Objective: The placenta constitutes a physical and immunological barrier against infectious agents. Toll-like receptors (TLRs) are essential components for the induction of innate immunity responses in different human tissues including the placenta. We investigated the expressions of TLR2 and TLR4 in the decidua and amniotic cells in non-infl amed placenta and placenta with infection. Materials and Methods: There were a total 74 placentas (37 with infection and 37 without infection- 25 bacterial, 10 viral and 2 toxoplasma). TLR2 and TLR4 expressions were assessed using immunohistochemical technique. Positive cells were indicated by cytoplasmic staining and the percentage of positive in 100 cells was recorded and graded. The grades were 1+ (<25%), 2+ (25-75%) and 3+ (>75%). Results: We found signifi cantly higher expression of TLR2 in the amniotic cells and decidua cells in infected placentas as compared to non-infl amed placentas among the preterm placenta. A higher number of cases have TLR4 expression in the amnion of preterm infected placenta than in term placenta. This, however, is not statistically signifi cant. Conclusion: Our fi ndings suggest that TLR2 plays a role in the innate immunity in bacterial and viral infection in the placenta, however, their role in protection against toxoplasma may be limited. This study further supports the observations that TLR2 expression was higher in placenta with infection which strengthened the role of TLR2 in the protection of preterm placenta against infection.

Purpose: Intestinal fibrosis is a common complication of inflammatory bowel diseases. However, the possible involvement of epithelial-mesenchymal transition (EMT) has been scarcely investigated. This systematic review aims to search through research papers that are focusing on messenger RNA (mRNA) and protein expression profile in EMT in fistula or in intestinal fibrosis. Methods: Electronic exploration was performed until April 24, 2019 through PubMed, Ovid, Science Direct, and Scopus databases with the terms of “fistula” OR “intestinal fibrosis” AND “epithelial-mesenchymal transition”. Two independent reviewers scrutinized the suitability of the title and abstract before examining the full text that met the inclusion criteria. For each study, the sample types that were used, methods for analysis, and genes expressed were identified. The list of genes was further analyzed using DAVID (Database for Annotation, Visualization, and Integrated Discovery) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway. Results: There were 896 citations found; however, only 3 studies fulfilled the requirements. Among the EMT-related genes, 5 were upregulated genes at mRNA level while 6 were at protein level. However, only 2 downregulated genes were found at each mRNA and protein level. Of the 4 inflammation-related genes found, 3 genes were upregulated at mRNA level and 1 at protein level. These genes were confirmed to be involved in the development of inflammatory induced fibrosis and fistula through EMT. Results from quantitative real-time polymerase chain reaction analysis were consistent with the process of EMT, confirmed by the western blot protein analysis. Conclusion Many significant genes which are involved in the process of EMT in fistula and intestinal fibrosis have been identified. With high-end technology many more genes could be identified. These genes will be good molecular targets in the development of biomarkers for precision drug targeting in the future treatment of intestinal fibrosis and fistula.

End of life care is framework to allow for a peaceful, comfortable and dignified death while considering the patients’ personal and religious values, bioethics and knowledge of the disease process. A well planned end of life pathway should allow for the flexibility to shift from an active (or aggressive) treatment approach to one of comfort and care when initial interventions have failed. The need for this pathway is most apparent in the intensive care setting. Implementation of a pathway will face various challenges due to religious and cultural beliefs, education of healthcare providers to carry out difficult discussions and larger socioeconomic implications. Clear medico-legal framework will be required to support this pathway. In conclusion, an end of life pathway tailored to our local needs is the way forward in allowing for dignified death of terminally ill patients; this will require the active participation of medical societies, religious leaders, healthcare providers, patients and their care givers.

Introduction: Health education is an essential part of controlling the risk of myocardial infarction (MI). This study evaluates the effects of one-on-one education programmes on the cardiovascular health index among patients with MI.Methods: A quasi-experimental study was conducted in Kuala Lumpur Hospital, Malaysia. Data were collected from November 2014 to January 2015 with a total of 58 respondents who met the inclusion criteria. The respondents received a 20-min one-on-one education programme regarding coronary heart disease, treatment and prevention, and healthy lifestyle. A questionnaire comprising demographic data was administered and the cardiovascular health index was measured before and after four weeks of the education programme. Data were analysed with descriptive and inferential statistics.Results: There were statistically significant decreases in the score of anxiety, stress, depression, body mass index, and smoking status (P < 0.001) between pre-test and post-test.Conclusion: The findings suggest that the one-on-one education programme could improve the cardiovascular health index of patients with MI. Furthermore, nurses need to develop and implement a standard education structure programme for patients with MI to improve health outcomes.

Antiphospholipid antibodies (aPL) are autoantibodies that attack phospholipid through anti-beta 2-glycoprotein 1. The actions of aPL are associated with events leading to thrombosis and morbidity in pregnancy. Antiphospholipid syndrome (APS) is diagnosed when a patient is persistently positive for aPL and also has recognised clinical manifestations such as recurrent pregnancy losses, arterial or venous thrombosis and in a catastrophic case, can result in death. Unfortunately, the pathogenesis of APS is still not well established. Recently, microRNA expressed in many types of diseased tissues were claimed to be involved in the pathological progression of diseases and has become a useful biomarker to indicate diseases, including APS. Objective: This systematic review aims to search for research papers that are focussing on microRNA expression profiles in APS. Method: Three search engines (Ebcohost, ProQuest and Ovid) were used to identify papers related to expression of specific microRNA in antiphospholipid syndrome. Results and Discussion: A total of 357 papers were found and screened, out of which only one study fulfilled the requirement. In this particular study blood samples from APS patients were tested. The microRNAs found to be related to APS were miR-19b and miR-20a. No data was found on specific microRNA being expressed in obstetric antiphospholipid syndrome. Analysis on the microRNA target genes revealed that most genes targeted by miR-19b and miR-20a involve in TGF-Beta Signalling and VEGF, hypoxia and angiogenesis pathways. Conclusion: In view of the limited data on the expressions of microRNA in APS we recommend further research into this field. Characterization of microRNA profile in blood as well as in placenta tissue of patients with APS could be useful in identifying microRNAs involved in obstetric APS.

Introduction: Glucose-6-phosphate dehydrogenase (G6PD) deficiency causes red blood cell destruction due to oxidative stress. G6PD is essential for NADPH conversion; which is critical for glutathione reductase to prevent damage to cellular structures. In Malaysia, blood donors are not routinely screened for G6PD deficiency. We hypothesise that G6PD-deficient red blood cells are more likely to haemolyse during storage due to increased oxidative molecules. The objectives of this study were to determine the prevalence of G6PD deficiency among blood donors, describe their characteristics and to evaluate the effects of storage on G6PD-deficient donated blood. Methods: This study was conducted at selected mobile donation centres in Terengganu. Consented blood donors were screened for G6PD status using fluorescent spot tests (FST). G6PD enzyme activities were measured for donors who were G6PD deficient. Effects of storage on haemolysis from G6PD-deficient donors were compared with non G6PD-deficient group. Sixty ml of blood was collected from blood unit to transfer pouch for estimation of haemoglobin (Hb), plasma Hb, percentage of haemolysis and plasma potassium. Serial sampling with a 7-day interval was done from Day 1 to Day 35. Statistical analysis was considered significant if p ≤0.05. Results: A total of 440 blood donors were screened and 12 male donors were found to be G6PD deficient by FST. Enzymatic activities were measured in 11 donors as one donor sample failed to be sent to the centre due to logistic problem. Their enzymatic activities ranged from 1.66-2.93 U/g Hb whereby 6 have severe deficiency and the other 5 were categorised as partial deficiency. Donors were asymptomatic for haemolytic episode. Serial sampling showed there was no significant difference of haemolytic parameters in blood units of G6PD-deficient donors as compared to control (p>0.05). Conclusion: Prevalence of G6PD blood donors in Terengganu mobile centres was 2.7%. G6PD enzyme activities did not correlate with clinical symptoms. Haemolytic parameters were not affected in blood units which were G6PD-deficient.