Molecular epidemiology of Plasmodium falciparum resistance to antimalarial drugs in Indonesia

The extent of gene polymorphisms associated with resistance to chloroquine and sulfadoxine-pyrimethamine was examined in field isolates of Plasmodium falciparum from Indonesia. Eight malaria-endemic areas, representing a broad region of the western and eastern Indonesian Archipelago were surveyed. Blood from 20-50 patients was collected at each site, DNA was isolated, and the sequences of four different genes (dihydrofolate reductase [dhfr], dihydropteroate synthase [dhps], P. falciparum multidrug resistance 1 [pfmdr1], and P. falciparum chloroquine resistance transporter [pfcrt]) were analyzed using polymerase chain reaction and restriction fragment length polymorphisms to detect polymorphisms previously shown to be associated with resistance. This analysis identified polymorphisms in dhfr at 108-Asn/Thr, 16-Val, and 59-Arg. Polymorphisms in dhps were found less frequently, either 437-Gly alone or paired with 540-Glu. The pfcrt 76-Thr polymorphism was fixed in all parasite populations and pfmdr1 86-Tyr polymorphisms in all populations except in the most eastern regions. The pfmdr1 1042-Asp polymorphism occurred less frequently. These findings indicate that polymorphisms in genes associated with drug resistance in P. falciparum are found across a broad region of Indonesia.     

National health accounts data from 1996 to 2010: a systematic review

Objective

To collect, compile and evaluate publicly available national health accounts (NHA) reports produced worldwide between 1996 and 2010.

Methods

We downloaded country-generated NHA reports from the World Health Organization global health expenditure database and the Organisation for Economic Co-operation and Development (OECD) StatExtract website. We also obtained reports from Abt Associates, through contacts in individual countries and through an online search. We compiled data in the four main types used in these reports: (i) financing source; (ii) financing agent; (iii) health function; and (iv) health provider. We combined and adjusted data to conform with OECD’s first edition of A system of health accounts manual, (2000).

Findings

We identified 872 NHA reports from 117 countries containing a total of 2936 matrices for the four data types. Most countries did not provide complete health expenditure data: only 252 of the 872 reports contained data in all four types. Thirty-eight countries reported an average not-specified-by-kind value greater than 20% for all data types and years. Some countries reported substantial year-on-year changes in both the level and composition of health expenditure that were probably produced by data-generation processes. All study data are publicly available at http://vizhub.healthdata.org/nha/.

Conclusion

Data from NHA reports on health expenditure are often incomplete and, in some cases, of questionable quality. Better data would help finance ministries allocate resources to health systems, assist health ministries in allocating capital within the health sector and enable researchers to make accurate comparisons between health systems.     

Potential of biofluid components to modify silver nanoparticle toxicity

Establishing realistic exposure scenarios is critical for cytotoxic investigation of silver nanoparticles (AgNP) in the gastrointestinal tract. This study investigated the potential interaction with and effect of biofluid components, namely cholic acid, deoxycholic acid and ursodeoxycholic acid, on AgNP toxicity. Two cell lines corresponding to organs related to the biofluid components were employed. These were HepG‐2 a hepatocellular carcinoma derived from liver tissue and Hep2 an epithelial cell line. Physiochemical and cytotoxic screening was performed and the ability of biofluid components to modify AgNP cytotoxicity was explored. No alteration to the physiochemical characteristics of AgNP by biofluid components was demonstrated. However, biofluid component addition resulted in alteration of AgNP toxicity. Greater reactive oxygen species induction was noted in the presence of cholic acid and deoxycholic acid. Ursodeoxycholic acid demonstrated no modification of toxicity in HepG‐2 cells; however, significant modification was noted in Hep2 cells. It is concluded that biofluid components can modify AgNP toxicity but this is dependent on the biofluid component itself and the location where it acts. Copyright © 2015 John Wiley & Sons, Ltd.     

Management of tandem occlusions in patients who receive rtPA

Journal of Thrombosis and Thrombolysis - Tandem occlusions exist in 17–32% of large vessel occlusion (LVO) strokes. A significant concern is bleeding when carotid stenting is performed in...     

Magnetic field interactions between current consumer electronics and cardiac implantable electronic devices

Journal of Interventional Cardiac Electrophysiology - Ablation index (AI) is a radiofrequency lesion quality marker. The AI value that allows effective and safe pulmonary vein isolation (PVI) is...     

Double Heterozygosity for Two Unstable Haemoglobins: Hb Sydney (β67[E11] Val→Ala) and Hb Coventry (β141[H19] Leu Deleted)

A 7-year-old English girl was found to have a lobar pneumonia with a marked haemolytic anaemia. Routine electrophoresis revealed no abnormal haemoglobin but, as anticipated, an unstable haemoglobin fraction readily formed in haemolysates on routine in vitro instability tests. From the subsequent structural and biosynthetic studies it was concluded that the propositus' red cells contained, in addition to Hbs A, A₂ and F, two unstable haemoglobins with abnormalities in the primary structure of their non α-chains: Hb Sydney and Hb Coventry. The first has an amino acid substitution Val→Ala at position β67 (E11), while the other, Hb Coventry, is a new variant with a non α-chain which resembles the β^A-chain except that the leucine residue at position β141(H19) is deleted. This suggests that, instead of the normal complement of two β-chain genes, the propositus' genome has three, i.e. β^A-, β^Sydney- and β^Coventry-chain genes. Evidence is presented from which it can be concluded that the non α-chain of Hb Coventry, whilst being structurally a β-chain variant is, in fact, a βδ fusion chain variant with 140β- and 5δ-chain residues. The oxygen dissociation curve of the propositus showed a reduced affinity at the upper part of the curve, a feature which she shared with a straightforward heterozygote for Hb Sydney, and a slight shift to the left in the lower part, a feature which she shared with her father who possessed Hb Coventry.