Methods: The 5-FU-loaded NPs were prepared utilizing a simple double emulsion method using polycaprolactone (PCL) and polylactic-co-glycolic acid (PLGA) with or without PEG 6000. The surface charge, particle size, and shape of NPs were evaluated by standard procedures. Both Fourier Transform Infrared Spectroscopy and X-ray diffraction spectra of the 5-FU loaded NPs were compared against the pure 5-FU. The in vitro release profile of 5-FU from the NPs was monitored by the dialysis tubing method. Cell death and apoptosis induction in response to 5-FU NP exposure were measured by MTT and Annexin-V/7-amino-actinomycin D (7-AAD) assays, respectively, in Daoy, HepG2, and HT-29 cancer cell lines.
Results: The 5-FU loaded NPs were found to be spherical in shape with size ranging between 176±6.7 and 253.9±8.6 nm. The zeta potential varied between -7.13± 0.13 and -27.06±3.18 mV, and the entrapment efficiency was between 31.96% and 74.09%. The in vitro release of the drug followed a two-phase mode characterized by rapid release in the first 8 hrs followed by a period of slow release up to 72 hrs with composition-based variable extents. Cells exposed to NPs demonstrated a significant cell death which correlated with the ratio of PEG in the formulations in Daoy and HepG2 cells but not in HT-29 cells. Formulations (F1-F3) significantly induced early apoptosis in HT-29 cell lines.
Conclusion: The physical PEGylation significantly enhanced the entrapment and loading efficiencies of 5-FU into NPs formulated with PLGA and PCL. It also fostered the in vitro cytotoxicity of 5-FU-loaded NPs in both Daoy and HepG2 cells. Induction of early apoptosis was confirmed for some of the formulations.
METHODS: The systematic review and meta-analysis were performed according to the previously published protocol. The PubMed, Web of Sciences, and Scopus databases were meticulously searched for relevant data, without time or language restriction, up to June 1, 2017. All clinical trials which assessed the effect of Se supplementation on antioxidant markers, including oxidative stress index (OSI), antioxidant potency composite (APC) index, plasma malonaldehyde (MDA), total antioxidant capacity (TAC), antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT)), and total antioxidant plasma (TAP), were included. The effect of Se supplementation on antioxidant markers was assessed using standardized mean difference (SMD) and 95% confidence interval (CI). The random-effect meta-analysis method was used to estimate the pooled SMD.
RESULTS: In total, 13 studies which assessed the effect of Se supplementation on antioxidant markers were included. The random-effect meta-analysis method showed that Se supplementation significantly increased GPX (SMD = 0.54; 95% CI = 0.21-0.87) and TAC (SMD = 0.39, 95% CI = 0.13, 0.66) levels and decreased MDA levels (SMD = - 0.54, 95% CI = - 0.78, - 0.30). The effect of Se supplementation on other antioxidant markers was not statistically significant (P > 0.05).
CONCLUSION: The findings showed that Se supplementation might reduce oxidative stress by increasing TAC and GPX levels and decreasing serum MDA, both of which are crucial factors for reduction of oxidative stress.
AIM: The aim of study was to evaluate the relationship of β-adrenergic receptors gene polymorphisms with low triiodothyronine syndrome in patients with a heart failure.
MATERIALS AND METHODS: 354 patients with HF on a background of postinfarction cardiosclerosis were included to the study. At 89 (25.1%) patients LT3S was diagnosed. The course of HF was studied for 2 years. Mean levels of thyroid stimulating hormone (TSH), free T3f and T4f were evaluated. Genotyping of 4 single nucleotide polymorphisms (Gly389Arg of β1-AR gene, Ser49Gly of β1-AR gene, Gln27Glu of β2- AR gene and Ser275 of GNβ3 gene) was performed by polymerase chain reaction. Genetic and epidemiological analysis was performed using the SNPStats program.
RESULTS: The risk of LT3S in patients with HF increases with homozygous G/G variant of Gln27Glu polymorphism of the β2-AR gene (OR=2.21, p=0.037), described as a recessive model of inheritance. There was a tendency to increase the risk of LT3S development in the presence of the genotype C/T of the Ser275 polymorphism of the GNb3 gene (OR=1.75, p=0.054), described as an over-dominant model. The genotype C/G of the Gln27Glu polymorphism of the β2-AR gene was associated with a decreased risk of LT3S development (OR=0.54, p=0.037), described as over-dominant model. Patients with HF carriers the A allele (A/GA/A) of the Ser49Gly polymorphism of the β1-AR gene have a lower risk of repeated hospitalization due to HF decompensation (OR=0.50, p=0.032), described as a dominant model. There was a tendency to increase the risk of re-hospitalization in the G-allele (C/GG/ G) variant of the Gln27Glu polymorphism of the β2-AR gene (OR=1.68, p=0.057), described as a dominant heredity model. At patients with HF in combination with LT3S the risk of re-hospitalization increases at C/G variant of the Gln27Glu polymorphism of β2-AR gene (OR=1.25, p=0.025), described as an over-dominant model.
CONCLUSIONS: The results suggest that congenital genetic alterations in β-adrenergic pathways may be associated with the development of LT3S in patients with HF and the features of the HF course.
Patients and methods: A cross-sectional study was conducted over five months among King Khalid University students, Abha, Saudi Arabia.
Results: Among all the study participants, nearly 98.7% were practicing self-medication. Headache (75.9%), cough and cold (52.5%), and fever (35.6%) and body pain (24.6%) were the most reported symptoms. Use of painkillers (91.6%) was significantly predominant among the medical students, whereas non-medical students used antibiotics (35.4%).Time saving (64.2%), mild symptom (51.7%) and quick relief (36.9%) were the reasons behind seeking self-medication in this study.
Conclusion: Self-medications was common in King Khalid University. Educational programs are highly recommended.
CASE SUMMARY: A 27-year-old male, who was exposed to cranial irradiation at the age of 4 years as part of the treatment for acute lymphoblastic leukaemia, presented with symptoms of raised intracranial pressure for one week. Brain magnetic resonance imaging revealed a heterogeneously enhancing lesion at the hypothalamus. Stereotactic biopsy was performed. Histopathological examination of the lesion showed malignant rhabdoid tumour. The disease progressed rapidly, with manifestation of leptomeningeal spread. He was started on craniospinal irradiation but treatment was suspended after 5.4 Gy, as he developed myelosuppression. His clinical condition deteriorated rapidly, and he succumbed to his illness within 2 mo.
CONCLUSION: This fifth case of radiation-induced central nervous system rhabdoid tumour re-enforces the aggressive nature of this disease with poor prognosis.