Tuesday, April 2, 2019
Role of Medicinal Plants for Health
Role of salubriousnessful Plants for HealthGeneralThe use of natural products with therapeutic properties is as quaint as human civilization. For a very capacious time, mineral, plant and creature products were the main radicals of drugs 1.The use of complementary medicate to alleviate and improve headspringness conditions is increasing in developed countries 2. New medicinal plants from different get out of the world ar being investigated with this purpose in mind 3. Although the physical exercise of botanicals has incr quiltd in the western world, there is a lack of reading close to implements of do and potential differences among species within the similar genus 4.Now-a-days, some(prenominal) plants cave in been identified for their anti kittycer and anti- inflammatory compounds. Scientific experiments on the anticancer properties of plants and their comp singlents experience been detected. Herbal medicines have been the basis of hidement and cure for ming led diseases and physiological conditions in handed-down methods practiced such(prenominal) as ayurveda, unani and siddha. However no systematic studies were conducted to evaluate the efficacy and safety of the formulations from the plant were undertaken. Also no attempts were made to isolate and identify the active principles problematical in these effect 5.As an evolutionary solvent plants were obliged to make and store a wide range of organic motes. These sum of moneys ar usually circumstanceed as unessential metabolites (SM). around of these compounds atomic number 18 involved in the survival of the plants as a defense mechanism against natural enemies. Many SM could actively move with leads in the human body inducing a bioactivity of interest 6. The bioactive compounds of medicinal plants are utilize as anti-diabetic, chem an different(prenominal)apeutic, anti-inflammatory drug, anti-arthritic agents where no satisfactory cure is bounty in modern medicines.Th e use of plants for medicinal purposes dates back to antiquity because they turn out components of therapeutic value 7. Medicinal plants are cheaper and much than accessible to near of the population in the world. The acceptance of traditional medicine as an substitute(a) form of health care and the development of microbial resistance to the accessible antibiotic drugs has led researchers to investigate various therapeutic uses of medicinal plants 8. Therefore, the quest for plants with medicinal properties continues to receive attention as scientists are in need of plants, oddly of ethno botanical significance for a complete range of biological activities, which ranges from antibiotic to anti-cancerous 9.Bangladesh features a sub-tropical climate and low-lying landmass bear-sizedly adjacent to e largeated river deltas. The country comprises very fertile soils and is home to some rare ecosystems such as the Sundarbans mangrove forests. Given the fertile plains and high po pulation density, the autochthonous vegetation has mostly given way to cropland and extensive cultivation. Today, almost 60% of the landmass is used for farming, which is a global maximum value. However, originally plumping parts of Bangladesh featured tropical forests and marshy jungle with highly bio-diverse flora being overly an excellent source for medicinal plants.The Bangladeshi traditional medicine is a unique conglomerate of different ethnomedical influences. Due to the geographic location and sociocultural characteristics of the country, it involves traditionally rooted elements influenced by local anaesthetic innate people and close-by Indian Ayurveda and Unani medicine 10, 11. Given its inexpensive, easily accessible and healthy up-established health services, the use of traditional medicine is an integral part of public health services in Bangladesh with its pass onrs being deeply embedded within the local community 12-14. Recent data suggest that the utilizatio n of traditional medicine health services in Bangladesh is widespread 15 and diarrheas a crucial image in providing health care for poor people, people in cracker-barrel field of operations and for tribal people 16.Antioxidant and anti-inflammatory activities of medicinal plantsThe anti-oxidative activity has been confirmed impart kinds of cancer and inflammatory stayions for its multiple functional roles. The work of oxidants is a classifiable event associated with aerobic metabolic movement. When atomic reckon 8 is supplied in excess or its decrement is insufficient, reactive group O species or stop radicals such as superoxide anion anions, hydroxyl group radicals and hydrogen peroxide are generated 17. Accumulation of the liberate radicals in body organs or threads can cause oxidative prostitute to biomolecules and membranes of cell, eventually postulateing to many chronic diseases, such as inflammatory, cancer, diabetes, aging, cardiac dysfunction and separat e degenerative diseases 18. In the last 50 years, antioxidant and anti-inflammatory activities of extracts from medicinal or food plants have been extensively investigated. Many pharmacological studies have bespeakn that extracts of some antioxidant plant possess anti-inflammatory, anti-allergic, anti-tumor, anti-bacterial, anti-mutagenic and anti-viral activities to a greater or lesser extent. Researchers reported that intake of fruits, vegetables and new(prenominal) foods having high antioxidant activity has been associated with decreased risks of cancer, cardiovascular disease, diabetes and other diseases 17. Trouillas et al. investigated the antioxidant, anti-inflammatory and anti-proliferative properties of sixteen French herbal teatime and form some herbs exhibited high antioxidant, anti-inflammatory and anti-proliferative activities 19. Antioxidant activities in twenty traditional anti-inflammatory herbs extracts were investigated. The results suggested that the anti-infl ammatory activities of these extracts could be explained, at least in part, by their antioxidant properties 20. Free radicals liberated from phagocyte cells are important in inflammatory servees, because they are implicated in the activation of nuclear factor kB, which induces the placement of inflammatory cytokines and cyclo oxygenase-2 21.Free radicals and oxidative stress reactive oxygen species (ROS) is a term that encompasses all highly reactive, oxygen containing molecules, including free radicals. Types of ROS take on the hydroxyl radical, the superoxide anion radical, hydrogen peroxide, singlet oxygen, nitric oxide radical, hypochlorite radical, and various lipide peroxides. All are capable of reacting with membrane lipids, nucleic loony toonss, proteins and enzymes, and other pure molecules, resulting in cellular damage. ROS are generated by a number of pathways. Most of the oxidants assertd by cells make it asA con place of normal aerobic metabolism approximately 9 0% of the oxygen utilized by the cell is consumed by the mitochondrial electron rape system.Oxidative burst from phagocytes (white assembly line cells) as part of the mechanism by which bacteria and viruses are killed, and by which foreign proteins (antigens) are denatured.Xenobiotic metabolism, i.e., detoxification of toxic substances.Consequently, things like vigorous exercise, which accelerates cellular metabolism chronic ardor, infections, and other illnesses exposure to allergens and the presence of leaky gut syndrome and exposure to drugs or toxins such as cigarette smoke, pollution, pesticides, and insecticides whitethorn all contribute to an change magnitude in the bodys oxidant load 22.Most reactive oxygen species are generated as by-products during mitochondrial electron transport. In adjunct ROS are formed as inevitable intermediates of metal catalyzed oxidation reactions. Atomic oxygen has two unpaired electrons in separate orbits in its outer electron shell. Thi s electron structure makes oxygen susceptible to radical make-up. The sequential reduction of oxygen through the addition of electrons leads to the formation of a number of ROS including superoxide hydrogen peroxide hydroxyl radical hydroxyl ion and nitric oxide.Free radicals and other ROS are derived all from normal essential metabolic processes in the human body or from external sources such as exposure to X-rays, ozone, cigarette smoking, air pollutants, and industrial chemicals. Free radical formation occurs continuously in the cells as a consequence of both enzymatic and non-enzymatic reactions. Enzymatic reactions, which serve as source of free radicals, include those involved in the respiratory chain, in phagocytosis, in prostaglandin synthesis, and in the cytochrome P-450 system. Free radicals can also be formed in non-enzymatic reactions of oxygen with organic compounds as well as those initiated by ionizing reactions. to the highest degree internally generated sources o f free radicals are Mitochondria, Xanthine oxidase, Peroxisomes, Inflammation, Phagocytosis, Arachidonate pathways, Exercise, Ischemia/reperfusion injury etceteraSome externally generated sources of free radicals are- Cigarette smoke, Environmental pollutants, Radiation, Certain drugs, pesticides, Industrial solvents, Ozone etc.Normally, cells defend themselves against ROS damage with enzymes such as alpha-1-microglobulin, superoxide dismutases, catalases, lactoperoxidases, glutathione peroxidases and peroxiredoxins. Small molecule antioxidants such as ascorbic acid (vitamin C), tocopherol (vitamin E), uric acid, and glutathione also play important roles as cellular antioxidants. In a similar manner, polyphenol antioxidants sanction in preventing ROS damage by scavenging free radicals. In contrast, the antioxidant ability of the extracellular space is less e.g., the most important plasma antioxidant in human beings is uric acid.Effects of ROS on cell metabolism are well documen ted in a variety of species. These include not provided roles in apoptosis (programmed cell death) but also positive cause such as the induction of host defense genes and militarisation of ion transport systems. This implicates them in control of cellular function. In particular, thrombocytes involved in smart repair and line of merchandise homeostasis release ROS to recruit supererogatory platelets to aims of injury. These also provide a link to the adaptive resistant system via the recruitment of leukocytes.Reactive oxygen species are implicated in cellular activity to a variety of inflammatory responses including cardiovascular disease. They whitethorn also be involved in hearing impairment via cochlear damage induced by elevated sound levels, in ototoxicity of drugs such as cisplatin, and in essential deafness in both animals and humans. ROS are also implicated in mediation of apoptosis or programmed cell death and ischemic injury. unique(predicate) examples include stro ke and heart attack.All the biological molecules accede in our body are at risk of being attacked by free radicals. Such damaged molecules can impair cell functions and even lead to cell death eventually resulting in diseased states.In late(a) years it has become apparent that the oxidation of lipids, or lipid peroxidation, is a crucial step in the pathogenesis of several disease states in openhanded and infant patients. lipid peroxidation is a process generated naturally in small amounts in the body, mainly by the effect of several reactive oxygen species (hydroxyl radical, hydrogen peroxide etc.). It can also be generated by the action of several phagocytes. These reactive oxygen species readily attack the polyunsaturated fat acids of the fatty acid membrane, initiating a self-propagating chain reaction. The destruction of membrane lipids and the end-products of such lipid peroxidation reactions are especially dangerous for the viability of cells, even meanders 23-25.Membrane lipids present in subcellular organelles are highly susceptible to free radical damage. Lipids when reacted with free radicals can undergo the highly damaging chain reaction of lipid peroxidation (LP) leading to both direct and indirect do. During LP a large number of toxic byproducts are also formed that can have cause at a site away from the area of generation, behaving as gage messengers. The damage caused by LP is highly detrimental to the functioning of the cell 26.Lipid peroxidation is a free radical mediated process. Initiation of a peroxidative sequence is due to the attack by any species, which can abstract a hydrogen atom from a methylene group (CH2), leaving easy an unpaired electron on the carbon paper atom (CH). The resultant carbon radical is stabilized by molecular rearrangement to take a leak a blend diene, which then can react with an oxygen molecule to give a lipid peroxyl radical (LOO). These radicals can further abstract hydrogen atoms from other lipid mo lecules to form lipid hydroperoxides (LOOH) and at the same time disseminate LP further.The process of LP, gives rise to many products of toxicological interest like malondialdehyde (MDA), 4-hydroxy no(prenominal)nal (4-HNE) and various 2-alkenals. Isoprostanes are unique products of lipid peroxidation of arachidonic acid and recently tests such as mass spectrometry and ELISA-assay kits are available to detect isoprostanes 27.Oxidation of proteins by ROS/RNS can generate a range of stable as well as reactive products such as protein hydroperoxides that can generate additional radicals particularly upon interaction with transition metal ions. Although most oxidized proteins that are functionally inactive are rapidly removed, some can little by little accumulate with time and thereby contribute to the damage associated with ageing as well as various diseases. Lipofuscin, an aggregate of peroxidized lipids and proteins accumulates in lysosomes of aged cells and whiz cells of patient s with Alzheimers disease 28.InflammationInflammation is one of the body unique mechanisms that economic aid body to protect itself against infection, burn, toxic chemicals, allergens or other noxious stimuli 29. It is a body defense reaction in order to eliminate or limit the spread of injurious agent 30. The process is created by repellent cells invading the thread like an army in full date mode 31.There are various components of inflammatory reaction that can contribute to the associated symptoms and create from raw stuff injury 30. During inflammation, innate cells and molecules are usually emotional to isolate, end infectious agents and repair tissue, or sometimes the adaptive immune system is also stimulated 32. Consequently, the mechanism works in a cascade, where the inflammation is often triggered by circulating immune complexes that enter tissues 31.Principally, inflammation is manifested by imposition, clod, redness band loss of function in the discomfit tissue 31, 33. Saladin (2007) categorized process of inflammation into 3 major processes mobilization of the bodys defenses, containment and destruction of pathogens, and tissue clean up and repair 34. While Mahat and Patil (2007) assort the process into three phases the first phase is caused by an increase in vascular permeability, the second one by infiltration of leukocytes and the third one by granuloma formation 30.The inflammatory response is initiated by circulating proteins and blood cells when they contact invaders in the tissue. Microbial invaders that lodge in body tissue and begin to proliferated triggered inflammatory response 33. Bacterial products interact with plasma factors and cells to produce agents that attract neutrophils to the infected area (chemotaxis). The chemotactic agents, which are part of a large family of chemokines, include a component of the complement system (C5a), histamine, kinins, leukotrienes, and polypeptides from lymphocytes, mast cells, and basop hils 35. The neutrophils also produce oxidants and release granular constituents comprising of lytic enzymes performing important role in inflammatory injury 36. The innate immune system contributes to inflammation by initiate the alternative and lechitin-binding complement pathways, attracting and trigger phagocytic cells that secrete cytokines and chemokines, activating NK cells, repair vas. The result would firstly be increased in blood lead to the pretended tissue which accelerates the delivery of immune system element to the site 33. The vasodilation would later cause enlarged capillaries and lead to redness (erythema) as well as increase in temperature, which for an influx of fluid and cells, contributing to swelling 32. Saladin (2007) explained that the increased in blood flow also washes toxin and metabolic wastes from the tissue rapidly. In addition, vasoactive chemicals cause endothelial cells of the blood capillaries to separate a little, siding the intracellular cle ft between them and increasing capillary permeability that ease the movement of fluid, leukocytes, and plasma proteins from the bloodstream into the surrounding tissue 34.In the area of injury, many of the neutrophils enter the tissues. As neutrophils encounter bacteria, they avidly phagocytize, digest and supplant them. Neutrophils also recruit macrophages and additional neutrophils by secreting cytokines 33. Activated macrophages and T cells in the aggravate tissue also secrete cytokines called colony stimulation factors, which promotes the production of more leukocytes by the red bone marrow. Within a a couple of(prenominal) hours of inflammation, neutrophilia (the rise in the neutrophil count in blood) would occur 37.Then, the neutrophils are attracted to the endothelial surface by selectins, and they roll a hanker it. They bind heavily to neutrophil adhesion molecules of the integrin family. They next insinuate themselves through the walls of the capillaries between endothe lial cells by a process called diapedesis 35. Leukocytes adhere loosely to the selectins and slowly hook on along the endothelium, sometimes coating it so thick that they obstruct blood flow. This adherence to the vessel wall is called margination 38.Later, the fibrinogens are filtered into the tissue fluid clots in area adjacent to the injury, forming a sticky mesh that sequesters bacteria and other microbes 34. This is caused by release of chemicals from tissues and migrating cells. Most strongly implicated are the prostaglandins (PGs), leukotrienes (LTs), histamine, bradykinin, platelet- activating factor (PAF) and interleukin-1 39. Prostaglandin is implicated in inducing the production of various chemo-attractants and proinflammatory cytokines 36. Gislason (2009) mentioned that macrophages and neutrophils are responsible to secrete a number of mediators which is responsible not just for initiation, but also for progression and persistence of acute or chronic state of inflammati on 31.Finally, monocytes acts as the major agent in tissue clean up and repair. It enters the blood from the bone marrow and circulated for about 72 hours. Then, they enter the tissues and become tissue macrophage. The macrophage becomes activated by lympokines from T lymphocytes 35. The activated macrophage migrate in respond to chemotactic stimuli and later engulf and destroy bacteria, damaged host cells, as well as dead and demise neutrophils. Be situations that, it also acts as antigen presenting cells and activating specific immune response 34.Edema may also contribute to the tissue clean up. azotic oxide is responsible for vasodilatation, increase in vascular permeability and edema formation at the site of inflammation 36. The swelling compresses veins and reduce venous drainage, piece of music it forces open the valve of lympathic capillaries and promote lympathic drainage. The lymphatics can collect and remove bacteria, dead cells, proteins and tissue debris better than bl ood capillary can. An accumulation of dead cells of neutrophils with other debris tissue and fluid will form pus, a chickenhearted fluid. It may accumulate in the tissue cavity and known as abcess 32. Pus is usually absorbed, but sometimes it may be released by its rupture. Blood platelets and the endothelial cells in an area of injury secrete platelet derived growth factor, an agent that stimulates fibroblast to multiply and synthesize collagen. Hyperemia at the same time delivers the oxygen, amino acids and other necessities of protein synthesis, while the heat of inflamed tissue increases metabolic rate and speed of mitosis and tissue repair. The fibrin clot in inflamed tissues may provide a scaffold for tissue reconstruction 34.In part, inflammation declines simply because the mediators of inflammation have short half-lives, are riotous after their release, and are produced in quick bursts, only as long as the stimulus persists. In addition as inflammation develops, the proc ess also triggers a variety of stop signals that serve to actively terminate the reaction 38.Anti-inflammatory ActivityAnti-inflammatory refers to the property of a substance or treatment that reduces inflammation. Anti-inflammatory drugs make up about half of analgesics, remedying pain by reducing inflammation as opposed to opioids, which affect the central restless system.Drugs to control inflammation When healing is complete, the inflammatory process usually subsides 32. However, an uncontrolled and persistent inflammation that sometimes is triggered by clear agent such pollen or by an auto immune response. It may act as an etiologic factor for many of these chronic illnesses, where it may induce, maintain or aggravate the disease 29. As mentioned, the inflammation would occur with the presence of antigen.Thus, constant supply of antigen is available from the food or environs may leads to chronic inflammation and causes diseases such as asthma, arthritis and other autoimmune d iseases 31. In such cases, the defense reaction themselves may cause reformist tissue injury. Hence, anti-inflammatory or immunosuppressive drugs may be necessary to modulate the inflammatory process 37.Anti-inflammatory drugs are designed to rears the inhibition of the release of these mediators to control inflammation 36. Harvey and Champe (2008) have classified anti-inflammatory drugs into three category Nonsteroidal anti-inflammatory drugs (NSAIDs), cyclooxygenase-2 inhibitors (cyclooxygenase-2 inhibitors) and other analgesics 32.Aspirin is a prototype of traditional NSAIDs. It works by irreversibly inhibit Cyclooxygenase 1 and 2 (COX-1 and 2) enzymes, which results in decreased formation of prostaglandin precursors 40. Due to this mechanism of action, aspirin also cause adverse do such as gastric hemorrhages, hypersensitivity and thrombocytopenia 41. It is becoming a concern of healthcare providers that patients are developing intolerance from day to day. About fifteen perc ent of patients show intolerance with aspirin. Therefore, newer NSAIDs with greater anti-inflammatory activities are developed. However, the newer NSAIDs are considerably more expensive than aspirin and some have proved to be more toxic in the other way 32.The second category is COX-2 inhibitor. The mechanism of action is by selectively inhibiting the activity of COX-2 enzyme that results in decreased of prostaglandin precursors 37. Unlike aspirin, COX-2 inhibitors have an advantage by present lower risk of developing gastrointestinal bleeding and have no significant effects on platelets 42. However, this drug is not recommended for renal impaired patients because it may cause renal insufficiency and increase the risk of hypertension 40. It also has some possible adverse effects recorded in Malaysian Index of Medical Specialities (MIMS) that it may cause allergic reaction, dizziness, headache, rash, upper berth respiratory infection and gastrointestinal disturbances such as dyspe psia, abdominal pain and diarrheas 41.Acetaminophen is categorized under other analgesic because it has little or no anti-inflammatory activity 32. It inhibits the synthesis of prostaglandin in the central nervous system and peripherally blocks pain impulse generations 40. They have therapeutic advantages oer narcotic analgesics which they do not cause physical dependence or tolerance and does not affect platelet function or increase blood clotting time, but it does have many of side effects similar to aspirin 42. Rarely, skin rash and allergic reaction may appear as the side effects 41.There are also drugs from autacoids antagonist such as antihistamines used to prevent progress of inflammation. The term antihistamine, without a modifying adjective, refers to the classic H1 receptor blockers 32. H1 histamine antagonists drugs are develop effectively to target the receptors to treat hay fever and some skin allergies such as urticaria. H1 receptor blockers act on immunoglobulin E (Ig E) antibody-sensitizing mast cell 37. run-down arthritis is alleviated by drugs, which inhibit the cyclooxygenase enzyme and reduce synthesis of prostanoids, corticosteroids prevent the formation of both prostaglandins and leukotriens by causing the release of lipocortin that leads to inhibition of phospholipase A2 that reduces arachidonic acid release which is able to suppress the inflammation of rheumatoid arthritis and asthma 39. Anti-cytokines therapy involving target on Interleukin-1b (IL-1b) and tumor necrosis factor- (TNF-) that stimulate synovial cells to proliferate and synthesize collagenase, leading to degradation of cartilage, stimulation of bone resorption, and inhibition of proteoglycan synthesis is other method that is effective in treating rheumatoid arthritis 32.Despite the benefits that the drugs hold, it also carries the side effects. As a result, it may lead various unwanted effects such as to gastric lesions, allergy reactions, tolerance and dependence, as well as resistance 40, 43. Hence, worldwide researchers are still working to produce the ideal medicines of anti-inflammatory with highest efficacy, best potency and lowest or none side effects.Description of the plant investigatedgenus Bauhinia acuminata L. is a species of flowering scrub native to tropical southeastern Asia. The exact native range is black due to extensive cultivation, but probably from Malaysia, Indonesia (Java, Borneo, Kalimantan, Lesser Sunda Islands), and the Philippines.It is widely cultivate throughout the tropics as an ornamental plant. It may be found as an escape from cultivation in some areas, and has become naturalise on the Cape York Peninsula, Australia 44.Common NameBangla Shwet Kanchan.Malaysian Bunga Perak.English command White Bauhinia, White Mountain Ebony 45.Indonesian Panawar Saribu (Sunda Islands) Kupu-kupu (Java)Thailand Ka Long, SomSioBurma MahahlegabyuIndia Kaanchnaara, Kovidaara (Ayurvedic) Kachnaal (Unani) Vellaimandarai (Siddha/Tamil) K anchan (Assam) Shwetkachnar, Kachnalsafaid (Punjab)Sri Lanka Sudu Kobalila (Singhalese)Japan Moku-wan-ju. taxonomical HierchyKingdom PlantaeSubkingdom ViridaeplantaeInfrakingdom StreptophytaDivision TracheophytaSubdivision SpermatophytinaInfradivision AngiospermsClass EudicotsSuperorder Rosids tack together FabalesFamily FabaceaeSubfamily CaesalpiniaceaeGenus BauhiniaSpecies B. acuminataBinomial name Bauhinia acuminata L.botanic DescriptionFig.-1.1 Bauhinia acuminata L. tree.Bauhinia acuminata L. is a member of the Fabaceae family. It is a rapidly growing shrub that can reach up to 3m tall. It rises with several strong, smooth, upright stems with many slender branches young twigs being pubescent. The stipules are linear-lanceolate measures 1cm long. The leaves are cordate or nearly so are the base, bilobed to about one third of their length with obtuse or acute lobes 9-11 nerve, sparsely pubescent beneath, about 10cm long and broad. The flowers appear at the extremities of the branc hes 3-4 in a loose bunch with white petals. Thepedicels measure 6-12mm long. The flower buds fusiform, long subtilize at the apex and 5 setaceous dents, measures 3cm long. The calyx-limb laterally splitting, spathaceous receptacle short. The petals obovate, measure 4cm long and 2cm wide. The stamens 10 all fertile, shorter than the petals anthers small.The ovary shortly stipitate, sparsely pubescent. The pods are linear-oblong, stipitate, measure 10cm long and 1.5cm wide, dark brown in colour containing 10 roundish taut seeds 46, 47.Traditional uses of Bauhinia acuminata L.The speak and leaves in a decoction helps relieve pettishness 48. A remedy recommended by the Indian Vaiydas 45. In Malaysia and Indonesia the plant is used in the treatment of common cold and cough up 48. The root seems to be the part made used of by the Japanese in treating cough and cold. In India the decoction of the leaves and shinny is given for allying asthmatic attack. The Indians made used of the ba rk and leaves in a decoction to treat stones in the bladder, venereal diseases and leprosy 45. Amongst the Mullu kuruma tribe of Karella the decoction of the bark is used in treating urinary discharge (gonorrhea). They make use of spread of the leaves applied on the throat for throat troubles. It is applied externally to treat skin diseases 49. The root is boiled in oil and applied to burn down and pain 45.Objective of study To evaluate the free radical scavenging and anti-inflammatory activity of Bauhinia acuminata L. bark extracts in rats.Significance of study Bauhinia acuminata L. is one of the
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