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Lists of 100 best books
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Many publishers have lists of 100 best books, defined by their own criteria. This article enumerates some lists of "100 best" books for which there are fuller articles.
Among them, Science Fiction: The 100 Best Novels (Xanadu, 1985) and Modern Fantasy: The 100 Best Novels (Grafton, 1988) are collections of 100 short essays by a single author, David Pringle, with moderately long critical introductory chapters also by Pringle. For publisher Xanadu, Science Fiction was the first of four "100 Best" books published from 1985 to 1988. The sequels covered crime & mystery, horror, and fantasy.
Lists[edit]
Publisher
Name
Published
Crime Writers' Association The Top 100 Crime Novels of All Time 1990
Grafton Books
by David Pringle Modern Fantasy: The 100 Best Novels 1988
Larry McCaffery 20th Century's Greatest Hits: 100 English-Language Books of Fiction 1999
Le Monde Le Monde's 100 Books of the Century 1999
Modern Library Modern Library 100 Best Nonfiction 1998
Modern Library Modern Library 100 Best Novels 1998
Mystery Writers of America The Top 100 Mystery Novels of All Time 1995
New York Times Book Review New York Times 100 Notable Books annually
Norwegian Book Club Bokklubben World Library since 2002
Nimbus Publishing Atlantic Canada's 100 Greatest Books 2009
Tidningen Boken Världsbiblioteket 1991
Time Time's List of the 100 Best Novels 2005
The Guardian The Guardian 100 best novels 2015
Shūkan Bunshun Tozai Mystery Best 100 1985
Xanadu
by David Pringle Science Fiction: The 100 Best Novels 1985
See also[edit]
Category:Top book lists
Western canon#Examples, a broader list of lists
List of best-selling books
List of literary awards
References[edit]
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High-density lipoprotein
From Wikipedia, the free encyclopedia
Jump to: navigation, search
High-density lipoproteins (HDL) are one of the five major groups of lipoproteins.[1] Lipoproteins are complex particles composed of multiple proteins which transport all fat molecules (lipids) around the body within the water outside cells. They are typically composed of 80-100 proteins per particle (organized by one, two or three ApoA; more as the particles enlarge picking up and carrying more fat molecules) and transporting up to hundreds of fat molecules per particle.
Contents
[hide]
1 Overview
2 Testing
3 Structure and function
3.1 Subfractions
3.2 Major lipids in the human body
4 Epimodility
5 Estimating HDL via associated cholesterol
5.1 Recommended ranges
6 Measuring HDL concentration and sizes
6.1 Electrophoresis measurements
6.2 NMR measurements
6.2.1 Optimal total and large HDL concentrations
7 Memory
8 Increasing HDL levels
8.1 Diet and exercise
8.2 Recreational drugs
8.3 Pharmaceutical drugs and niacin
9 See also
10 Notes and references
11 External links
Overview[edit]
HDL particles have long been divided into 5 subgroups, by density/size (an inverse relationship), which also correlates with function and incidence of cardiovascular events. Unlike the larger lipoprotein particles which deliver fat molecules to cells, HDL particles remove fat molecules from cells which need to export fat molecules. The lipids carried include cholesterol, phospholipids, and triglycerides; amounts of each are quite variable.
Increasing concentrations of HDL particles are strongly associated with decreasing accumulation of atherosclerosis within the walls of arteries. This is important because atherosclerosis eventually results in sudden plaque ruptures, cardiovascular disease, stroke and other vascular diseases. HDL particles are sometimes referred to as "good cholesterol" because they can transport fat molecules out of artery walls, reduce macrophage accumulation, and thus help prevent or even regress atherosclerosis. However, studies have shown that HDL-lacking mice still have the ability to transport cholesterol to bile, suggesting that there are alternative mechanisms for cholesterol removal.[2]
Testing[edit]
Because of the high cost of directly measuring HDL and LDL protein particles, blood tests are commonly performed for the surrogate value, HDL-C, i.e. the cholesterol associated with ApoA-1/HDL particles. In healthy individuals, about 30% of blood cholesterol, along with other fats, is carried by HDL.[3] This is often contrasted with the amount of cholesterol estimated to be carried within low-density lipoprotein particles, LDL, and called LDL-C. HDL particles remove fats and cholesterol from cells, including within artery wall atheroma, and transport it back to the liver for excretion or re-utilization; thus the cholesterol carried within HDL particles (HDL-C) is sometimes called "good cholesterol" (despite being the same as cholesterol in LDL particles). Those with higher levels of HDL-C tend to have fewer problems with cardiovascular diseases, while those with low HDL-C cholesterol levels (especially less than 40 mg/dL or about 1 mmol/L) have increased rates for heart disease.[4] Higher native HDL levels are correlated with better cardiovascular health;[5] however, it does not appear that further increasing one's HDL improves cardiovascular outcomes.[6]
The remainder of the serum cholesterol after subtracting the HDL is the non-HDL cholesterol. The concentration of these other components, which may cause atheroma, is known as the non-HDL-C. This is now preferred to LDL-C as a secondary marker as it has been shown to be a better predictor and it is more easily calculated.[7]
Structure and function[edit]
HDL is the smallest of the lipoprotein particles. It is the densest because it contains the highest proportion of protein to lipids. Its most abundant apolipoproteins are apo A-I and apo A-II.[8] A rare genetic variant, ApoA-1 Milano, has been documented to be far more effective in both protecting against and regressing arterial disease; atherosclerosis. The liver synthesizes these lipoproteins as complexes of apolipoproteins and phospholipid, which resemble cholesterol-free flattened spherical lipoprotein particles, whose NMR structure was recently published;[9] the complexes are capable of picking up cholesterol, carried internally, from cells by interaction with the ATP-binding cassette transporter A1 (ABCA1).[10] A plasma enzyme called lecithin-cholesterol acyltransferase (LCAT) converts the free cholesterol into cholesteryl ester (a more hydrophobic form of cholesterol), which is then sequestered into the core of the lipoprotein particle, eventually causing the newly synthesized HDL to assume a spherical shape. HDL particles increase in size as they circulate through the bloodstream and incorporate more cholesterol and phospholipid molecules from cells and other lipoproteins, for example by the interaction with the ABCG1 transporter and the phospholipid transport protein (PLTP).
HDL transports cholesterol mostly to the liver or steroidogenic organs such as adrenals, ovary, and testes by both direct and indirect pathways. HDL is removed by HDL receptors such as scavenger receptor BI (SR-BI), which mediate the selective uptake of cholesterol from HDL. In humans, probably the most relevant pathway is the indirect one, which is mediated by cholesteryl ester transfer protein (CETP). This protein exchanges triglycerides of VLDL against cholesteryl esters of HDL. As the result, VLDLs are processed to LDL, which are removed from the circulation by the LDL receptor pathway. The triglycerides are not stable in HDL, but are degraded by hepatic lipase so that, finally, small HDL particles are left, which restart the uptake of cholesterol from cells.
The cholesterol delivered to the liver is excreted into the bile and, hence, intestine either directly or indirectly after conversion into bile acids. Delivery of HDL cholesterol to adrenals, ovaries, and testes is important for the synthesis of steroid hormones.
Several steps in the metabolism of HDL can participate in the transport of cholesterol from lipid-laden macrophages of atherosclerotic arteries, termed foam cells, to the liver for secretion into the bile. This pathway has been termed reverse cholesterol transport and is considered as the classical protective function of HDL toward atherosclerosis.
However, HDL carries many lipid and protein species, several of which have very low concentrations but are biologically very active. For example, HDL and its protein and lipid constituents help to inhibit oxidation, inflammation, activation of the endothelium, coagulation, and platelet aggregation. All these properties may contribute to the ability of HDL to protect from atherosclerosis, and it is not yet known which are the most important. In addition, a small subfraction of HDL lends protection against the protozoan parasite Trypanosoma brucei brucei. This HDL subfraction, termed trypanosome lytic factor (TLF), contains specialized proteins that, while very active, are unique to the TLF molecule.[11]
In the stress response, serum amyloid A, which is one of the acute-phase proteins and an apolipoprotein, is under the stimulation of cytokines (interleukin 1, interleukin 6), and cortisol produced in the adrenal cortex and carried to the damaged tissue incorporated into HDL particles. At the inflammation site, it attracts and activates leukocytes. In chronic inflammations, its deposition in the tissues manifests itself as amyloidosis.
It has been postulated that the concentration of large HDL particles more accurately reflects protective action, as opposed to the concentration of total HDL particles.[12] This ratio of large HDL to total HDL particles varies widely and is measured only by more sophisticated lipoprotein assays using either electrophoresis (the original method developed in the 1970s) or newer NMR spectroscopy methods (See also nuclear magnetic resonance and spectroscopy), developed in the 1990s.
Subfractions[edit]
Five subfractions of HDL have been identified. From largest (and most effective in cholesterol removal) to smallest (and least effective), the types are 2a, 2b, 3a, 3b, and 3c.[13]
Major lipids in the human body[edit]
Lipids are a heterogeneous group of compounds which are relatively insoluble in water and soluble in non-polar solvents. Triglycerides (TGs), cholesterol, and phospholipids are the major lipids in the body. They are transported as complexes of lipid and proteins known as lipoproteins.
TGs (triglycerides): TGs are formed by combining glycerol with three molecules of fatty acid. TGs, as major components of VLDL and chylomicrons, play an important role in metabolism. When the body requires fatty acids as an energy source, the hormone glucagon signals the breakdown of the TGs by lipase to release free fatty acids (FFA). TGs are water-insoluble, non-polar neutral fats. These are not the structural components of biological membranes.TGs synthesis and storage mostly occurs in liver and adipose tissue. FFA and glycerol must be activated prior to the synthesis of TGs into Acyl-CoA and glycerol-3-phosphate respectively.
Cholesterol: The name cholesterol originates from the Greek chole- (bile) and stereos (solid), and the chemical suffix-ol for an alcohol. It is an essential structural component of cell membrane, where it is required to establish proper membrane permeability and fluidity. In addition, cholesterol is an important component for the manufacture of bile acids, steroid hormones, and vitamin D. Although cholesterol is an important and necessary molecule, a high level of serum cholesterol is an indicator for diseases such as heart disease. About 20-25% of total daily cholesterol production occurs in the liver.
Phospholipids: Phospholipids are TGs that are covalently bonded to a phosphate group by an ester linkage. Phospholipids perform important functions including regulating membrane permeability and in maintaining electron transport chain in mitochondria. They participate in the reverse cholesterol transport and thus help in the removal of cholesterol from the body. They are involved in signal transmission across membranes and they act as detergents and help in solubilization of cholesterol.
Lipoprotein: These consist of a central core of a hydrophobic lipid (including TGs and cholesteryl esters) encased in a hydrophilic coat of polar phospholipid, free cholesterol and apolipoprotein. There are six main classes of lipoprotein, differing in the relative proportion of the core lipids and in the type of apoprotein.
Chylomicrons
VLDL-C particiles
IDL-C particles
LDL-C particles
HDL-C particle
Lipoprotein (a) [LP(a)]
Epimodility[edit]
Men tend to have noticeably lower HDL levels, with smaller size and lower cholesterol content, than women. Men also have an increased incidence of atherosclerotic heart disease. Alcohol consumption tends to raise HDL levels,[14] and moderate alcohol consumption is associated with lower cardiovascular and all-cause mortality. Recent studies confirm the fact that HDL has a buffering role in balancing the effects of the hypercoagulable state in type 2 diabetics and decreases the high risk of cardiovascular complications in these patients. Also, the results obtained in this study revealed that there was a significant negative correlation between HDL and activated partial thromboplastin time (APTT).[15]
Epidemiological studies have shown that high concentrations of HDL (over 60 mg/dL) have protective value against cardiovascular diseases such as ischemic stroke and myocardial infarction. Low concentrations of HDL (below 40 mg/dL for men, below 50 mg/dL for women) increase the risk for atherosclerotic diseases.
Data from the landmark Framingham Heart Study showed that, for a given level of LDL, the risk of heart disease increases 10-fold as the HDL varies from high to low. On the converse, however, for a fixed level of HDL, the risk increases 3-fold as LDL varies from low to high.[16][17]
Even people with very low LDL levels are exposed to increased risk if their HDL levels are not high enough.[18]
Estimating HDL via associated cholesterol[edit]
Clinical laboratories formerly measured HDL cholesterol by separating other lipoprotein fractions using either ultracentrifugation or chemical precipitation with divalent ions such as Mg2+, then coupling the products of a cholesterol oxidase reaction to an indicator reaction. The reference method still uses a combination of these techniques.[19] Most laboratories now use automated homogeneous analytical methods in which lipoproteins containing apo B are blocked using antibodies to apo B, then a colorimetric enzyme reaction measures cholesterol in the non-blocked HDL particles.[20] HPLC can also be used.[21] Subfractions (HDL-2C, HDL-3C) can be measured,[22] but clinical significance of these subfractions has not been determined.[23] The measurement of apo-A reactive capacity can be used to measure HDL cholesterol but is thought to be less accurate.
Recommended ranges[edit]
The American Heart Association, NIH and NCEP provide a set of guidelines for fasting HDL levels and risk for heart disease.[24][25][26]
Level mg/dL
Level mmol/L
Interpretation
<40 for men, <50 for women <1.03 Low HDL cholesterol, heightened risk for heart disease
40–59 1.03–1.55 Medium HDL level
>60 >1.55 High HDL level, optimal condition considered protective against heart disease
High LDL with low HDL level is an additional risk factor for cardiovascular disease.[27]
Measuring HDL concentration and sizes[edit]
As technology has reduced costs and clinical trials have continued to demonstrate the importance of HDL, methods for directly measuring HDL concentrations and size (which indicates function) at lower costs have become more widely available and increasingly regarded as important for assessing individual risk for progressive arterial disease and treatment methods.
Electrophoresis measurements[edit]
Since the HDL particles have a net negative charge and vary by density & size, ultracentrifugation combined with electrophoresis have been utilized since before 1950 to enumerate the concentration of HDL particles and sort them by size with a specific volume of blood plasma. Larger HDL particles are carrying more cholesterol.
NMR measurements[edit]
Concentration and sizes of lipoprotein particles can be estimated using nuclear magnetic resonance fingerprinting.[28]
Optimal total and large HDL concentrations[edit]
The HDL particle concentrations are typically categorized by event rate percentiles based on the people participating and being tracked in the MESA[29] trial, a medical research study sponsored by the United States National Heart, Lung, and Blood Institute.
Total HDL particle Table
MESA Percentile
Total HDL particles μmol/L
Interpretation
>75% >34.9 Those with highest (Optimal) total HDL particle concentrations & lowest rates of cardiovascular disease events
50–75% 30.5–34.5 Those with moderately high total HDL particle concentrations & moderate rates of cardiovascular disease events
25–50% 26.7–30.5 Those with lower total HDL particle concentrations & Borderline-High rates of cardiovascular disease
0–25% <26.7 Those with lowest total HDL particle concentrations & Highest rates of cardiovascular disease events
Large (protective) HDL particle Table
MESA Percentile
Large HDL particles μmol/L
Interpretation
>75% >7.3 Those with highest (Optimal) Large HDL particle concentrations & lowest rates of cardiovascular disease events
50–75% 4.8–7.3 Those with moderately high Large HDL particle concentrations & moderate rates of cardiovascular disease events
25–50% 3.1–4.8 Those with lower Large HDL particle concentrations & Borderline-High rates of cardiovascular disease
0–25% <3.1 Those with lowest Large HDL particle concentrations & Highest rates of cardiovascular disease events
The lowest incidence of atherosclerotic events over time occurs within those with both the highest concentrations of total HDL particles (the top quarter, >75%)[clarification needed] and the highest concentrations of large HDL particles. Multiple additional measures, including LDL particle concentrations, small LDL particle concentrations, VLDL concentrations, estimations of insulin resistance and standard cholesterol lipid measurements (for comparison of the plasma data with the estimation methods discussed above) are routinely provided in clinical testing.
Memory[edit]
Fasting serum lipids have been associated with short term verbal memory. In a large sample of middle aged adults, low HDL cholesterol was associated with poor memory and decreasing levels over a five-year follow-up period were associated with decline in memory.[30]
Increasing HDL levels[edit]
While higher HDL levels are correlated with cardiovascular health, no medication used to increase HDL has been proven to improve health.[31] In other words, while high HDL levels might correlate with better cardiovascular health, specifically increasing one's HDL might not increase cardiovascular health.[6] The remaining possibilities are that either good cardiovascular health causes high HDL levels, there is some third factor which causes both, or this is a coincidence with no causal link.
HDL lipoprotein particles that bear apolipoprotein C3 are associated with increased, rather than decreased, risk for coronary heart disease.[32]
Diet and exercise[edit]
Certain changes in diet and exercise may have a positive impact on raising HDL levels:[33]
Decreased intake of simple carbohydrates.[34][35][36][37]
Aerobic exercise[38]
Weight loss[39]
Magnesium supplements raise HDL-C.[40]
Addition of soluble fiber to diet[41]
Consumption of omega-3 fatty acids such as fish oil[42] or flax oil[43]
Consumption of pistachio nuts.[44]
Increased intake of cis-unsaturated fats[45]
Consumption of medium-chain triglycerides (MCTs) such as caproic acid, caprylic acid, capric acid, and lauric acid.
Removal of trans fatty acids from the diet[46]
Most saturated fats increase HDL cholesterol to varying degrees but also raise total and LDL cholesterol.[47] A high-fat, adequate-protein, low-carbohydrate ketogenic diet may have similar response to taking niacin (vitamin B3) as described below (lowered LDL and increased HDL) through beta-hydroxybutyrate coupling the Niacin receptor 1.[48]
Recreational drugs[edit]
HDL levels can be increased by smoking cessation,[39] or mild to moderate alcohol intake.[49][50][51][52][53][54]
Cannabis in unadjusted analyses, past and current cannabis use was not associated with higher HDL-C levels.[55] A study performed in 4635 patients demonstrated no effect on the HDL-C levels (P=0.78) [the mean (standard error) HDL-C values in control subjects (never used), past users and current users were 53.4 (0.4), 53.9 (0.6) and 53.9 (0.7) mg/dL, respectively].[55]
Pharmaceutical drugs and niacin[edit]
Pharmacological therapy to increase the level of HDL cholesterol includes use of fibrates and niacin. Fibrates have not been proven to have an effect on overall deaths from all causes, despite their effects on lipids.[56]
Niacin (vitamin B3) increases HDL by selectively inhibiting hepatic diacylglycerol acyltransferase 2, reducing triglyceride synthesis and VLDL secretion through a receptor HM74[57] otherwise known as niacin receptor 2 and HM74A / GPR109A,[48] niacin receptor 1.
Pharmacologic (1- to 3-gram/day) niacin doses increase HDL levels by 10–30%,[58] making it the most powerful agent to increase HDL-cholesterol.[59][60] A randomized clinical trial demonstrated that treatment with niacin can significantly reduce atherosclerosis progression and cardiovascular events.[61] However, niacin products sold as "no-flush", i.e. not having side-effects such as "niacin flush", do not contain free nicotinic acid and are therefore ineffective at raising HDL, while products sold as "sustained-release" may contain free nicotinic acid, but "some brands are hepatotoxic"; therefore the recommended form of niacin for raising HDL is the cheapest, immediate-release preparation.[62] Both fibrates and niacin increase artery toxic homocysteine, an effect that can be counteracted by also consuming a multivitamin with relatively high amounts of the B-vitamins[citation needed], however multiple European trials of the most popular B-vitamin cocktails, trial showing 30% average reduction in homocysteine, while not showing problems have also not shown any benefit in reducing cardiovascular event rates. A 2011 niacin study was halted early because patients adding niacin to their statin treatment showed no increase in heart health, but did experience an increase in the risk of stroke.[63]
In contrast, while the use of statins is effective against high levels of LDL cholesterol, most have little or no effect in raising HDL cholesterol.[59] However, several statins – rosuvastatin and pitavastatin – have been demonstrated to significantly raise HDL levels. As statins are associated with side effects like myopathy which causes sore muscles, patients who experience these side effects may need to be given a lower dose of statin to control cholesterol.[64]
Lovaza has been shown to increase HDL-C.[65] However, the best evidence to date suggests it has no benefit for primary or secondary prevention of cardiovascular disease.
Though it hasn't been FDA the PPAR Modulator (Sometimes referred to as a SARM) GW501516, Currently a research chemical (Not for human consumption), Has shown a positive effect on HDL-C[66] and an antiatherogenic where LDL is an issue.[67]
See also[edit]
Asymmetric dimethylarginine
Cardiovascular disease
Cholesteryl ester storage disease
Endothelium
Lipid profile
Low-density lipoprotein
Lysosomal acid lipase deficiency
Notes and references[edit]
Jump up ^ "LDL and HDL: Bad and Good Cholesterol". Centers for Disease Control and Prevention. CDC. Retrieved 11 September 2017.
Jump up ^ Betteridge; et al. (2008). "Structural requirements for PCSK9-mediated degradation of the low-density lipoprotein receptor". PNAS. 105 (35): 13045–13050. doi:10.1073/pnas.0806312105. CS1 maint: Explicit use of et al. (link)
Jump up ^ "LDL and HDL Cholesterol: What's Bad and What's Good?". American Heart Association. 2 July 2009. Retrieved 8 October 2009.
Jump up ^ Toth PP (Feb 2005). "Cardiology patient page. The "good cholesterol": high-density lipoprotein". Circulation. 111 (5): e89–e91. doi:10.1161/01.CIR.0000154555.07002.CA. PMID 15699268.
Jump up ^ Sirtori, Cesare R. (October 2006). "HDL and the progression of atherosclerosis: new insights". European Heart Journal Supplements.
^ Jump up to: a b "NIH stops clinical trial on combination cholesterol treatment". National Institute of Health. National Heart, Lung, and Blood Institute (NHLBI). Retrieved 2 June 2011.
Jump up ^ M.J. Sorrentino (2011), "Non-HDL-Cholesterol", Hyperlipidemia in Primary Care, pp. 86–87, ISBN 978-1-60327-502-6
Jump up ^ Després, Jean-Pierre. "The Atherogenic Triad of New Metabolic Risk Factors: Importance of Waist and Fasting Triglycerides as Screening Tools". Visceral Adipose Tissue and Cardiometabolic Risk: Does It Really Matter? Part 2. Retrieved 8 October 2009. [self-published source?]
Jump up ^ Bibow S et. al. (2017), "Solution structure of discoidal high-density lipoprotein particles with a shortened apolipoprotein A-I", Nature Structural & Molecular Biology, 24 (6): 187–93, doi:10.1038/nsmb.3345 CS1 maint: Uses authors parameter (link)
Jump up ^ Huang CX, Zhang YL (2013). "The target of regulating the ATP-binding cassette A1 protein (ABCA1): promoting ABCA1-mediated cholesterol efflux in different cells". Current Pharmaceutical Biotechnology. 14 (6): 623–31. doi:10.2174/138920101131400228. PMID 24016265.
Jump up ^ Stephens NA, Kieft R, Macleod A, Hajduk SL (Dec 2012). "Trypanosome resistance to human innate immunity: targeting Achilles' heel". Trends in Parasitology. 28 (12): 539–45. doi:10.1016/j.pt.2012.09.002. PMC 4687903  . PMID 23059119.
Jump up ^ Kwiterovich PO (Dec 2000). "The metabolic pathways of high-density lipoprotein, low-density lipoprotein, and triglycerides: a current review". The American Journal of Cardiology. 86 (12A): 5L–10L. doi:10.1016/S0002-9149(00)01461-2. PMID 11374859.
Jump up ^ HDL, HDL2, and HDL3 subfractions, and the risk of acute myocardial infarction. A prospective population study in eastern Finnish men.
Jump up ^ Ruidavets JB, Ducimetière P, Arveiler D, Amouyel P, Bingham A, Wagner A, Cottel D, Perret B, Ferrières J (Jan 2002). "Types of alcoholic beverages and blood lipids in a French population". Journal of Epidemiology and Community Health. 56 (1): 24–8. doi:10.1136/jech.56.1.24. PMC 1732002  . PMID 11801616.
Jump up ^ Mard-Soltani M, Dayer MR, Shamshirgar-Zadeh A, Ali-Bahar H, Nasirbagheban Z (April 2012). "The Buffering Role of HDL in Balancing the Effects of Hypercoagulable State in Type 2 Diabetes". J Applied sciences. 12 (8): 745–52. doi:10.3923/jas.2012.745.752.
Jump up ^ Rahilly-Tierney CR, Spiro A, Vokonas P, Gaziano JM (Apr 2011). "Relation between high-density lipoprotein cholesterol and survival to age 85 years in men (from the VA normative aging study)". The American Journal of Cardiology. 107 (8): 1173–7. doi:10.1016/j.amjcard.2010.12.015. PMID 21296318.
Jump up ^ Rubins HB, Robins SJ, Collins D, Nelson DB, Elam MB, Schaefer EJ, Faas FH, Anderson JW (2002). "Diabetes, plasma insulin, and cardiovascular disease: subgroup analysis from the Department of Veterans Affairs high-density lipoprotein intervention trial (VA-HIT)". Archives of Internal Medicine. 162 (22): 2597–604. doi:10.1001/archinte.162.22.2597. PMID 12456232.
Jump up ^ Barter P, Gotto AM, LaRosa JC, Maroni J, Szarek M, Grundy SM, Kastelein JJ, Bittner V, Fruchart JC (Sep 2007). "HDL cholesterol, very low levels of LDL cholesterol, and cardiovascular events". The New England Journal of Medicine. 357 (13): 1301–10. doi:10.1056/NEJMoa064278. PMID 17898099.
Jump up ^ "National Reference System for Cholesterol – Cholesterol Reference Method Laboratory Network – HDL Cholesterol Certification Protocol for Manufacturers" (PDF). CDC. Retrieved 10 November 2013.
Jump up ^ Warnick GR, Nauck M, Rifai N (Sep 2001). "Evolution of methods for measurement of HDL-cholesterol: from ultracentrifugation to homogeneous assays". Clinical Chemistry. 47 (9): 1579–1596. PMID 11514391.
Jump up ^ Okazaki M, Sasamoto K, Muramatsu T, Hosaki S (Oct 1997). "Evaluation of precipitation and direct methods for HDL-cholesterol assay by HPLC". Clinical Chemistry. 43 (10): 1885–90. PMID 9342008.
Jump up ^ Hirano T, Nohtomi K, Koba S, Muroi A, Ito Y (May 2008). "A simple and precise method for measuring HDL-cholesterol subfractions by a single precipitation followed by homogenous HDL-cholesterol assay". Journal of Lipid Research. 49 (5): 1130–6. doi:10.1194/jlr.D700027-JLR200. PMID 18223297.
Jump up ^ Superko HR, Pendyala L, Williams PT, Momary KM, King SB 3rd, Garrett BC (2012). "High-density lipoprotein subclasses and their relationship to cardiovascular disease". Journal of Clinical Lipidology. 6 (6): 496–523. doi:10.1016/j.jacl.2012.03.001. PMID 23312047.
Jump up ^ "Cholesterol Levels". American Heart Association. Archived from the original on 8 February 2010. Retrieved 14 November 2009.
Jump up ^ "What Do My Cholesterol Levels Mean?" (PDF). American Heart Association. September 2007. Archived from the original (PDF) on 3 December 2008. Retrieved 14 November 2009.
Jump up ^ "Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Executive Summary" (PDF). National Heart, Lung, and Blood Institute (NHLBI). National Institutes of Health. May 2001.
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External links[edit]
Adult Treatment Panel III Full Report – National Heart, Lung, and Blood Institute
ATP III Update 2004 – National Heart, Lung, and Blood Institute
HDL: The good, but complex, cholesterol – Harvard Heart Letter
HDL Cholesterol at Lab Tests Online
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Lipids: lipoprotein particle metabolism
Lipoprotein particle classes and subclasses
delivery of TGs: Chylomicron
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Are You Sitting Comfortably? (song)
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"Are You Sitting Comfortably?"
Song by The Moody Blues
from the album On the Threshold of a Dream
Released
25 April 1969
Recorded
January 1969
Length
3:30
Label
Deram Records
Songwriter(s)
Justin Hayward
Ray Thomas
Producer(s)
Tony Clarke
On the Threshold of a Dream track listing
Side one
"In the Beginning"
"Lovely to See You"
"Dear Diary"
"Send Me No Wine"
"To Share Our Love"
"So Deep Within You"
Side two
"Never Comes the Day"
"Lazy Day"
"Are You Sitting Comfortably?"
"The Dream"
"Have You Heard (Part 1)"
"The Voyage"
"Have You Heard (Part 2)"
"Are You Sitting Comfortably?" is a 1969 song by the progressive rock band The Moody Blues. It was written jointly by band members Justin Hayward and Ray Thomas. It was recorded and released in 1969 on the Moody Blues Album On the Threshold of a Dream.
The lyrics of "Are You Sitting Comfortably?" refer heavily to the legend of King Arthur, and include direct references to Camelot, and to the characters Merlin and Guinevere, all of which are part of the legend.
The song itself is primarily driven by Justin Hayward's vocal performance and Ray Thomas's flute, which gives it a sound similar to Hayward and Thomas's collaboration, "Visions of Paradise," from the Moody Blues previous album, In Search of the Lost Chord.
Personnel[edit]
Justin Hayward: lead vocals, acoustic guitar
John Lodge: bass guitar, backing vocals
Mike Pinder: mellotron, backing vocals
Ray Thomas: flute, backing vocals
Graeme Edge: tambourine, bass drum
External links[edit]
"Are You Sitting Comfortably?" being performed in 1970 on YouTube
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Aravalli Range
From Wikipedia, the free encyclopedia
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This article is about the mountain range in western India. For information about the district in Gujarat state, see Aravali district.
Aravalli Range
The Aravali Range in Rajasthan
Highest point
Peak
Guru Shikhar, Mount Abu
Elevation
1,722 m (5,650 ft)
Coordinates
24°35′33″N 74°42′30″E / 24.59250°N 74.70833°E / 24.59250; 74.70833
Dimensions
Length
692 km (430 mi)
Naming
Pronunciation
Hindustani pronunciation: [ aa ra vli]
Geography
Topographic map of India showing the range
Country
India
States
Rajasthan, Haryana, Delhi and Gujarat
Region
North India, Western India
Settlement
Delhi, Gurgaon, Mount Abu
Range coordinates
25°00′N 73°30′E / 25°N 73.5°E / 25; 73.5Coordinates: 25°00′N 73°30′E / 25°N 73.5°E / 25; 73.5
Rivers
Banas, Luni, Sakhi and Sabarmati
Geology
Orogeny
Aravalli-Delhi Orogen
Age of rock
Precambrian
Type of rock
Fold mountains from Plate tectonics
The Aravalli Range is a range of mountains running approximately 692 km (430 mi) in a southwest direction, starting in North India from Delhi and passing through southern Haryana,[1] through to Western India across the states of Rajasthan and ending in Gujarat.[2][3]
Contents
[hide]
1 Etymology
2 Natural History
2.1 Geology
2.2 Minerals
2.3 Mining
2.4 Geographical features
3 Human history
3.1 Early stone age
3.2 Mid-stone age
3.3 Post stone age
3.3.1 Ganeshwar sunari Cultural Complex
4 Environment
4.1 Climate
4.2 Rivers
5 Ecology
5.1 Flora
5.2 Fauna
5.3 Concerns
6 Economy
7 Tourism
8 Concerns
9 Gallery
10 See also
11 Further reading
11.1 External links
11.2 Books
12 References
Etymology[edit]
Aravalli, a composite Sanskrit word from "ara" and "vali", literally means the "line of peaks".[4][5]
Natural History[edit]
Geology[edit]
Main article: Tectonic evolution of the Aravalli Mountains
Map of prominent mountain ranges in India, showing Aravalli in north-west India
The Aravalli Range, an eroded stub of ancient mountains, is the oldest range of fold mountains in India.[6] The natural history of the Aravalli Range dates back to times when the Indian Plate was separated from the Eurasian Plate by an ocean. The Proterozoic Aravalli-Delhi orogenic belt in north west India is similar to the younger Himalayan-type orogenic belts of the Mesozoic-Cenozoic era (of the Phanerozoic) in terms of component parts and appears to have passed through a near-orderly Wilson supercontinental cycle of events. The range rose in a Precambrian event called the Aravalli-Delhi Orogen. The Aravalli Range is a northeast-southwest trending orogenic belt that is located in the northwestern part of Indian Peninsula. It is part of the Indian Shield that was formed from a series of cratonic collisions.[7] In ancient times, Aravalli were extremely high but since have worn down almost completely by millions of years of weathering, where as the Himalayas being young fold mountains are still continuously rising. Aravalli, being the old fold mountains, have stopped growing higher due to the cessation of upward thrust caused by the stopping of movement of the tectonic plates in the Earth's crust below them. The Aravalli Range joins two of the ancient earth's crust segments that make up the greater Indian craton, the Aravalli Craton which is the Marwar segment of earth's crust to the northwest of the Aravalli Range, and the Bundelkand Craton segment of earth's crust to the southeast of the Aravalli Range. Cratons, generally found in the interiors of tectonic plates, are old and stable parts of the continental lithosphere that has remained relatively undeformed during the cycles of merging and rifting of continents.
volcanic arc and geological process of undersea subduction during tactonic collusion
global convergent boundary of plate margins
It consists of two main sequences formed in Proterozoic eon, metasedimentary rock (sedimentary rocks metamorphised under pressure and heat without melting) and metavolcanic rock (metamorphised volcanic rocks) sequences of the Aravalli Supergroup and Delhi Supergroup. These two supergroups rest over the Archean Bhilwara Gneissic Complex basement, which is a gneissic (high-grade metamorphism of sedimentary or igneous rocks) basement formed during the archean eon 4 Ga ago. It started as an inverted basin, that rifted and pulled apart into granitoid basement, initially during Aravalli passive rifting around 2.5 to 2.0 Ga years ago and then during Delhi active rifting around 1.9 to 1.6 Ga years ago. It started with rifting of a rigid Archaean continent banded gneissic complex around 2.2 Ga with the coexisting formation of the Bhilwara aulacogen in its eastern part and eventual rupturing and separation of the continent along a line parallel to the Rakhabdev (Rishabhdev) lineament to the west, simultaneous development of a passive continental margin with the undersea shelf rise sediments of the Aravalli-Jharol belts depositing on the attenuated crust on the eastern flank of the separated continent, subsequent destruction of the continental margin by accretion of the Delhi island arc (a type of archipelago composed of an arc-shaped chain of volcanoes closely situated parallel to a convergent boundary between two converging tectonic plates) from the west around 1.5 Ga. This tectonic plates collision event involved early thrusting with partial obduction (overthrusting of oceanic lithosphere onto continental lithosphere at a convergent plate boundary) of the oceanic crust along the Rakhabdev lineament, flattening and eventual wrenching (also called strike-slip plate fault, side ways horizontal movement of colliding plates with no vertical motion) parallel to the collision zone. Associated mafic igneous rocks show both continental and oceanic tholeiitic geochemistry (magnesium and iron rich igneous rocks) from phanerozoic eon (541–0 million) with rift-related magmatic rock formations.[8]
The Aravalli-Delhi Orogen is an orogen event that led to a large structural deformation of the Earth's lithosphere (crust and uppermost mantle, such as Aravalli and Himalayas fold mountains) due to the interaction between tectonic plates when a continental plate is crumpled and is pushed upwards to form mountain ranges, and involve a great range of geological processes collectively called orogenesis.[9][10]
Minerals[edit]
The archean basement had served as a rigid indentor which controlled the overall wedge shaped geometry of the orogen. Lithology of area shows that the base rocks of Aravalli are of Mewar Gneiss formed by high-grade regional metamorphic processes from preexisting formations that were originally sedimentary rock with earliest life form that were formed during the archean eon, these contain fossils of unicellular organism such as green algae and cyanobacteria in stromatolitic carbonate ocean reefs formed during the paleoproterozoic era. Sedimentary exhalative deposits of base metal sulfide ores formed extensively along several, long, linear zones in the Bhilwara aulacogen or produced local concentration in the rifted Aravalli continental margin, where rich stromatolitic phosphorites also formed. Tectonic evolution of the Aravalli Mountains shows Mewar Geniss rocks are overlain by Delhi Supergroup type of rocks that also have post-Aravalli intrusions. Metal sulfide ores were formed in two different epocs, lead and zinc sulfide ores were formed in the sedimentary rocks around 1.8 Ga years ago during Paleoproterozoic phase. The tectonic setting of Zinc-lead-copper sulfides mineralization in Delhi supergroup rocks in Haryana-Delhi were formed in mantle plume volcanic action around 1 Ga years ago covering Haryana and Rajasthan during mesoproterozoic. In the southern part of Aravalli supergroup arc base metal sulfides were generated near the subduction zone on the western fringe and in zones of back-arc extension to the south-east. Continued subduction produced W-Sn (Tungsten-Tin) mineralisation in S-type (sedimentary unmetamorphosed rock) felsic (volcanic rock) plutons (underground crystallised solidified magma). This includes commercially viable quantities of minerals, such as rock phosphate, lead-zinc-silver mineral deposits at Zawar, Rikahbdev serpentinite, talc and pyrophyllite) and asbestos, apatite, kyanite and beryl.[11][12]
Mining[edit]
Mining of copper and other metals in the Aravalli range dates back to at least the 5th century BCE, based on carbon dating.[13][14] Recent research indicates that copper was already mined here during the Sothi-Siswal period going back to c. 4000 BCE. Ancient Kalibangan and Kunal, Haryana settlements obtained copper here.[15]
Geographical features[edit]
See also: Tectonic evolution of the Aravalli Mountains § General formation
The Aravalli Range, seen from the range's highest point at Guru Shikhar, in Rajasthan.
The Aravalli Range can be divided into the following parts (north to south direction):
Archean basement, is a Banded Gneissic Complex (BGC) with schists (medium grade metamorphic rock), gneisses (high grade regional metamorphic rock), composite gneiss and quartzites. It forms the basement rock for both Delhi Supergroup and Aravalli Supergroup.
Delhi Supergroup
Alwar Group, with arenaceous and mafic volcanic rocks
Delhi Ridge, in north
Haryana Aravalli ranges, in the west
Tosham Hill range, basement rocks are quartzite with chiastolite, the upper layers of quartz porphyry ring dyke, felsite, welded tuff and muscovite biotite granite rocks have commercially nonviable tin, tungsten and copper.
Rajasthan Alwar range, in the east
Ajabgarh Group-Kumbhalgarh Group, with Carbonate, mafic volcanic and argillaceous rocks
Raialo Group, with Mafic volcanic and calcareous rocks
Aravalli Supergroup
Debari Group, with Carbonates, quartzite, and pelitic rocks
Jharol Group, with Turbidite facies and argillaceous rocks
The Delhi Ridge is the northernmost end of the Aravalli range, which begins in Central Delhi at Raisina hill. The ridge diagonally traverses to the South Delhi (hills of Asola Bhatti Wildlife Sanctuary), where at the hills of Bandhwari, it meets the Haryana Aravalli range consisting of various isolated hills and rocky ridges passing along the southern border of Haryana.[16]
The Aravalli supergroup passes through Rajasthan state, dividing it into two halves, with three-fifths of Rajasthan on the western side towards Thar Desert and two third on the eastern side consisting of the catchment area of Banas and Chambal rivers bordering the state of Madhya Pradesh. Guru Shikhar, the highest peak in the Aravalli Range at 5650 feet (1722 meters) in Mount Abu of Rajasthan, lies near the south-western extremity of the Central Aravalli range, close to the border with Gujarat state. The southern Aravalli Supergroup enters the northeast of Gujarat near Modasa where it lends its name to the Aravalli district, and ends at the center of the state at Palanpur near Ahmedabad.
Human history[edit]
The Aravalli Range has been site of three broad stages of human history, early stone age saw the use of flint stones; mid-stone age starting from 20,000 BP saw the domestication of cattle for agriculture; and post stone age starting from 10,000 BP saw the development of the Kalibangan civilization, 4,000 years old Aahar civilization and 2,800 years old Gneshwar civilization, Aarayan civilization and Vedic era civilizations.
Early stone age[edit]
Mid-stone age[edit]
Post stone age[edit]
Ganeshwar sunari Cultural Complex[edit]
Ganeshwar sunari Cultural Complex (GSCC) is a collection of third millennium BC settlements in the area of the Aravalli Hill Range. Among them, there are similarities in material culture, and in the production of copper tools. They are located near the copper mines.
"The GSCC is east of the Harappan culture, to the north-east of Ahar-Banas Complex, north/north west to the Kayatha Culture and at a later date, west of the OCP-Copper Hoard sites (Ochre Coloured Pottery culture-Copper Hoard Culture). Located within the regions of the Aravalli Hill Range, primarily along the Kantli, Sabi, Sota, Dohan and Bondi rivers, the GJCC is the largest copper producing community in third millennium BC South Asia, with 385 sites documented. Archaeological indicators of the GSCC were documented primarily in Jaipur, Jhunjhunu, and Sikar districts of Rajasthan, India ..."[17]
Among their pottery, we find the incised ware, and reserved slip ware.
There are two main type sites, Ganeshwar, and Sunari, in Tehsil Kot Putli, Jaipur District (Geo coordinates: N 27° 35' 51", 76° 06' 85" E).
Environment[edit]
A lake nested within Aravali Hills.
Climate[edit]
The Northern Aravalli range in Delhi and Haryana has humid subtropical climate and hot semi-arid climate continental climate with very hot summers and relatively cool winters.[18] The main characteristics of climate in Hisar are dryness, extremes of temperature, and scanty rainfall.[19] The maximum daytime temperature during the summer varies between 40 and 46 °C (104 and 115 °F). During winter, its ranges between 1.5 and 4 °C.[20]
The Central Aravalli range in Rajasthan has an arid and dry climate.
The Southern Aravalli range in Gujarat has a tropical wet and dry climate
Rivers[edit]
Following rivers flow from the Aravalli range.
North-to-south flowing rivers, originate from the western slopes of Aravalli range in Rajasthan, pass through the southeastern portion of the Thar Desert, and end into Gujarat.
Luni River, originates in the Pushkar valley near Ajmer, ends in the marshy lands of Rann of Kutch.
Sakhi river, ends in the marshy lands of Rann of Kutch.
Sabarmati River, originates one the western slopes of Aravalli range of the Udaipur District, end into the Gulf of Cambay of Arabian Sea.
West to north-west flowing rivers, originate from the western slopes of Aravalli range in Rajasthan, flow through semi-arid historical Shekhawati region, drain into southern Haryana. Several Ochre Coloured Pottery culture sites, also identified as late Harappan phase of Indus Valley Civilisation culture,[21] has been found along the banks of these rivers.
Sahibi River, originates near Manoharpur in Sikar district flows through Haryana, along with its following tributaries:[22][23][24][25]
Dohan river, tributary of Sahibi river, originates near Neem Ka Thana in Sikar district).
Sota River, tributary of Sahibi river, merges with Sahibi river at Behror in Alwar district.
Krishnavati river, former tributary of Sahibi river, originates near Dariba copper mines in Rajsamand district of Rajasthan, flows through Patan in Dausa district and Mothooka in Alwar district, then disappears in Mahendragarh district in Haryana much before reaching Sahibi river.
West to north-east flowing rivers, originating from the eastern slopes of Aravalli range in Rajasthan, flow northwards to Yamuna.
Chambal River, a southern-side tributary of Yamuna river.
Banas River, a northern-side tributary of Chambal river.
Berach River, a southern-side tributary of Banas River, originates in the hills of Udaipur District.
Ahar River, a right-side (or eastern side) tributary of the Berach river, originates in the hills of Udaipur District, flows through Udaipur city forming the famous Lake Pichola.
Wagli River, a right-side tributary of the Berach River.
Wagon River, a right-side tributary of the Berach River.
Gambhiri River, a right-side tributary of the Berach river.
Orai River, a right-side tributary of the Berach River.
Ecology[edit]
Flora[edit]
The Aravalli Range has several forests with a diversity of environment.[26]
Fauna[edit]
Ranthambore National Park, in Rajasthan.
The Aravalli Range is rich in wildlife. The first ever 2017 wildlife survey of 200 square meter area cross five districts (Gurgaon, Faridabad, Mewat, Rewari and Mahendergarh) of Haryana done by the Wildlife Institute of India (WII) found 14 species, including leopards, striped hyena (7 sightings), golden jackal (9 sightings, with 92% occupancy across the survey area), nilgai (55 sightings), palm civet (7 sightings), wild pig (14 sightings), rhesus macaque (55 sightings), peafowl (57 sightings) and Indian crested porcupine (12 sightings). Encouraged by first survey, wildlife department has prepared a plan for the comprehensive study and census of wildlife across the whole Aravalli range, including radio collar tracking of the wild animals.[26]
Concerns[edit]
In May 1992, some parts of the Aravalli hills in Rajasthan and Haryana were protected from mining through the Ecologically Sensitive Areas clauses of Indian laws. In 2003, the central government of India prohibited mining operations in these areas. In 2004, India's Supreme Court banned mining in the notified areas of Aravalli Range. In May 2009, the Supreme Court extended the ban on mining in an area of 448 km2 across the Faridabad, Gurgaon and Mewat districts in Haryana, covering the Aravalli Range.[27][28]
A 2013 report used high resolution Cartosat-1 & LISS-IV satellite imaging to determine the existence and condition of mines in the Aravalli Range. In the Guru Gram district, the Aravalli hills occupy an area of 11,256 hectares, of which 491 (4.36%) hectares had mines, of which 16 hectares (0.14%) were abandoned flooded mines. In the Faridabad and Mewat districts, about 3610 hectares were part of mining industry, out of a total of 49,300 hectares. These mines were primarily granite and marble quarries for India's residential and real estate construction applications.[29] In the Central Rajasthan region, Sharma states that the presence of some mining has had both positive and negative effects on neighboring agriculture and the ecosystem. The rain induced erosion brings nutrients as well as potential contaminants.[30]
Economy[edit]
The Aravali Range is the source area of many rivers, resulting in development of human settlements with sustainable economy since pre-historic times. The Delhi Mumbai Industrial Corridor Project, Western Dedicated Freight Corridor, Mumbai–Ahmedabad high-speed rail corridor, North Western Railway network, Jaipur-Kishangarh Expressway and Delhi-Jaipur Expressway, all run parallel to the length of the Aravalli Range providing an economic boost.[31]
Tourism[edit]
Aravali range is the home of several forests, wildlife and protected areas, UNESCO heritage listed forts, hundreds of rivers and ancient history to sustain a large tourism industry.
Concerns[edit]
Damage to the environment and ecology from the unorganised urbanisation, overexploitation of the natural resources including water and minerals, mining, untreated human waste and disposal, pollution, loss of forest cover and wildlife habitat, unprotected status of most of the Aravalli and the lack of an integrated Aravalli management agency are the major causes of concern.
Gallery[edit]
The Aravali Range inside Ranthambhore National Park, in Rajasthan.
Aravalli range near Udaipur Rajasthan
See also[edit]
Mountains portal
Environment portal
Ecology portal
Asola Bhatti Wildlife Sanctuary, Delhi
Aravali Biodiversity Park
Arid Forest Research Institute
Hill Forts of Rajasthan
Pinangwan
Further reading[edit]
External links[edit]
Wikimedia Commons has media related to Aravalli Range.
Wikivoyage has a travel guide for Western India.
Aravali Range Homepage India Environment Portal
Rainfall
Books[edit]
Watershed Management in Aravali Foothills, by Gurmel Singh, S. S. Grewal, R. C. Kaushal. Published by Central Soil & Water Conservation Research & Training Institute, 1990.
References[edit]
Jump up ^ "Aravalli Biodiversity Park, Gurgaon". Archived from the original on 2012-05-28.
Jump up ^ Kohli, M.S. (2004), Mountains of India: Tourism, Adventure, Pilgrimage, Indus Publishing, pp. 29–, ISBN 978-81-7387-135-1
Jump up ^ Dale Hoiberg; Indu Ramchandani (2000). "Aravali Range". Students' Britannica India. Popular Prakashan. pp. 92–93. ISBN 0-85229-760-2.
Jump up ^ George Smith (1882). The Geography of British India, Political & Physical. J. Murray. p. 23.
Jump up ^ "Aravali Range". Britannica.com.
Jump up ^ Roy, A. B. (1990). Evolution of the Precambrian crust of the Aravalli Range. Developments in Precambrian Geology, 8, 327-347.
Jump up ^ Mishra, D.C.; Kumar, M. Ravi. Proterozoic orogenic belts and rifting of Indian cratons: Geophysical constraints. Geoscience Frontiers. 2013 March. 5: 25–41.
Jump up ^ P. K. VermaR. O. Greiling, December 1995, "Tectonic evolution of the Aravalli orogen (NW India): an inverted Proterozoic rift basin?", Geologische Rundschau, Volume 84, Issue 4, pp 683–696.
Jump up ^ Tony Waltham (2009). Foundations of Engineering Geology (3rd ed.). Taylor & Francis. p. 20. ISBN 0-415-46959-7.
Jump up ^ Philip Kearey; Keith A. Klepeis; Frederick J. Vine (2009). "Chapter 10: Orogenic belts". Global Tectonics (3rd ed.). Wiley-Blackwell. p. 287. ISBN 1-4051-0777-4.
Jump up ^ M. Deb and Wayne David Goodfellow, 2004, "Sediment Hosted Lead-Zinc Sulphide Deposits", Narosa Publishing, pp 260.
Jump up ^ Naveed Qamar, "Indian shield rocks".
Jump up ^ SM Gandhi (2000) Chapter 2 – Ancient Mining and Metallurgy in Rajasthan, Crustal Evolution and Metallogeny in the Northwestern Indian Shield: A Festschrift for Asoke Mookherjee, ISBN 978-1842650011
Jump up ^ Shrivastva, R. (1999). Mining of copper in ancient India. Indian Journal of History of Science, 34, 173-180
Jump up ^ Jane McIntosh, The Ancient Indus Valley: New Perspectives. Understanding ancient civilizations. ABC-CLIO, 2008 ISBN 1576079074 p77
Jump up ^ Bhuiyan, C., Singh, R. P., & Kogan, F. N. (2006). Monitoring drought dynamics in the Aravalli region (India) using different indices based on ground and remote sensing data. International Journal of Applied Earth Observation and Geoinformation, 8(4), 289-302
Jump up ^ Uzma Z. Rizvi (2010) Indices of Interaction: Comparisons between the Ahar-Banas and Ganeshwar Jodhpura Cultural Complex Archived May 9, 2016, at the Wayback Machine., in EASAA 2007: Special Session on Gilund Excavations, edited by T. Raczek and V. Shinde, pp. 51-61. British Archaeological Reports: ArchaeoPress
Jump up ^ "Climate of Hisar". PPU. Archived from the original on 5 May 2012. Retrieved 27 May 2012.
Jump up ^ "Climate of Hisar". District Administration, Hisar. Retrieved 27 May 2012.
Jump up ^ "More snowfall in Himachal". The Hindu. Retrieved 24 March 2016.
Jump up ^ Gupta, S.P. (ed.) (1995), The lost Sarasvati and the Indus Civilization, Jodhpur: Kusumanjali Prakashan CS1 maint: Extra text: authors list (link)
Jump up ^ Cultural Contours of India: Dr. Satya Prakash Felicitation Volume, Vijai Shankar Śrivastava, 1981. ISBN 0391023586
Jump up ^ Sahibi river
Jump up ^ Google Books: Page 41, 42, 43, 44, 47 (b) Sahibi Nadi (River), River Pollution, By A.k.jain
Jump up ^ Minerals and Metals in Ancient India: Archaeological evidence, Arun Kumar Biswas, Sulekha Biswas, University of Michigan. 1996. ISBN 812460049X.
^ Jump up to: a b Aravalis in Gurugram, Faridabad core area for leopards, finds survey, The Times of India, 17 June 2017
Jump up ^ SC bans all mining activity in Aravali hills area of Haryana, 9 May 2009.
Jump up ^ Mission Green: SC bans mining in Aravali hills Hindustan Times, 9 May 2009.
Jump up ^ Rai and Kumar, MAPPING OF MINING AREAS IN ARAVALLI HILLS IN GURGAON, FARIDABAD & MEWAT DISTRICTS OF HARYANA USING GEO-INFORMATICS TECHNOLOGY, International Journal of Remote Sensing & Geoscience, Volume 2, Issue 1, Jan. 2013
Jump up ^ Sharma, K. C. (2003). Perplexities and Ecoremediation of Central Aravallis of Rajasthan. Environmental Scenario for 21st Century, ISBN 978-8176484183, Chapter 20
Jump up ^ Jha, Bagis, TNN. 195-km super expressway to link Delhi, Jaipur, The Economic Times, 21 March 2017, Accessed on 20 June 2017.
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Retrieved from "https://en.wikipedia.org/w/index.php?title=Aravalli_Range&oldid=848748675"
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