Dyslipidemia

Dyslipidemia has a complex pathophysiology consisting of various genetic, lifestyle, and environmental factors. It has many adverse health impacts, notably in the development of chronic non-communicable diseases. Significant ethnic differences exist due to the prevalence and types of lipid disorders. While elevated serum total- and LDL-cholesterol are the main concern in Western populations, in other countries hypertriglyceridemia and low HDL-cholesterol are more prevalent. The latter types of lipid disorders are considered as components of the metabolic syndrome. The escalating trend of obesity, as well as changes in lifestyle and environmental factors will make dyslipidemia a global medical and public health threat, not only for adults but for the pediatric age group as well. Several experimental and clinical studies are still being conducted regarding the underlying mechanisms and treatment of dyslipidemia. The current book is providing a general overview of dyslipidemia from diverse aspects of pathophysiology, ethnic differences, prevention, health hazards, and treatment

Diagnostic role of systemic inflammation, blood coagulation and padua prediction score in lung thrombosis risk estimation in hospitalized patients with community-acquired pneumonia

Introduction: Some coagulation and thrombotic disorders during severe CAP could lead to some intravascular disorders and even be the reason of lethal end in hospitalized patients with CAP. But this fact hadn’t been established to the end yet.The aim was to study the intravascular changes in patients with severe CAP and to estimate the role of parameters of systemic inflammation (procalcitonin (PCT), C-reactive protein (CRP)), blood coagulation test (fibrinogen, D-dimer, heparin time, prothrombin time) and risk of thrombosis in patients with moderate and severe CAP.Materials and methods: The main group was 63 patients with moderate to severe CAP. The mean age was 54.0 [37.0–63.0] years old, men – 46 (73.0%)). Depending on the severity all patients of the main group were divided into 2 subgroups: subgroup 1 – 36 patients with moderate CAP (the mean age was 51.0 [32.5–62.5] years old, men – 29 (80.5%)), subgroup 2 – 27 patients with severe CAP (the mean age was 56.0 [46.0–68.0] years old, men – 17 (63.0%). Subgroups had no significant difference according to age (p=0,348) and sex (p=0,237). Received results were compared with values in control group. The control group was 10 healthy people (the mean age was 52.0 [35.6–62.0] years old, men – 5 (50.0%)).Results and conclusions: Patients with severe CAP had significantly higher levels of PCT, CRP, D-dimer, prothrombin time, heparin index and the lowest level of heparin time. This fact shows the highest risk of thrombosis in patients with severe CAP on the background of severe systemic inflammation. The mean level of scores by Padua scale in patients with severe CAP was 5.0 [5.0–6.0] scores, which was significantly higher than in patients with moderate CAP, who had 1.0 [1.0–2.0] scores.On autopsy of 5 died patients with severe CAP we found thrombosis of lung vessels which differ from embolism or post-mortem blood clots. These changes maybe reflect systemic thrombosis at patients with severe CAP and could be the reasons of increased mortality in this category of patients

Obesity-induced chronic inflammation in C57Bl6J mice, a novel risk factor in the progression of renal AA amyloidosis?

Background: Compelling evidence links obesity induced systemic inflammation to the development of chronic kidney disease (CKD). This systemic inflammation may result from exacerbated adipose inflammation. Besides the known detrimental effects of typical pro-inflammatory factors secreted by the adipose tissue (TNF-α, MCP-1 and IL-6) on the kidney, we hypothesize the enhanced obesity-induced secretion of serum amyloid A (SAA), an acute inflammatory protein, to play a key role in aggravating obesity-induced CKD. Methods: Groups of male C57Bl/6J mice (n = 99 in total) were fed a low (10% lard) or high (45% lard) fat diet for a maximum of 52 weeks. Mice were sacrificed after 24, 40 and 52 weeks. Whole blood samples, kidneys and adipose tissues were collected. The development of adipose and renal tissue inflammation was assessed on gene expression and protein level. Adipocytokine levels were measured in plasma samples. Results: A distinct inflammatory phenotype was observed in the adipose tissue of HFD mice prior to renal inflammation, which was associated with an early systemic elevation of TNF-α, leptin and SAA (1A-C). With aging, sclerotic lesions appeared in the kidney, the extent of which was severely aggravated by HFD feeding. Lesions exhibited typical amyloid characteristics (2A) and pathological severity positively correlated with bodyweight (2B). Interestingly, more SAA protein was detected in lesions of HFD mice. Conclusion: Our data suggest a causal link between obesity induced chronic inflammation and AA amyloidosis in C57Bl/6J mice. Though future studies are necessary to prove this causal link and to determine its relevance for the human situation, obesity may hence be considered a risk factor for the development and progression of renal AA amyloidosis in the course of CKD. (Figure Presented)

Drug Discovery

Natural products are a constant source of potentially active compounds for the treatment of various disorders. The Middle East and tropical regions are believed to have the richest supplies of natural products in the world. Plant derived secondary metabolites have been used by humans to treat acute infections, health disorders and chronic illness for tens of thousands of years. Only during the last 100 years have natural products been largely replaced by synthetic drugs. Estimates of 200 000 natural products in plant species have been revised upward as mass spectrometry techniques have developed. For developing countries the identification and use of endogenous medicinal plants as cures against cancers has become attractive. Books on drug discovery will play vital role in the new era of disease treatment using natural products