The anticancer activities of turmeric include inhibiting cell proliferation and inducing apoptosis of cancer cells. Ar-turmerone, which is isolated from turmeric, induced apoptosis in human leukemia Molt 4B and HL-60 cells by fragmenting DNA to oligonucleosome-sized fragments, a known step in the process of apoptosis (Aratanechemuge et al. 2002). Moreover, the nucleosomal DNA fragmentation induced by ar-turmerone was associated with induction of Bax and p53 proteins, rather than B cell lymphoma 2 (Bcl-2) and p21, and activation of mitochondrial cytochrome c and caspase-3 (Lee 2009). This study showed that turmeric extract repressed the production and secretion of hepatitis B surface antigen from HepG 2.2.15 cells, an activity that is mediated through the enhancement of cellular accumulation of p53 protein by transactivating the transcription of the p53 gene as well as increasing the stability of the p53 protein (Kim et al. 2009).
Process Control By K Krishnaswamy Pdf 27
Turmeric showed antioxidant potential by lowering oxidative stress in animals. A study showed that a diet containing 0.1% turmeric fed for 3 weeks to retinol-deficient rats lowered lipid peroxidation rates by 22.6% in liver, 24.1% in kidney, 18.0% in spleen, and 31.4% in brain (Kaul and Krishnakantha 1997). A study conducted on mice showed that turmeric extract inhibited membrane phospholipid peroxidation and increased liver lipid metabolism, which indicates turmeric extract has the ability to prevent the deposition of triacylglycerols in the liver. Dietary supplementation for one week (1% w/w of diet) with a turmeric extract showed lower phospholipids hydroperoxide level in mice red blood cells (RBC). The liver lipid peroxidizability induced with Fe2+/ascorbic acid was effectively suppressed by dietary supplementation with turmeric (Asai, Nakagawa, and Miyazawa 1999). Oral administration of a nutritional dose of turmeric extract decreased susceptibility to oxidation of erythrocyte and liver microsome membranes in vitro. When turmeric hydroalcoholic extract (1.66 mg/kg of body weight) was given to rabbits fed a high-fat diet, oxidation of erythrocyte membranes was found to be significantly lower than that in membranes of control animals. Levels of hydroperoxides and thiobarbituric acid-reactive substances in liver microsomes were also low (Mesa et al. 2003). Turmeric also seems beneficial in preventing diabetes-induced oxidative stress. In diabetic rats, an AIN93 diet containing 0.5% turmeric was found to control oxidative stress by inhibiting increases in thiobarbituric acid-reactive substances and protein carbonyls and reversing altered antioxidant enzyme activities without altering the hyperglycemic state (Arun and Nalini 2002; Suryanarayana et al. 2007). This diet also inhibited expression of vascular endothelial growth factor in diabetic rats (Mrudula et al. 2007). Further, it suppressed increase in blood glucose level in type 2 diabetic KK-Ay mice. A dose of 0.2 or 1.0 g of ethanol extract, 0.5 g of hexane extract, and 0.5 g of hexane-extraction residue per 100 g of diet in the mice feed suppressed significant increase in blood glucose levels. The ethanol extract of turmeric also stimulated human adipocyte differentiation, and it showed human peroxisome proliferator-activated receptor-gamma (PPAR-γ) ligand-binding activity (Nishiyama et al. 2005). Further, turmeric appeared to minimize osmotic stress. Most importantly, aggregation and insolubilization of lens proteins due to hyperglycemia was prevented by turmeric, indicating that it prevents or delays the development of cataracts (Suryanarayana et al. 2005).
Abstract:Food safety is imperative, especially for infants and young children because of their underdeveloped immune systems. This requires adequate nutritious food with appropriate amounts of macro- and micronutrients. Currently, a well-established system for infant food is enforced by the regulatory bodies, but no clear system exists for complementary food, which is consumed by children from the age of 6 month to 24 months. As the child grows beyond 6 months, the need for nutrients increases, and if the nutritional needs are not fulfilled, it can lead to health problems, such as stunted growth, weak immune system, and cardiovascular diseases. Hence, it is important to have regulatory bodies monitoring complementary food in a similar capacity as is required for infant formula. The objective of this review is to provide an overview of the existing regulatory bodies, such as the Codex Alimentarius, International Standard Organization (ISO), Food and Drug Administration (FDA), etc., and their regulations specifically for infant formula that can be adopted for complementary foods. This study focuses on the development of a hazard analysis and risk-based preventive controls (HARPC)-based food safety plan to ensure safe food processing and prevent any possible outbreaks.Keywords: complementary food; infants; FSMA; HACCP; regulations
Overall this systematic review demonstrates that ASPs can offset or reduce costs while improving some patient outcomes, thereby suggesting high value for certain healthcare systems. The findings also suggest that costs associated with start-up and implementation of ASPs are potentially offset by subsequent cost-savings. Additionally, numerous systematic reviews and meta-analyses have demonstrated that such programs have beneficial effects on hospital LOS [149, 150], resistance patterns [63, 150], and infection incidence [151]. This data supports the value of ASPs in tandem with infection control measures [1]. However, for the findings to be globally relevant, more studies, particularly in real world settings across a diverse range of geographies and resource settings are required, so that a full critical appraisal of the true value of these programs can be made. This will not only allow our ability to develop high value bespoke models of ASP based on robust clinical and economic data but also consider creating benchmarks, an area fraught with challenges [152, 153].
processing.... Drugs & Diseases > Cardiology Heart Failure Treatment & Management Updated: Jul 02, 2022 Author: Ioana Dumitru, MD; Chief Editor: Gyanendra K Sharma, MD, FACC, FASE more...
Share Email Print Feedback Close Facebook Twitter LinkedIn WhatsApp webmd.ads2.defineAd(id: 'ads-pos-421-sfp',pos: 421); Sections Heart Failure Sections Heart Failure Overview Practice Essentials
Background Pathophysiology Etiology Epidemiology Prognosis Patient Education Show All Presentation History
Physical Examination Predominant Right-Sided Heart Failure Heart Failure in Children Heart Failure Criteria, Classification, and Staging ACC/AHA Staging Show All DDx Workup Approach Considerations
Routine Laboratory Tests Natriuretic Peptides Genetic Testing Assessment of Hypoxemia Electrocardiography Chest Radiography Echocardiography CT Scanning and MRI Nuclear Imaging Catheterization and Angiography Assessment of Functional Capacity Show All Treatment Approach Considerations
Nonpharmacologic Therapy Pharmacologic Therapy Acute Heart Failure Treatment Treatment of Heart Failure with Preserved LVEF Treatment of Right Ventricular Heart Failure Electrophysiologic Intervention Revascularization Procedures Valvular Surgery Ventricular Restoration Extracorporeal Membrane Oxygenation Ventricular Assist Devices Heart Transplantation Total Artificial Heart Show All Guidelines Guidelines Summary
Screening and Genetic Testing Diagnostic Procedures Nonpharmacologic Therapy Pharmacologic Therapy Electrophysiologic Intervention Revascularization Procedures Valvular Surgery Mechanical Circulatory Support Devices Heart Transplantation Management of Acute Decompensated Heart Failure (ADHF) Show All Medication Medication Summary
Beta-Blockers, Alpha Activity Beta-Blockers, Beta-1 Selective ACE Inhibitors ARBs Inotropic Agents Vasodilators Nitrates B-type Natriuretic Peptides I(f) Inhibitors Angiotensin Receptor-Neprilysin Inhibitors (ARNi) Diuretics, Loop Diuretics, Thiazide Diuretics, Other Diuretics, Potassium-Sparing Aldosterone Antagonists, Selective SGLT2 Inhibitors Soluble Guanylate Cyclase Stimulators Alpha/Beta Adrenergic Agonists Calcium Channel Blockers Anticoagulants, Cardiovascular Opioid Analgesics Show All Questions & Answers Media Gallery Tables References Treatment Approach Considerations Medical care for heart failure (HF) includes a number of nonpharmacologic, pharmacologic, and invasive strategies to limit and reverse its manifestations. [3, 8, 116] Depending on the severity of the illness, nonpharmacologic therapies include dietary sodium and fluid restriction; physical activity as appropriate; and attention to weight gain. Pharmacologic therapies include the use of diuretics, vasodilators, inotropic agents, anticoagulants, beta blockers, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs), digoxin, nitrates, B-type natriuretic peptides (BNPs), I(f) inhibitors, angiotensin receptor-neprilysin inhibitors (ARNIs), soluble guanylate cyclase stimulators, sodium-glucose cotransporter-2 inhibitors (SGLT2Is), and mineralocorticoid receptor antagonists (MRAs).
Although there are no reports of controlled trials evaluating heart failure without angina and their outcomes with coronary revascularization, surgical revascularization is recommended in those with significant left main stenosis and in those with extensive noninfarcted but hypoperfused and hypocontractile myocardium on noninvasive testing. [3] In patients with heart failure and reduced LVEF but without angina, it has not yet been determined whether routine evaluation of possible myocardial ischemia/viability and coronary artery disease should be performed. [3] 2ff7e9595c