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Diet, exercise, and education remain the foundation of any type 2 diabetes treatment program. Ultimately, many patients will require insulin therapy alone or in combination with other agents to maintain glucose control. The American Diabetes Association and the European Association for the Study of Diabetes have updated guidelines on the management of hyperglycemia in nonpregnant adults with type 2 diabetes. The novel position statement on the management of hyperglycemia in type 2 diabetes was necessary because since the last similar treatment algorithm, which is more than 3 years old, a lot of new insights have been generated that required an update. According to the ADA, to reduce the incidence of macrovascular disease, HbA1c should be lowered to less than 7% in most patients. For strong recommendations in favour (or against) certain diabetes medications, the evidence is not strong enough; choices and preferences will differ with different patients, their characteristics and attitudes. Several therapeutic options were discussed, including lifestyle interventions to change physical activity levels and food intake; oral agents and noninsulin injectables, as well as insulin. The second step can be a dipeptidyl peptidase-4 inhibitor, it can be a glucagon-like peptide-1 (GLP-1) receptor agonist, it can be a thiazolidinedione, it can be a sulfonylurea agent, or it could be basal insulin.
If a patient needs a more intensive insulin regimen, then it is recommended to add 1 or 2 - maybe even 3 - doses of mealtime insulin. The position statement lists all commonly used medications with all their properties (positive and negative), and gives all the information to make good choices based on priorities (ie, avoiding hypoglycemia at all costs) and preferences.
Overall, comparative evidence for antihyperglycemic treatment of type 2 diabetes is lacking, and there is a considerable need for high-quality, comparative-effectiveness research on costs and outcomes important to patients, including quality of life and the avoidance of life-limiting complications such as cardiovascular disease.
Because of the rapid change in lifestyle in China, there is concern that diabetes may become epidemic.
A nationally representative sample of 46,239 adults, 20 years of age or older, from 14 provinces and municipalities participated in the study.
These results indicate that diabetes has become a major public health problem in China and that strategies aimed at the prevention and treatment of diabetes are needed.
In an editorial comment in the European Heart Journal, some opinion leaders indicate what might be the reasons for the failure of the dal-HEART programme.Both the on-treatment vascular effects and the underlying molecular mechanism causing increased HDL-c are important in determining the vascular effects of an HDL-c raising therapy.
The Treatment Options for Type 2 Diabetes in Adolescents and Youth (TODAY) study assessed how to manage diabetes in children and adolescents. The China National Survey of Chronic Kidney disease was a cross-sectional study to evaluate the prevalence of CKD and associated factors in Chinese adults between 2007 and 2010.CKD has become an important public health issue in China, maybe as a consequence of increased diabetes and hypertension. DPP-4 inhibitors can be used as second line treatment in patients with type 2 diabetes who do not achieve their glycaemic targets with metformin alone. The study was set up to determine all cause mortality and deaths from cardiovascular events related to intensive glucose lowering treatment in people with type 2 diabetes.
In GPRD data, current use of sulphonylureas only (with active or inactive metabolites) was associated with an increased risk of hypoglycaemic events, as compared with current use of metformin. Recent outcome trials of novel antidiabetic drugs shed new light on why diabetes patients develop heart disease. Out of 18 biomarkers, Lp-PLA2 and adiponectin were independently associated with a decreased risk for T2DM. In females with gestational diabetes, the future risk of developing type 2 diabetes depends on certain pregnancy-related and maternal factors that could be used for postnatal counselling. After cleansing and toning routine, apply gently on to the face in an upward and outward motion. Helps improve the appearance of sagging facial contours, while sealing in lasting moisture. Diabetes mellitus is a metabolic disease characterized by hyperglycemia that results from defects in insulin secretion, insulin action, or both. A variety of pathogenic processes are involved in the development of different forms of diabetes. Acute life-threatening consequences of diabetes mellitus are ketoacidosis and nonketotic hyperglycemic hyperosmolar coma. Specific long-term complications of diabetes include (l) retinopathy with potential loss of vision, (2) nephropathy leading to end stage renal disease (ESRD), and (3) neuropathy with risk of foot ulcers, amputation, Charcot joints, sexual dysfunction, and potentially disabling dysfunction of the stomach, bowel, and bladder.
Sufficient hyperglycemia to cause pathologic and functional changes in target tissues may be present for some time before clinical symptoms lead to a diagnosis of diabetes in many patients. The classification of diabetes mellitus has recently been revised by a task force of the American Diabetes Association that included representation from Europe.1 Major etiologic classes of the disease, along with more esoteric examples, have been categorized [see Table 1]. Type 1 and type 2 diabetes were formerly known as insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM), respectively. Gestational diabetes mellitus (GDM) constitutes a separate category for cases of diabetes first detected during pregnancy.3 When diabetes is detected early in pregnancy, it is likely to be type 1 or type 2 diabetes mellitus that is presenting symptomatically and was probably precipitated or worsened by the pregnant state. Of the categories of secondary diabetes [see Table 1], endo-crinopathies and drug- or chemical-induced diabetes are noteworthy because they represent instances of diabetes that are potentially reversible if they are recognized and the physician can cure the endocrinopathy or discontinue the offending drug.
Diabetes caused by chronic pancreatitis, pancreatectomy, or occasionally carcinoma of the pancreas is usually type 1 in character.
Although many individual drugs have been incriminated as a cause of hyperglycemia, the continued use of pharmacologic anti-inflammatory or immunosuppressive doses of synthetic gluco-corticoids is an especially important continuing problem. Screening for type 1 diabetes mellitus by office glucose testing is currently indicated in high-risk patients. Figure 1 The opposing actions of insulin and glucagon, particularly within the liver, on substrate flow and plasma levels are seen here. Annual incidence of type 2 diabetes mellitus per 100,000 population ranges from 180 in 25 to 44 year olds to a peak of 860 in 65 to 74 year olds. Figure 2 Plasma glucose (a) is normally kept within a narrow range throughout the day, largely because of beta cell function. A proper balance between insulin and glucagon is one crucial hormonal regulator of basal metabolic homeostasis.20 Insulin primarily facilitates storage of glucose as glycogen, free fatty acids in triglycerides, and amino acids in protein, and it inhibits glycogenolysis, lipolysis, ketogenesis, proteolysis, and gluconeogenesis [see Figure 1]. Insulin is synthesized in pancreatic islet beta cells from a larger molecule called proinsulin, which is then split to yield insulin and an intramolecular connecting peptide called C-peptide [see Figure 3].
Insulin acts via a plasma insulin receptor that leads to the generation of multiple mediators of insulin’s numerous intracellular cytoplasmic and nuclear effects [see Figure 4].
A feedback loop exists between insulin responsiveness in target tissues and insulin secretion by beta cells. A distinctive feature of diabetes—the microvascular complications—were only revealed or commonly appreciated after the introduction of insulin therapy in 1922 allowed patients with type 1 diabetes mellitus to live long enough to experience these complications.
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Trulicity is once-a -week glucagon-like peptide-1 (GLP-1) receptor agonist in solution formulation for the treatment of type-II diabetes mellitus. The Ohio State University Wexner Medical Center endocrinologist, associate professor, and lead study author Kathleen Dungan M.D. This Phase 3, randomized, double-blind, and placebo-controlled, a 24-week study was done on a total of 299 patients, having a mean HbA1c of 8.4 percent. Glucagon-like peptide-1 (GLP-1) is derived from the transcription product of the proglucagon gene. GLP-1 secretion by L cells is dependent on the presence of nutrients in the lumen of the small intestine. GLP-1 possesses several physiological properties that make it a subject of intensive investigation as a potential treatment of diabetes mellitus.[1][2][3]. DPP-4 inhibitors, also known as ‘gliptins’, are a class of oral glucose-lowering agents that block the DPP-4 enzyme.
Onglyza has a mechanism of action that acts through the incretin pathway, impacting on both the pancreatic ?-cells and ?-cells. Combination therapy with an additional 1–2 oral or injectable agents is reasonable, aiming to minimize side effects where possible. The update is based on new evidence of risks and benefits of glycemic control, evidence on safety and efficacy of new drug classes, the withdrawal and restriction of other drug classes and the increasing need for a more patient-centered approach to care. However, data from type 2 diabetes cardiovascular trials have demonstrated that not all patients benefit from aggressive glucose maintenance, again pointing toward a more individualized approach to treatment. In contrast to previous statements, the present one is based on a patient-centered approach.
According to the guidelines, when it comes to prescribing oral agents and noninsulin injectables, agent- and patient-specific properties, such as dosing frequency, side effect profiles, cost and other benefits, are often used to guide drug selection.
Anticipated glucose-lowering effects should be balanced with the convenience of the regimen, in the context of an individual’s specific therapy goals. We conducted a national study from June 2007 through May 2008 to estimate the prevalence of diabetes among Chinese adults. These processes range from autoimmune destruction of the beta cells of the pancreatic islets with consequent insulin deficiency to mutations in the insulin receptor gene with consequent resistance to insulin action.


Overtreatment of hyperglycemia can lead to hypoglycemia, which may be severe enough to cause seizures and loss of consciousness. Numerous mechanisms have been discovered that may mediate the specific tissue damage caused by hyper-glycemia. At an even earlier stage, an incipient abnormality in glucose metabolism can be identified on plasma glucose testing, which indicates that the patient is at considerably increased risk for the full clinical disorder. The vast majority of cases of diabetes mellitus are either type 1 (insulin-dependent) or type 2 ( non-insulin-dependent) in an approximate ratio of 1:9. This classification was abandoned largely because it was difficult to distinguish patients with IDDM from those patients with NIDDM who eventually required insulin treatment to mitigate hyperglycemia. The category of genetic defects in beta cell function illustrates how the classification will grow ever more detailed as knowledge increases. Because patients with this disease have glucagon as well as insulin deficiency, they are somewhat less likely to go into ke-toacidosis4 but are quite vulnerable to hypoglycemia.
Current American Diabetes Association criteria for office screening of asymptomatic individuals for type 2 diabetes mellitus employ FPG levels.1 Screening is recommended in all individuals 45 years of age and older at 3-year intervals. Current estimates of annual incidence are 18 per 100,000 population in the 0- to 19-year age range and 9 per 100,000 population in those older than 20 years.8 Approximately 30,000 cases of type 1 diabetes mellitus are estimated to occur yearly in the United States, and it is more common in whites than in African Americans. A prevalence of 12.3% (diagnosed plus undiagnosed) was estimated for individuals 40 to 74 years of age.
The two hormones have directly opposite effects on key enzymes, such as glycogen synthase and phosphorylase.
Approximately 625,000 cases of type 2 diabetes mellitus develop yearly in the United States.10 The prevalence is expected to rise from 15 million in the year 2000 to 21 million in 2025. Plasma insulin (b) and plasma C-peptide (c) rise sharply from their basal levels with each meal and, after reaching peaks, return promptly to basal levels, which are maintained throughout the night.
Glucagon stimulates mobilization of glucose, free fatty acids, and glycerol and stimulates hepatic uptake of amino acids and the conversion of their carbon skeletons to glucose.
The two molecules are stored in the same granules and secreted in an equimolar ratio when the beta cell is stimulated. This relation operates to increase insulin secretion in individuals relatively resistant to insulin action and to decrease insulin release in individuals very sensitive to insulin action. It should be borne in mind that the descriptions and pathogenetic sequences presented below reflect a former commonly practiced degree of metabolic control no longer considered acceptable. The peptide that connects the amino terminus (NH2-) of the A chain to the carboxyl terminus (-COOH) of the B chain is called connecting peptide (C-peptide). If you require further details regarding the transaction data, please contact the supplier directly. It comes in a form of a pen and the patient does not require the drug to mix, measure, or handle the needle problems. The scientific data proves that Trulicity 1.5 mg plus sulfonylurea showed a superior HbA1c reduction from baseline as compared to sulfonylurea with placebo. Trulicity proved its efficacy profile at a dosage of 1.5 mg to placebo with the reduction of HbA1c, when compared in patients with sulfonylurea alone. The major source of GLP-1 in the body is the intestinal L cell that secretes GLP-1 as a gut hormone. Based on work by Cafer Zorkun, Navin, Scott Williams and Alexandra Almonacid, wikidoc user WikiBot and wikidoc anonymous user Wkong. Genetic heterogeneity of autoimmune diabetes: Age of presentation in adults is influenced by HLA DRB1 and DQB1 genotypes (UKPDS 43). Metabolic and immune parameters at clinical onset of insulin-dependent diabetes: A population-based study.
Antibodies to glutamic acid decarboxylase reveal latent autoimmune diabetes mellitus in adults with a non-insulin-dependent onset of disease. Islet cell antibodies and fasting C-peptide predict insulin requirement at diagnosis of diabetes mellitus.
Time to insulin initiation cannot be used in defining latent autoimmune diabetes in adults. Prevalence of type 1 diabetes autoantibodies (GADA, IA2,and IAA) in overweight and obese children. Guidelines and recommendations for laboratory analysis in the diagnosis and management of diabetes mellitus. C-peptide is the appropriate outcome measure for type 1 diabetes clinical trials to preserve B-cell function report of an ADA workshop, 21-22 October 2001. Complete long-term recovery of beta-cell function in autoimmune type 1 diabetes after insulin treatment. Islet autoantibodies in clinically diagnosed type 2 diabetes: Prevalence and relationship with metabolic control (UKPDS 70). Autoimmune diabetes not requiring insulin at diagnosis (latent autoimmune diabetes of the adult) definition, characterization, and potential prevention.
The role of sulphonylurea in combination therapy assessed in a trial of sulphonylurea withdrawal. Rosiglitazone prevents diabetes by increasing beta-cell mass in an animal model of type 2 diabetes characterized by reduced beta-cell mass at birth.
Rosiglitazone combined with insulin preserves islet beta cell function in adult-onset latent autoimmune diabetes (LADA). Beta-cell function in new-onset type 1 diabetes and immunomodulation with a heat-shock protein peptide (diaPep277): A randomised, double blind, phase II trial.
Clinical evidence for the safety of GAD65 immunomodulation in adult-onset autoimmune diabetes. The authors recommend combination therapy with the addition of one to two oral or injectable agents, with the goal of reducing side effects when possible.
The prevalence of diabetes was higher among urban residents than among rural residents (11.4% vs. The basis for the metabolic abnormalities of diabetes mellitus is deficient action of insulin on its major target tissues, including skeletal muscle, cardiac muscle, adipose tissue, and liver. Symptoms of poorly controlled hyperglycemia include polyuria, polydipsia, blurred vision, weight loss, polypha-gia, stunting of growth, and vulnerability to infections or susceptibility to a more virulent or chronic course when infected. Diabetic patients are also at increased risk for atherosclerotic cardiovascular, peripheral vascular, and cerebrovascu-lar disease.
Physicians, nurses, hospital-record-room personnel, health insurers, and even sometimes researchers were hard put to distinguish between these two forms of diabetes using the old terminology. However, GDM is associated with a high risk of future diabetes, especially in women who have IGT post partum or who remain obese.3 Permanent diabetes will develop in approximately 50% of patients within 10 years of GDM.
For example, the single diabetes mellitus phenotype formerly called maturity-onset diabetes of the young (MODY) can now be more precisely classified into at least four genetic varieties, each of which arises from mutation of a different gene. Because they are deficient in pancreatic enzymes, their digestion and subsequent absorption of nutrients is somewhat erratic, even though replacement enzymes are ingested with meals. Worldwide, the highest annual incidence of type 1 diabetes mellitus is found in Finland (35 cases per 100,000) and the lowest is found in Korea (< 1 per 100,000).
Thus, stimulatory effects of glucagons on glucose and ketoacid production are magnified when insulin is deficient, as in type 1 diabetes mellitus. Worldwide, the prevalence of type 2 diabetes mellitus will likely increase from 150 million to 300 million during that time.11 The increase42 reflects aging of the population, strikingly increased obesity,13 and a sedentary lifestyle. Many patients with type 2 diabetes mellitus have a strong family history of that disease in first-degree relatives. To understand the pathogenesis of diabetes, it is useful to start with a brief review of normal metabolism. Note also that plasma insulin and C-peptide levels are elevated in obese individuals who are insulin resistant.
The result is one critical mechanism for maintaining fasting and postprandial plasma glucose levels within narrow normal ranges.
Prevention of these complications is a major goal of current therapeutic policy and recommendations for all but transient forms of diabetes [see Prevention and Treatment of Microvascular Complications, below]. Proinsulin is converted to insulin and C-peptide, and these two molecules are packaged together in the secretory granule. As expected, patients suffered from a bout of hypoglycemiawhen treated with Trulicity plus a sulfonylurea in comparison to those treated with sulfonylurea alone in both groups during the study.
The clinical risk score cannot by itself predict autoantibodies, but highly indicates for antibody testing and helps early diagnosis.DiagnosisLADA was first identified in a subset of phenotypic T2DM individuals with positive ICAs. Part 1: Diagnosis and classification of diabetes mellitus provisional report of a WHO consultation.
Insulin therapy, whether alone or in combination, will ultimately be required to maintain glucose control for many patients.


The chronic hyperglycemia of diabetes mellitus is specifically associated with long-term damage, dysfunction, and failure of various organs, especially the retina and lens of the eye, the kidneys, and both somatic and autonomic nervous systems. Loss of proper insulin regulation of metabolism results from inadequate secretion of insulin, from diminished tissue responses to insulin at one or more points in the complex pathways of insulin action, or from both processes.
These conditions may be related to hyperglycemia as well as to hypertension and abnormal lipoprotein profiles that are often found in diabetic patients. The new classification, dependent on etiology rather than mode of treatment, puts a greater emphasis on the history and characteristics of the patients to determine the probable etiology and type. The greatest importance of any single episode of GDM lies in the risks it poses to the fetus.
If alcoholism, often the cause of chronic pancreatitis, is irremediable, it also contributes to blood glucose instability, as does the often accompanying irregular lifestyle.
Although insulin resistance in the liver and muscle is a well-recognized effect of glucocorticoids, an action on the beta cells to limit the compensatory response to hyperglycemia7 adds to the diabetogenic effect at higher steroid doses. An extraordinary example is found among the Arizona Pima Indians on the Gila River reservation, where 50% of the adult population has type 2 diabetes mellitus.
Insulin sensitivity is best measured in humans by infusing insulin to establish steady-state plasma insulin levels [see Figure 5].
On stimulation of the beta cell, C-peptide and insulin are secreted in equimolar proportions.
There was no imbalance in CV deaths due to heart failure (0.5% in each group according to 2-year Kaplan-Meier estimates). The prevalence of isolated impaired glucose tolerance was higher than that of isolated impaired fasting glucose (11.0% vs. Impairment of insulin secretion and defects in insulin action coexist in many patients, and in these patients, it is often unclear which abnormality is the primary cause of the hyperglycemia. These risks include intrauterine mortality, neonatal mortality, respiratory distress syndrome, hypoglycemia, hypocalcemia, jaundice, and macrosomia, which can cause trauma such as shoulder dystocia during passage through the birth canal.
Small frequent doses of lispro insulin should be helpful, but safety may require less stringent blood glucose goals in such patients. Patients treated with glucocorticoids for more than a few days need to be warned to watch for and report clinical symptoms of hyperglycemia promptly.
Non-Hispanic African-American and Mexican-American women have nearly twice the prevalence of diabetes as non-Hispanic white women. Other risk factors for the disease include physical inactivity, hypertension, dyslipidemia, gestational diabetes, low birth weight, low income, low level of education, and low socioeconomic status.
After a mixed meal, plasma insulin rises sharply [see Figure 2] and, with it, the insulin-glucagon ratio.
Simultaneously, the baseline plasma glucose is maintained at a constant level by a variable glucose infusion.
For the first time, this data is presented at the 2015 International Diabetes Federation (IDF) World Diabetes Congress in Vancouver, Canada. Non-Hispanic African-American men have a slightly higher risk than non-Hispanic white men, but Mexican-American men have about a 50% greater risk than non-Hispanic white men. The amount of glucose required to prevent plasma glucose from decreasing under the effect of insulin is equal to the increased amount of glucose being used per unit time under insulin stimulation (assuming that insulin has completely suppressed hepatic glucose output by the liver).
Dietary carbohydrate is stored in muscle and liver glycogen, free fatty acids are reesteri-fied and stored as triglycerides in adipose tissue, and protein metabolism shifts back toward anabolism. The quantity of glucose used per unit time divided by the plasma insulin level provides an index of whole body sensitivity to insulin in the sphere of glucose metabolism. When all the nutrients have been assimilated and plasma glucose returns to its basal preprandial level, plasma insulin [see Figure 2] and the in-sulin-glucagon ratio promptly return to basal levels, preventing an overshoot of insulin action that would otherwise cause hy-poglycemia. In most instances, steroid diabetes is transient, but in a minority of cases, diabetes persists even after withdrawal of the glucocorticoids. Thus, an immediate rise, an early peak, and a prompt fall in insulin secretion are requisite to normal postprandial metabolism [see Figure 2]. Epitope specificity, antibody levels, and concomitant presence of ICAs subcategorize LADA with a different risk toward insulin dependency.
Therefore, islet autoantibodies are currently not recommended in diagnosis or routine management of adult patients with diabetes. Although autoantibody-positive diabetic patients progress to absolute insulin deficiency faster, many antibody-negative patients also progress to insulin dependency with time. The clinical benefits from institution of insulin therapy to these patients are based on careful monitoring and treatment of hyperglycemia rather than diagnosis of antibodies itself. An adult patient with T2DM who has single antibody is probably at no greater risk of early insulin requirement than the one of the same age without antibodies.
However, a young person with multiple autoantibodies is almost certain to need insulin soon. These factors need to be taken into consideration in counseling patients, and antibody testing will benefit in such cases.
Lifestyle modification, medical nutrition therapy, screening and treatment of hypertension, hyperlipidemia, nephropathy, retinopathy, and every overall aspect of comprehensive diabetes care should be followed. Investigations should also include antibody testing for diagnosis and C-peptide levels for β-cell status.
Overweight adults are presumed to have T2DM and are not tested, whereas normal-weight adults are considered to potentially have LADA and may be tested. Disease risk is associated with organ-specific autoantibodies, which can be used to screen the subjects.
These agents stimulate insulin secretion by interacting with ATP-sensitive potassium channels in β-cells, and are very effective in treating T2DM of recent onset.
Despite their initial efficacy, there is progressive deterioration in β-cells and glycemic control over time.
The cause might be exhaustion or desensitization of β-cells by prolonged exposure to sulfonylurea and possibly accelerated oxidative stress and apoptosis. A total of 60% of the autoantibody-positive patients treated with sulfonylureas progressed to insulin requirement within 2 years compared with 15% of the autoantibody-negative patients. It acts by decreasing the hepatic glucose output and sensitizing peripheral tissues to the action of insulin. But there is a potential risk of lactic acidosis in patients who progress toward insulin dependency. They decrease insulin resistance and enhance glucose uptake by upregulating GLUT4 channels via peroxisome proliferator activated receptor-γ. The rationale for early insulin therapy though would be to improve glycemic control while protecting β-cells.
Also, as insulin itself is an autoantigen, immunization with exogenous insulin is thought to initiate an immune modulation possibly by tolerance induction or "bystander" suppression of autoreactive T-cells through release of regulatory cytokines. Subgroup analysis suggested that patients with high anti-GAD titers and preserved C-peptide response at baseline were less likely to progress to the insulin dependency, with early initiation of insulin. If rapid loss of insulin release occurs early in LADA, replacement with multiple doses of insulin might be beneficial. However, from a practical point of view, it is difficult to initiate multiple insulin injection therapy very early in LADA patients, especially if their blood glucose levels are not severely elevated.
Since progression of LADA is slower than T1DM, windows of opportunities for treatment are better. But there are no standard guidelines currently as its pathogenesis and natural history is yet to be fully understood. Since our main target in management of LADA is the possible preservation of β-cells to prolong insulin independency, we should be able to predict the at-risk group for early intervention. Sulfonylureas should not be used as first-line therapy, and not at all if possible since they further exhaust β-cells. Metformin may be used, especially in obese subjects with insulin resistance, but the possibility of lactic acidosis with insulin dependency should always be kept in mind. Based on C-peptide levels, insulin should be initiated as early as needed, and as early as possible.
Patients are always reluctant to start insulin, especially if they have to switch from OHA very early, so educating and counseling the patients is very important. Immunomodulatory agents might be of benefit, but clinical studies are yet to clearly demonstrate their benefit in LADA.
More studies are needed to come to a definite conclusion, which, if successful, may also help in preventing insulin dependency in younger individuals who are susceptible to type 1 diabetes.



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