text:
Available structures
Ortholog search: PDBe RCSB
1BWX, 1ET1, 1FVY, 1HPH, 1HPY, 1HTH, 1ZWA, 1ZWB, 1ZWD, 1ZWE, 1ZWF, 1ZWG, 2L1X, 3C4M
PTH, PTH1, parathyroid hormone, Parathyroid hormone
External IDs
MGI: 97799 HomoloGene: 266 GeneCards: PTH
Gene location (Human)
Chr.
Chromosome 11 (human)[1]
11p15.3
13,492,054 bp[1]
Gene location (Mouse)
Chromosome 7 (mouse)[2]
7 F1|7 59.19 cM
113,385,580 bp[2]
Molecular function
• transcription factor activity, RNA polymerase II distal enhancer sequence-specific binding
• hormone activity
• parathyroid hormone receptor binding
• type 1 parathyroid hormone receptor binding
• protein N-terminus binding
• receptor ligand activity
• peptide hormone receptor binding
• RNA polymerase II transcription factor activity, sequence-specific DNA binding
• protein binding
Cellular component
• intracellular
• cell
• extracellular region
• extracellular space
Biological process
• positive regulation of signal transduction
• positive regulation of cell proliferation in bone marrow
• positive regulation of osteoclast proliferation
• response to drug
• response to fibroblast growth factor
• hormone-mediated apoptotic signaling pathway
• cAMP metabolic process
• response to ethanol
• response to parathyroid hormone
• skeletal system development
• positive regulation of ossification
• response to lead ion
• response to nutrient levels
• G-protein coupled receptor signaling pathway
• response to vitamin D
• negative regulation of apoptotic process in bone marrow
• negative regulation of transcription from RNA polymerase II promoter
• cellular macromolecule biosynthetic process
• cellular calcium ion homeostasis
• homeostasis of number of cells within a tissue
• response to cadmium ion
• Rho protein signal transduction
• positive regulation of glucose import
• positive regulation of glycogen biosynthetic process
• bone resorption
• positive regulation of bone mineralization
• regulation of gene expression
• positive regulation of transcription from RNA polymerase II promoter
• cell-cell signaling
• activation of phospholipase C activity
• negative regulation of chondrocyte differentiation
• positive regulation of inositol phosphate biosynthetic process
• negative regulation of bone mineralization involved in bone maturation
• regulation of receptor activity
• adenylate cyclase-activating G-protein coupled receptor signaling pathway
• positive regulation of cAMP biosynthetic process
• calcium ion transport
• magnesium ion homeostasis
• bone mineralization
• phosphate ion homeostasis
• calcium ion homeostasis
• negative regulation of calcium ion transport
Sources:Amigo / QuickGO
Q9Z0L6
RefSeq (protein)
Location (UCSC)
Chr 11: 13.49 – 13.5 Mb Chr 7: 113.39 – 113.39 Mb
PubMed search
View/Edit Human View/Edit Mouse
Parathyroid hormone (PTH), also called parathormone or parathyrin, is a hormone secreted by the parathyroid glands that regulates the serum calcium through its effects on bone, kidney, and intestine.[5]
PTH influences bone remodeling, which is an ongoing process in which bone tissue is alternately resorbed and rebuilt over time. PTH is secreted in response to low blood serum calcium (Ca2+) levels. PTH indirectly stimulates osteoclast activity within the bone matrix (osteon), in an effort to release more ionic calcium (Ca2+) into the blood to elevate a low serum calcium level. The bones act as a (metaphorical) "bank of calcium" from which the body can make "withdrawals" as needed to keep the amount of calcium in the blood at appropriate levels despite the ever-present challenges of metabolism, stress, and nutritional variations. PTH is "a key that unlocks the bank vault" to remove the calcium.
PTH is secreted primarily by the chief cells of the parathyroid glands. It is a polypeptide containing 84 amino acids, which is a prohormone. It has a molecular mass around 9500 Da.[6] Its action is opposed by the hormone calcitonin.
There are two types of PTH receptors. Parathyroid hormone 1 receptors, activated by the 34 N-terminal amino acids of PTH, are present at high levels on the cells of bone and kidney. Parathyroid hormone 2 receptors are present at high levels on the cells of central nervous system, pancreas, testes, and placenta.[7] The half-life of PTH is about 4 minutes.[8]
Disorders that yield too little or too much PTH, such as hypoparathyroidism, hyperparathyroidism, and paraneoplastic syndromes can cause bone disease, hypocalcaemia, and hypercalcaemia.
1 Structure
2.1 Regulation of serum calcium
2.2 Regulation of serum phosphate
2.3 Vitamin D synthesis
2.3.1 Interactive pathway map
3 Regulation of PTH secretion
3.1 Stimulators
3.2 Inhibitors
4 Disorders
5 Measurement
5.1 Interpretive Guide
6 Model organisms
8 Footnote
Structure[edit]
hPTH-(1-34) crystallizes as a slightly bent, long, helical dimer. The extended helical conformation of hPTH-(1-34) is the likely bioactive conformation.[9] The N-terminal fragment 1-34 of parathyroid hormone (PTH) has been crystallized and the structure has been refined to 0.9 Å resolution.
helical dimer structure of hPTH-(1-34)[10]
Function[edit]
Regulation of serum calcium[edit]
The Parathyroid Gland releases PTH which keeps Calcium in homeostasis.
Main article: Calcium metabolism
A diagrammatic representation of the movements of calcium ions into and out of the blood plasma (the central square labeled PLASMA Ca2+) in an adult in calcium balance: The widths of the red arrows indicating movement into and out of the plasma are roughly in proportion to the daily amounts of calcium moved in the indicated directions. The size of the central square in not in proportion to the size of the diagrammatic bone, which represents the calcium present in the skeleton, and contains about 25,000 mmol (or 1 kg) of calcium compared to the 9 mmol (360 mg) dissolved in the blood plasma. The differently colored narrow arrows indicate where the specified hormones act, and their effects ("+" means stimulates; "-" means inhibits) when their plasma levels are high. PTH is parathyroid hormone, 1,25 OH VIT D3 is calcitriol or 1,25 dihydroxyvitamin D3, and CALCITONIN is a hormone secreted by the thyroid gland when the plasma ionized calcium level is high or rising. The diagram does not show the extremely small amounts of calcium that move into and out of the cells of the body, nor does it indicate the calcium that is bound to the extracellular proteins (in particular the plasma proteins) or to plasma phosphate.[11][12][13][14][15]
Parathyroid hormone regulates serum calcium through its effects on bone, kidney, and the intestine:[5]
In bone, PTH enhances the release of calcium from the large reservoir contained in the bones.[16] Bone resorption is the normal destruction of bone by osteoclasts, which are indirectly stimulated by PTH. Stimulation is indirect since osteoclasts do not have a receptor for PTH; rather, PTH binds to osteoblasts, the cells responsible for creating bone. Binding stimulates osteoblasts to increase their expression of RANKL and inhibits their secretion of Osteoprotegerin (OPG). Free OPG competitively binds to RANKL as a decoy receptor, preventing RANKL from interacting with RANK, a receptor for RANKL. The binding of RANKL to RANK (facilitated by the decreased amount of OPG available for binding the excess RANKL) stimulates these osteoclast precursors to fuse, forming new osteoclasts, which ultimately enhances bone resorption. Another mechanism to regulate this pathways as PTH does is by estrogen. Estrogen suppresses T cell TNF production by regulating T cell differentiation and activity in the bone marrow, thymus, and peripheral lymphoid organs. In the bone marrow, estrogen downregulates the proliferation of hematopoietic stem cells through an IL-7 dependent mechanism.[17]
In the kidney, around 250 mmol of calcium ions are filtered into the glomerular filtrate per day. Most of this (245 mmol/d) is reabsorbed from the tubular fluid, leaving about 5 mmol/d to be excreted in the urine. This reabsorption occurs throughout the tubule (most, 60-70%, of it in the proximal tubule), except in the thin segment of the loop of Henle.[11] Circulating parathyroid hormone only influences the reabsorption that occurs in the distal tubules and the renal collecting ducts[11] (but see Footnote[nb 1]). A more important effect of PTH on the kidney is, however, its inhibition of the reabsorption of phosphate (HPO42−) from the tubular fluid, resulting in a decrease in the plasma phosphate concentration. Phosphate ions form water-insoluble salts with calcium. Thus, a decrease in the phosphate concentration of the blood plasma (for a given total calcium concentration) increases the amount of calcium that is ionized.[20][21] A third important effect of PTH on the kidney is its stimulation of the conversion of 25-hydroxy vitamin D into 1,25-dihydroxy vitamin D (calcitriol), which is released into the circulation. This latter form of vitamin D is the active hormone which stimulates calcium uptake from the intestine.[22]
Via the kidney, PTH enhances the absorption of calcium in the intestine by increasing the production of activated vitamin D. Vitamin D activation occurs in the kidney. PTH up-regulates 25-hydroxyvitamin D3 1-alpha-hydroxylase, the enzyme responsible for 1-alpha hydroxylation of 25-hydroxy vitamin D, converting vitamin D to its active form (1,25-dihydroxy vitamin D). This activated form of vitamin D increases the absorption of calcium (as Ca2+ ions) by the intestine via calbindin.
PTH was one of the first hormones to be shown to use the G-protein, adenylyl cyclase second messenger system.
Regulation of serum phosphate[edit]
PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney,[23] which means more phosphate is excreted through the urine.
However, PTH enhances the uptake of phosphate from the intestine and bones into the blood. In the bone, slightly more calcium than phosphate is released from the breakdown of bone. In the intestines, absorption of both calcium and phosphate is mediated by an increase in activated vitamin D. The absorption of phosphate is not as dependent on vitamin D as is that of calcium. The end result of PTH release is a small net drop in the serum concentration of phosphate.
Vitamin D synthesis[edit]
PTH upregulates the activity of 1-α-hydroxylase enzyme, which converts 25-hydroxycholecalciferol, the major circulating form of inactive vitamin D, into 1,25-dihydroxycholecalciferol, the active form of vitamin D, in the kidney.
Interactive pathway map[edit]
Click on genes, proteins and metabolites below to link to respective articles. [§ 1]
|{{{bSize}}}px|alt=Vitamin D Synthesis Pathway (view / edit)]]
Vitamin D Synthesis Pathway (view / edit)
^ The interactive pathway map can be edited at WikiPathways: "VitaminDSynthesis_WP1531".
Regulation of PTH secretion[edit]
Secretion of parathyroid hormone is determined chiefly by serum ionized calcium concentration through negative feedback. Parathyroid cells express calcium-sensing receptors on the cell surface. PTH is secreted when [Ca2+] is decreased (calcitonin is secreted when serum calcium levels are elevated). The G-protein-coupled calcium receptors bind extracellular calcium and may be found on the surface on a wide variety of cells distributed in the brain, heart, skin, stomach, C cells, and other tissues. In the parathyroid gland, high concentrations of extracellular calcium result in activation of the Gq G-protein coupled cascade through the action of phospholipase C. This hydrolyzes phosphatidylinositol 4,5-bisphosphate (PIP2) to liberate intracellular messengers IP3 and diacylglycerol (DAG). Ultimately, these two messengers result in a release of calcium from intracellular stores into the cytoplasmic space. Hence a high extracellular calcium concentration leads to an increase in the cytoplasmic calcium concentration. In contrast to the mechanism that most secretory cells use, this high cytoplasmic calcium concentration inhibits the fusion of vesicles containing granules of preformed PTH with the membrane of the parathyroid cell, and thus inhibits release of PTH.
In the parathyroids, magnesium serves this role in stimulus-secretion coupling. A mild decrease in serum magnesium levels stimulates the resorptive activity PTH has on the kidneys. Severe hypomagnesemia inhibits PTH secretion and also causes resistance to PTH, leading to a form of hypoparathyroidism that is reversible.[24]
Stimulators[edit]
Decreased serum [Ca2+].
Mild decreases in serum [Mg2+].
An increase in serum phosphate (increased phosphate causes it to complex with serum calcium, forming calcium phosphate, which reduces stimulation of Ca-sensitive receptors (CaSr) that do not sense calcium phosphate, triggering an increase in PTH).
Inhibitors[edit]
Increased serum [Ca2+].
Severe decreases in serum [Mg2+], which also produces symptoms of hypoparathyroidism (such as hypocalcemia).[25]
Disorders[edit]
Hyperparathyroidism, the presence of excessive amounts of parathyroid hormone in the blood, occurs in two very distinct sets of circumstances. Primary hyperparathyroidism is due to autonomous, abnormal hypersecretion of PTH from the parathyroid gland, while secondary hyperparathyroidism is an appropriately high PTH level seen as a physiological response to hypocalcaemia. A low level of PTH in the blood is known as hypoparathyroidism and is most commonly due to damage to or removal of parathyroid glands during thyroid surgery.
There are a number of rare but well-described genetic conditions affecting parathyroid hormone metabolism, including pseudohypoparathyroidism, familial hypocalciuric hypercalcaemia, and autosomal dominant hypercalciuric hypocalcemia. Of note, PTH is unchanged in pseudopseudohypoparathyroidism. In osteoporotic women, administration of an exogenous parathyroid hormone analogue (teriparatide, by daily injection) superimposed on estrogen therapy produced increases in bone mass and reduced vertebral and nonvertebral fractures by 45 to 65%.[26]
Measurement[edit]
PTH can be measured in the blood in several different forms: intact PTH; N-terminal PTH; mid-molecule PTH, and C-terminal PTH, and different tests are used in different clinical situations.
The average PTH level is 8–51 pg/mL.[27] Normal total plasma calcium level ranges from 8.5 to 10.2 mg/dL (2.12 mmol/L to 2.55 mmol/L).[28]
Interpretive Guide[edit]
The intact PTH and calcium normal ranges are different for age; calcium is also different for sex. [29][30]
Intact PTH
Normal Parathyroid Normal Normal
Hypoparathyroidism Low or Low Normal [note 1] Low
- Primary High or Normal [note 1] High
- Secondary High Normal or Low
- Tertiary [note 2] High High
Non-Parathyroid Hypercalcaemia Low or Low Normal [note 1] High
^ a b c Low Normal or Normal only for Quest Lab, not LabCorp
^ Both primary and tertiary hyperparathyroidism may have high PTH and high calcium. Tertiary is differentiated from primary hyperparathyroidism by a history of chronic kidney failure and secondary hyperparathyroidism.
Model organisms[edit]
Model organisms have been used in the study of PTH function. A conditional knockout mouse line called Pthtm1a(EUCOMM)Wtsi was generated at the Wellcome Trust Sanger Institute.[31] Male and female animals underwent a standardized phenotypic screen[32] to determine the effects of deletion.[33][34][35][36] Additional screens performed: - In-depth immunological phenotyping[37]
Pth knockout mouse phenotype
All data available at.[32][37]
Insulin Normal
Homozygous viability at P14 Normal
Homozygous Fertility Normal
Body weight Normal
Neurological assessment Normal
Grip strength Normal
Dysmorphology Normal
Indirect calorimetry Normal
Glucose tolerance test Normal
Auditory brainstem response Normal
DEXA Normal
Radiography Normal
Eye morphology Normal
Clinical chemistry Abnormal
Haematology 16 Weeks Normal
Peripheral blood leukocytes 16 Weeks Normal
Salmonella infection Normal
Disorders of calcium metabolism
Parathyroid hormone family
Parathyroid hormone-related protein
Footnote[edit]
^ This reduction in the rate of calcium excretion via the urine is a minor effect of high parathyroid hormone levels in the blood. The main determinant of the amount of calcium excreted into the urine per day is the plasma ionized calcium concentration itself. The plasma parathyroid hormone (PTH) concentration only increases or decreases the amount of calcium excreted at any specified plasma ionized calcium concentration. Thus, in primary hyperparathyroidism, the quantity of calcium excreted in the urine per day is increased despite the high levels of PTH in the blood, because hyperparathyroidism results in hypercalcemia, which increases the urinary calcium concentration (hypercalcuria) despite the moderately increased rate of calcium reabsorption from the renal tubular fluid caused by PTH's direct effect on those tubules. Renal stones are, therefore, often a first indication of hyperparathyroidism, especially since the hypercalcuria is accompanied by an increase in urinary phosphate excretion (a direct result of the high plasma PTH levels). Together the calcium and phosphate tend to precipitate out as water-insoluble salts, which readily form solid "stones".[11][18][19]
^ a b c GRCh38: Ensembl release 89: ENSG00000152266 - Ensembl, May 2017
^ a b c GRCm38: Ensembl release 89: ENSMUSG00000059077 - Ensembl, May 2017
^ "Human PubMed Reference:".
^ "Mouse PubMed Reference:".
^ a b Coetzee M, Kruger MC (May 2004). "Osteoprotegerin-receptor activator of nuclear factor-kappaB ligand ratio: a new approach to osteoporosis treatment?". Southern Medical Journal. 97 (5): 506–11. doi:10.1097/00007611-200405000-00018. PMID 15180028.
^ Brewer HB, Fairwell T, Ronan R, Sizemore GW, Arnaud CD (1972). "Human parathyroid hormone: amino-acid sequence of the amino-terminal residues 1-34". Proceedings of the National Academy of Sciences of the United States of America. 69 (12): 3585–8. doi:10.1073/pnas.69.12.3585. PMC 389826. PMID 4509319.
^ Essentials of Human Physiology by Thomas M. Nosek. Section 5/5ch6/s5ch6_11.
^ Bieglmayer C, Prager G, Niederle B (Oct 2002). "Kinetic analyses of parathyroid hormone clearance as measured by three rapid immunoassays during parathyroidectomy". Clinical Chemistry. 48 (10): 1731–8. PMID 12324490.
^ Jin L, Briggs SL, Chandrasekhar S, Chirgadze NY, Clawson DK, Schevitz RW, Smiley DL, Tashjian AH, Zhang F (Sep 2000). "Crystal structure of human parathyroid hormone 1-34 at 0.9-A resolution". The Journal of Biological Chemistry. 275 (35): 27238–44. doi:10.1074/jbc.M001134200. PMID 10837469.
^ PDB: 1ETE; Savvides SN, Boone T, Andrew Karplus P (Jun 2000). "Flt3 ligand structure and unexpected commonalities of helical bundles and cystine knots". Nature Structural Biology. 7 (6): 486–91. doi:10.1038/75896. PMID 10881197.
^ a b c d Blaine J, Chonchol M, Levi M (2015). "Renal control of calcium, phosphate, and magnesium homeostasis". Clinical Journal of the American Society of Nephrology. 10 (7): 1257–72. doi:10.2215/CJN.09750913. PMC 4491294. PMID 25287933.
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^ Guyton A (1976). ''Medical Physiology''. p.1062; New York, Saunders and Co.
^ Barrett KE, Barman SM, Boitano S, Brooks H. "Chapter 23. Hormonal Control of Calcium & Phosphate Metabolism & the Physiology of Bone". In Barrett KE, Barman SM, Boitano S, Brooks H (eds.). Ganong's Review of Medical Physiology (23e ed.).
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^ "Symptoms of Hyperparathyroidism and Symptoms of Parathyroid Disease". Parathyroid.com. Norman Parathyroid Center. Retrieved 2015-12-30.
^ Haldimann B, Vogt K (1983). "[Hyperphosphatemia and tetany following phosphate enema]". Schweizerische Medizinische Wochenschrift (in French). 113 (35): 1231–3. PMID 6623048.
^ Sutters M, Gaboury CL, Bennett WM (1996). "Severe hyperphosphatemia and hypocalcemia: a dilemma in patient management". Journal of the American Society of Nephrology. 7 (10): 2056–61. PMID 8915965.
^ Stryer L (1995). Biochemistry (Fourth ed.). New York: W.H. Freeman and Company. p. 707. ISBN 978-0-7167-2009-6.
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^ Agus ZS (Jul 1999). "Hypomagnesemia". Journal of the American Society of Nephrology. 10 (7): 1616–22. PMID 10405219.
^ Costanzo, Linda S. (2007). BRS Physiology. Lippincott, Williams, & Wilkins. p. 260. ISBN 978-0-7817-7311-9.
^ Neer RM, Arnaud CD, Zanchetta JR, Prince R, Gaich GA, Reginster JY, Hodsman AB, Eriksen EF, Ish-Shalom S, Genant HK, Wang O, Mitlak BH (May 2001). "Effect of parathyroid hormone (1-34) on fractures and bone mineral density in postmenopausal women with osteoporosis". The New England Journal of Medicine. 344 (19): 1434–41. doi:10.1056/NEJM200105103441904. PMID 11346808.
^ Longo DL, Fauci A, Kasper D, Hauser S, Jameson J, Loscalzo J (2012). Harrison's Principles of Internal Medicine (18th ed.). New York: McGraw-Hill. p. 3594. ISBN 978-0-07-174889-6.
^ Zieve D. "MedlinePlus Medical Encyclopedia: Serum calcium". National Library of Medicine, National Institutes of Health. Retrieved 2009-02-01.
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^ Parathyroid Hormone (PTH) Plus Calcium. LabCorp. Accessed 2019-07-02.
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Media related to Parathyroid hormone at Wikimedia Commons
Parathyroid hormone: analyte monograph - the Association for Clinical Biochemistry and Laboratory Medicine
PDB gallery
1bwx: THE SOLUTION STRUCTURE OF HUMAN PARATHYROID HORMONE FRAGMENT 1-39, NMR, 10 STRUCTURES
1et1: CRYSTAL STRUCTURE OF HUMAN PARATHYROID HORMONE 1-34 AT 0.9 A RESOLUTION
1fvy: SOLUTION STRUCTURE OF THE OSTEOGENIC 1-31 FRAGMENT OF THE HUMAN PARATHYROID HORMONE
1hph: STRUCTURE OF HUMAN PARATHYROID HORMONE 1-37 IN SOLUTION
1hpy: THE SOLUTION STRUCTURE OF HUMAN PARATHYROID HORMONE FRAGMENT 1-34 IN 20% TRIFLUORETHANOL, NMR, 10 STRUCTURES
1zwa: STRUCTURE OF HUMAN PARATHYROID HORMONE FRAGMENT 1-34, NMR, 10 STRUCTURES
1zwb: STRUCTURE OF HUMAN PARATHYROID HORMONE FRAGMENT 2-37, NMR, 10 STRUCTURES
1zwc: STRUCTURE OF BOVINE PARATHYROID HORMONE FRAGMENT 1-37, NMR, 10 STRUCTURES
1zwd: STRUCTURE OF HUMAN PARATHYROID HORMONE FRAGMENT 3-37, NMR, 10 STRUCTURES
1zwe: STRUCTURE OF HUMAN PARATHYROID HORMONE FRAGMENT 4-37, NMR, 10 STRUCTURES
1zwf: STRUCTURE OF N-TERMINAL ACETYLATED HUMAN PARATHYROID HORMONE, NMR, 10 STRUCTURES
1zwg: SUCCINYL HUMAN PARATHYROID HORMONE 4-37, NMR, 10 STRUCTURES
Hypothalamic-
GnRH
GHRH
Somatostatin (GHIH)
Posterior pituitary
Anterior pituitary
POMC
Endorphins
Lipotropin
Adrenal axis
Aldosterone
DHEA-S
Adrenal medulla
Epinephrine
Norepinephrine
Thyroid hormones
Thyroid axis
Gonadal axis
Inhibin
Activin
Relaxin
GnSAF
Amylin
Somatostatin
Pancreatic polypeptide
Pineal gland
N,N-Dimethyltryptamine
5-Methoxy-N,N-dimethyltryptamine
Thymosins
Thymosin α1
Beta thymosins
Thymopoietin
Thymulin
Ghrelin
Incretins
GLP-1
Motilin
Enteroglucagon
Peptide YY
Liver/other
Insulin-like growth factor
Osteocalcin
Renin
Prostaglandin
Natriuretic peptide
Signaling peptide/protein receptor modulators
AdipoR1
Agonists: Peptide: Adiponectin
ADP-355
ADP-399; Non-peptide: AdipoRon
(–)-Arctigenin
Arctiin
Gramine
Matairesinol
Antagonists: Peptide: ADP-400
Deoxyschizandrin
Parthenolide
Syringing
Taxifoliol
Angiotensin
See here instead.
Bradykinin
Agonists: Bradykinin
Kallidin
Antagonists: FR-173657
Icatibant
LF22-0542
CGRP
Agonists: Amylin
Pramlintide
Antagonists: Atogepant
BI 44370 TA
CGRP (8-37)
Olcegepant
Rimegepant
SB-268262
Telcagepant
Ubrogepant
Antibodies: Eptinezumab
Erenumab
Fremanezumab
Galcanezumab
Agonists: Cholecystokinin
Antagonists: Amiglumide
Asperlicin
Devazepide
Dexloxiglumide
Lintitript
Lorglumide
Loxiglumide
Pranazepide
Proglumide
Tarazepide
Tomoglumide
Pentagastrin (CCK-5)
Antagonists: Ceclazepide
CI-988 (PD-134308)
Itriglumide
L-365,360
Netazepide
Spiroglumide
Antagonists: Nastorazepide
Agonists: Cortagine
Corticorelin
Corticotropin releasing hormone
Sauvagine
Stressin I
Urocortin
Antagonists: Antalarmin
Astressin-B
CP-154,526
Emicerfont
Hypericin
LWH-234
NBI-27914
Pexacerfont
Verucerfont
Agonists: Corticorelin
Antagonists: Astressin-B
Endothelin
Agonists: Endothelin 1
Endothelin 2
IRL-1620
Sarafotoxin
Antagonists: A-192621
ACT-132577
Ambrisentan
Aprocitentan
Atrasentan
Avosentan
Bosentan
BQ-123
Clazosentan
Darusentan
Edonentan
Enrasentan
Fandosentan
Feloprentan
Macitentan
Nebentan
Sitaxentan
Sparsentan
Tezosentan
Zibotentan
Agonists: Galanin
Galanin (1-15)
Galanin-like peptide
Galmic
Galnon
NAX 810-2
Antagonists: C7
Dithiepine-1,1,4,4-tetroxide
Galantide (M15)
SCH-202596
GalR3ant
SNAP-37889
SNAP-398299
Ghrelin/GHS
Agonists: Albiglutide
Beinaglutide
Dulaglutide
Efpeglenatide
Exenatide
Langlenatide
Lixisenatide
Oxyntomodulin
Pegapamodutide
Semaglutide
Taspoglutide
Agonists: Apraglutide
Elsiglutide
Glepaglutide
Teduglutide
Propeptides: Preproglucagon
Proglucagon
Agonists: Dasiglucagon
Antagonists: Adomeglivant
LGD-6972
Gonadotropin
Agonists: Chaetochromin (4548-G05)
Insulin-like growth factor 1
Insulin aspart
Insulin degludec
Insulin detemir
Insulin glargine
Insulin lispro
Mecasermin
Mecasermin rinfabate
Antagonists: BMS-754807
Kinase inhibitors: Linsitinib
Antibodies: Xentuzumab (against IGF-1 and IGF-2)
Kisspeptin
Agonists: Kisspeptin
Kisspeptin-10
Antagonists: Kisspeptin-234
Agonists: Leptin
Metreleptin
Agonists: Melanin concentrating hormone
Antagonists: ATC-0065
ATC-0175
GW-803430
NGD-4715
SNAP-7941
Melanocortin
Neuropeptide FF
Agonists: Neuropeptide AF
Neuropeptide SF (RFRP-1)
Neuropeptide VF (RFRP-3)
Antagonists: BIBP-3226
Neuropeptide S
Agonists: Neuropeptide S
Antagonists: ML-154
SHA-68
Agonists: Neuropeptide Y
Antagonists: BIBO-3304
BIBP-3226
BVD-10
GR-231118
PD-160170
Agonists: 2-Thiouridine 5'-triphosphate
Neuropeptide Y (13-36)
Peptide YY (3-36)
Antagonists: BIIE-0246
JNJ-5207787
Agonists: GR-231118
Antagonists: UR-AK49
Agonists: BWX-46
Antagonists: CGP-71683
FMS-586
Lu AA-33810
NTNCB
Velneperit (S-2367)
Neurotensin
Agonists: Neurotensin
Neuromedin N
Antagonists: Meclinertant
SR-142948
Antagonists: Levocabastine
Orexin
Agonists: Orexin (A, B)
Antagonists: ACT-335827
Almorexant
Filorexant
Lemborexant
Nemorexant
RTIOX-276
Suvorexant
TCS-1102
EMPA
JNJ-10397049
Seltorexant
TCS-OX2-29
Agonists: Growth hormone
Human placental lactogen
Placental growth hormone (growth hormone variant)
S179D-hPRL
Somatotropin
Antagonists: Δ1–9-G129R-hPRL
Δ1–14-G129R-hPRL
G120K-hGH
G129R-hPRL
Prolactin modulators: Prolactin inhibitors: D2 receptor agonists (e.g., bromocriptine, cabergoline); Prolactin releasers: D2 receptor antagonists (e.g., domperidone, metoclopramide, risperidone)
Estrogens (e.g., estradiol)
Progestogens (e.g., progesterone)
Agonists: Abaloparatide
Parathyroid hormone-related protein (PTHrP)
Semparatide
Teriparatide
Agonists: Insulin-like factor 3
Relaxin (1, 2, 3)
Serelaxin
Tachykinin
Agonists: Azetirelin
Fertirelin
Montirelin
Orotirelin
Posatirelin
Protirelin
Rovatirelin
Taltirelin
TRH (TRF)
Agonists: Thyrotropin alfa
TSH (thyrotropin)
VIP/PACAP
VIPR1
Agonists: Peptide: Bay 55-9837
LBT-3393
PACAP
Agonists: Peptide: LBT-3627
Agonists: PACAP
PACAP (1-27)
Antagonists: PACAP (6-38)
PHV
Endogenous: Adrenomedullin
Asprosin
DSIP
Formyl peptide
Integrin ligands (collagens, fibrinogen, fibronectin, laminins, ICAM-1, ICAM-2, osteopontin, VCAM-1, vitronectin)
Kininogens
Natriuretic peptides (ANP, BNP, CNP, urodilatin)
Neuromedin B
Neuromedin S
Neuromedin U
Obestatin
Urotensin-II
Exogenous: Lifitegrast (LFA-1 antagonist)
Receptor/signaling modulators
Retrieved from "https://en.wikipedia.org/w/index.php?title=Parathyroid_hormone&oldid=905872647"
Genes on human chromosome 11
Parathyroid hormone receptor agonists
Hormones of the parathyroid glands
Hormones of calcium metabolism


NG: As responsible gun owners, we need to keep our firearms accessible for protection while also ensuring they are safely secured, especially when children and guests are visiting our homes. We must also help ensure our firearms are not accessible to criminals and people who are not trained in safe firearm handling.
NG: In 2013, I started The Well Armed Woman Chapter in Yuma. All three chapter co-leaders—Jan Ennenga, Joanne Schickle and myself—are NRA Certified Basic Pistol Instructors and Range Safety Officers. We offer free firearms safety training in our community with a focus on women, especially military spouses who frequently have firearms in their home. We also target local "mom's clubs" to encourage responsible firearms safety in the home and around children. All of our courses cover the basic firearms safety rules, include proper handling and storage. To date, we have taught more than 400 members of our community.
NG: Project ChildSafe is an important program that provides educational resources for firearms owners, options for safe storage and overall important information for those who own guns. The program highlights the importance of responsible firearms ownership, including our obligation to help prevent guns from being accessible to children and other unauthorized individuals.


Glucose is a type of sugar. It comes from food and also is created in the liver. Glucose travels through the body in the blood. It moves from the blood to cells with the help of a hormone called insulin. Once glucose is in those cells, it can be used for energy. Diabetes mellitus is a condition that causes a buildup of glucose in the blood and makes it difficult for the body's cells to get enough energy. There are two primary kinds of diabetes mellitus, type 1 and type 2.
Type 1—An autoimmune disease occurs when there is an abnormal immune response to a normal part of the body. Type 1 diabetes is an autoimmune disorder caused by destruction of the cells that secrete insulin from the pancreas. This results in too little insulin being produced to support the body's needs. Type 1 diabetes is usually diagnosed in children and young adults, and was previously known as juvenile diabetes.
Without insulin, glucose from the carbohydrate foods you eat cannot enter cells. This causes glucose to build up in the blood, leaving your body's cells and tissues starved for energy. While a variety of tissue transplantation and genetically-based treatments are being studied, at this point the only widely-available treatments for type 1 diabetes are the injection of insulin and inhaled insulin.
Type 2—Type 2 is the most common form of diabetes and can be caused by a combination of factors. One factor is that your body begins to make less insulin. A second is that your body becomes resistant to insulin. This means there is insulin in your body, but your body cannot use it effectively. Insulin resistance is often related to excess body fat. Medication, lifestyle changes, and monitoring can help control blood glucose levels in those with type 2 diabetes.
Other autoimmune conditions such as Hashimoto disease, Graves's disease, lupus, and rheumatoid arthritis.
Type 1—Type 1 diabetes is a chronic disease that has no cure, but it can be managed with proper treatment and care. The goal of diabetes treatment is to maintain blood glucose levels before and after meals within a healthy range. By doing so, you will feel better on a daily basis and will help prevent or delay complications of diabetes. Talk to your doctor about what a healthy blood glucose range is for you.
Follow a balanced meal plan that includes carbohydrates, proteins, and fats.
Eat normal serving sizes. Measure your food control portion sizes, if necessary.
Do not skip meals. Having meals throughout the day can maintain steady glucose levels.
Limit the amount of fat, especially saturated and trans fats, in your foods.
Keep a record of your food intake and create a meal plan with your dietician or doctor.
Medication—Certain medications will help to manage blood glucose levels. Talk to your doctor about special medication to help control your diabetes.
Blood Glucose Testing—You can check the level of glucose in your blood with a blood glucose meter. Checking your blood glucose levels during the day can help you stay on track. It will also help your doctor determine if your treatment is working. Keeping track of blood sugar levels is especially important if you take insulin.
More information can be found on the American Diabetes Association website www.diabetes.org. For individual diagnosis and treatment recommendations for type 1 and type 2 diabetes, please consult your physician. Joyce Vivian, MSN, NP, is available to screening, treatment options, and lifestyle tips. To schedule an appointment, call the office at (540) 772-3490 or schedule an appointment online.


Looking for a bed and breakfast in Bangladesh? Look no further! Bangladesh B&Bs offer a great value and a great alternative to hotels. Some Bangladesh B&Bs' are even of a higher quality than 5 stars hotels (while costing less). Select a B&B Bangladesh from the list below, to book it online in advance.


Tucson, Ariz. According to the Association of American Physicians and Surgeons, on Nov 1, 2012 vascular surgeon John Natale, M.D., 63, of Arlington, Ill., reported to the federal Bureau of Prisons to serve a 10-month sentence. According to a U.S. Department of Justice press release, he was convicted on two counts of making false statements in connection with surgeries performed between August 2002 and October 2004, and acquitted on two counts of Medicare fraud.
Physicians are required to use AMA-copyrighted codes in their billings. These codes are frequently changed or added to, and Natale testified that he had been taught at seminars to pick the most similar code if there wasn't one precisely matching the procedure.
Because Dr. Natale testified on his own behalf and gave a lengthy explanation of the reasons for the mistakes, the prosecution demanded a sentencing enhancement for obstruction of justice. This could have resulted in 5 years in prison.
The Complexity Of The Medicare Rules For "Incident To" Billing Is Continued As You Look At Other Insurance Payers. Non-physician Practitioners (NPP) are being utilized in more and more practice situations to help ease the workload and allow for expansion of the practice. Many practices have taken an "all or nothing" approach to NPP reimbursements: billing all services directly or all services "incident to". Neither of these is correct. The supervision of NPP's has seen numerous comments and clarifications from the OPPS in the past 3 years. The impact of this information should not be viewed negatively. The concept of "Split shared visits" is relatively easy to understand but the practical use and documentation requirements become the challenge. Non-physician Practitioners (NPP) reimbursement & billing rules are variable.
Join us for this On Demand Webinar "Incident To Services: Compliant Use of Non-Physician Practitioners" tomorrow Friday, 14th Dec, 2012. This webinar can be accessed anytime of the day once registered.
History of Non-Physician Practitioner (NPP) Services & State Scope of Practice/License.
Where do you find the most current and best resources for billing NPP services.
Which services can your NPP perform and options for billing them.
Levels of Supervision required at the various locations for a NPP to provide services.
Required Qualifications, Employment Relationships, Service Payment Methodology.
What can your NPP do to help with New Patient and Consultation visits.
Tips to consider if looking for an NPP to help your practice make the most informed decision.
Types of Nurse Practitioner Services That May Be Covered Under Medicare Reimbursement Rules.
Services Otherwise Excluded From Medicare's Coverage.
Collaboration & Collaborative Agreements between a PA and one or more physicians (MD/DO).
Incident To Services under Medicare Benefit Policy Manual.
Integral Activities of the Physician's/NPP's Professional Service.
Plan of Care – What is it?
Inappropriate Documentation & Direct Billing.
FAQs on the most pressing and compelling challenges faced today.
Please apply discount code "SAVE20" at checkout to get an additional $20 discount on registration.
Looking forward to having you onboard here.
This is a huge cottage industry, born out of the fear physicians have for suffering the fate of the doctor mentioned in Dr. Orient's story. I think more and more physicians will reject the money of the state purely out of fear.


Darling of the festival circuit the world over - The Famous Spiegeltent is one of Traffic Design Studios largest event clients. We have designed event programs and all promotional material for almost 20 seasons Worldwide since 2000 including Melbourne, Sydney, Canberra, Edinburgh and Brighton UK. During this time we have produced a wide range of designs, many with the use of paintings (2002 by Deborah Ladd and all later painings by Mark Ogge - artist of the Spiegeltent facade). We have also organised photoshoots to produce new imagery to work with.


text:
Newsmax Health | Drs. Mehmet Oz and Dr. Mike Roizen
Dr. Mehmet Oz is host of the popular TV show "The Dr. Oz Show." He is a professor in the Department of Surgery at Columbia University and directs the Cardiovascular Institute and Complementary Medicine Program and New York-Presbyterian Hospital.
Dr. Mike Roizen is chief medical officer at the Cleveland Clinic Wellness Institute, an award-winning author, and has been the doctor to eight Nobel Prize winners and more than 100 Fortune 500 CEOs.
Dr. Mehmet Oz,Dr. Mike Roizen
Home | Dr. Oz
Tags: youtube | junk food | kids health | dr. oz
Beware of Bad Influence From YouTube
By Dr. Oz and Michael Roizen, M.D. Monday, 23 November 2020 12:07 PM Current | Bio | Archive
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In 1965, Soupy Sales was suspended for two weeks from his children's TV show for telling kids to go to their parents' wallets and take out funny green pieces of paper with pictures of U.S. presidents and mail them to him. Thousands of dollars poured in.
In contrast, today's celebrities who may negatively influence kids' behaviors are often kids themselves.
And they get big bucks in return. The highest-paid YouTube influencer last year was an 8-year-old, who earned $26 million.
According to a study in the journal Pediatrics, youngsters from 3 to 14 whose parents post entertaining videos of them aren't just delivering bad jokes with unexpected consequences; they're part of a carefully crafted marketing push for junk food that targets young kids.
New York University researchers found that YouTube "shows" hosted by kids have garnered more than 1 billion views, and almost half promote food and drinks — more than 90% of which are fast foods, candies, sodas, or fast-food toys.
The persuasive juxtaposition of adorable kids and lousy food promotes obesity. "Numerous studies have shown that children who see food ads consume more calories than children who see non-food ads," explains the study's senior author.
Don't plop your child down in front of YouTube kids' shows without finding out what products they're pushing. And talk to your youngster about what makes certain foods unhealthy.
These days, to raise a smart consumer — and a healthy child — you have to talk about nutrition and how to evaluate media early and often.
Posts by Dr. Oz and Michael Roizen, M.D.
Social Interaction Helps Prevent Falls
Cold-Weather Exercise Burns More Fat
View More Posts by Dr. Oz and Michael Roizen, M.D.
© King Features Syndicate
Dr-Oz
Numerous studies have shown that children who see food ads consume more calories than children who see non-food ads.
youtube, junk food, kids health, dr. oz
Monday, 23 November 2020 12:07 PM

redpajama_set_name: RedPajamaCommonCrawl


Eating "low-fat": Low-fat or fat-free foods replace harmless fats with low-performing carbohydrates that digest quickly, causing a sugar rush and, immediately afterward, rebound hunger.
Sleeping too little or too much: Dieters who sleep five hours or less put on 2 and a half times more belly fat, while those who sleep more than eight hours pack on only slightly less than that.
Drinking soda -- even diet soda: Drinking one to two sodas per day increases your chances of being overweight or obese by nearly 33 percent. And diet soda is no better.
Eating too quickly: It takes 20 minutes for your stomach to tell your brain that it's had enough.
Watching too much TV: A study found that overweight participants who reduced their TV time by just 50 percent burned an additional 119 calories a day on average.
Eating off larger plates: One study found that when given an option, a whopping 98.6 percent of obese individuals opt for larger plates.
Taking big bites: Research shows that people who take large bites of food consume 52 percent more calories in one sitting.
Eating too late: A recent study found that those who ate after 8 PM took in the most daily calories and had the highest BMIs.
Drinking fruity beverages: All juice is high sugar, and the ones that use viscous syrups made mostly from high fructose corn syrup and thickening agents are even worse.
To see the rest of their list, you can click on the link below. Another reason you may want to be sure your diet includes healthy fats? A recent study investigated the effects of dietary medium-chain triglycerides on liver fat accumulation in growing rats with protein malnutrition. Weaning rats were fed either a low-protein diet or control protein diet, either in combination with or without medium-chain triglycerides.
After four weeks, liver fat increased in the low-protein groups compared with the control groups. However, the liver fat content in the low-protein group fed medium-chain triglycerides was significantly decreased compared with that in the other low-protein group.
"These results suggest that ingestion of a low-protein diet caused fatty liver in growing rats. However, when rats were fed the low-protein diet with [medium-chain triglycerides], hepatic triglyceride deposition was attenuated, and mRNA levels encoding CPT1a and CPT2 were preserved at the levels of rats fed control protein diets."
Over two-thirds of American adults are now overweight or obese, and one-third of adults, along with 17 percent of children and teens, are obese. In fact, in 2010, data from the U.S. Centers for Disease Control and Prevention (CDC) showed that no state had a prevalence of obesity less than 20 percent, and 36 states had an obesity prevalence of 25 percent or more.
Clearly overweight and obesity are at epidemic proportions, and this trend is putting both adults and children at risk of serious, chronic disease ranging from high blood pressure and heart disease to diabetes and cancer. As for what's causing so many Americans to gain excess weight, it's a complex situation.
Why are So Many Americans Overweight and Obese?
There's the fact that the U.S. government heavily subsidizes the very foods that contribute to weight gain (i.e. corn). There's the problem with environmental chemicals, like phthalates, which can interfere with the hormonal mechanisms that control your weight. There's the abundance of stress that many people live with on a daily basis, which leads to emotional eating as well as chronic elevations of the hormone cortisol, that in turn leads to weight gain around your midsection.
But there's also another issue that cannot be ignored: misinformation. Many Americans are seriously confused about what a truly healthful food is, and this is partly the result of clever and deceptive marketing that makes junk foods and synthetic substances, like artificial sweeteners, appear healthy. Further, fats in general are still considered the dietary villains by many people.
A Consumer Reports survey found that 51 percent said they are limiting their consumption of fat in belief that this is a healthy choice. Changes are this lumps ALL fats into one evil category, when in reality the only types of fats you should really be limiting are man-made varieties like trans-fats and rancid, refined polyunsaturated fats in vegetable oils.
It's encouraging to see mainstream media outlets like Yahoo busting the prevalent myth that fat must be avoided if you want to lose weight. In fact, research suggests that eating healthy fats is actually conducive to weight loss. When you eat fats as part of your meal, they actually slow down your food absorption so that you can go longer without feeling hungry. The fatty acid conjugated linoleic acid (CLA), found in grass-fed beef and full-fat dairy products from grass-fed cows (butter, milk, cheese, etc.), is also associated with reduced body fat and weight.
For instance, a study in the American Journal of Clinical Nutrition found that people who ate 3.2 grams of CLA a day had a drop in fat mass of about 0.2 pounds a week (that's about one pound a month) compared to those given a placebo. Research also shows that women who ate at least one serving of full-fat dairy a day gained 30 percent less weight over a nine-year period than women who ate only low-fat (or no) dairy products.
Unfortunately, many people are still shunning healthy foods like raw butter and grass-fed beef, which contain saturated fat, because they believe it will cause heart disease. In reality, saturated fats are among the healthiest fats you can consume.
Could this Saturated Fat Actually Prevent Liver Disease?
Saturated fats provide the building blocks for your cell membranes and a variety of hormones and hormone-like substances that are essential to your health, and saturated fats from animal and vegetable sources (such as meat, dairy, certain oils, and tropical plants like coconut) provide a concentrated source of energy in your diet that has far-reaching health benefits.
Unfortunately nearly the entire conventional media and nearly every health "expert" will disagree with the above and use statements that all the research supports their belief. Well the truth of the matter is that it doesn't. Gary Taubes has provided the best rebuttal to this concept in the book he wrote Good Calories Bad Calories. Gary is one of the leading science journalists and he devoured the literature on this and reviewed all the studies and he expertly debunks their flawed logic and details how this misunderstanding has contributed to the epidemic of chronic disease in the U.S.
Additionally, new research this year showed that medium-chain triglycerides, such as those found in coconut oil, helped to stop the development of fatty liver in rats. Saturated fats also act as carriers for important fat-soluble vitamins A, D, E and K. Dietary fats are also needed for the conversion of carotene to vitamin A, for mineral absorption, and for a host of other biological processes.
"… there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD [coronary heart disease] or CVD [stroke and cardiovascular disease]."
What is the True Dietary Villain for Your Weight?
If you are serious about losing weight, you have got to strictly limit the amount of fructose in your diet, as evidence is mounting that excess sugar, and fructose in particular, is the primary factor in the obesity epidemic. The central issue is that fructose is now used in virtually all processed foods (whether you'd suspect the food would contain a sweetener or not).
If you want to lose weight, cutting soda from your diet is essential … but -- and this is a point many fail to appreciate -- you've got to cut other sources of fructose, too, including that in processed foods, fruit juice, excessive fruit and so-called "healthy" sweeteners like agave. Ideally you should keep your total fructose consumption below 25 grams per day and this includes fruits. This is especially true if you have insulin resistance and are overweight, have high blood pressure, diabetes or high cholesterol.
Rapidly leads to weight gain and abdominal obesity ("beer belly"), decreased HDL, increased LDL, elevated triglycerides, elevated blood sugar, and high blood pressure—i.e., classic metabolic syndrome.
Over time leads to or worsens preexisting insulin resistance, which is not only an underlying factor of type 2 diabetes and heart disease, but also many cancers.
According to Dr. Robert Lustig, fructose is 'isocaloric but not isometabolic." This means you can have the same amount of calories from fructose or glucose, fructose and protein, or fructose and fat, but the metabolic effect will be entirely different despite the identical calorie count.
Fructose is "isocaloric but not isometabolic."
This means you can have the same amount of calories from fructose or glucose, fructose and protein, or fructose and fat, but the metabolic effect will be entirely different despite the identical calorie count.
This is largely because different nutrients provoke different hormonal responses, and those hormonal responses determine, among other things, how much fat you accumulate.
Even the most popular calorie-counting weight loss program, Weight Watchers, recently admitted this fact and changed their wildly successful formula. The new system instead tries to encourage dieters to consume more natural, less processed food, which I believe is the crux of any long-term weight loss program.
As you cut these dietary villains from your meals, you need to replace them with healthy substitutes like vegetables, proteins and fats. Your body prefers the carbohydrates in vegetables rather than grains and sugars because it slows the conversion to simple sugars like glucose, and decreases your insulin level. When you cut grains and sugar from your meals, you typically will need to radically increase the amount of vegetables you eat, as well as make sure you are also consuming protein and healthy fats regularly.
Finally, remember that the foods you choose to eat will be the driving force behind successfully achieving your weight loss goals -- even more so than exercise. It's important to realize that exercise -- even if you incorporate exercises like Peak 8 into your routine -- will NOT compensate for fructose use and can destroy many of the benefits of your hard work. Exercise is still important for weight loss and optimal health … but it will generally not be enough to make up for the damage done by a poor, fructose-rich diet.


Persuasive Essay Example ... The United States is the only modernized Western nation that does not offer publicly funded health care to all its citizens; the costs of health care for the uninsured ... One of the most common arguments against providing universal health care coverage (UHC) is that it will cost too much money.
universal healthcare essaysIn this paper, I will discuss the reasons why America should convert to a universal healthcare system, and reveal the pros and cons behind the problems that America faces without a universal plan. My argument is based on these major issues: the people involved and their ex.
Universal health care is the special coverage system that ensures that all residents of the country have an access to the medical facilities and assistance. Universal health care is funded through a variety of different programs worldwide. All of the developed states, accept for the USA, have universal health care system.


The Piper Partners Team and First Equity Residential Mortgage are holding a free home buyer seminar Tuesday, March 26th at the Chelsea District Library.
If you're thinking of buying a home in the next two years, you will not want to miss this event.
This event is absolutely free and we are even offering refreshments. Come learn everything you need to know about the home buying process and have all your questions answered by professionals in the real estate industry. Andy Piper, Julie Lemorie and Lender Bob Yopko will be there to answer all your real estate and financial questions.
Who: Andy Piper and Julie Lemorie with the Piper Partners Team at Keller Williams Realty and Bob Yopko with First Equity Residential Mortgage.
If you have questions, call us at (734) 845-9700.
If you have questions about qualifying for a mortgage, are wondering about low or no down payment mortgage options or are just wondering what the home buying process looks like, we hope to see you there!


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Average Cargo Theft Costs Around $77K, Says TT Club Survey
Posted on 18 June 2019 by InsuranceEdgeEditor in Global insurance trends // 0 Comments
This Monday Aug. 28, 2017 image provided by the Port of Virginia shows the CMA CGM Theodore Roosevelt being unloaded at the Virginia International Gateway in Norfolk, Va. The arrival of the ship breaks the record for largest container ship ever to visit the Port of Virginia and the East Coast. (Keith Lanpher/Port of Virginia via AP)
TT Club and BSI have issued the second edition of their report on global cargo theft, the first to cover a full year. Highlighted findings include: theft from road vehicles once more accounts for the highest proportion at 84%; Slash and Grab the largest type of cargo theft at 26% globally but with significant regional variations; the combination of food, beverage, alcohol and tobacco making up the most common commodity group at 34% and South America topping the regional analysis of median value for each theft at $77,000.
Leading international transport and logistics insurer, TT Club and global provider of supply chain intelligence, BSI produced their first regular Semi-Annual Global Cargo Theft Intelligence and Advisory Report late last year but this second edition is the first to cover a complete twelve-month (2018) period.
TT Club's Mike Yarwood, explains the rationale behind the initiative, "Our report brings together threat and intelligence data from BSI's supply chain security country risk intelligence tool, SCREEN and TT Club's insurance risk management and loss prevention insights. It demonstrates the shared goal we possess of educating supply chain professionals in the threat of cargo theft across the globe. We aim to engage in a proactive approach in preventing cargo crime and also minimising the financial loss resulting from cargo crime."
The report, which is available as a free download https://www.ttclub.com/loss-prevention/publications/tt-club-bsi-cargo-theft-report-2018/ analyses cargo theft by modality, theft type (modus operandi), commodities targeted and the value of losses across the major regions of the world.
While the research found a consistency across the regions in terms of the most common modality involved (road transport) and in the commodities targeted, there was some variation in the median value of the cargo affected. This ranged from just under $19,000 in Asia, to around $60,000 in both Europe and North America to a high of $77,000 in South America.
The methods used in the majority of cases, however varied significantly across the regions. The global aggregation resulted in Slash and Grab at 26% topping the list, with Theft from Vehicle (19%) and Hijacking (17%) making up second and third spot. In North and South America Hijacking was the most common method at 37% and 52% respectively. In Asia methodology was quite different with Theft from a Facility being the most common, at 43% compared with just 19% from Hijacking.
The report includes several pieces of loss prevention advice to counter the identified threats. The risk mitigation advisory sections have been co-authored by BSI's Advisory Supply Chain Security team and the TT Club's claims and loss prevention team.
Yarwood goes on to say "In particular we would wish to emphasise The Insider Threat. As security measures become more sophisticated and widespread in practice, criminal organisations are increasingly recruiting employees of targeted companies to gain data, cargo information, delivery routes and destinations and access to IT systems. Due diligence in recruiting and managing staff is paramount. In general full or part-time salaried staff are less of a security risk than sub-contractors."
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text:
David Ruffin (né Davis Eli Ruffin) est un chanteur américain de soul né le  et mort le . Il est le chanteur principal du groupe The Temptations de 1964 à 1968, pendant la période dite « Classic Five » du groupe. Parmi ses interprétations de chansons du groupe, on peut citer My Girl ou encore Ain't Too Proud to Beg. Il quitte le groupe en 1969 pour mener une carrière solo pendant laquelle il sortira une dizaine d'albums.

Sa voix de baryton lui vaut d'être classé en 2008 parmi les 100 meilleurs chanteurs de tous les temps () par le magazine Rolling Stone. Il entre en 1989 au Rock and Roll Hall of Fame.

Marvin Gaye dit de lui : « J'ai entendu dans sa voix une force que la mienne n'a pas ».

Aretha Franklin et Stevie Wonder chantent pendant ses obsèques, financées en partie par Michael Jackson. Il est enterré au  à Détroit..

Éléments de biographie
David Ruffin est né le  à Whynot (Mississippi) d'un père pasteur baptiste, Éli, et d'Ophélia Davis, qui meurt quelques mois après sa naissance. Son père se remarie très rapidement, en 1942, avec Earline, une institutrice. Le jeune David Ruffin voyage avec son père, ses frères Quincy et Jimmy, ainsi que sa sœur Rita Mae à travers les États-Unis pour chanter dans une chorale de gospel, en première partie de Mahalia Jackson et des The Five Blind Boys of Mississippi. Il chante aussi entre autres dans la chorale de l'église Méthodiste de Mount Salem. Il quitte le domicile familial en 1955, alors âgé de 14 ans, avec pour objectif de continuer son ministère à Memphis.

Durant l'été 1969, il se produit en solo au Harlem Cultural Festival.

Discographie autre qu'avec les Temptations

Albums
 My Whole World Ended (1969)
 Feelin' Good (1969)
 David Ruffin (1973)
 Me And Rock N Roll Are Here To stay (1974)
 Who I Am (1975)
 Everything´s Coming Up Love (1976)
 In My Stride (1977)
 At His Best (1978)
 So Soon We Change (1979)
 Gentleman Ruffin (1981)
 David (2004)

avec Jimmy Ruffin
 I Am My Brothers Keeper (1970)

avec Eddie Kendricks
 Ruffin & Kendrick (1987)

avec Hall & Oates
 Live At The Apollo with David Ruffin & Eddie Kendrick (1985)

Solo-Hits
 My Whole World Ended (USA # 10) (1969)
 Walk Away From Love (USA # 8) (1975)

Notes et références

Liens externes

Naissance en janvier 1941
Décès en juin 1991
Artiste de Motown
Musicien afro-américain
Chanteur américain du XXe siècle
Personnalité inhumée au cimetière de Woodlawn
Décès à 50 ans
Artiste de Warner Bros. Records
Chanteur de soul

redpajama_set_name: RedPajamaWikipedia


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Andy Clachers is currently Chief Operating Officer of AXA China Region (Hong Kong). A results orientated senior operations executive, Andy has more than 15 years experience working at executive level within Financial Services in Hong Kong, Indonesia and Mainland China. Known for a positive 'can do' attitude, he has a strong track record of building businesses through a clear understanding of customer needs.
Among Andy's achievements are the successful development and implementation of operational strategies, including the strategic selection and implementation of IT systems. He's a strong communicator with an ability to develop people and teams to realise corporate objectives, and execute company strategy.
At AXA China Region (Hong Kong), Andy is responsible for leading Operations, including the Business Transformation and Operational Excellence functions. His ability to form relationships at many levels of the company allow him to have a positive influence on the overall development of the business.
Previously he served as Chief Operating Officer for AXA Indonesia where he had responsibility for leading operations across AXA's four business entities, as well as IT, Project Management Office, Operations Improvement and Health Claims functions within the shared service centre.
Prior to this he served as the COO at Standard Life Asia in Hong Kong and Operations Director at Heng An Standard Life in Tianjin, China. In Tianjin, Andy was a member of the original team formed to establish Standard Life's joint venture. Filling several different roles, he was responsible for implementing the operational strategy that supported the successful establishment of operations across 25 cities in China.
Andy thoroughly enjoyed his four years in Jakarta. This was thanks to the people, the food and the feeling of vibrancy from a city that's going places! One of the best parts is that Jakarta is a fantastic base to explore the beauty, the history and the culture of a nation of 250 million spread across 17,000 Islands!
While living there, he had the chance to experience the world class diving around Komodo Island; the magnificent history of Borobudur and the chilled out beauty of Bali. On such trips, he often feels as though he's living in an episode of the National Geographic channel.
However, the people are even more special; they are warm, friendly and always smiling. He feels that he has been taught to smile more and admires the openness of his Indonesian friends to other cultures. He's been taught that smiling is contagious and that we should all do it more.
And of course the people love to eat. So much street food and so many restaurants. The variety reflects the diversity of the country and its population. Overall, it's tremendously exciting to live in a place that is being transformed. Jakarta is already the Twitter capital of the world. Yes, Andy and his fellow Jakarta citizens collectively tweet more than any other city. In fact they embrace all forms of social media with a thirst for ideas that will transform the country in the next 15 years. It has one of the youngest populations in the world who are now approaching a 'sweet spot' in terms of the large proportion of the country who will be of working age. They are all contributing to the growth and transformation of the country. Jakarta is buzzing and you can feel the energy! To life in Jakarta is to feel alive in Jakarta! For that, Andy feels very fortunate.
It's not for nothing that Hong Kong is described as 'Asia's World City'! A truly cosmopolitan city, dynamic and diverse, Andy was delighted with the opportunity the return to Hong Kong.
From skyscrapers to fishing villages, and selection of every type of food possible, there is never a dull moment in Hong Kong. Amongst Andy's favourites are Cha Siu Bao and Egg Tarts! Hong Kong is also one of the best places in the world to enjoy photography!
Copyright © Andy Clachers 2015.


If carbon atoms 1, 2, 4 and 5 of cyclohexane occupy coplanar positions and when carbon atoms 3 and 6 are on opposite sides of the plane the conformation (of symmetry group D3d) is called a chair form. The same term is applied to similar conformations of analogous saturated six-membered ring structures containing hetero-atoms and/or bearing substituent groups, but these conformations may be distorted from the exact D3d symmetry. For cyclohexane and most such analogues, the chair form is the most stable conformation. If the cyclohexane conformation has no centre of symmetry but possesses two planes of symmetry, one of them bisecting the bonds between atoms 1 and 2 and between 4 and 5 and the other plane passing through atoms 3 and 6 (which lie out of the plane and on the same side of the plane containing 1, 2, 4 and 5), that conformation (of symmetry group C2v) is called a boat form and it is generally not a stable form. Again, this term is also applied to structural analogues. The conformation of D2 symmetry passed through in the interconversion of two boat forms of cyclohexane is called the twist form (also known as skew boat, skew form and stretched form).
In a five-membered ring a conformation in which two adjacent atoms are maximally displaced, in opposite directions, relative to the plane containing the other three carbon atoms has been called a half-chair but is better called a twist conformation.
In carbohydrate chemistry the term twist refers to a five-membered ring and the D2 symmetry six-membered ring is referred to as skew.