disease and other dementias, epilepsy, and Parkinson's disease are significant risk factors for severity of COVID-19 infection and mortality in the acute infectious period. Given that 61.5% (24/39) of the current evidence only includes data from 2020, further updated literature is crucial to identify the relationship between chronic neurological conditions and clinical characteristics of COVID-19 variants.

  19. Passmore MR, Byrne L, Obonyo NG, See Hoe LE, Boon AC, Diab SD, et al.
    Respir Res, 2018 Nov 22;19(1):231.
    PMID: 30466423 DOI: 10.1186/s12931-018-0935-4
    BACKGROUND: Sepsis is a multi-system syndrome that remains the leading cause of mortality and critical illness worldwide, with hemodynamic support being one of the cornerstones of the acute management of sepsis. We used an ovine model of endotoxemic shock to determine if 0.9% saline resuscitation contributes to lung inflammation and injury in acute respiratory distress syndrome, which is a common complication of sepsis, and investigated the potential role of matrix metalloproteinases in this process.

    METHODS: Endotoxemic shock was induced in sheep by administration of an escalating dose of lipopolysaccharide, after which they subsequently received either no fluid bolus resuscitation or a 0.9% saline bolus. Lung tissue, bronchoalveolar fluid (BAL) and plasma were analysed by real-time PCR, ELISA, flow cytometry and immunohistochemical staining to assess inflammatory cells, cytokines, hyaluronan and matrix metalloproteinases.

    RESULTS: Endotoxemia was associated with decreased serum albumin and total protein levels, with activated neutrophils, while the glycocalyx glycosaminoglycan hyaluronan was significantly increased in BAL. Quantitative real-time PCR studies showed higher expression of IL-6 and IL-8 with saline resuscitation but no difference in matrix metalloproteinase expression. BAL and tissue homogenate levels of IL-6, IL-8 and IL-1β were elevated.

    CONCLUSIONS: This data shows that the inflammatory response is enhanced when a host with endotoxemia is resuscitated with saline, with a comparatively higher release of inflammatory cytokines and endothelial/glycocalyx damage, but no change in matrix metalloproteinase levels.

  20. Aljabali AAA, Bakshi HA, Hakkim FL, Haggag YA, Al-Batanyeh KM, Zoubi MSA, et al.
    Cancers (Basel), 2020 Nov 30;12(12).
    PMID: 33266353 DOI: 10.3390/cancers12123587
    The authors wish to make the following corrections to this paper [...].
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