Intro to PSL

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Negative Feedback: A product of target cell and will inhibit the anterior pituitary.
Positive Feedback: Rare but important, a change is kept moving in the direction of the initial change
The content of the interstitial fluid is maintained by: Homeostasis
Cytosol: the liquid portion of the cell.
Metabolism: involves thousands of reactoins that are carried out by enzymes with are protein catalysts.
Protein Synthesis: protein is made in the cytosol by the ribosomes which are attached to the ER.
Ribosomes: make proteins that must be folded by the help of chaperone proteins.
Endoplasmic Reticulum: is a complex that has a lot of interconnected tubes
Rough ER: ribosomes sit on a hole and new protein will enter the tube so Oxygen crosses easily.
Smooth ER: mesh of interconnected tubules. It makes the new membrane and doesn't contain ribosomes.
lysosomes: the ezymes convert proteins to amino acids and they reduce complex carbs to simple sugars. they digest new food.
Mitochondria: energy organelles or power plants of the cell. take nutrients in food and change into form for cell activity
ATP: adenosine with 3 tri phosphates attached. When this is split a lot of energy is released.
Glycolysis: the process of splitting sugar or glucose into pyruvic adic to produce energy.
Endocrine Disorders: arises b/c target cell responsiveness to the hormone is abnormally low and produces no response to normal hormone levels.
Hyposecretion: low secretion of a hormone
Hypersecretion: too much hormone secreted,
Cell responsiveness is controlled by: the number of available receptors.
Down regulation: occurs when there is desensitization of receptors due to chronic exposure of an agonist.
Processes consist of internalization of receptors or chemical modification of receptors.
Permissiveness: occurs when one hormone maximizes the effect of a second hormone.
Synergism: when two hormones effect each other's activity
Antagonism: one hormone decreases the activity of a second hormone.
Pineal Gland: it releases melatonin to regulate circadian rhythms.
Biological Clocks: SCN regulates protein production over a day's length. Light entraains the SCN to a 24 hour day.
Melatonin: Is controlled by light and is released in high amounts in the dark and less in the light. It also controls other hormone release. It is an antioxidant that damages free radicals which are found in cancer, coronary artery disease and aging. Melatonin will slow the aging process.
Plasma Calcium: Plasma in Calcium is about 2.5mM and is free inside the cells.
Parathyroid hormone: These are 4 spots found on the thyroid which increase Calcium reabsorption from bone then from calcium phosphate.
Hypocalcemia: You have this if you don't have a parathyroid hormone (no blood calcium).
Vitamin D: Used as a steriod hormone and increases the effectiveness of the parathyroid hormone.
Osteoporosis: A decrease in bone density. Weight bearing work and exercise will increase bone density.
Hypothalamus: Controls homeostasis.
Pituitary: Contains the Posterior and Anterior pituitary.
Posterior Pituitary: It releases hormones made int he hypothalamus.
Vasopressin: Increases water reabsorption by the kidneys.
Oxytocin: It causes uterin contractions during child birth and milk ejection in the breast during lactation.
Hypothalamic Releasing and Inhibiting Hormones: The hypothalamus produces reales hormones and inhibiting hormones that are released in small amounts in the anterior pituitary.
Portal System: It carries releasing and inhibiting hormones to the anterior pituitary.
Anterior Pituitary Hormone Release: amounts released are controlled by the balance of the releasing and inhibiting hormones.
Growth Control: Genetic and nutrition must have sufficiant amino acids and vitamins to maximize growth.
Growth Hormone: it activates 2nd messengers in many tissues and circulates for 15 mins. and metabolizes the liver.
Non-Growth Related Effects: it increases liver glucose production and increases fatyy acid release from adipose tissue.
Growth-Promoting Actions: GH promotes soft tissues by Hyperplasia-increase the number of cells or mitosis and hypertrophy- increase the size of the cells or protein synthesis.
Bone Growth: contains growth hormone that will stimulate the bone thickness and length.
Bone Composition: Outer layer contains compact bone containing calcium phosphate. Inner layers are spongy bone containing lighten bones.
Osteoblasts: cells that form bone and secrete calcium phosphate and make collagen.
Osteroclasts: creates space in the bone that is digested hard bone.
Bone Length Growth: osteoclasts eat away epiphyseal plates and osteoblasts will add bone to the diaphysis.
Control of GH release: the hypothalamus gets multiple inputs and produces GHRA which will increase GH release and GHIH which will decrease GH release
GH Deficiency in children and adults: Children-produces dwarfism by a decrease in bone growth.
Adults there is no effect.
GH Excess before puberty and after puberty: Before puberty there is increased but proportional growth.
After puberty there is acromegaly or and increase in facial bone growth and extremities such as the hands and feet.
Thyroid Hormone: Increase results in poor mental health, poor physical funtion, less cold resistance, and mental retardation. Increase in TH results in wasting, nervousness and increase in heat production.
TH hormone synthesis: Iodine is added to tyrosine in thyroglobulin which moves by exocytosis into a colloid or liquid. Then with these added it moves by endocytosis to follicular cells which digest TGB and T3 and T4 number of iodines.
TH secretion: Occurs when T3 and T4 are secreeted into the blood. They are not stored.
TH transport: T3 and 4 are bound to protien in plasma. Most T4 is converted to T3 in plasma.
TH buffering: As TH is lost in urine or enters cells the bound TH will release some TH to become free TH and replace the lost TH.
TH effects: Maximizes GH effects on bone and protein synthesis.
Calorogenic TH Effect: Increase in heat production. TH will bind to nuclear receptors and increase gene activity, cell activity, fatty acid metabolism, and Sodium pump activity by making more pumps.
TH Effects: Sympathomimetic Function: TH is required for a full sympathetic response b/c TH increases the production of adrenergic receptors.
TH Effects on the Heart: Increase in beta and adrenergic receptor number so and increase in heart rate and the increase on the force of contraction takes place.
TH Effects on Neural Tissue: TH is nessecary for CNS development in children. It maximizes RAS activity or a switch in the brain that keeps you awake.
Regulation of TH secretion: Regulation is by Thyroid Stimulating Hormone from the anterior pituitary.
TSH regulation (Thyroid Stimulating Hormone): An increase in blood TH causes the release of TSH from the anterior pituitary which will increase TSH production. An increase in blood TH will cause a decrease in TSH production
Hypothytroidism: Results in Thyroid gland disease, low TSH production, and a lack of iodine. The symptoms are a decrease in BMR and in mental and physical functions.
Graves Disease: Produces hyperthyroidism b/c you produce TSI or T. S. Immunoglobulin. Symptoms are increase in BMR, nervousness, wasting, and bulging eyes.
Hashimoto's Syndrome: An autoimmune attack on the thyroid gland which produces hypothyroidism.
Goiter: An enlarged thyroid that occurs due to excess TSH or TSI.
Adrenal Medulla: is the inner layer of hte adrenal gland
AD Secretions: Consist of epinephrine and norepinephrine that are stored in granules 4:1.
AD Effects of Catecholamines: E. release causes an increasse in HR, a decrease in total peripheral resistance and increase in cardiac output. N.E. causes vasoconstriction except in heart and skeletal muscles. A large increase in BP and Metabolic Rate.
AD on Neural Control: Decrease in E. and N.E. release to increase BP. and Increase these to decrease BP.
Adrenal Cortex: The outer layer has many endocrine secretions.
AC Secretions: are all steriods or derivatives of cholesterol-Mineralcorticoids or aldosterone, glucocorticoids or cortisol a stress hormone, and androgens or male hormones which produce DHEA similar to testosterone.
ACTH Effects and Control (Adrenocorticotropic Hormone): Increase in ACTH causes a release of all adrenal cortex hormones. Decrease on ACTH causes negative feedback by cortisol.
Circulation of Glucocorticoids: most circulate bound to globulin proteins and only the free form are active for about an hour.
Glucocorticoid Effects: Cortisol is a stress hormone which is necessary for survival it binds to nuclear receptors to increase synthesis.
Anabolism: The buildup of large macromolecules (proteins and glycogen)
Catabolism: Is the breakdown of large macromolecules
Essential Nutrients: these are ones the body can't make but must have. You must also have enough calories.
Nutrient Storage: Glycogen is stored in muscle and in liver.
Fats in adipose tissue/ carbs can be converted to fats to go into adipose tissue.
Amino Acids made in proteins used for energy during starvation.
Brain Glucose Supply: B/w meals glycogen from the liver maintains plasma glucos for the brain. Proteins can be made into glucose but fats can't.
Apsorptive State: Post meal time lasts about 4 hours.
Post-Abosorptive State: Fasting b/w meals
Islet Cells: They secrete hormones into the blood.
Alpha cells secrete glucagon and beta cells secrete insulin which is more important.
Insulin Effects: All are aimed at storing energy for future use
Insulin Effects on Carbs: In seconds it will increase number of glucose transporters in cell membranes and causes an increase in glucose entry.
Insulin Effects on Fats: Takes hours for insulin to increase lipid storage.
Insulin Effects on Proteins: Within seconds you increas amino acid entry and over the course of minutes you increase protein synthesis.
Regulation of Insulin Secretion: is by plasma glucose which is increase and causes insulin release for 1 hour.
Sugar rapidly increases plasma glucose and causes increase in insulin. There is hyperglycemia.
Starch slowly increases plasma glucose and insulin there is no hypoglycemia.
Glucagon: Does the opposite of insulin. It decreases plasma glucose which causes glucagon release and glucose increases plasma glucose.
Diabetes Mellitus: Is characterized by the presences of glucose in urine. There are two types: Type 1: 10% is autoimmune attack on B cells of pancreas and Type 2: 90% due to obesity and age-down regulate the number of insulin receptor.
Hyperglycemia: High plasma glucose. Increase plasma osmolarity which exceeds the transport maximum for glucose in kidneys.
Dehydration: Increase in glucose excretion causes an increase in water excretion. Water follows glucose osmotically.
Protein Metabolism: Amino Acids are used for energy and to make glucose in your liver. Negative protein balance leads to muscle wasting.
Fat Utilization: Use fats in most cells when glucose is not present. Increase fat use in body leads to increase in plasma fatty acids and cholesterol which leads to atherosclerosis and a decreaes in blood flow.
Acidosis: You use 2 carbon segments each time for energy and are left with 4c remnants which are ketoacids which produce acidosis and a decrease in neural function in the CNS which leads to coma.
Coma: Occurs b/c of acidosis, dehydration, and hyperosmolarity.
Type 1 Diabetes Mellitus: Juvenille diabetes-the most prominent onset in early teens but can occur at other ages.
Type 2 Diabetes Mellitus: Occurs b/c the loss of insulin receptors due to excess caloric intake. A prolonged increase in insulin causes down regulation of insulin receptors which causes lots of insulin and no glucose entry.
Obesity: Type 2 diabetes occurs under 40 years old has the same symptoms as type 1.
Age: Type 2 diabetes occurs in the elderly. They lose insulin receptors but the reason why is unknown.
Insulin injections are sometimes used to maximize the available receptors.
Muscle Effects: Taking heavy loads will disrupt your muscle filaments and causes an increase in free myosin leads to hypertrophy and more filaments.
Carbohydrate Loading: Exercise decreases glycogen in muscle and enzymes will replace the glycogen when at rest.
Cardiovascular Effects: Estrogen increases cardiovascular health.
Increase in cardio disease in women after menopause.
Decrease in HDL and increase in vascular reactivity and increase in BP.
Muscle Blood Flow: this will increase depending on the kind of exercise.
Cardiac Changes: the thought of exercise with decrease parasympathetic activity and increase your HR.
Isometric exercise (try to lift very heavy weights) you get a huge increase in systolic pressure and increase in diastolic pressure.
Isotonic exercise causes an increase in systolic and diastolic pressure.
Training: increases stroke volume and decreases HR, increases extraction of oxygen from blood by muscle, increases mitochondrial oxygen use when you're fit.
Effects on Pathology: Isotonic or rhythmic exercise is better than isometric for health. It produces fewer and less severe heart attacks. There's more blood flow to the heart and increase in heart attack risk 30 mins after heavy exercise by sedentary people.
Heat Disspation: Lose heat through skin and lungs when you exercise
Skin Blood Flow: There is an icrease in dermal heat gradient and in heat transfer thru the skin by convection and radiation.
Sweat: Convert liquid water to vapor, exercise will decrease sodium content of sweat so it's easier to vaporize.
Respiratory Effects from Exercise: increase in delivery of oxygen to the blood, increase in removal of carbon dioxide, and increase in heat loss.
Changes in Ventilation: When exercising you increase oxygen delivery so you must have more oxygen transfer at alveoli into the blood.
Oxygen Debt: When exercising you increase lactate and most is remade into glucose the rest goes to pyruvate then to mitochondria and is used to make ATP to use oxygen.
Fatigue: The sensation of fatigue is dyspnea or difficulty in breathing, neural pain, acidosis or decrease in neural function, and an increase in temperature.
Connective Tissue: Collagen-strong linear protein polymer. An important component of cartilage-squishy material which cushions your joints.
Tendons connect bone to muscle.
Ligaments connect bone to bone.
Arthritis: Osteoartheritis is caused by repetitive motion with medium to heaby weights.
Cancer Incidence: In males: prostate>lung>colon>bladder
In females: breast>lung>colon>uterine
Death:
Males: lung-100 prostate 16 colon 45 pancreas 100
Females: lung 90 breast 22 colon 45 pancreas 100
Benign Cancer: Growth is localized and can be treated with surgery. Causes problems if a decrease in blood flow or space of adjacent healthy tissues.
Malignant Cancer: need surgery to remove primary tumor and treat it with radiation or chemo.
Diagnosis of Cancer: Need a biopsy- increase use of MRI
Genetics: A single cell will generate a tumor.
Surgery for Cancer: Remove the tumor with extra tissue and look for clear edges.
Radiation: Kill fast growing cells.
Side Effects: bone marrow decrease (RBC, WBC, and platelets) and small intestine mucosa and decrease absorption.
Chemotherapy: A poison with multiple targets such as DNA and a mitotic spindle.
Biologic Therapy: Shift balance of host and tumor toward the host. Increase cell activity, antibody activity and cytokines.
Mutation of Cancer: Usually need 5 to 10 mutations to become malignant. DNA alterations
Tumor Viruses: RNA virus is linked to luekemia.
DNA virus is linked to cervical cancer, liver, and some lymphomas.
Cell Biology: Uncontrolled mitosis, cell division. Cells are non functional and immature that are produced.
p53 Mutations: Controls normal mitosis and acts as a tumor suppressant.
Mutation leads to genomic instability and resistance to apetosis
Environmental Signals: Cytokines and paracrines can alter G proteins and other enzymes. These increase or decrease mitosis rate.
Loss of cell to cell connection and increases metastasis.
Transcription Factors: Alter tumor growth in positive or negative way. Targets of new cancer research.
Apoptosis Regulation: a decrease in tumor cells and its not eliminated.
Targets of new therapies for cancer.
Angiogenesis: Tumors get high blood flow and starve healthy tissues. Therapy is to decrease tumor blood flow to starve the tumor.
Prevention of Cancer: Prevent multiple mutations necessary to get cancer such as smoking, diet, and sun avoidance.
Smoking Cessation: nearly 500,000 premature deaths per year. Linked to lung, larynx, esophagus, bladder, and pancreatic cancers.
Smoking increases cadiovascular and colonary disease.
Diet: If you decrease fat intake you will decrease your risk for cancer.
Eat fiber to decrease risk for colon cancer.
Sun Avoidance: UV Rays can break DNA and cause mutations.
Chemoprevention: Try to decrease mutation risk in susceptible people. Tomoxifen decreases the risk of breast cancer in high risk women.
Chromosomes: 23 pairs, 22 are somatic
X and Y Chromosomes: X is large with many genes on it
Y is small with relatively few genes and has SRY gene which starts reproduction.
Gonads in Embryo: Testes and ovaries. In the 7th week of development the gonadal medulla develops into the testes and the cortex will regress. Develops into ovaries and the medulla will regress.
Puberty: Maturation of the reproductive system.
GnRH and Leptins: GnRH is Gonadotropin Releasing Hormones produced by the hypothalamus which travel to the anterior pituitary to release of FSH and LSH.
Leptins might be necessary for menarchy the onset of mensturation.
Menopause: 400 cycles in lifetime
7 million oo cytes at birth. 1/400 start to develop at each cycle and 1 cell is released at ovulation.
Hormone Replacement: Decrease menopause symptomes
Increase risk of Heart disease, stroke, breast cancer.
Pituitary Gonadotropins: Controlled by neg. feedback of testosterone, estrogen and progesterone.
FSH: Females: causes growth and development of ovarian follicles.
Males: causes development and maturation of sperm cells by activating sertolli cells.
LH: Females: responsible for ovulation, causes estrogen secretion and ovarian maturation
Males: causes testosterone secretion from the laydig cells.
Prolacin: Females: Responsible for milk secretion
Secretion will peak at parturition or child birth.
Testes: Seminiferous tubules are the site of sperm production
Sortoli cells assist sperm production
Laydig cells produce testosterone.
Spermatogenesis: Formation of sperm cells from spermatocytes
Sperm Formation: Spermatocyte mitosis one stays and one migrates to seminiferous tubule lumen.
Sertoli cells absorb most of spermatocyte cytoplasm.
Sperm Structure: Head-tip is a chromosome that contains digestive enzyme which will allow sperm penetration of the ovary.
Midpiece-mitochondria-ATO-Fructose
Tail-contains microtubules involved in propulsion into the ovary.
Temperature of scrotum: In cold testes ascend closer to body.
In warm testes will descend.
Undescended testicles are normally infertile.
Semen: a liquid that mixes with the sperm during emission.
Male with less than 20,000 sperm/ejaculate is infertile
Erection: Arteriolar dialation and venous compression result in engorgment.
Emission: The mixing of sperm with semen from the accessory organs. Controlled by sympathetic nerves.
Ejaculation: Requires skeletal muscle contractionActive delivery of sperm into the vagina.
Testosterone: steriod hormone that increases protein production and is released 1st before birth in utero. This allows development of male reproductive structures.
Testosterone Secretion: Is from the laydig cells in the testes. Released as it is made continuously.
98% us bound to protein in plasma. 2% is free and active
Secondary Sex Characteristics: Male hair pattern, penile/genitalia enlargment, thickening fo the vocal chords, increase in mental aquity, increase in sex drive, and increase in growth.
Anabolic Effects: Growth spurt the epiphyseal closure and increase in musculature and increase in kidney size.
Control of Testicular Function: Negative feedback to the anterior piruitary and the hypothalamus
Teste FSH: Increase in GnRH from the hypothalamus which causes the FSH release from the anterior pituitary.
FSH will activate sertoli cells to remodel sperm and release fructose.
Teste LH: Increase GnRH causes LH Testosterone release from laydig cells, testosterone inhibits LH and GnRH
Teste Inhibin: It inhibits FSH released.
Menstrual Cycle: Ovum is prepared for release from the follicle. Uterus is prepard for implantation of the embryo.
Ovarian Cycle: Ovum growth, release, and follicular changes.
Follicular Phase: Dominated by FSH release. Multiple follicles will enlarge and form the antrum. One follicle will outgrow the others. The otehrs regress or die out called atresia.
Estrogen released from granulosa and fecal cells surround ovum.
Ovulation: LH surge from anterior pituitary causes the antrum to rupture. Ovum is released into the abdomen. The fimbria will sweep the ovum into the oviduck and takes 5 days to migrate to the uterus.
Luteal Phase: Corpus Luteum forms from cells left in the follicle. It will secrete progesterone and estrogen. Progesterone prepares the uterus for embryp implantation.
Uterine Cycle: It's changes will supply implanted embryp with energy until the placenta forms.
Proliferative Phase: Estrogen dominated, repair of the uterine surface after menstration. Increase in uterine lining thickness and increase in blood supply.
Secretory Phase: Great increase in vascularization and thickness. Progesterone dominates increased growth. It also decreases uterine contractions, uters secretes glycogen.
Menstruation: Sloughing off of uterine lining if there's no implantaino. If there in implantation, there will be hormonal changes that signal that pregnancy has occured.
Cervix: Opening b/w the vagina and the uterus, usually blocked with mucus. Estrogen thin mucus at ovulation. Pregnancy increases mucus production.
Indicators of Ovulation: Pregnancy -increase in body temperature, thinning of mucus.
Ovarian Hormones: Estrogen and progesterone have multiple effects.
Estrogens: Formed from testosterone and androstenedione.
Effects of Estrogens: Increase follicle development and inhibit FSH.
Increase ciliary motion in the oviducts and increases uterin size and causes the LH surge that produces ovulation. Increase in neural plasticity.
Progesterone: Increase size and secretions of the uters and cervical mucus and inhibits LH. It decreases contractions of the uterus during pregnancy and increases heat production.
Relaxin: Increases digestion of connective tissue in the cervix so the baby can squeeze through. It softens the pelvis for delivery.
Control of Ovarian Funcion: Negative feedback to the anterior pituitary and hypothalamus. GnRH
Pituitary Controls in the Follicular Phase: Increases estrogen release and decreases FSH release. FSH stimulates granulosa cells and LH stimulates both granulosa and fecal cells.
Pituitary Controls in the Luteal Phase: Increases in progesterone that inhibits GnRH and FSH and LH release.
Embryo Development: Cells surround the embryo and invade the uterine wall and become the placenta. Folice acid is important b/c it helps mitosis occur and prevents birth defects.
Corpus Luteum: hCG is released from the uterus and maintains the CL. Progesterone stays high and the uterus stays quiet.
Placental Hormones: Function to maintain pregnancy.
Placental Hormones: hCG: Maintains Corpus Luteum and is used for pregnancy tests.
Placental Hormones: Progesterone: Is released by placenta in large amounts within weeks after implantation. A decrease in progesterone release starts uterine contractions at parturition or child birth.
Placental Hormones: Relaxin: Softens the pelvis and increases digestion of connective tissue in the cervix.
Placental Functions: Supplies steroids for fetal cortisol. It's involved in the exchange of gases, nutrients, and waste products. There's increase in maternal respiration and renal output.
Parturition: Exact initiator is unknown. Increase in estrogen leads to an increase in uterine excitability leads to an increase in the number of gap junctions and an increase in the number of oxytocin receptors.
Fertilization: Cepacitation is the increase in sperm motility, which occurs in the female reproductive tract. Sperm break through granulosa cells, fecal cels, and zoma pollucida (a gell that surrounds the ovum where sperm enters) Membrane of ovum repells other sperm.
Progesterone in Parturition: Decrease in progesterone which allows urerine contractions.
Oxytocin in Parturition: Levels are high in the blood throughout pregnancy. Increase number of uterine oxytocin receptors when near term and increase uterine contractions and cervical dialation.
Labor: Start uterine contractions increase pressure and increase prostaglandin release and increase in ocytocin release which increases contractions.
Very strong contractions lead to spiral reflexes which increase abdominal contractions-delivery head first the body then the placenta.
Lactation: Milk production for newborn infant.
Breast Development: Estrogen increases mammory duct size. Progesterone increases mamory lobule size and prolactin completes structural changes.
Milk Secretion: 1st 2 weeks is colostrum which contains nutriets, lactoferrin and antibiotic, and antibodies.
Milk Ejection: Sucking will increase oxytocin release. Oxytocin will contract mammory lobules and contract the uterus. Milk at the nipple is not sucked out. It is secreted and lapped up.
GnRH Effects: Prolactin (PRL) decreases GnRH release and decreases FSH and LH and there is no ovulation during breast feeding.
Glucocorticoid Effects: Metabolism: Increase protein metabolism leads to free amino acids for protein repair in damaged areas. Cortisol causes increase in plasma glucose and increase plasma fatty acides. Liverates energy for repair.
Glucocorticoid Effects: Permissive Actions: Cortisol assists glucagon in increase plasma glucose and it increases activity of calcium echolomines-Epi and N.E. Increase vasoconstriction and Bronchoconstriction.
Glucocorticoid Effects: Stress: Increase in ACTH release and cortisol release.
Short Term increases energy availability and amino acids and catecholamine and cortisol to the breakdown of protein which causes pain (slow).
Glucocorticoid Effects: Anti-Inflammatory Effects: Only at high glucocorticoid levels. Decrease swelling and histamine to work in the CNS. Cortisol will block the immune system. Apoptosis of WBC's must use antibiotics to block infection. Not for routine use.
Mineralcorticoids: Aldosterone increase. Sodium reabsorption in the kindney.
Adrenal Androgens: DHRA is swamped by effects of testosterone.
DHEA and Androstenedione
Adrenal Androgens: DHEA: It causes the growth spurt that occurs at puberty Estrogen caps the growth spurt in females.
Adrenal Androgens: Androstenedione: No effects, 1 reaction into testosterone in females is converted into estradial.

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