/library/oar/handle/123456789/15049 2026-08-14T11:43:52Z 2026-08-14T11:43:52Z /library/oar/handle/123456789/15584 2017-01-19T12:55:51Z 2016-01-01T00:00:00Z

Title: Enhancing fibroblast proliferation for wound healing through chemical and physical methods Abstract: When tissue damaged is incurred a wound healing cascade is activated, consisting of rapid haemostasis, appropriate inflammation, effective proliferation/repair and organised maturation/remodelling which together should led to an appropriate resolution. However in some situations, the wound healing process becomes jammed in a cycle of pathogenic inflammation, leading to the formation of chronic wounds which, through standard treatment fail to resolve accordingly, or relapse. This is a serious issue which costs many lives and billions of euros worldwide. The goal of this study was to delve into the effect of specific chemicals and electromagnetic frequencies on fibroblast proliferation, which is quintessential for normal wound healing as well as the resolution of chronic wounds. To test the effect of these novel approaches, a scratch assay screening method, as well as MTT proliferation assay were utilized to identify the best chemicals and frequencies and to determine whether the chemicals can be used together in synergistic fashion. The outcome of these experiments, was the identification of potential adjuvant pharmaceutical options for the treatment of chronic wounds in the form of chemical 198 (0.1μM) and chemical 273 (1μM) and Padina Pavonica Extract (PPE) (2ug/ml). However apart from the chemicals, two electromagnetic frequencies were identified as potential adjuvant treatment options and these were the 875 MHz frequency at 20 minutes exposure & 750 MHz frequency at 5 minute exposure and could possibly pave the way to a new and exciting field of electroceuticals, the use of electromagnetic frequencies to manage a pathology, or in this case chronic wound management. However for these chemicals and physical methods to advance from the theoretical to practical, further study is required, to first and foremost ensure that the observed proliferative effect is maintainable and does not cause long term-damage to the Human Dermal Fibroblasts (HDFs). Description: B.SC.(HONS)BIOMED.SCI.

2016-01-01T00:00:00Z /library/oar/handle/123456789/15581 2018-05-28T08:43:08Z 2016-01-01T00:00:00Z

Title: The effect of Survival Motor Neuron (SMN) : gemins complex disruption on Drosophila behaviour Abstract: Spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS) are motor neuron diseases which cause progressive loss of movement and eventually paralysis. In the case of SMA, this is due to the loss of motor neurons from the spinal cord, secondary to a Survival of Motor Neuron (SMN) gene mutation. This is commonly a deletion in the SMN1 gene. Humans possess a second gene, SMN2, which produces a truncated protein that cannot compensate for the nonfunctional SMN protein produced by the mutated SMN1 gene. Therefore the patient is left without functional SMN, which leads to SMA. SMN is not found alone, but complexed with Gemins 2-8 and Unr-interacting protein (UNRIP). Together, these proteins are involved in the biosynthesis of small nuclear ribonucleoproteins (snRNPs), which make up the spliceosome. On the other hand, one of the causes of ALS is the formation of cytoplasmic aggregates of transactive response DNA binding protein 43 (TDP-43) in neuronal cells, resulting in neurodegeneration. In this study, Drosophila melanogaster was used as a model to investigate the effect of two Gemin3 transgenes: Gem3ΔN and Gem3BART on Drosophila behaviour when expressed in different tissues. Gem3BART was found to have grievous effects on larval behaviour when expressed both muscularly and neuronally. Gem3ΔN on the other hand, had no significant effect on behaviour when expressed in the brain of adult flies. However, Gemin3 aggravated behaviour in flies expressing TDP-43 in the brain, showing commonalities in the pathways underlying SMA and ALS, which may suggest that these two diseases are linked. These findings suggest that treatments that are effective in SMA patients can also be targeted to treat ALS. Description: B.SC.(HONS)BIOMED.SCI.

2016-01-01T00:00:00Z /library/oar/handle/123456789/15580 2017-01-19T12:50:44Z 2016-01-01T00:00:00Z

Title: Genotyping of the human CTBP2 3’UTR SNP in the Maltese population Abstract: Patients suffering from sickle cell disease or β-thalassaemia would benefit greatly from the reactivation of foetal haemoglobin (Hb F) synthesis in order to alleviate the symptoms in affected adults. To accomplish this, it is essential to gain the necessary knowledge on the genetic switch from foetal to adult haemoglobin also known as the γ to β globin gene switching. In recent years considerable progress has been made in this field; however the exact mechanism remains elusive. The combination of clinical research coupled with basic research should help in this regard. In a previous research project around 259 patients with borderline HbA2/HbF levels were identified and stored into the Malta BioBank. Extensive molecular studies conducted on these samples so far, have revealed a number of KLF1 and VEGF-A mutations, which are partially responsible for the borderline parameters observed. However, these data were still not sufficient to explain the heterogeneous distribution of HbF in different family members with KLF1 haploinsufficiency, with a range of 3.3 to 20% HbF and in the collection of patients with borderline HbA2/HbF. A polymorphism (rs3781408) was the centre of this project and depending on which CtBP2 transcript is quoted, can be either reported to be in the 3’UTR of the gene or else in an amino acid changing domain of the CtBP2 gene. During the course of Whole Genome Sequence analysis of family members with hereditary persistence of foetal haemoglobin, the CtBP2 polymorphism appeared to be tightly linked with a phenotype exhibiting an increase in HbF levels in vivo. This was genotyped by Sanger's DNA sequencing in a collection of patients exhibiting borderline HbA2/HbF, haemoglobin variants and in additional prospective patient DNA known to carry β-thalassaemia mutations. Description: B.SC.(HONS)BIOMED.SCI.

2016-01-01T00:00:00Z /library/oar/handle/123456789/15579 2017-01-19T12:49:34Z 2016-01-01T00:00:00Z

Title: Frequency of the Factor XIII Val34Leu polymorphism in a Maltese Myocardial Infarction case-control collection Abstract: Fibrin clot structure is dependent upon the ability of coagulation factor XIII (FXIII) to crosslink fibrin polymers providing resistance to improper activation of chemical, mechanical and enzymatic processes. The F13A1 gene is highly polymorphic and one of the commonest polymorphisms is FXIII Valine34Leucine (FXIII Val34Leu) which is caused by a G to T transition in codon 34 resulting the substitution of valine by leucine in the FXIIIA subunit. FXIII Val34Leu polymorphism accelerates the rate by which thrombin activates FXIII. The influence of FXIII Val34Leu polymorphism on the risk of Myocardial infarction (MI) has not been established yet since inconsistent results have been obtained from different studies. In this study, samples from the Maltese Acute Myocardial Infarction (MAMI) collection were tested for the FXIII Val34Leu (rs5985) using Polymerase Chain reaction (PCR), Restriction Fragment Length Polymorphism (RFLP) using HhaI and electrophoresis. FXIII activity (%) assays were carried out by Prof Lisman as part of an ongoing collaboration. The allele frequencies of the FXIII Val34Leu polymorphisms were 80% (wildtype allele) and 20% (mutant allele). Median FXIII median activity was similar in males and females and also no correlation was found with the different metabolic and environmental factors. The median FXIII activity was almost identical in cases, controls and relatives. However on carrying out stratification based on the FXIII Val34Leu genotype, it was noted that median FXIII activity was markedly higher in individuals possessing the variant Leu allele. The FXIII Val34Leu does not appear to change the risk of MI when the collection was analysed as a whole, but on combining genotype and smoking, it was noted that smokers have an increased risk of MI with increasing number of Leu alleles. Combination of high fibrinogen levels and an increasing number of Leu alleles increase risk of MI in males but not in females. Description: B.SC.(HONS)BIOMED.SCI.

2016-01-01T00:00:00Z