document_title: Road speed limits in the Republic of Ireland

question_text: what is the maximum speed limit on national roads in ireland

text: History[edit]

text: The first speed limits in Ireland were introduced prior to independence, by regulations made in 1876 under the Dublin Traffic Act 1875, which prescribed speed limits of 6 mph (9.7 km/h) for certain vehicles. The Light Locomotives on Highways (Ireland) Order 1896 then set a maximum national speed limit of 12 mph (19 km/h) with a speed limit of 6 mph (9.7 km/h) for traffic in villages, towns and the Dublin Metropolitan Police District. Vehicles weighing more than 2 tons (unladen) were restricted to 5 mph (8.0 km/h) in these areas. This situation was updated in 1933 with Road Traffic Act 1933 [1] prescribing an ordinary speed limit of 25 mph (40 km/h) for light motor vehicles or heavy motor vehicles fitted with pneumatic tyres. Lower speed limits were applied for heavy motor vehicles without some pneumatic tyres, or used for pulling another vehicle. Road signage was established by the Traffic Signs Regulations, 1956.[2]

text: However, the main piece of legislation responsible for the introduction of speed limits in Ireland was Part IV of the Road Traffic Act, 1961.[3] This repealed the 1933 Act and allowed the Minister for the Environment to prescribe a general speed limit through regulations made under this Act. It also allowed local authorities to specify special speed limits through regulations made under this Act. The first regulations made were the Road Traffic (Speed Limits) Regulations, 1963 [4] which set down a speed limit of 50 mph (80 km/h) for all roads except those subject to a built up area speed limit of 30 mph (48 km/h) or special speed limit of 40 mph (64 km/h). Throughout the mid to late 1960s local authorities studied roads in their areas and had regulations drafted specifically for their county which prescribed speed limits of 30 mph (48 km/h) and 40 mph (64 km/h) along specifically named roads in their administrative area.

text: On 1 April 1969 the Minister for the Environment through the Road Traffic (General Speed Limit) Regulations, 1969 [5] finally prescribed a general national speed limit of 60 mph (97 km/h) on all roads except those subject to special and built up area speed limits of 40 mph (64 km/h) and 30 mph (48 km/h). This replaced the 50 mph (80 km/h) speed limit in all but a few cases where regulations had been drafted specifically to impose a 50 mph (80 km/h) limit. While the built up area and special speed limits were clearly indicated to motorists by the number 30, 40 or 50 in black numbers on a white circular background with a red outline, there was no such signage for the general 60 mph (97 km/h) speed limit. This was indicated to motorists by a "general speed limit" applies sign which consisted of a circular white sign with a black diagonal line bisecting it. The general limit was reduced to 55 mph (89 km/h) in 1979[6] as an energy conservation measure during the 1979 energy crisis.[7] Some drivers remained unaware of this change.[8] A review of speed limits from 1990-92 restored the 60 mph limit.[9][10]

text: It was not until 1992 that a 70 mph (113 km/h) speed limit was authorised on the State's motorways. This occurred through the Road Traffic (Speed Limits) (County of Kildare) (Amendment) Regulations, 1992 [11] and the similar Road Traffic (Speed Limits) (County Borough of Dublin and County of Dublin) (Amendment) Regulations, 1992.[12] This authorised traffic on the M1, M7, M11 and M50 to travel at 70 mph (113 km/h) where signposted. This was extended to motorways in general by the Road Traffic Act, 1994.[13] A minimum speed limit of 30 mph (48 km/h) had previously been set in 1974 through the Local Government (Roads and Motorways) Act, 1974.[14]

text: On 20 January 2005, Ireland adopted metric speed limits.[15] Around 35,000 existing signs were replaced and a further 23,000 new signs erected bearing the speed limit in kilometres per hour. To avoid confusion with the old signs, each speed limit sign now has "km/h" beneath the numerals.

text: During the period 2000-2010, the state underwent a massive road building programme which included the construction of a national motorway network. Many sections of this "motorway network" such as the N6 from Kinnegad to Kilbeggan were originally built to high quality dual carriageway standard. The Roads Act, 2007 enacted in July 2007 made a provision for the redesignation of dual carriageways to motorway. This meant the hard shoulder of the high quality dual carriageways chosen to be redesignated, had to be changed from a broken yellow line to a continuous yellow line. Green signage also had to be changed to blue. In some instances the cost of this retrofit ran to millions of euro as it involved the replacement of existing gantry and large panel signage as well as the application of hundreds of kilometres of thermoplastic road paint. In September 2008, the Cahir to Cashel stretch of the M8 had its gantry signage changed and hard shoulder re-painted. Parts of the M6 also underwent the same process.

text: In February 2012 Leo Varadkar, the Minister for Transport, Tourism and Sport, tasked a working group with reviewing speed-limit policy and implementation.[16] Its report, published in 2013, identified two key issues: inconsistency of limits between similar roads, and inappropriateness of limits on some roads.[17] It found the default limits were unsafely high on many minor roads where they applied. It recommended the introduction of a "rural speed limit" sign, to emphasise that the statutory maximum speed was not necessarily a safe speed, which would comprise an "end of speed limit" circular sign over a "Slow" rectangular plate.[18] This was introduced in 2016 as a combination of Sign RUS 041A and Plate P 080 (bilingually reading SLOW and Go Mall); it can only be used on local secondary and tertiary roads (not on national, regional, or local primary roads).[19]

text: Signs[edit]

text: RUS 041A

text: Ordinary speed limits[edit]

text: Different default speed limits apply to particular categories of roads. Default speed limits are termed as "ordinary speed limits" by the Road Traffic Act 2004. There are also speed restrictions for certain classes of vehicles. As of 2007, the ordinary speed limits are as follows:

text:
120 km/h (75 mph) for motorways
100 km/h (62 mph) for National Routes (Primary and Secondary) that are not motorway status.
80 km/h (50 mph) for local and regional roads.
50 km/h (31 mph) in built up areas.

text: Special speed limits[edit]

text:
120 km/h (75 mph) (for Dual Carriageways forming part of a national road only)
60 km/h (37 mph)
40 km/h (25 mph)
30 km/h (19 mph)

text: There are particular powers available to local county councils under the Road Traffic Act 2004 [20] to apply "special speed limits" to particular stretches of road. Special speed limits of 30, 50, 60, 80, 100 and 120 km/h (19, 31, 37, 50, 62 and 75 mph) can be imposed, but only 30 and 60 km/h (19 and 37 mph) are exclusively "special" as opposed to the others which are "ordinary". The 120 km/h (75 mph) limit is ordinary for motorways but can be special for dual carriageways forming part of a national primary road. Special speed limits are usually lower than normal, for schools, etc. One instance of higher speed limits being applied is that of the new N2 route from the M50 motorway in Fingal (Dublin) to north of Ashbourne, County Meath where a special speed limit of 120 km/h (75 mph) was imposed from 15 June 2006, therefore becoming the first non-motorway road in Ireland to obtain this speed limit. According to the project engineers, the National Roads Authority decided due to the lack of available space at the M50 junction to accommodate a parallel joining non-motorway route that they would designate the new road as high quality dual carriageway and block off the existing road from the M50. The 2004 Act has therefore allowed Local Authorities to get around such issues as the implications of motorway restrictions on learner drivers as under this act such drivers are now permitted to travel at speeds up to 120 km/h (75 mph) on such roads as this section of the N2. The N1 dual carriageway north of Dundalk has also recently been granted a special speed limit of 120 km/h (75 mph), in line with its preceding M1 motorway. As of 2 March 2007, Cork County Council and Limerick city and county councils have published amendments to local bye-laws to adjust several High Quality Carriageways' speed limits to 120 km/h (75 mph).[21] S.I. No. 331 of 2012 allowed a new speed limit of 40km/h to be applied by a city or county council.[22]

text: Cautionary speed limits[edit]

text: The Minister for Transport issued a direction to road authorities under section 95(16) of the Road Traffic Act 1961 in February 2007 with respect to a range of non-regulatory traffic signs. Chapter 8 of the Traffic Signs Manual was superseded by an updated version which allowed for the erection of signage stating a cautionary speed limit in the vicinity of Road Works. These speed limits are purposely different from legal speed limits and always display a speed limit that ends in 5, for example 35 km/h (22 mph), 45 km/h (28 mph), etc. They are not legally binding on drivers but it is likely that in the event of a road traffic accident that the issue of if they were being complied with, would be taken into account.

text: Road works speed limits[edit]

text: The Manager of a City or County Council can reduce the speed limit on a road undergoing road works for a stated period of time by executive order under powers available to him/her under the Road Traffic Act 2004. The reduced speed limits are typically 30, 50 or 90 km/h (19, 31 or 56 mph). These are different from Cautionary Speed Limits as they are binding on drivers and it is an offence to exceed a road works speed limit.


document_title: Cellular respiration

question_text: how many net molecules of atp are produced from the complete oxidation of one molecule of glucose

root

text: Cellular respiration

text: Aerobic respiration

text: Aerobic respiration requires oxygen (O2) in order to create ATP. Although carbohydrates, fats, and proteins are consumed as reactants, it is the preferred method of pyruvate breakdown in glycolysis and requires that pyruvate enter the mitochondria in order to be fully oxidized by the Krebs cycle. The products of this process are carbon dioxide and water, but the energy transferred is used to break bonds in ADP as the third phosphate group is added to form ATP (adenosine triphosphate), by substrate-level phosphorylation, NADH and FADH2

tag: p

text:
Simplified reaction:
C6H12O6 (s) + 6 O2 (g) → 6 CO2 (g) + 6 H2O (l) + heat

ΔG = −2880 kJ per mol of C6H12O6

tag: table

text: The negative ΔG indicates that the reaction can occur spontaneously.

text: The potential of NADH and FADH2 is converted to more ATP through an electron transport chain with oxygen as the "terminal electron acceptor". Most of the ATP produced by aerobic cellular respiration is made by oxidative phosphorylation. This works by the energy released in the consumption of pyruvate being used to create a chemiosmotic potential by pumping protons across a membrane. This potential is then used to drive ATP synthase and produce ATP from ADP and a phosphate group. Biology textbooks often state that 38 ATP molecules can be made per oxidised glucose molecule during cellular respiration (2 from glycolysis, 2 from the Krebs cycle, and about 34 from the electron transport system).[2] However, this maximum yield is never quite reached because of losses due to leaky membranes as well as the cost of moving pyruvate and ADP into the mitochondrial matrix, and current estimates range around 29 to 30 ATP per glucose.[2]

text: Aerobic metabolism is up to 15 times more efficient than anaerobic metabolism (which yields 2 molecules ATP per 1 molecule glucose). However some anaerobic organisms, such as methanogens are able to continue with anaerobic respiration, yielding more ATP by using other inorganic molecules (not oxygen) as final electron acceptors in the electron transport chain. They share the initial pathway of glycolysis but aerobic metabolism continues with the Krebs cycle and oxidative phosphorylation. The post-glycolytic reactions take place in the mitochondria in eukaryotic cells, and in the cytoplasm in prokaryotic cells.

text: Aerobic Respiration Summed Up

text: 1. Glycosis:

text: --- 2 ATPs + Glucose → 2 Pyruvic Acid + 4 Hydrogen + 4 ATPs

text: 2. Formation of Acetyl CoA:

text: --- 2 Pyruvic Acid + 2 CoA → 2 Acetyl CoA + 2 Carbon Dioxide + 2 Hydrogen

text: 3. Krebs Cycle:

text: --- 2 Acetyl CoA + 3 O2 → 6 Hydrogen + 4 Carbon Dioxide + 2 ATPs

text: 4. Electron Transport System:

text: --- 12 Hydrogen + 3 O2 → 6 Water + 32 ATPs

text: Overall Reaction:

text: --- Glucose + 6 O2 → 6 Carbon Dioxide + 6 Water + 36 ATPs

text: Glycolysis

text: Glycolysis is a metabolic pathway that takes place in the cytosol of cells in all living organisms. This pathway can function with or without the presence of oxygen. In humans, aerobic conditions produce pyruvate and anaerobic conditions produce lactate. In aerobic conditions, the process converts one molecule of glucose into two molecules of pyruvate (pyruvic acid), generating energy in the form of two net molecules of ATP. Four molecules of ATP per glucose are actually produced, however, two are consumed as part of the preparatory phase. The initial phosphorylation of glucose is required to increase the reactivity (decrease its stability) in order for the molecule to be cleaved into two pyruvate molecules by the enzyme aldolase. During the pay-off phase of glycolysis, four phosphate groups are transferred to ADP by substrate-level phosphorylation to make four ATP, and two NADH are produced when the pyruvate are oxidized. The overall reaction can be expressed this way:

text: Starting with glucose, 1 ATP is used to donate a phosphate to glucose to produce glucose 6-phosphate. Glycogen can be converted into glucose 6-phosphate as well with the help of glycogen phosphorylase. During energy metabolism, glucose 6-phosphate becomes fructose 6-phosphate. An additional ATP is used to phosphorylate fructose 6-phosphate into fructose 1,6-disphosphate by the help of phosphofructokinase. Fructose 1,6-diphosphate then splits into two phosphorylated molecules with three carbon chains which later degrades into pyruvate.

text: Glycolysis can be literally translated as "sugar splitting".[3]

text: Oxidative decarboxylation of pyruvate

text: Pyruvate is oxidized to acetyl-CoA and CO2 by the pyruvate dehydrogenase complex (PDC). The PDC contains multiple copies of three enzymes and is located in the mitochondria of eukaryotic cells and in the cytosol of prokaryotes. In the conversion of pyruvate to acetyl-CoA, one molecule of NADH and one molecule of CO2 is formed.

text: Citric acid cycle

text: This is also called the Krebs cycle or the tricarboxylic acid cycle. When oxygen is present, acetyl-CoA is produced from the pyruvate molecules created from glycolysis. Once acetyl-CoA is formed, aerobic or anaerobic respiration can occur.[4] When oxygen is present, the mitochondria will undergo aerobic respiration which leads to the Krebs cycle. However, if oxygen is not present, fermentation of the pyruvate molecule will occur. In the presence of oxygen, when acetyl-CoA is produced, the molecule then enters the citric acid cycle (Krebs cycle) inside the mitochondrial matrix, and is oxidized to CO2 while at the same time reducing NAD to NADH. NADH can be used by the electron transport chain to create further ATP as part of oxidative phosphorylation. To fully oxidize the equivalent of one glucose molecule, two acetyl-CoA must be metabolized by the Krebs cycle. Two waste products, H2O and CO2, are created during this cycle.

text: The citric acid cycle is an 8-step process involving 18 different enzymes and co-enzymes.[4] During the cycle, acetyl-CoA (2 carbons) + oxaloacetate (4 carbons) yields citrate (6 carbons), which is rearranged to a more reactive form called isocitrate (6 carbons). Isocitrate is modified to become α-ketoglutarate (5 carbons), succinyl-CoA, succinate, fumarate, malate, and, finally, oxaloacetate.

text: The net gain of high-energy compounds from one cycle is 3 NADH, 1 FADH2, and 1 GTP; the GTP may subsequently be used to produce ATP. Thus, the total yield from 1 glucose molecule (2 pyruvate molecules) is 6 NADH, 2 FADH2, and 2 ATP.

text: Oxidative phosphorylation

text: In eukaryotes, oxidative phosphorylation occurs in the mitochondrial cristae. It comprises the electron transport chain that establishes a proton gradient (chemiosmotic potential) across the boundary of inner membrane by oxidizing the NADH produced from the Krebs cycle. ATP is synthesized by the ATP synthase enzyme when the chemiosmotic gradient is used to drive the phosphorylation of ADP. The electrons are finally transferred to exogenous oxygen and, with the addition of two protons, water is formed.

text: Efficiency of ATP production

text: The table below describes the reactions involved when one glucose molecule is fully oxidized into carbon dioxide. It is assumed that all the reduced coenzymes are oxidized by the electron transport chain and used for oxidative phosphorylation.

text:
Step
coenzyme yield
ATP yield
Source of ATP

Glycolysis preparatory phase

−2
Phosphorylation of glucose and fructose 6-phosphate uses two ATP from the cytoplasm.

Glycolysis pay-off phase

4
Substrate-level phosphorylation

2 NADH
3 or 5
Oxidative phosphorylation : Each NADH produces net 1.5 ATP (instead of usual 2.5) due to NADH transport over the mitochondrial membrane

Oxidative decarboxylation of pyruvate
2 NADH
5
Oxidative phosphorylation

Krebs cycle

2
Substrate-level phosphorylation

6 NADH
15
Oxidative phosphorylation

2 FADH2
3
Oxidative phosphorylation

Total yield
30 or 32 ATP
From the complete oxidation of one glucose molecule to carbon dioxide and oxidation of all the reduced coenzymes.

text: Although there is a theoretical yield of 38 ATP molecules per glucose during cellular respiration, such conditions are generally not realized because of losses such as the cost of moving pyruvate (from glycolysis), phosphate, and ADP (substrates for ATP synthesis) into the mitochondria. All are actively transported using carriers that utilize the stored energy in the proton electrochemical gradient.

text:
Pyruvate is taken up by a specific, low Km transporter to bring it into the mitochondrial matrix for oxidation by the pyruvate dehydrogenase complex.
The phosphate carrier (PiC) mediates the electroneutral exchange (antiport) of phosphate (H2PO4−; Pi) for OH− or symport of phosphate and protons (H+) across the inner membrane, and the driving force for moving phosphate ions into the mitochondria is the proton motive force.
The ATP-ADP translocase (also called adenine nucleotide translocase, ANT) is an antiporter and exchanges ADP and ATP across the inner membrane. The driving force is due to the ATP (−4) having a more negative charge than the ADP (−3), and thus it dissipates some of the electrical component of the proton electrochemical gradient.

tag: ul

text: The outcome of these transport processes using the proton electrochemical gradient is that more than 3 H+ are needed to make 1 ATP. Obviously this reduces the theoretical efficiency of the whole process and the likely maximum is closer to 28–30 ATP molecules.[2] In practice the efficiency may be even lower because the inner membrane of the mitochondria is slightly leaky to protons.[5] Other factors may also dissipate the proton gradient creating an apparently leaky mitochondria. An uncoupling protein known as thermogenin is expressed in some cell types and is a channel that can transport protons. When this protein is active in the inner membrane it short circuits the coupling between the electron transport chain and ATP synthesis. The potential energy from the proton gradient is not used to make ATP but generates heat. This is particularly important in brown fat thermogenesis of newborn and hibernating mammals.

text: According to some of newer sources the ATP yield during aerobic respiration is not 36–38, but only about 30–32 ATP molecules / 1 molecule of glucose [6], because:

text:
ATP : NADH+H+ and ATP : FADH2 ratios during the oxidative phosphorylation appear to be not 3 and 2, but 2.5 and 1.5 respectively. Unlike in the substrate-level phosphorylation, the stoichiometry here is difficult to establish.

ATP synthase produces 1 ATP / 3 H+. However the exchange of matrix ATP for cytosolic ADP and Pi (antiport with OH− or symport with H+) mediated by ATP–ADP translocase and phosphate carrier consumes 1 H+ / 1 ATP as a result of regeneration of the transmembrane potential changed during this transfer, so the net ratio is 1 ATP : 4 H+.
The mitochondrial electron transport chain proton pump transfers across the inner membrane 10 H+ / 1 NADH+H+ (4 + 2 + 4) or 6 H+ / 1 FADH2 (2 + 4).

text:
ATP : NADH+H+ coming from glycolysis ratio during the oxidative phosphorylation is

1.5, as for FADH2, if hydrogen atoms (2H++2e−) are transferred from cytosolic NADH+H+ to mitochondrial FAD by the glycerol phosphate shuttle located in the inner mitochondrial membrane.
2.5 in case of malate-aspartate shuttle transferring hydrogen atoms from cytosolic NADH+H+ to mitochondrial NAD+

text: So finally we have, per molecule of glucose

text:
Substrate-level phosphorylation: 2 ATP from glycolysis + 2 ATP (directly GTP) from Krebs cycle
Oxidative phosphorylation

2 NADH+H+ from glycolysis: 2 × 1.5 ATP (if glycerol phosphate shuttle transfers hydrogen atoms) or 2 × 2.5 ATP (malate-aspartate shuttle)
2 NADH+H+ from the oxidative decarboxylation of pyruvate and 6 from Krebs cycle: 8 × 2.5 ATP
2 FADH2 from the Krebs cycle: 2 × 1.5 ATP

text: Altogether this gives 4 + 3 (or 5) + 20 + 3 = 30 (or 32) ATP per molecule of glucose

text: The total ATP yield in ethanol or lactic acid fermentation is only 2 molecules coming from glycolysis, because pyruvate is not transferred to the mitochondrion and finally oxidized to the carbon dioxide (CO2), but reduced to ethanol or lactic acid in the cytoplasm.[6]

text: Fermentation

text: Without oxygen, pyruvate (pyruvic acid) is not metabolized by cellular respiration but undergoes a process of fermentation. The pyruvate is not transported into the mitochondrion, but remains in the cytoplasm, where it is converted to waste products that may be removed from the cell. This serves the purpose of oxidizing the electron carriers so that they can perform glycolysis again and removing the excess pyruvate. Fermentation oxidizes NADH to NAD+ so it can be re-used in glycolysis. In the absence of oxygen, fermentation prevents the buildup of NADH in the cytoplasm and provides NAD+ for glycolysis. This waste product varies depending on the organism. In skeletal muscles, the waste product is lactic acid. This type of fermentation is called lactic acid fermentation. In strenuous exercise, when energy demands exceed energy supply, the respiratory chain cannot process all of the hydrogen atoms joined by NADH. During anaerobic glycolysis, NAD+ regenerates when pairs of hydrogen combine with pyruvate to form lactate. Lactate formation is catalyzed by lactate dehydrogenase in a reversible reaction. Lactate can also be used as an indirect precursor for liver glycogen. During recovery, when oxygen becomes available, NAD+ attaches to hydrogen from lactate to form ATP. In yeast, the waste products are ethanol and carbon dioxide. This type of fermentation is known as alcoholic or ethanol fermentation. The ATP generated in this process is made by substrate-level phosphorylation, which does not require oxygen.

text: Fermentation is less efficient at using the energy from glucose: only 2 ATP are produced per glucose, compared to the 38 ATP per glucose nominally produced by aerobic respiration. This is because the waste products of fermentation still contain chemical potential energy that can be released by oxidation. Ethanol, for example, can be burned in an internal combustion engine like gasoline. Glycolytic ATP, however, is created more quickly. For prokaryotes to continue a rapid growth rate when they are shifted from an aerobic environment to an anaerobic environment, they must increase the rate of the glycolytic reactions. For multicellular organisms, during short bursts of strenuous activity, muscle cells use fermentation to supplement the ATP production from the slower aerobic respiration, so fermentation may be used by a cell even before the oxygen levels are depleted, as is the case in sports that do not require athletes to pace themselves, such as sprinting.

text: Anaerobic respiration

text: Cellular respiration is the process by which biological fuels are oxidised in the presence of an inorganic electron acceptor (such as oxygen) to produce large amounts of energy, to drive the bulk production of ATP.

text: Anaerobic respiration is used by some microorganisms in which neither oxygen (aerobic respiration) nor pyruvate derivatives (fermentation) is the final electron acceptor. Rather, an inorganic acceptor such as sulfate or nitrate is used. Such organisms are typically found in unusual places such as underwater caves or near hydrothermal vents at the bottom of the ocean.


document_title: List of presidents of Southern University

question_text: who is the president of southern university baton rouge

text: This article does not cite any sources. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (September 2018) (Learn how and when to remove this template message)

text: This article needs more links to other articles to help integrate it into the encyclopedia. Please help improve this article by adding links that are relevant to the context within the existing text. (June 2016) (Learn how and when to remove this template message)

text: This is a list of presidents of Southern University and A&M College in Baton Rouge, Louisiana. It was designated as a land grant college in 1890, to serve black students in the state. It added Agricultural and Mechanical College to its title. In 1914 it relocated to Scotlandville, Louisiana in East Baton Rouge Parish, where the state had bought several hundred acres to support the new campus and its agricultural program.

text:
President

Term

Dr. Joseph S. Clark

1914–1938

Dr. Felton G. Clark

1938–1969

Dr. G. Leon Netterville

1969–1974

Dr. Jesse N. Stone, Jr.

1974–1985

Dr. Joffre T. Whisenton

1985–1988

Dr. Dolores R. Spikes*

1988–1996

Dr. Leon R. Tarver II

1997–2005

Dr. Edward Jackson, (interim)

2005–2006

Dr. Ralph Slaughter

2006–2009

Dr. Ronald Mason Jr.

2010–2015

Dr. Ray Belton

2015–present

*First female head of any college system in the U.S.


document_title: Kidney

question_text: the initial stage of blood filtration in the kidneys occurs in which portion of the nephron

question_tokens: the initial stage of blood filtration in the kidneys occurs in which portion of the nephron

text: Kidney

text: Structure[edit]

text: In humans, the kidneys are located high in the abdominal cavity, one on each side of the spine, and lie in a retroperitoneal position at a slightly oblique angle.[2] The asymmetry within the abdominal cavity, caused by the position of the liver, typically results in the right kidney being slightly lower and smaller than the left, and being placed slightly more to the middle than the left kidney.[3][4][5] The left kidney is approximately at the vertebral level T12 to L3,[6] and the right is slightly lower. The right kidney sits just below the diaphragm and posterior to the liver. The left sits below the diaphragm and posterior to the spleen. On top of each kidney is an adrenal gland. The upper parts of the kidneys are partially protected by the 11th and 12th ribs. Each kidney, with its adrenal gland is surrounded by two layers of fat: the perirenal fat present between renal fascia and renal capsule and pararenal fat superior to the renal fascia.

text: The kidney is a bean-shaped structure with a convex and a concave border. A recessed area on the concave border is the renal hilum, where the renal artery enters the kidney and the renal vein and ureter leave. The kidney is surrounded by tough fibrous tissue, the renal capsule, which is itself surrounded by perirenal fat, renal fascia, and pararenal fat. The anterior (front) surface of these tissues is the peritoneum, while the posterior (rear) surface is the transversalis fascia.

text: The superior pole of the right kidney is adjacent to the liver. For the left kidney, it is next to the spleen. Both, therefore, move down upon inhalation.

text: In adult males, the kidney weighs between 125 and 170 grams. In females the weight of the kidney is between 115 and 155 grams.[7] A Danish study measured the median renal length to be 11.2 cm (4.4 in) on the left side and 10.9 cm (4.3 in) on the right side in adults. Median renal volumes were 146 cm3 on the left and 134 cm3 on the right.[8]

text: Gross anatomy[edit]

text: The substance, or parenchyma, of the kidney is divided into two major structures: the outer renal cortex and the inner renal medulla. Grossly, these structures take the shape of eight to 18 cone-shaped renal lobes, each containing renal cortex surrounding a portion of medulla called a renal pyramid.[7] Between the renal pyramids are projections of cortex called renal columns. Nephrons, the urine-producing functional structures of the kidney, span the cortex and medulla. The initial filtering portion of a nephron is the renal corpuscle which is located in the cortex. This is followed by a renal tubule that passes from the cortex deep into the medullary pyramids. Part of the renal cortex, a medullary ray is a collection of renal tubules that drain into a single collecting duct.

text: The tip, or papilla, of each pyramid empties urine into a minor calyx; minor calyces empty into major calyces, and major calyces empty into the renal pelvis. This becomes the ureter. At the hilum, the ureter and renal vein exit the kidney and the renal artery enters. Hilar fat and lymphatic tissue with lymph nodes surrounds these structures. The hilar fat is contiguous with a fat-filled cavity called the renal sinus. The renal sinus collectively contains the renal pelvis and calyces and separates these structures from the renal medullary tissue.[9]

text: The kidneys possess no overtly moving structures

text: Blood supply[edit]

text: The renal circulation supplies the blood to the kidneys via the renal arteries, left and right, which branch directly from the abdominal aorta. Despite their relatively small size, the kidneys receive approximately 20% of the cardiac output.[7]

text: Each renal artery branches into segmental arteries, dividing further into interlobar arteries, which penetrate the renal capsule and extend through the renal columns between the renal pyramids. The interlobar arteries then supply blood to the arcuate arteries that run through the boundary of the cortex and the medulla. Each arcuate artery supplies several interlobular arteries that feed into the afferent arterioles that supply the glomeruli.

text: After filtration occurs, the blood moves through a small network of venules that converge into interlobular veins. As with the arteriole distribution, the veins follow the same pattern: the interlobular provide blood to the arcuate veins then back to the interlobar veins, which come to form the renal vein exiting the kidney for transfusion for blood.

text: The table below shows the path that blood takes when it travels through the glomerulus, traveling "down" the arteries and "up" the veins. However, this model is greatly simplified for clarity and symmetry. Some of the other paths and complications are described at the bottom of the table. The interlobar artery and vein (not to be confused with interlobular) are between two renal lobes, also known as the renal column (cortex region between two pyramids).

text:
Arteries (down)
Veins (up)

Abdominal aorta
Vena cava

Renal artery (Note 1)
Renal vein

Segmental arteries (Note 2)
–

Lobar arteries
–

Interlobar artery
Interlobar vein

Afferent arterioles
Efferent arterioles (Note 4)

Glomerulus
Glomerulus

text:
Note 1: The renal artery also provides a branch to the inferior suprarenal artery to supply the adrenal gland.
Note 2: Each renal artery partitions into an anterior and posterior branch. The anterior branch further divides into the superior (apical), anterosuperior, anteroinferior and inferior segmental arteries. The posterior branch continues as the posterior segmental artery.
Note 3: Also called the cortical radiate arteries. The interlobular artery also supplies to the stellate veins.
Note 4: The efferent arterioles do not directly drain into the interlobular vein, but rather they go to the peritubular capillaries first. The efferent arterioles of the juxtamedullary nephron drain into the vasa recta.

text: Nerve supply[edit]

text: The kidney and nervous system communicate via the renal plexus, whose fibers course along the renal arteries to reach each kidney.[10] Input from the sympathetic nervous system triggers vasoconstriction in the kidney, thereby reducing renal blood flow.[10] The kidney also receives input from the parasympathetic nervous system, by way of the renal branches of the vagus nerve; the function of this is yet unclear.[10][11] Sensory input from the kidney travels to the T10-11 levels of the spinal cord and is sensed in the corresponding dermatome.[10] Thus, pain in the flank region may be referred from corresponding kidney.[10]

text: Microanatomy[edit]

text: Renal histology studies the microscopic structure of the kidney. Distinct cell types include:

text:
Kidney glomerulus parietal cell
Kidney glomerulus podocyte
Kidney proximal tubule brush border cell
Loop of Henle thin segment cell
Thick ascending limb cell
Kidney distal tubule cell
Collecting duct principal cell
Collecting duct intercalated cell
Interstitial kidney cells

text: Gene and protein expression[edit]

text: About 20,000 protein coding genes are expressed in human cells and almost 70% of these genes are expressed in normal, adult kidneys.[12][13] Just over 300 genes are more specifically expressed in the kidney, with only some 50 genes being highly specific for the kidney. Many of the corresponding kidney specific proteins are expressed in the cell membrane and function as transporter proteins. The highest expressed kidney specific protein is uromodulin, the most abundant protein in urine with functions that prevent calcification and growth of bacteria. Specific proteins are expressed in the different compartments of the kidney with podocin and nephrin expressed in glomeruli, Solute carrier family protein SLC22A8 expressed in proximal tubules, calbindin expressed in distal tubules and aquaporin 2 expressed in the collecting duct cells.[14]

text: Development[edit]

text: The mammalian kidney develops from intermediate mesoderm. Kidney development, also called nephrogenesis, proceeds through a series of three successive developmental phases: the pronephros, mesonephros, and metanephros. The metanephros are primordia of the permanent kidney.[15]

text: Function[edit]

text: The microscopic structural and functional unit of the kidney is the nephron. It processes the blood supplied to it via filtration, reabsorption, secretion and excretion; the consequence of those processes is the production of urine.

text: Mechanism[edit]

text: Filtration[edit]

text: Filtration, which takes place at the renal corpuscle, is the process by which cells and large proteins are filtered from the blood to make an ultrafiltrate that eventually becomes urine. The kidney generates 180 liters of filtrate a day. The process is also known as hydrostatic filtration due to the hydrostatic pressure exerted on the capillary walls.

text: Reabsorption[edit]

text: Reabsorption is the transport of molecules from this ultrafiltrate and into the peritubular capillary. It is accomplished via selective receptors on the luminal cell membrane. Water is 99% reabsorbed in the proximal tubule. Glucose at normal plasma levels is completely reabsorbed in the proximal tubule. The mechanism for this is the Na+/glucose cotransporter. A plasma level of 350 mg/dL will fully saturate the transporters and glucose will be lost in the urine. A plasma glucose level of approximately 160 is sufficient to allow glucosuria, which is an important clinical clue to diabetes mellitus. Amino acids are reabsorbed by sodium dependent transporters in the proximal tubule. Hartnup disease is a deficiency of the tryptophan amino acid transporter, which results in pellagra.[16]

text:
Location of Reabsorption
Reabsorbed nutrient
Notes

Early proximal tubule
Glucose (100%), amino acids (100%), bicarbonate (90%), Na+ (65%), Cl−, phosphate and H2O (65%)

PTH will inhibit phosphate reabsorption.
AT II stimulates Na+, H2O and HCO3− reabsorption.

Thin descending loop of Henle
H2O

Reabsorbs via medullary hypertonicity and makes urine hypertonic.

Thick ascending loop of Henle
Na+ (10–20%), K+, Cl−; indirectly induces para cellular reabsorption of Mg2+, Ca2+

This region is impermeable to H2O and the urine becomes less concentrated as it ascends.

Early distal convoluted tubule
Na+, Cl−

PTH causes Ca2+ reabsorption.

Collecting tubules
Na+(3–5%), H2O

Na+ is reabsorbed in exchange for K+, and H+, which is regulated by aldosterone.
ADH acts on the V2 receptor and inserts aquaporins on the luminal side

Source:[16]

text: Secretion[edit]

text: Secretion is the reverse of reabsorption: molecules are transported from the peritubular capillary through the interstitial fluid, then through the renal tubular cell and into the ultrafiltrate.

text: Excretion[edit]

text: Homeostasis[edit]

text: The kidney participates in whole-body homeostasis, regulating acid-base balance, electrolyte concentrations, extracellular fluid volume, and blood pressure. The kidney accomplishes these homeostatic functions both independently and in concert with other organs, particularly those of the endocrine system. Various endocrine hormones coordinate these endocrine functions; these include renin, angiotensin II, aldosterone, antidiuretic hormone, and atrial natriuretic peptide, among others.

text: The kidneys excrete a variety of waste products produced by metabolism into the urine. These include the nitrogenous wastes urea, from protein catabolism, and uric acid, from nucleic acid metabolism. The ability of mammals and some birds to concentrate wastes into a volume of urine much smaller than the volume of blood from which the wastes were extracted is dependent on an elaborate countercurrent multiplication mechanism. This requires several independent nephron characteristics to operate: a tight hairpin configuration of the tubules, water and ion permeability in the descending limb of the loop, water impermeability in the ascending loop, and active ion transport out of most of the ascending limb. In addition, passive countercurrent exchange by the vessels carrying the blood supply to the nephron is essential for enabling this function.

text: Acid-base balance[edit]

text: Two organ systems, the kidneys and lungs, maintain acid-base homeostasis, which is the maintenance of pH around a relatively stable value. The lungs contribute to acid-base homeostasis by regulating carbon dioxide (CO2) concentration. The kidneys have two very important roles in maintaining the acid-base balance: to reabsorb and regenerate bicarbonate from urine, and to excrete hydrogen ions and fixed acids (anions of acids) into urine.

text: Regulation of osmolality[edit]

text: Maintaining water and salt level of the body. Any significant rise in plasma osmolality is detected by the hypothalamus, which communicates directly with the posterior pituitary gland. An increase in osmolality causes the gland to secrete antidiuretic hormone (ADH), resulting in water reabsorption by the kidney and an increase in urine concentration. The two factors work together to return the plasma osmolality to its normal levels.

text: ADH binds to principal cells in the collecting duct that translocate aquaporins to the membrane, allowing water to leave the normally impermeable membrane and be reabsorbed into the body by the vasa recta, thus increasing the plasma volume of the body.

text: There are two systems that create a hyperosmotic medulla and thus increase the body plasma volume: Urea recycling and the 'single effect.'

text: Urea is usually excreted as a waste product from the kidneys. However, when plasma blood volume is low and ADH is released the aquaporins that are opened are also permeable to urea. This allows urea to leave the collecting duct into the medulla creating a hyperosmotic solution that 'attracts' water. Urea can then re-enter the nephron and be excreted or recycled again depending on whether ADH is still present or not.

text: The 'single effect' describes the fact that the ascending thick limb of the loop of Henle is not permeable to water but is permeable to sodium chloride. This allows for a countercurrent exchange system whereby the medulla becomes increasingly concentrated, but at the same time setting up an osmotic gradient for water to follow should the aquaporins of the collecting duct be opened by ADH.

text: Blood pressure regulation[edit]

text: Although the kidney cannot directly sense blood, long-term regulation of blood pressure predominantly depends upon the kidney. This primarily occurs through maintenance of the extracellular fluid compartment, the size of which depends on the plasma sodium concentration. Renin is the first in a series of important chemical messengers that make up the renin-angiotensin system. Changes in renin ultimately alter the output of this system, principally the hormones angiotensin II and aldosterone. Each hormone acts via multiple mechanisms, but both increase the kidney's absorption of sodium chloride, thereby expanding the extracellular fluid compartment and raising blood pressure. When renin levels are elevated, the concentrations of angiotensin II and aldosterone increase, leading to increased sodium chloride reabsorption, expansion of the extracellular fluid compartment, and an increase in blood pressure. Conversely, when renin levels are low, angiotensin II and aldosterone levels decrease, contracting the extracellular fluid compartment, and decreasing blood pressure.

text: Hormone secretion[edit]

text: The kidneys secrete a variety of hormones, including erythropoietin, and the enzyme renin. Erythropoietin is released in response to hypoxia (low levels of oxygen at tissue level) in the renal circulation. It stimulates erythropoiesis (production of red blood cells) in the bone marrow. Calcitriol, the activated form of vitamin D, promotes intestinal absorption of calcium and the renal reabsorption of phosphate. Part of the renin–angiotensin–aldosterone system, renin is an enzyme involved in the regulation of aldosterone levels.

text: Calculations of function[edit]

text: Calculations of kidney performance are an important part of physiology and can be estimated using the calculations below.

text: Filtration fraction[edit]

text: The filtration fraction is the amount of plasma that is actually filtered through the kidney. This can be defined using the equation:

text: FF=GFR/RPF

text:
FF is the filtration fraction
GFR is the glomerular filtration rate
RPF is the renal plasma flow

text: Normal human FF is 20%.

text: Renal clearance[edit]

text: Renal clearance is the volume of plasma from which the substance is completely cleared from the blood per unit time.

text: Cx=(Ux)V/Px

text:
Cx is the clearance of X (normally in units of mL/min.
Ux is the urine concentration of X.
Px is the plasma concentration of X.
V is the urine flow rate.

text: Mathematical modelling of function[edit]

text: The kidney is a very complex organ and mathematical modelling has been used to better understand kidney function at several scales, including fluid uptake and secretion.[17][18]

text: Clinical significance[edit]

text: Kidney disease is an abnormal structure, function or process in the kidney(s). Nephrosis is non-inflammatory nephropathy and nephritis is inflammatory kidney disease. Nephrology is the speciality that deals with kidney function and disease. Medical terms related to the kidneys commonly use terms such as renal and the prefix nephro-. The adjective renal, meaning related to the kidney, is from the Latin rēnēs, meaning kidneys; the prefix nephro- is from the Ancient Greek word for kidney, nephros (νεφρός).[19] For example, surgical removal of the kidney is a nephrectomy, while a reduction in kidney function is called renal dysfunction.

text: Acquired[edit]

text:
Diabetic nephropathy
Glomerulonephritis
Hydronephrosis is the enlargement of one or both of the kidneys caused by obstruction of the flow of urine.
Interstitial nephritis
Kidney stones (nephrolithiasis) are a relatively common and particularly painful disorder. A chronic condition can result in scars to the kidneys. The removal of kidney stones involves ultrasound treatment to break up the stones into smaller pieces, which are then passed through the urinary tract. One common symptom of kidney stones is a sharp to disabling pain in the middle and sides of the lower back or groin.
Kidney tumour

Wilms tumor
Renal cell carcinoma

Lupus nephritis
Minimal change disease
In nephrotic syndrome, the glomerulus has been damaged so that a large amount of protein in the blood enters the urine. Other frequent features of the nephrotic syndrome include swelling, low serum albumin, and high cholesterol.
Pyelonephritis is infection of the kidneys and is frequently caused by complication of a urinary tract infection.
Renal failure

Acute renal failure
Stage 5 Chronic Kidney Disease

Renal artery stenosis
Renovascular hypertension

text: Kidney injury and failure[edit]

text: Generally, humans can live normally with just one kidney, as one has more functioning renal tissue than is needed to survive. Only when the amount of functioning kidney tissue is greatly diminished does one develop chronic kidney disease. Renal replacement therapy, in the form of dialysis or kidney transplantation, is indicated when the glomerular filtration rate has fallen very low or if the renal dysfunction leads to severe symptoms.

text: Dialysis[edit]

text: Dialysis is a treatment that takes over jobs that healthy kidneys normally do. Kidneys are in need of dialysis when approximately 85%-90% of kidney function is lost, in addition to a Glomerular Filtration Rate (GFR) of less than 15. Dialysis maintains homeostasis by removing excess water and other salts, regulating blood pressure, and maintaining chemical levels within the body. Dialysis is a treatment that does not cure kidney disease, a kidney transplant will cure kidney disease. While a costly procedure, Dialysis has a life expectancy of 5-10 years with patients having lived up to 30 years while receiving treatment. However, patients receiving the dialysis treatments are able to lead normal lives, despite the regular appointments. [20]

text: This section needs expansion. You can help by adding to it. (August 2017)

text: Congenital disease[edit]

text:
Congenital hydronephrosis
Congenital obstruction of urinary tract
Duplex kidneys, or double kidneys, occur in approximately 1% of the population. This occurrence normally causes no complications, but can occasionally cause urinary tract infections.[21][22]
Duplicated ureter occurs in approximately one in 100 live births
Horseshoe kidney occurs in approximately one in 400 live births
Nutcracker syndrome
Polycystic kidney disease

Autosomal dominant polycystic kidney disease afflicts patients later in life. Approximately one in 1000 people will develop this condition
Autosomal recessive polycystic kidney disease is far less common, but more severe, than the dominant condition. It is apparent in utero or at birth.

Renal agenesis. Failure of one kidney to form occurs in approximately one in 750 live births. Failure of both kidneys to form used to be fatal; however, medical advances such as amnioinfusion therapy during pregnancy and peritoneal dialysis have made it possible to stay alive until a transplant can occur.
Renal dysplasia
Unilateral small kidney
Multicystic dysplastic kidney occurs in approximately one in every 2400 live births
Ureteropelvic Junction Obstruction or UPJO; although most cases appear congenital, some appear to be an acquired condition[23]

text: Diagnosis[edit]

text: Many renal diseases are diagnosed on the basis of a detailed medical history, and physical examination.[citation needed] The medical history takes into account present and past symptoms, especially those of kidney disease; recent infections; exposure to substances toxic to the kidney; and family history of kidney disease.

text: Kidney function is tested for using blood tests and urine tests. A usual blood test is for urea and electrolytes, known as a U and E. Creatinine is also tested for. Urine tests such as urinalysis can evaluate for pH, protein, glucose, and the presence of blood. Microscopic analysis can also identify the presence of urinary casts and crystals.[24] The glomerular filtration rate (GFR) can be calculated.[24]

text: Imaging[edit]

text: Imaging studies are important in the evaluation of structural renal disease caused by urinary tract obstruction, renal stones, renal cyst, mass lesions, renal vascular disease, and vesicoureteral reflux.[24]

text: Imaging techniques used most frequently include renal ultrasound and helical CT scan.

text: Biopsy[edit]

text: The role of the renal biopsy is to diagnose renal disease in which the etiology is not clear based upon noninvasive means (clinical history, past medical history, medication history, physical exam, laboratory studies, imaging studies). In general, a renal pathologist will perform a detailed morphological evaluation and integrate the morphologic findings with the clinical history and laboratory data, ultimately arriving at a pathological diagnosis. A renal pathologist is a physician who has undergone general training in anatomic pathology and additional specially training in the interpretation of renal biopsy specimens.

text: Ideally, multiple core sections are obtained and evaluated for adequacy (presence of glomeruli) intraoperatively. A pathologist/pathology assistant divides the specimen(s) for submission for light microscopy, immunofluorescence microscopy and electron microscopy.

text: The pathologist will examine the specimen using light microscopy with multiple staining techniques (hematoxylin and eosin/H&E, PAS, trichrome, silver stain) on multiple level sections. Multiple immunofluorescence stains are performed to evaluate for antibody, protein and complement deposition. Finally, ultra-structural examination is performed with electron microscopy and may reveal the presence of electron-dense deposits or other characteristic abnormalities that may suggest an etiology for the patient's renal disease.

text: Other animals[edit]

text: In the majority of vertebrates, the mesonephros persists into the adult, albeit usually fused with the more advanced metanephros; only in amniotes is the mesonephros restricted to the embryo. The kidneys of fish and amphibians are typically narrow, elongated organs, occupying a significant portion of the trunk. The collecting ducts from each cluster of nephrons usually drain into an archinephric duct, which is homologous with the vas deferens of amniotes. However, the situation is not always so simple; in cartilaginous fish and some amphibians, there is also a shorter duct, similar to the amniote ureter, which drains the posterior (metanephric) parts of the kidney, and joins with the archinephric duct at the bladder or cloaca. Indeed, in many cartilaginous fish, the anterior portion of the kidney may degenerate or cease to function altogether in the adult.[25]

text: In the most primitive vertebrates, the hagfish and lampreys, the kidney is unusually simple: it consists of a row of nephrons, each emptying directly into the archinephric duct. Invertebrates may possess excretory organs that are sometimes referred to as "kidneys", but, even in Amphioxus, these are never homologous with the kidneys of vertebrates, and are more accurately referred to by other names, such as nephridia.[25] In amphibians, kidneys and the urinary bladder harbour specialized parasites, monogeneans of the family Polystomatidae.[26]

text: The kidneys of reptiles consist of a number of lobules arranged in a broadly linear pattern. Each lobule contains a single branch of the ureter in its centre, into which the collecting ducts empty. Reptiles have relatively few nephrons compared with other amniotes of a similar size, possibly because of their lower metabolic rate.[25]

text: Birds have relatively large, elongated kidneys, each of which is divided into three or more distinct lobes. The lobes consists of several small, irregularly arranged, lobules, each centred on a branch of the ureter. Birds have small glomeruli, but about twice as many nephrons as similarly sized mammals.[25]

text: The human kidney is fairly typical of that of mammals. Distinctive features of the mammalian kidney, in comparison with that of other vertebrates, include the presence of the renal pelvis and renal pyramids, and of a clearly distinguishable cortex and medulla. The latter feature is due to the presence of elongated loops of Henle; these are much shorter in birds, and not truly present in other vertebrates (although the nephron often has a short intermediate segment between the convoluted tubules). It is only in mammals that the kidney takes on its classical "kidney" shape, although there are some exceptions, such as the multilobed reniculate kidneys of pinnipeds and cetaceans.[25]

text: Evolutionary adaptation[edit]

text: Kidneys of various animals show evidence of evolutionary adaptation and have long been studied in ecophysiology and comparative physiology. Kidney morphology, often indexed as the relative medullary thickness, is associated with habitat aridity among species of mammals,[27] and diet (e.g., carnivores have only long loops of Henle).[18]

text: Society and culture[edit]

text: Significance[edit]

text: Egyptian[edit]

text: In ancient Egypt, the kidneys, like the heart, were left inside the mummified bodies, unlike other organs which were removed. Comparing this to the biblical statements, and to drawings of human body with the heart and two kidneys portraying a set of scales for weighing justice, it seems that the Egyptian beliefs had also connected the kidneys with judgement and perhaps with moral decisions.[28]

text: Hebrew[edit]

text: According to studies in modern and ancient Hebrew, various body organs in humans and animals served also an emotional or logical role, today mostly attributed to the brain and the endocrine system. The kidney is mentioned in several biblical verses in conjunction with the heart, much as the bowels were understood to be the "seat" of emotion – grief, joy and pain.[29] Similarly, the Talmud (Berakhoth 61.a) states that one of the two kidneys counsels what is good, and the other evil.

text: In the sacrifices offered at the biblical Tabernacle and later on at the temple in Jerusalem, the priests were instructed [30] to remove the kidneys and the adrenal gland covering the kidneys of the sheep, goat and cattle offerings, and to burn them on the altar, as the holy part of the "offering for God" never to be eaten.[31]

text: India: Ayurvedic system[edit]

text: In ancient India, according to the Ayurvedic medical systems, the kidneys were considered the beginning of the excursion channels system, the 'head' of the Mutra Srotas, receiving from all other systems, and therefore important in determining a person's health balance and temperament by the balance and mixture of the three 'Dosha's – the three health elements: Vatha (or Vata) – air, Pitta – bile, and Kapha – mucus. The temperament and health of a person can then be seen in the resulting color of the urine.[32]

text: Modern Ayurveda practitioners, a practice which is characterized as pseudoscience,[33] have attempted to revive these methods in medical procedures as part of Ayurveda Urine therapy.[34] These procedures have been called "nonsensical" by skeptics.[35]

text: Medieval Christianity[edit]

text: The Latin term renes is related to the English word "reins", a synonym for the kidneys in Shakespearean English (e.g. Merry Wives of Windsor 3.5), which was also the time when the King James Version of the Bible was translated. Kidneys were once popularly regarded as the seat of the conscience and reflection,[36][37] and a number of verses in the Bible (e.g. Ps. 7:9, Rev. 2:23) state that God searches out and inspects the kidneys, or "reins", of humans, together with the heart.

text: As food[edit]

text: The kidneys, like other offal, can be cooked and eaten.

text: Kidneys are usually grilled or sautéed, but in more complex dishes they are stewed with a sauce that will improve their flavor. In many preparations, kidneys are combined with pieces of meat or liver, as in mixed grill. Dishes include the British steak and kidney pie, the Swedish hökarpanna (pork and kidney stew), the French rognons de veau sauce moutarde (veal kidneys in mustard sauce) and the Spanish riñones al Jerez (kidneys stewed in sherry sauce) .[38]

text: Additional images[edit]

text:
Kidney Posterior View

Anterior relation of Left Kidney

Structure of a Kidney

Kidney Anatomy

Kidneys of a mammal after the technique of vinylite and corrosion.

Kidney Cross Section

text:
[show]Dissection images

Right Kidney

Kidney

Right Kidney

Right kidney

Left kidney

Kidneys

Left kidney


document_title: Fastest goals in association football

question_text: who has scored the fastest goal in champions league

text: Fastest goals in association football

text: This article lists goals which have been considered among the fastest ever scored in association football matches. The records concerning the fastest goals are disputed for a number of reasons. Ray Spiller of the Association of Football Statisticians has argued that as there is no official system for recognizing the timing of goals there are always going to be disputes concerning these records.[1]

text: In addition, many of the goals listed in the Guinness Book of World Records as being among the fasted were not filmed preventing the precise timing of goals from being assessed.[1] The status of Nawaf Al Abed's goal which is credited as being scored after two seconds is also disputed given that the match was later declared void due to ineligible players, when several players over the age of 23 were found to have played in the age restricted game.

text: Marc Burrows' goal has also been considered the fastest ever but it was scored in an amateur reserve game. As there is no standard size for a football pitch some of the goals listed benefit from being played on smaller pitches that require the ball to travel a shorter distance before reaching the goal. Furthermore, many of the records listed come from English language publications and reflect a bias towards English football within the sources.

text: Under The Laws of the Game, specifically Law 8, goals may be scored directly from the kick-off. Some of the fastest goals on the list below are shots taken directly from the kick-off. [2]

text: Goals[edit]

text: The following is a list of 49 goals scored by any kind of players, including juniors, amateurs, semi-professionals, professionals, women football, in any football league, cup or other competition around the world.

text:
Player
Year
Match
Result
Time
Ref.
Notes

Nawaf Al Abed
2017
v Al Shoalah
4–0
2 sec
[3][4]
This match was later declared void as ineligible players had been fielded. As such the status of this goal as the fastest ever has been disputed.

Gavin Stokes
2017
Maryhill v Clydebank
3–0
2.1 sec
[5][6]
This match was a junior football match (non-league) involving two teams from the West of Scotland Super League First Division in Scottish football.

Vuk Bakic
2012
GSP Polet v FK Dorćol
4–1
2.2 sec
[7]
[8]
This match was a junior match of the Serbian 2. League. Immediately after the referee whistled the beginning of the meeting, Vuk Bakic sent the ball into the goal. Distance from the centre and goal was approximately 50 meters.

Marc Burrows
2004
Cowes Sports Res. v Eastleigh Res.
5–3
2.56 sec
[9]
[10]
This match was an amateur match but the record has been recognised by The Football Association. Eye-witness reports state the goal was aided by a particularly strong following wind.

Ricardo Olivera
1998
Rio Negro Capital v Soriano Interior
1–1
2.8 sec
[11][12]
The goal was listed in the Guinness World Records prior to 2004.

Cheung Sai Ho
1993
Portsmouth Cup

2.8 sec
[13]
Cheung scored for the Hong Kong youth team 2.8 seconds after the start of a match in the Portsmouth Cup in 1993. It was the world record in 1993.

Carlos Almeida
2011
Oliveira do Hospital v Associação Atlética de Arganil
3–0
3 sec
[14]
[15]
Occurred during a match in the first tier of Coimbra Football Association, the fourth tier of Portuguese football.

Frederico Chaves
2003
América Mineiro v Vila Nova
1–5
3.17 sec
[10][16]
Fastest Goal in Brazilian Football.

Colin Cowperthwaite
1979
Barrow v Kettering Town
0-4
3.55 sec
[17]
Fastest Goal in association football at the time.

Richard Wetton
2017
Oakwood FC v Lingfield FC
2-6
3.57 sec
[18]
Not only a fast goal but also a contender for the TWO fastest goals from Kick Off! The equalizer coming on just 40 seconds into the match. 22 August 2017 in the Peter Bentley Challenge Cup. Both teams play in the Southern Combination Football League Division One.

Bart van der Veer
2014
LTC v Oeverzwaluwen
2–4
3.6 sec
[19]
[20]
Occurred during a match in the Saturdays 1e Klasse, the fifth tier of Dutch football and the third tier of Dutch amateur football. It was Van der Veer's last match for Oeverzwaluwen before his retirement.

Damian Mori
1995
Adelaide City v Sydney United
2–2
3.69 sec
[21]
[22]
According to the Guinness Book of Records, Mori held the record from 1995 to 1998 when Ricardo Olivera scored a goal in 2.8 sec.

Yael Averbuch
2006
North Carolina v Yale Bulldogs
4–0
3.9 sec
[23][24]
Goal occurred in a women's college football match.

Jim Fryatt
1964
Bradford Park Avenue v Tranmere
4–2
4 sec
[25]
[26]
[21]
According to the sources some onlookers say that this goal took closer to 10 seconds. However, there is no film evidence to contradict the assessment of the referee Bob Simons who said: "I blew my whistle for the start and still had my stopwatch in my hand when the ball entered the net. The scoring time is exactly four seconds – no question of it."

Gareth Morris
2001
Ashton United v Skelmersdale United
4–2
4 sec
[27]
[21]
This goal is likely to be the fastest ever scored in the FA Cup although the lack of records dating back to the formation of the competition make this impossible to verify.

Gustavo Ramírez
2014
Mineros de Zacatecas v Club Necaxa
2–0
4 sec
[28]
Goal occurred in the first match of the season in Ascenso MX.

Albert Mundy
1958
Aldershot Town v Hartlepool United
3–0
6 sec
[1][29]
Fastest Goal in association football at the time.

Barrie Jones
1962
Notts County v Torquay United
2–0
6 sec
[1]
[30]
[31]
[32]
Jones kicked the match off, tapping the ball to a teammate. He set off, running diagonally to the right, towards the centre of the 18 yard box. Bob Forrest had received the ball by now and he rolled it perfectly into Jones's path. The Torquay keeper was out to the edge of his box but he hit it under him with his first touch, helping the ball on from the direction of Forrest's pass.

Keith Smith
1964
Crystal Palace v Derby County
3–3
6 sec
[1][33]

Tommy Langley
1980
QPR v Bolton Wanderers
3–1
6 sec
[1][34]

Alexandros Zafeiris
1980
Irodotos v Kifisia
3–1
6 sec
[35]
Fastest goal scored in the third tier of Greek Football League 2.

Lukas Podolski
2013
Germany v Ecuador
4–2
6 sec
[36][37]
Fastest goal ever scored in an international match.

Ghazi ayedi
2017
Club Africain vs CS Sfaxien
2-1
6 sec

Fastest goal ever scored in Tunisien super ligue

Ji Xiang
2012
Jiangsu Sainty v Guangzhou Evergrande
1–1
7 sec
[38]
Fastest goal ever scored in Chinese Super League.

Andreas Labropoulos
2013
Olympiacos v OFI Crete
5–1
7 sec
[39]
Fastest goal ever scored in Greek Super League.

Jerome Martelli
2014
Leyton U18 v Dagenham & Redbridge U18
4–1
7 sec
[40]
Fastest goal ever scored in an U18 Association football game.

Mike Grella
2015
New York Red Bulls v Philadelphia Union
4–1
7 sec
[41]
Fastest goal ever scored in Major League Soccer.

Joseba Llorente
2008
Real Valladolid v Espanyol
2–1
7.22 sec
[42]
Fastest goal ever scored in La Liga.

Roman Yaremchuk
2016
Vorskla Poltava v Oleksandriya
2–2
7.27 sec
[43][44]
Fastest goal ever scored in the Ukrainian Premier League.

Carlos Aguiar
2010
Huachipato v Universidad de Chile
1–2
7.3 sec
[45][46]
Fastest goal ever scored in the Chilean Primera División.

Miroslav Manolov
2012
Cherno More Varna v Montana
3–1
7.42 sec
[47]
Fastest goal ever scored in Bulgarian A Football Group.

Seydou Keita
2014
Valencia CF v UD Almería
2–2
7.66 sec
[42]

Gholamreza Rezaei
2012
Persepolis v Fajr Sepasi
2–0
8 sec
[48]
Fastest goal ever scored in Persian Gulf Pro League.

Tim Cahill
2013
Houston Dynamo v New York Red Bulls
0–3
8 sec
[49]
Second fastest goal ever scored in Major League Soccer.

Zaur Sadayev
2014
Lech Poznań v Jagiellonia Białystok
4–2
8 sec
[50]
Fastest goal ever scored in Polish Cup.

Marco Tavares
2017
Maribor v Domžale
1–0
8 sec
[51]
Fastest goal ever scored in Slovenian FirstLeague.

Tom Morgan
2014
Turton v Lytham
4–1
8 sec
[52]
[53]
[54]
West Lancashire Football League Division One – Level 12 – The kick off was quickly taken with a pass intended for a Turton player hitting a Lytham player hard on the shin and bobbling up. Tom Morgan struck the ball in the air about 45 metres from goal and the ball cannoned in off the underside of the crossbar. The referee, Simon Robinson timed the goal at exactly eight seconds.

Paolo Poggi
2001
Piacenza v Fiorentina
3–1
8.1 sec
[55]
Fastest goal ever scored in Serie A.

Christian Benteke
2016
Gibraltar v Belgium
0–6
8.1 sec
[56]
Fastest goal ever scored in a FIFA World Cup qualification game.

Davide Gualtieri
1993
San Marino v England
1–7
8.3 sec
[36][57]

Hisato Satō
2006
Sanfrecce Hiroshima v Cerezo Osaka
1–1
8.7 sec
[58]
Fastest goal ever scored in J.League Division 1.

Kevin Volland
2015
TSG Hoffenheim v Bayern München
1–2
9 sec
[59]

Karim Bellarabi
2014
Borussia Dortmund v Bayer Leverkusen
0–2
9 sec
[60][61]
Fastest goal scored in the history of the Bundesliga.

Ledley King
2000
Tottenham Hotspur v Bradford City
3–3
9.9 sec
[62]
Fastest goal ever scored in the Premier League.

Uroš Đurđević
2016
Čukarički v Partizan
1–3
10 sec
[63]
Fastest goal scored in the history of the Serbian SuperLiga

Julian Kristoffersen
2016
FC Copenhagen U19 v Leicester City U19
3–2
10 sec
[64]
UEFA Youth League

Justin Meram
2015
Columbus Crew v New York Red Bulls
2–0
10 sec
[65]
Fastest goal ever scored in the MLS Cup Playoffs.

Roy Makaay
2007
Bayern München v Real Madrid
3–2
10.1 sec
[66]
Fastest goal ever scored in the UEFA Champions League.

Hakan Şükür
2002
Korea Republic v Turkey
2–3
10.8 sec
[67]
Fastest goal ever scored in the FIFA World Cup finals.

Diego Souza
2017
Brazil v Australia
1-0
11 sec
[68]

Simone Magill
2016
Northern Ireland v Georgia
4-0
11 sec
[69]
Fastest goal ever scored in Women's International History.

Christian Eriksen
2017
Tottenham v Manchester United
2-0
11 sec

Juan Cazares
2016
Atletico Mineiro v Botafogo
5–3
12 sec

Fastest Atlético Mineiro goal in Campeonato Brasileiro Série A

Ahmad Fakri Saarani
2015
Kelantan v Terengganu
1–2
12 sec

Fastest goal ever scored in Malaysia Super League

Ian Bogie
1996
Port Vale v Stoke City
1–0
12 sec
[70][71]

I. M. Vijayan
1999
India v Bhutan
3–0
12 sec
[72][73]
Scored in the group stage of the football competition in the 8th South Asian Federation Games, 1999.

Maheta Molango
2004
Reading v Brighton & Hove Albion
3–2
12 sec
[74][75]
Fastest goal ever scored from Offside.

Stevan Račić
2014
Partizani Tirana v Elbasani
1–0
12 sec
[76][77]
Fastest goal ever scored in the history of Albanian Superliga.

Asmir Begović
2013
Stoke City v Southampton
1–1
13 sec
[78]
Begović scored against Southampton at a distance of 97.5 yards, after his long kick downfield deceived Artur Boruc. His goal against earned him a place in the Guinness World Records for the longest goal scored in football.

Neymar
2016
Brazil v Honduras
6–0
14 sec
[79][80]
Fastest goal ever scored in the history of Olympic Football Competition.


document_title: Ten-code

question_text: where does the term ten four come from

question_tokens: where does the term ten four come from

text: Ten-code

text: History[edit]

text: APCO first proposed Morse code brevity codes in the June 1935 issue of The APCO Bulletin, which were adapted from the procedure symbols of the U.S. Navy.[2]

text: The development of the APCO Ten Signals began in 1937 to reduce use of speech on the radio at a time when police radio channels were limited. Credit for inventing the codes goes to Charles "Charlie" Hopper, communications director for the Illinois State Police, District 10 in Pesotum, Illinois. Hopper had been involved in radio for years and realized there was a need to abbreviate transmissions on State Police bands.[3] Experienced radio operators knew the first syllable of a transmission was frequently not understood because of quirks in early electronics technology. Radios in the 1930s were based on vacuum tubes powered by a small motor-generator called a dynamotor. The dynamotor took from 1/10 to 1/4 of a second to "spin up" to full power. Police officers were trained to push the microphone button, then pause briefly before speaking; however, sometimes they would forget to wait. Preceding each code with "ten-" gave the radio transmitter time to reach full power. An APCO Bulletin of January 1940 lists codes assigned as part of standardization;[4]

text: The Ten Signals were included in APCO Project Two (1967), "Public Safety Standard Operating Procedures Manual", published as study cards in APCO Project 4 (1973), "Ten Signal Cards", and then revised in APCO Project 14 (1974).[5][6][7][8]

text: In popular culture[edit]

text: Ten-codes, especially "10-4" (meaning "understood") first reached public recognition in the mid- to late-1950s through the popular television series Highway Patrol, with Broderick Crawford. Crawford would reach into his patrol car to use the microphone to answer a call and precede his response with "10-4".

text: Ten-codes were adapted for use by CB radio enthusiasts. C. W. McCall's hit song "Convoy" (1975), depicting conversation among CB-communicating truckers, put phrases like 10-4 and what's your twenty? (10-20 for "where are you?") into common use in American English.

text: The movie Convoy (1978), loosely based on McCall's song, further entrenched ten-codes in casual conversation.

text: Replacement with plain language[edit]

text: While ten-codes were intended to be a terse, concise, and standardized system, the proliferation of different meanings can render them useless in situations when officers from different agencies and jurisdictions need to communicate.

text: In the fall of 2005, responding to inter-organizational communication problems during the rescue operations after Hurricane Katrina, the United States Federal Emergency Management Agency (FEMA) discouraged the use of ten-codes and other codes due to their wide variation in meaning.[9][10] The Department of Homeland Security's SAFECOM program, established in response to communication problems experienced during the September 11 attacks also advises local agencies on how and why to transition to plain language,[11] and their use is expressly forbidden in the nationally standardized Incident Command System, as is the use of other codes.[12]

text: APCO International's current position states that plain speech communications over public safety radio systems is preferred over the traditional 10-Codes and dispatch signals,[13] As of 2011[update], ten-codes remain in common use in many areas, but are increasingly being phased out in favor of plain language,[1] with nineteen states planning to change to plain English as of the end of 2009[update].[14]

text: Examples of ten-codes[edit]

text: Some examples of the codes are:[15]

text:
10-1 Bad reception
10-4 I acknowledge/Affirmative/Copy
10-9 Say again
10-20 Advise to location
10-21 Call
10-33 Emergency: all units stand by
10-36 Correct time

text: Many additional codes have been added by individual local or regional first-response agencies; these are not standard across jurisdictions and may be problematic if multiple organizations must respond to the same incident.

text: Related codes[edit]

text:
The California Highway Patrol uses ten-codes, along with an additional set of eleven- and higher codes.[16]
California Penal Code sections were in use by the Los Angeles Police Department as early as the 1940s, and these Hundred Code numbers are still used today instead of the corresponding ten-code. Generally these are given as two sets of numbers[citation needed]—"One Eighty-Seven" or "Fifty-One Fifty"—with a few exceptions such as "459"—Burglary, which is given as "Four-Five-Nine". The American public was made aware of these California Penal Code references as a result of the TV series Adam-12, which used them habitually in radio communications and in the main title of the show. The best-known include:

"187": Homicide
Further information: 187 (slang)

"211": Robbery
"415": Disturbance
"417": Person with a weapon
"502": Intoxicated Driver
"5150": Mentally disturbed person (actually a reference to the California Welfare and Institutions Code)

The New York Fire Department uses its own ten-code system.[17]
The New Zealand Fire Service uses a system of "K-codes" to pass fire appliance availability statuses as well as operational messages. For example, "K1" means "proceeding to incident", while "K99" means "Structure fire, well involved".[18][19] The New Zealand Police also use some K-codes,[20] with completely unrelated meanings to those used by NZFS; Police code "K1" means "no further police action required".
Telegraph and teletype procedures

Q code and prosigns for Morse code are used in amateur radio, aviation and marine radio. They provide specific abbreviations for concepts related to aviation, shipping, RTTY, radiotelegraph and amateur radio.[21] In radiotelegraph operation, a Q code is often shorter (as ten-codes require transmission of three prefix characters: 1, 0, hyphen) and provides standardization of codes, essential in international and shortwave communications.
Z codes are used by NATO countries in military radio communications.