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Human rights violations against women: acid violence in Bangladesh

Haque SE, Ahsan H

Am J Prev Med, 2014 Feb;46(2):216-7.
PMID: 24439357 DOI: 10.1016/j.amepre.2013.10.013
Fulltext Transient pain and discomfort when wearing high-heeled shoes

Almadhaani HMA, Goonetilleke RS, Wijeweera A, Jayaraman R, Ameersing L, Khandoker AH, et al.

Sci Rep, 2024 Apr 23;14(1):9291.
PMID: 38654097 DOI: 10.1038/s41598-024-59966-9

In the dynamic world of fashion, high-heeled footwear is revered as a symbol of style, luxury and sophistication. Yet, beneath the facade of elegance of classy footwear lies the harsh reality of discomfort and pain. Thus, this study aims to investigate the influence of wearing high-heeled shoes on the sensation of pain across different body regions over a period of 6 h. It involved fifty female participants, all habitual wearers of high-heeled shoes, aged between 20 and 30 years. Each participant kept a record of their perceptions of pain and discomfort every hour for a total of 6 h using a 0-10 pain scale with 0 indicating no pain and 10 indicating severe pain. The findings reveal a progressive rise in pain throughout wear, with the most intense pain reported in the back, calcaneus, and metatarsals. The analysis shows that after approximately 3.5 h, participants experience significant increases in pain levels. However, the relationship between heel height and pain is not linear. It appears that a heel height of 7.5 cm is the threshold where overall body pain becomes significant. The study suggests that a duration of 3.5 h of wear and a heel height of 7.5 cm serve as critical points to decrease overall body pain. Moreover, beyond this heel height, knee pain diminishes compared to other body areas possibly due to the shift towards a more neutral posture. The study findings, coupled with the recommendations, can assist footwear designers in crafting not only stylish but also comfortable shoes.
Rational use of antibiotics in an intensive care unit: a retrospective study of the impact on clinical outcomes and mortality rate

Ali M, Naureen H, Tariq MH, Farrukh MJ, Usman A, Khattak S, et al.

Infect Drug Resist, 2019;12:493-499.
PMID: 30881054 DOI: 10.2147/IDR.S187836

Background: Intensive care units (ICUs) are specialized units where patients with critical conditions are admitted for getting specialized and individualized medical treatment. High mortality rates have been observed in ICUs, but the exact reason and factors affecting the mortality rates have not yet been studied in the local population in Pakistan.
Aim: This study was aimed to determine rational use of antibiotic therapy in ICU patients and its impact on clinical outcomes and mortality rate.
Methods: This was a retrospective, longitudinal (cohort) study including 100 patients in the ICU of the largest tertiary care hospital of the capital city of Pakistan.
Results: It was observed that empiric antibiotic therapy was initiated in 68% of patients, while culture sensitivity test was conducted for only 19% of patients. Thirty-percent of patients developed nosocomial infections and empiric antibiotic therapy was not initiated for those patients (P<0.05). Irrational antibiotic prescribing was observed in 86% of patients, and among them, 96.5% mortality was observed (P<0.05). The overall mortality rate was 83%; even higher mortality rates were observed in patients on a ventilator, patients with serious drug-drug interactions, and patients prescribed with irrational antibiotics or nephrotoxic drugs. Adverse clinical outcomes leading to death were observed to be significantly associated (P<0.05) with irrational antibiotic prescribing, nonadjustment of doses of nephrotoxic drugs, use of steroids, and major drug-drug interactions.
Conclusion: It was concluded that empiric antibiotic therapy is beneficial in patients and leads to a reduction in the mortality rate. Factors including irrational antibiotic selection, prescribing contraindicated drug combinations, and use of nephrotoxic drugs were associated with high mortality rate and poor clinical outcomes.
Observation of the seleno bis-(S-glutathionyl) arsinium anion in rat bile

George GN, Gailer J, Ponomarenko O, La Porte PF, Strait K, Alauddin M, et al.

J Inorg Biochem, 2016 05;158:24-29.
PMID: 26883676 DOI: 10.1016/j.jinorgbio.2016.01.022

Certain arsenic and selenium compounds show a remarkable mutual cancelation of toxicities, where a lethal dose of one can be voided by an equimolar and otherwise lethal dose of the other. It is now well established that the molecular basis of this antagonism is the formation and biliary excretion of seleno bis-(S-glutathionyl) arsinium anion [(GS)2AsSe](-). Previous work has definitively demonstrated the presence of [(GS)2AsSe](-) in rabbit bile, but only in the presence of other arsenic and selenium species. Rabbits have a gall bladder, which concentrates bile and lowers its pH; it seems likely that this may be responsible for the breakdown of biliary [(GS)2AsSe](-). Since rats have no gall bladder, the bile proceeds directly through the bile duct from the hepatobiliary tree. In the present work we have shown that the primary product of biliary co-excretion of arsenic and selenium in rats is [(GS)2AsSe](-), with essentially 100% of the arsenic and selenium present as this species. The chemical plausibility of the X-ray absorption spectroscopy-derived structural conclusions of this novel arsenic and selenium co-excretion product is supported by density functional theory calculations. These results establish the biomolecular basis to further explore the use of selenium dietary supplements as a possible palliative for chronic low-level arsenic poisoning of human populations.
Selenium-mediated arsenic excretion in mammals: a synchrotron-based study of whole-body distribution and tissue-specific chemistry

Ponomarenko O, La Porte PF, Singh SP, Langan G, Fleming DEB, Spallholz JE, et al.

Metallomics, 2017 Nov 15;9(11):1585-1595.
PMID: 29058732 DOI: 10.1039/c7mt00201g

Arsenicosis, a syndrome caused by ingestion of arsenic contaminated drinking water, currently affects millions of people in South-East Asia and elsewhere. Previous animal studies revealed that the toxicity of arsenite essentially can be abolished if selenium is co-administered as selenite. Although subsequent studies have provided some insight into the biomolecular basis of this striking antagonism, many details of the biochemical pathways that ultimately result in the detoxification and excretion of arsenic using selenium supplements have yet to be thoroughly studied. To this end and in conjunction with the recent Phase III clinical trial "Selenium in the Treatment of Arsenic Toxicity and Cancers", we have applied synchrotron X-ray techniques to elucidate the mechanisms of this arsenic-selenium antagonism at the tissue and organ levels using an animal model. X-ray fluorescence imaging (XFI) of cryo-dried whole-body sections of laboratory hamsters that had been injected with arsenite, selenite, or both chemical species, provided insight into the distribution of both metalloids 30 minutes after treatment. Co-treated animals showed strong co-localization of arsenic and selenium in the liver, gall bladder and small intestine. X-ray absorption spectroscopy (XAS) of freshly frozen organs of co-treated animals revealed the presence in liver tissues of the seleno bis-(S-glutathionyl) arsinium ion, which was rapidly excreted via bile into the intestinal tract. These results firmly support the previously postulated hepatobiliary excretion of the seleno bis-(S-glutathionyl) arsinium ion by providing the first data pertaining to organs of whole animals.
Fulltext Genome-wide association analysis of more than 120,000 individuals identifies 15 new susceptibility loci for breast cancer

Michailidou K, Beesley J, Lindstrom S, Canisius S, Dennis J, Lush MJ, et al.

Nat Genet, 2015 Apr;47(4):373-80.
PMID: 25751625 DOI: 10.1038/ng.3242

Genome-wide association studies (GWAS) and large-scale replication studies have identified common variants in 79 loci associated with breast cancer, explaining ∼14% of the familial risk of the disease. To identify new susceptibility loci, we performed a meta-analysis of 11 GWAS, comprising 15,748 breast cancer cases and 18,084 controls together with 46,785 cases and 42,892 controls from 41 studies genotyped on a 211,155-marker custom array (iCOGS). Analyses were restricted to women of European ancestry. We generated genotypes for more than 11 million SNPs by imputation using the 1000 Genomes Project reference panel, and we identified 15 new loci associated with breast cancer at P < 5 × 10(-8). Combining association analysis with ChIP-seq chromatin binding data in mammary cell lines and ChIA-PET chromatin interaction data from ENCODE, we identified likely target genes in two regions: SETBP1 at 18q12.3 and RNF115 and PDZK1 at 1q21.1. One association appears to be driven by an amino acid substitution encoded in EXO1.
Fulltext Identification of four novel susceptibility loci for oestrogen receptor negative breast cancer

Couch FJ, Kuchenbaecker KB, Michailidou K, Mendoza-Fandino GA, Nord S, Lilyquist J, et al.

Nat Commun, 2016 Apr 27;7:11375.
PMID: 27117709 DOI: 10.1038/ncomms11375

Common variants in 94 loci have been associated with breast cancer including 15 loci with genome-wide significant associations (P<5 × 10(-8)) with oestrogen receptor (ER)-negative breast cancer and BRCA1-associated breast cancer risk. In this study, to identify new ER-negative susceptibility loci, we performed a meta-analysis of 11 genome-wide association studies (GWAS) consisting of 4,939 ER-negative cases and 14,352 controls, combined with 7,333 ER-negative cases and 42,468 controls and 15,252 BRCA1 mutation carriers genotyped on the iCOGS array. We identify four previously unidentified loci including two loci at 13q22 near KLF5, a 2p23.2 locus near WDR43 and a 2q33 locus near PPIL3 that display genome-wide significant associations with ER-negative breast cancer. In addition, 19 known breast cancer risk loci have genome-wide significant associations and 40 had moderate associations (P<0.05) with ER-negative disease. Using functional and eQTL studies we implicate TRMT61B and WDR43 at 2p23.2 and PPIL3 at 2q33 in ER-negative breast cancer aetiology. All ER-negative loci combined account for ∼11% of familial relative risk for ER-negative disease and may contribute to improved ER-negative and BRCA1 breast cancer risk prediction.
Fulltext Identification of ten variants associated with risk of estrogen-receptor-negative breast cancer

Milne RL, Kuchenbaecker KB, Michailidou K, Beesley J, Kar S, Lindström S, et al.

Nat Genet, 2017 Dec;49(12):1767-1778.
PMID: 29058716 DOI: 10.1038/ng.3785

Most common breast cancer susceptibility variants have been identified through genome-wide association studies (GWAS) of predominantly estrogen receptor (ER)-positive disease. We conducted a GWAS using 21,468 ER-negative cases and 100,594 controls combined with 18,908 BRCA1 mutation carriers (9,414 with breast cancer), all of European origin. We identified independent associations at P < 5 × 10-8 with ten variants at nine new loci. At P < 0.05, we replicated associations with 10 of 11 variants previously reported in ER-negative disease or BRCA1 mutation carrier GWAS and observed consistent associations with ER-negative disease for 105 susceptibility variants identified by other studies. These 125 variants explain approximately 16% of the familial risk of this breast cancer subtype. There was high genetic correlation (0.72) between risk of ER-negative breast cancer and breast cancer risk for BRCA1 mutation carriers. These findings may lead to improved risk prediction and inform further fine-mapping and functional work to better understand the biological basis of ER-negative breast cancer.
Fulltext Association analysis identifies 65 new breast cancer risk loci

Michailidou K, Lindström S, Dennis J, Beesley J, Hui S, Kar S, et al.

Nature, 2017 Nov 02;551(7678):92-94.
PMID: 29059683 DOI: 10.1038/nature24284

Breast cancer risk is influenced by rare coding variants in susceptibility genes, such as BRCA1, and many common, mostly non-coding variants. However, much of the genetic contribution to breast cancer risk remains unknown. Here we report the results of a genome-wide association study of breast cancer in 122,977 cases and 105,974 controls of European ancestry and 14,068 cases and 13,104 controls of East Asian ancestry. We identified 65 new loci that are associated with overall breast cancer risk at P