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Fulltext An audit of upper gastrointestinal bleeding at Seremban Hospital

Lim TM, Lu PY, Meheshinder S, Selvindoss P, Balasingh D, Ramesh J, et al.

Med J Malaysia, 2003 Oct;58(4):522-5.
PMID: 15190627

We retrospectively analyzed all patients presenting with upper gastrointestinal bleeding to Seremban Hospital over a one-year period. A quarter of the oesophagogastro-duodenoscopies (OGD) performed were performed as emergency for upper gastrointestinal tract bleeding. Gastric ulcers and duodenal ulcers were the two most common findings. Our results suggest that there is a male preponderance of 2:1, the Chinese were more likely to be affected and the elderly (> 60 years) were at highest risk.
Identification and validation of mRNA profiles linked to ATP- induced cell death represent a novel prognostic model for breast cancer

Zhang Z, Zhang H, Zhang Z, Sandai D, Lu P, Zhang H, et al.

Front Immunol, 2024;15:1483498.
PMID: 39555060 DOI: 10.3389/fimmu.2024.1483498

BACKGROUND: Cell death mechanisms are integral to the pathogenesis of breast cancer (BC), with ATP-induced cell death (AICD) attracting increasing attention due to its distinctive specificity and potential therapeutic applications.
METHODS: This study employed genomic methodologies to investigate the correlation between drug sensitivity and types of AICD in BC. Initially, data from TCGA were utilized to construct a prognostic model and classification system for AICD. Subsequently, a series of bioinformatics analyses assessed the prognostic and clinical significance of this model within the context of BC.
RESULTS: Analysis revealed a cohort of 18 genes associated with AICD, exhibiting prognostic relevance. Survival analyses indicated that overall survival rates were significantly lower in high-risk populations compared to their low-risk counterparts. Furthermore, prognostic indicators linked to AICD demonstrated high accuracy in predicting survival outcomes in BC. Immunological assessments indicated heightened expression of anti-tumor infiltrating immune cells and immune checkpoint molecules in low-risk populations, correlating with various anti-tumor immune functions. Ultimately, a comprehensive prognostic model related to AICD was developed through univariate analysis, least absolute shrinkage and selection operator (LASSO), and multivariate Cox regression analysis. As Adenosine triphosphate (ATP) concentration increased, the viability of BC cells exhibited a general decline at each time point. Notably, ATP diminished the mitochondrial membrane potential in BC cells while enhancing it in normal breast epithelial cells. Additionally, ATP inhibited the migration of BC cells and promoted their apoptosis. ATP also stimulated reactive oxygen species (ROS) production in MCF-10A cells, with implications for the immune response in BC cells. Compared to the control group, expression levels of CLIC6, SLC1A1, and CEMIP were significantly reduced in the ATP intervention group, whereas ANO6 expression was elevated. ANO6, CEMIP, and CLIC6 share genetic variants with BC, while SLC1A1 does not exhibit genetic causal variation with the disease.
CONCLUSION: A valuable prognostic model associated with AICD has been established, capable of accurately predicting BC prognosis. The induction of cell death by ATP appears to play a protective role in BC progression. These findings carry significant implications for the implementation of personalized and tailored treatment strategies for BC patients.
Differential expression and geographic variation of the venom phospholipases A2 of Calloselasma rhodostoma and Trimeresurus mucrosquamatus

Tsai IH, Chen YH, Wang YM, Liau MY, Lu PJ

Arch Biochem Biophys, 2001 Mar 15;387(2):257-64.
PMID: 11370849

To investigate the geographic variations in venoms of two medically important pitvipers, we have purified and characterized the phospholipases A2 (PLA2s) from the pooled venoms of Calloselasma rhodostoma from Malaysia, Thailand, Indonesia, and Vietnam, as well as the individual venom of Trimeresurus mucrosquamatus collected from both North and South Taiwan. Enzymatic and pharmacological activities of the purified PLA2s were also investigated. The complete amino acid sequences of the purified PLA2s were determined by sequencing the corresponding cDNAs from the venom gland and shown to be consistent with their molecular weight data and the N-terminal sequences. All the geographic venom samples of C. rhodostoma contain a major noncatalytic basic PLA2-homolog and two or three acidic PLA2s in different proportions. These acidic PLA2s contain Glu6-substitutions and show distinct inhibiting specificities toward the platelets from human and rabbit. We also found that the T. mucrosquamatus venoms from North Taiwan but not those from South Taiwan contain an Arg6-PLA2 designated as TmPL-III. Its amino acid sequence is reported for the first time. This enzyme is structurally almost identical to the low- or nonexpressed Arg6-PLA2 from C. rhodostoma venom gland, and thus appears to be a regressing venom component in both of the Asian pitvipers.
Fulltext Validation of the Malay Version of the Shame and Stigma Scale among Cancer Patients in Malaysia

Zhang Z, Azman N, Eyu HT, Nik Jaafar NR, Mohd Salleh Sahimi H, Mohamad Yunus MR, et al.

Int J Environ Res Public Health, 2022 Nov 01;19(21).
PMID: 36361144 DOI: 10.3390/ijerph192114266

The assessment of stigma among cancer patients is of the utmost importance as stigma may lead to various psychological sequelae and a lower quality of life. This study aimed to translate the English version of the Shame and Stigma Scale (SSS) into Malay and validate the Malay version of the SSS (SSS-M) to assess the degree of stigma among cancer patients in Malaysia. Initially, the concurrent translation and back translation of the SSS-M were performed, and the face and content validity were assessed. Subsequently, the SSS-M was administered to a total of 234 patients with mixed types of cancer to assess its reliability (internal consistency and test-retest reliability), construct validity (convergent and discriminant validity), and conduct an exploratory factor analysis (EFA) and a confirmatory factor analysis (CFA). The SSS-M total score registered a good internal consistency (a Cronbach's α of 0.881) and test-retest reliability (an intraclass correlation coefficient of 0.876, p < 0.001). The EFA and CFA confirmed that the SSS-M consisted of 16 items in 3 domains. Its convergent and discriminant validity were achieved. Hence, the SSS-M demonstrated good psychometric properties and is available for use to assess stigma among cancer patients in Malaysia.
Microbial metabolites in tumor epigenetic regulation

Zhang W, Zhang H, Liao Y, Jiang S, Zhang H, Huang C, et al.

Imeta, 2026 Feb;5(1):e70115.
PMID: 42974449 DOI: 10.1002/imt2.70115

With an increasing global cancer burden, the regulatory function of the human microbiome and its metabolites in tumor epigenetics has garnered significant interest. Microbial metabolites are not merely passive byproducts but serve as signaling molecules and epigenetic modulators, contributing to tumor progression through multiple overlapping pathways. Short-chain fatty acids (SCFAs) such as butyrate directly inhibit histone deacetylases to reactivate tumor suppressor genes, while secondary bile acids (BAs) induce gene silencing via DNA methylation remodeling by altering the FXR/TGR5 signaling pathway. Folate and vitamin B12 serve as substrates for DNA and histone methylation through one-carbon metabolism. A complex bidirectional feedback loop exists between microbial metabolism and tumor epigenetics: reprogramming driven by hypoxia or oncogenes alters metabolite flux, generating molecules such as lactate and succinate that not only remodel chromatin and the tumor microenvironment (TME) but also selectively promote the growth of metabolically adapted microbial species, thereby reinforcing epigenetic dysregulation. Despite growing mechanistic insights, establishing causality and correlating spatiotemporal dynamics and dose responses within the highly heterogeneous TME remain major challenges. Data integration across multi-omics remains limited by methodological and computational constraints. Resolving these issues will be critical for understanding the microbe-metabolite-epigenetic axis and advancing personalized precision oncology.