The clinical significance of osteoporosis lies in the fractures that arise, but the diagnosis of osteoporosis relies on the quantitative assessment of bone mineral density. There are a number of other indications for bone densitometry including monitoring of treatment, determining the extent of bone loss and assessment of suitability for certain treatments. Most commonly, bone density is used to determine eligibility for treatment. However, diagnostic thresholds differ from intervention thresholds for several reasons. Firstly, the fracture risk varies at different ages, even with the same T-score. Other factors that determine intervention thresholds include the presence of clinical risk factors such as a prior fracture, a family history of hip fracture, smoking and high alcohol consumption and secondary causes of osteoporosis. Algorithms that integrate the weight of clinical risk factors for fracture risk have been developed by the World Health Organization. This FRAX^® tool (www.shef.ac.uk/FRAX) computes the 10-year probability of hip fracture or a major osteoporotic fracture (clinical spine, hip, forearm or humerus). Probability-based intervention thresholds are now being incorporated into new management guidelines that integrate FRAX^® with clinical management algorithms.

The discovery of leptin has led to the elucidation of a robust physiologic system that maintains fat stores at a relatively constant level. Leptin is a peptide hormone secreted by adipose tissue in proportion to its mass. This hormone circulates in blood and acts on the hypothalamus to regulate food intake and energy expenditure. When fat mass falls, plasma leptin levels fall stimulating appetite and suppressing energy expenditure until fat mass is restored. When fat mass increases, leptin levels increase, suppressing appetite until weight is lost. By such a mechanism total energy stores are stably maintained within a relatively narrow range. Recessive mutations in the leptin gene are associated with massive obesity in mice and some humans. Treatment with recombinant leptin markedly reduces food intake and body weight. The low leptin levels in patients with leptin mutations are also associated with multiple abnormalities including infertility, diabetes and immune abnormalities all of which are corrected by leptin treatment. These findings have established important links between energy stores and many other physiologic systems and led to the use of leptin as a treatment for an increasing number of other human conditions including a subset of obesity, some forms of diabetes including lipodystrophy and hypothalamic amennorhea, the cessation of menstruation seen in extremely thin women. Identification of a physiologic system that controls energy balance establishes a biologic basis for obesity and further establishes links between leptin and numerous other physiologic responses.

Humans, mice and rats are susceptible to autoimmune diabetes we believe due to common molecular sequences of the trimolecular complex targeting of insulin, when tolerance mechanisms fail. The disease is now predictable in man, preventable in animal models, and recent trials indicate the potential for preventive therapy in man.

Parkinson's disease (PD) is one of the most common neurodegenerative disorders featuring the cardinal symptoms of resting tremors, postural instability, rigidity, bradykinesia and akinesia treated with a range of medicinal agents. The traditional drug therapy usually involves levodopa, the most potent drug for controlling PD symptoms, along with catechol-O-methyl-transferase inhibitors (COMTI), dopamine agonists and nondopaminergic drugs. For the last few years the treatment includes surgical techniques specially deep-brain stimulation, subthalamotomy, pallidotomy, thalamotomy, etc. The lay literature and mass media descriptions of surgery for PD often give patients and their families the impression that today's surgical procedures offer miraculous results to all patients undergoing this treatment. However, it is an important fact that these new treatments are not necessarily better than the established conventional drug therapy and that the treatment options must be selected according to the need of individual patient.

Background: Hypertension is a major cause of morbidity and mortality in the United Arab Emirates (UAE). However, little is known regarding vasoactive biomarkers and lipid profiles in hypertensives versus normotensives in this heterogeneous ethnic population. Aims: This study aimed to evaluate plasma endothelin-1 (ET-1), homocysteine (Hcy), nitric oxide (NO), and lipid parameters among hypertensive subjects and normotensives controls in a heterogeneous ethnic population from the UAE. Methods: We collected venous samples from 164 hypertensive and 112 normotensive subjects matched for age, gender and ethnicity to determine their plasma levels of ET-1, Hcy and NO as well as their lipid profile. Results: Hypertensive subjects displayed significantly higher plasma levels of ET-1 (p < 0.001) and NO (p < 0.001) but lower insulin levels (P<0.006) than normotensives. In contrast, there was no statistically significant difference with regard to Hcy concentrations. Very low-density lipoprotein (VLDL) and triglycerides (TG) levels were significantly (p < 0.01) higher in hypertensives than controls. Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and non-esterified fatty acids (NEFA) were significantly lower (p < 0.01) in hypertensives than normotensives. Conclusion: In our heterogeneous ethnic population, levels of ET-1 and NO, but not of Hcy, were found to be associated with hypertension and may possibly contribute to an increased systemic vascular resistance among hypertensives. Whether the elevated ET-1 results are because of overproduction or decreased clearance remains to be ascertained Elevated levels of TG and VLDL, alongside with unaltered TC levels, seem to indicate the presence of type IV hypertriglyceridaemia.

Objective: To review literature and assess whether adjunctive therapy with polyclonal and or enriched intravenous immunoglobulin (IVIG) reduces mortality in neonates with sepsis. Data Source: MEDLINE, EMBASE and Cochrane systematic review. Study Selection: All studies published in English language evaluating IVIG treatment in neonatal sepsis. Data Synthesis: Effect of all cause mortality was quantified using fixed-effect meta-analysis. Results: Fifteen studies published between 1986 and 2006 were identified of which fourteen reported mortality and were included in the analysis. Most studies involved small number of neonates, used different preparations and dosing regimens of IVIG, however, there was significant reduction in all cause mortality associated with use of IVIG in neonatal sepsis with pooled odds ratio of 0.41 (95% confidence interval 0.29-0.58) and a risk ratio of 0.52 (95% confidence interval 0.40-0.67; p < 0.00001). There was no statistically significant difference between-study heterogeneity for the outcome of mortality in the two analyses. I² = 0%. Number required to treat 7. Conclusion: This analysis shows that addition of polyclonal or enriched IVIG as adjunct to standard therapy significantly reduces all cause mortality in neonatal sepsis.