ABSTRACT
Diabetes mellitus is a metabolic disease which poses a major challenge to healthcare and is characterized by elevated blood glucose levels resulting from either an underproduction or underutilization of the insulin hormone. The actual cause of Type 1 diabetes is unknown, but it most likely results from an autoimmune mediated destruction of the insulin producing pancreatic beta cells that reduces or terminates insulin production. On the other hand, type 2 diabetes is often caused by obesity and induces a gradual desensitization of the body’s cells to insulin. Recent advances in diagnostic methods have heralded in a new era of diabetes management with improved glucose control, reduced fear of complications and better compliance with intensive therapies. Additional efforts are being made to refine these methods to allow their implementation into clinical practice and gain universal acceptance. Advances in diagnostic methods for insulin delivery and glucose monitoring are an important step forward in greatly improving the lives of diabetic patients.
ABSTRACT
Obesity is a major health concern worldwide as it provokes other health issues. The rise of obesity cases has started public concern as chronic obesity incidences are closely related to significantly shortened life expectancy. Coronary artery disease, hypertension, liver/biliary disease, osteoarthritis, strokes and type 2 diabetes are the common comorbidities which are closely associated with obesity. Adiponectin is the copious adipokine secreted by the adipose tissue in a human body. It is an anti-inflammatory and vasculoprotective cytokine whereas Serotonin, 5-hydroxytryptamine (5-HT) is a bio amine derived product of the amino acid tryptophan. Adiponectin and serotonin are observed to be the parts of the obesity by indirectly acting on the adipose tissues. The association of adiponectin and serotonin is based on the effect of adiponectin and serotonin on each other activity. Studies showed an elevation of serotonin may down-regulated the expression of adiponectin, which is normally seen in the case of obesity. Also, the factors affecting their activity vary from the molecular to the physical level.
ABSTRACT
Background: In view of the impact of hypertension on public health, the objective of this study was to determine whether having had a cup of coffee in an everyday life setting raises blood pressure significant enough to make it a methodological issue in routine sphygmomanometry. Methods: Healthy normotensive volunteers from a private university in Malaysia were recruited. After an overnight fast, seated systolic and diastolic blood pressures (SBP and DBP) of habitual coffee drinkers (n=16) were measured (Omron HEM 7080 automated monitor) in the laboratory 15 min. before and every 15 min. up to 90 min. after drinking strong coffee. This was repeated on non-habitual drinkers (n=16) who also underwent a control study (decaffeinated coffee). To see whether the laboratory findings could be extrapolated to everyday life setting, the pre-coffee BP and 30 min.- and 60 min.- post-coffee BPs were measured on habitual coffee drinkers (n=18) who consumed self-prepared coffee and who carried on with routine office work between BP measurements taken in a nearby room. Results: In the laboratory setting, coffee significantly increased SBP and DBP at all time-points in non-habitual drinkers (e.g.11.38+/- 8.2 and 10.75+/-5.7 mm Hg at 75 min; P<0.01, repeated measures ANOVA and Dunnett's test); in habitual drinkers, SBP only was increased (7.23+/-4.7 at 90 min; P<0.05). In the office setting, smaller but significant DBP elevations (3.72+/-5.1 at 60 min; P<0.05) were observed. Conclusion: The results indicate that having had a cup of coffee could be a methodological issue in routine sphygmomanometry, particularly with non-habitual coffee drinkers consuming strong coffee. However, caution should be exercised in drawing conclusions because of the small sample size.
ABSTRACT
Autism is a neurodevelopmental disorder that predominantly affects the younger generation. The etiology which contributes to the occurrence of autism is not well defined. However, apart from genetic factors, environmental factors such as metal exposure have been controversial from the last decade. Contamination of several metals was proposed to be responsible for oxidative stress production, mitochondria dysfunction and immune abnormalities which lead to characteristics of autism in children. Objective of review is to analyze the relationship between the most studied toxic metals namely mercury, lead, cadmium and arsenic. Based on the findings, metal toxicity due to lead, mercury and aluminum are clearly exhibited meanwhile insufficient data were available on arsenic and cadmium. In addition, lack of essential minerals in autistic children who were exposed to heavy metals has also precipitated the autistic disorder. However, high quality epidemiological studies with minimal biasness should be conducted to support the correlation of heavy metal with autism.
ABSTRACT
Aim: Breast cancer is a major health issue for women worldwide. The potential anti-tumor effect of snake venom, has been studied and evidences showed reducing tumor size and inhibition of angiogenesis. Present study aims to study the antitumor effect of Calloselasma rhodostoma venom on MDA-MB-231 cells. Methods: The morphological changes of venom-treated MDA-MB-231 and MCF-10A cells in various incubation time were studied. Cytotoxicity of the venom on both cell lines were determined using Cytotoxicity 96® Non-radioactive cytotoxicity assay. Results: Based on the morphology study and cytotoxicity assay study, MDA-MB-231 cells were killed at venom concentration of 10 μg/ml, started at 12 h post treatment and significant killing dose at venom concentration of 20 μg/ml. Cell morphology study of MCF-10A showed that the cells were also killed at venom concentration of 10 μg/ml, started at 12 h post. However, viable MCF-10A cells were observed 48 h post treatment. Conclusion: C. rhodostoma venom can kills both non-tumorgenic breast cells MCF-10A and tumorgenic breast cancer cells MDA-MB-231. However, the venom kills MDA-MB-231 cells at lower concentration than MCF-10A cells. More studies are needed to study antitumor effect of the venom.