Advanced meat recovery

China Product


Products

Finely Textured Beef (FTB), Lean Finely Textured Beef (LFTB), Premium Black Angus Finely Textured Beef (PBAFTB), Angus Finely Textured Beef (AFTB), Beef Trimmings, Finely Textured (BTFT) and Partially Defatted Chopped Beef (PDCB) are edible beef products derived from beef-fat trimmings.

Regulation alpha lipoic acid source

In the United States, USDA regulations stipulate that AMR machinery cannot grind, crush, or pulverize bones to remove edible meat tissue, and bones must emerge intact. The meat produced in this manner can contain no more than 150(30) milligrams of calcium per 100 grams product, as calcium in such high concentrations in the product would be indicative of bone being mixed with the meat. Products that exceed the calcium content limit must be labeled "mechanically separated beef or pork" in the ingredients statement. chaste berry extract

In 1994, the Food Safety and Inspection Service (FSIS) issued a rule allowing such meat to be labeled as meat for human consumption, providing that the bones from which it was removed were still intact after processing. In 1997, following tests indicating that central nervous system (CNS) tissue was showing up in mechanically removed meat, FSIS issued a directive to its inspectors instructing them to ensure that spinal cord tissue was removed from bones before the AMR process. Following the identification of a BSE-infected U.S. dairy cow in December 2003, FSIS issued new regulations expanding the definition of prohibited CNS tissue to include additional cattle parts. Furthermore, all AMR-processed product from cattle more than 30 months old now is prohibited from being used for food, and such product from younger cattle and from other livestock species also is prohibited if it contains CNS material. xanthones xango

See also

Specified risk material (SRM)

Mechanically separated meat (MSM)

References

^ USDA Purchases of Ground Beef Items Frozen Technical Requirements Schedule GB-2003 / USDA 29may03

^ Finely Textured Lean Beef as an Ingredient for Processed Meats, Ying He and Joseph G. Sebranek

^ US Patent 5725897 - Low temperature rendering process, US Patent issued March 10, 1998

^ Products, HRR Enterprises, Inc.

^ USDA Regulations

^ CRS Report for Congress: Agriculture: A Glossary of Terms, Programs, and Laws, 2005 Edition - Order Code 97-905

External links

United States Department of Agriculture Fact Sheet on Advanced Meat Recovery

Categories: Meat processing | Industrial agricultureHidden categories: Articles with limited geographic scope | USA-centric

Kowata Station

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Lines

Keihan Electric Railway

Uji Line force fx lightsabers

Layout varactor diodes

The station has two side platforms. shelf storage bin

Around the station

Panasonic Electronic Devices Co., Ltd. (Capacitor Business Unit)

Kyoto Animation studio

Kohata Station on the JR Nara Line

Adjacent stations

Service

Keihan Uji Line

Rokujiz

-

baku

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Stations of the Keihan Uji Line

Chshojima - Kangetsuky - Momoyama-minamiguchi - Rokujiz - Kowata - baku - Mimurodo - Uji

Coordinates: 345532.39 1354746.07 / 34.9256639N 135.7961306E / 34.9256639; 135.7961306

This Kyoto Prefecture railroad station-related article is a stub. You can help Wikipedia by expanding it.

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Categories: Stations of Keihan Electric Railway | Railway stations in Kyoto Prefecture | Kyoto Prefecture railway station stubs

Railroad engineer

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Duties

This section does not cite any references or sources.

Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (December 2009) coconut candle

The cab of a CountryLink Xplorer diesel multiple unit rose floating candles

An engineer is responsible for preparing equipment for service, checking paperwork and the condition of the locomotives. His or her duties require that s/he control acceleration, braking and handling of the train underway. S/he must know the physical characteristics of the railroad, including passenger stations, the incline and decline of the right-of-way and speed limits. Along with the conductor, the engineer monitors time to not fall behind schedule, nor leave stations early. The train's speed must be reduced when following other trains, approaching route diversions, or regulating time over road to avoid arriving too early. The engineer assumes the duties of the conductor if the conductor is incapacitated. led votive

The locomotive engineer is required to have an intimate knowledge of track geometry including signal placement so as to be able to safely control their train.

Maintaining concentration is of critical importance in this role.

Train handling

A workplace in Rigi cogwheel electric train

Train dynamics can be extreme and therefore an engineer must be familiar with train handling techniques so as to avoid train partings, derailments and not exceeding line speed.

Freight trains typically have different train forces from passenger trains. A typical freight train may have 500 tonnes of locomotive weight at the front. That may be followed by 1500m of wagons. The wagons may or may not be uniformly loaded and may brake differently.

Severe brake applications can combine with these factors to cause a train parting. Therefore good train handling practice for freight trains is usually to keep the consist (rail vehicles which make up a train) stretched. This is achieved by keeping the consist in power while a brake application is made and by bleeding the air off the locomotives brakes before they apply. It is not possible to do this with the use of dynamic brake, which presents its own train handling challenges.

When there are multiple locomotives, some may be set up to brake like wagons instead of locomotives, as too many locomotives on the front of the train (all with brakes bled off) would require too heavy an application from the rest.

On shorter passenger trains, this is even more noticeable, requiring the first application of the brake to be bled off on the locomotive, applying locomotive brakes with subsequent increases in application. The length and make-up of the slowing or stopping distance dictates just how much locomotive brake application should be allowed to apply.

The use of dynamic brake can result in a severe slack action, When engaged run in is highly possible if brought in at an inappropriate time (regarding track geometry and train speed) and if disengaged at an inappropriate time can result in a run out. Both can potentially snap train drawgear.

Straightlining is a potential cause of derailment that train handling techniques must take into account in order to reduce the likelihood of occurrence. When a train rounds a curve basic physics dictates the trailing wagons in the consist will try to take the shortest route and the flange on some of the wheels within the consist could potentially fail to prevent this occurring with the resultant effect being a derailment.

Track geometry is also critical to train handling. It is desirable to have brakes releasing at the bottom of steep grades rather than applied. And at the top of a steep grade it is desirable to have a fully charged brake pipe.

Serial braking is where a train descends a grade on the air brake alone. The brake pipe application is gradually increased to slow down and if required (depending on the weight of the train and on the grade) stop the train so as to allow the locomotive compressors to recharge the brake pipe throughout the consist. In these cases it is permissible to use the locomotive brakes (which are independent of the train brake and charged through the main reservoir directly) to hold the train (In some cases the weight of the trailing consist will not be held on the locomotive brakes alone) slowing the rate of acceleration and giving more time to recharge the brake pipe to give a better application in the next subsequent train brake application. A runaway can occur if a brake application is required before the train pipe has recharged (as happened at Cima Hill in the United States).

A split reduction is where a train brake application is made and gradually increased as the train descends the grade. It is different to serial braking in that with Serial Braking the application is released, the brake pipe recharged then reapplied.

The dynamic brake when operable slows down the rate of acceleration and allows longer for a train brake pipe to be recharged before being required to be re applied. When a train descends a grade utilizing both the dynamic and air brakes the procedure is known as 'maintaining braking'.

In the case of severe grades (for example the Westmere Bank in New Zealand, which is a 1:33 grade with a 40 km/h (25 mph)speed limit) a trains allowable speed is lower for a train that doesn't have dynamic brake than for one that does.[citation needed]

In freight train marshalling yards the wagon brakes are sometimes bled off so they can be easily loose shunted. However when a shunt locomotive moves large numbers of wagons around with no brakes the locomotive must brake for the entire train. This can result in severe slack action and wheel slip. Damage to goods and rolling stock is possible. Also, with unbraked wagons there is potential for a runaway.[citation needed]

Famous railroad engineers

Casey Jones

John Axon (UK)

Wallace Oakes

Norman Kirk, former Prime Minister of New Zealand

Jeanice McMillan

References

^ "2003 CFR Title 49, Volume 4; Part 240: Qualification and Certification of Locomotive Engineers". Code of Federal Regulations. United States National Archives and Records Administration. http://www.access.gpo.gov/nara/cfr/waisidx_03/49cfr240_03.html. Retrieved 2007-11-14. 

^ "Train Crew". FAQ: Railway Operations. Indian Railways Fan Club. 2007. http://www.irfca.org/faq/faq-ops.html#crew. Retrieved 2007-11-14. 

External links

A detailed explanation of what train driving involves, and becoming a train driver in the UK

Run-A-Locomotive. Link to a site that offers an engineer experience program at a museum in California.

Categories: Railroad engineers | Transportation occupationsHidden categories: Articles needing additional references from December 2009 | All articles needing additional references | All articles with unsourced statements | Articles with unsourced statements from June 2009

Stichodactyla toxin

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Source

The stichodactyla toxin stems from the sea anemone Stichodactyla helianthus. The Stichodactyla helianthus is a large, green, sessile, carpet-like sea anemone, from the Caribbean. It lives in shallow areas with mild to strong currents, and associates with clown fish. It is believed that it excretes toxins mainly to protect itself from the spiny lobster.

Helianthus stems from the Greek words (meaning sun), and , meaning flower. Therefore, S. helianthus is also named the sun anemone. clear glass dinnerware

Structure white porcelain plates

ShK is a 35-residue basic peptide first discovered by Professor Olga Castaneda from the University of Havana, Cuba, and her collaborators in Sweden. It is cross-linked by three disulfide bridges: Cys3-Cys35, Cys12-Cys28, and Cys17-Cys32 (see figure below). The amino acid sequence of the ShK toxin is Arg-Ser-Cys-Ile-Asp-Thr-Ile-Pro-Lys-Ser-Arg-Cys-Thr-Ala-Phe-Gln-Cys-Lys-His-Ser-Met-Lys-Tyr-Arg-Leu-Ser-Phe-Cys-Arg-Lys-Thr-Cys-Gly-Thr-Cys. ShK is stabilized by three disulfide bridges and consists of two short -helices comprising residues 14-19 and 21-24. The N-terminal eight residues of ShK adopt an extended conformation, followed by a pair of interlocking turns that resemble a 310 helix, while its C-terminal Cys35 residue forms a nearly head-to-tail cyclic structure through a disulfide bond with Cys3. Protein domains with structural resemblance to ShK have been described in 402 proteins, most of them from C. elegans (IPR003582). Other proteins containing domains with similar structures include the snake toxins natrin, triflin, and stecrisp, the Toxocara canis mucins and the human protein Tpx-1. stainless steel chafing

Schematic diagram of the primary structure of the ShK peptide highlighting the three disulfide () linkages.

Target

ShK toxin blocks the K+ channels Kv1.1, Kv1.3, Kv1.6 and Kv3.2 The peptide binds to all four subunits in the Kv1.3 tetramer through its interaction with the shallow vestibule at the outer entrance of the ion conduction pathway. The peptide's Lysine22 residue occludes the channel pore like a "cork in a bottle". This blocks the entrance to the pore.

ShK blocks the Kv1.3 channel in T cells with a Kd of about 11 pM. It blocks the neuronal Kv1.1 and Kv1.6 channels with Kds of 16 pM and 200 pM respectively. The Kv3.2 and KCa3.1 channels are more than 1000 times less sensitive to the peptide.

Several ShK analogs have been generated to enhance specificity for the Kv1.3 channel over the Kv1.1, Kv1.6 and Kv3.2 channels. The first analog that showed some degree of specificity was ShK-Dap22. Attaching a fluorescein to the N-terminus of the peptide via a hydrophilic AEEA linker (2-aminoethoxy-2-ethoxy acetic acid; mini-PEG) resulted in a peptide, ShK-F6CA, with 100-fold specificity for Kv1.3 over Kv1.1 and related channels. Based on this surprising finding additional analogs were made. ShK-170 [a.k.a ShK(L5)],contains a L-phosphotyrosine in place of the fluorescein in ShK-F6CA. It blocks Kv1.3 with a Kd of 69 pM and shows exquisite specificity for Kv1.3. However, it is chemically unstable. To improve stability a new analog, ShK-186 [a.k.a. SL5], was made with the C-terminal carboxyl of ShK-170 replaced by an amide; ShK-186 is otherwise identical to ShK-170. However, ShK-186 is also chemically unstable. ShK-192 is a new analog with increased stability. It contains norleucine21 in place of methionine21 to avoid methionine oxidation, and the terminal phosphotyrosine is replaced by a non-hydrolyzable para-phosphonophenylalanine (Ppa) group. The D-diasteromer of ShK is also stable but blocks Kv1.3 with 2800-fold potency than the L-form (Kd = 36 nM) and it only exhibits 2-fold specificity for Kv1.3 over Kv1.1.

Kv1.3 and KCa3.1 regulate membrane potential and calcium signaling of T cells. Calcium entry through the CRAC channel is promoted by potassium efflux through the Kv1.3 and KCa3.1 potassium channels. Blockade of Kv1.3 channels in effector-memory T cells by ShK-186 suppresses calcium signaling, cytokine production (interferon-gamma, interleukin 2) and cell proliferation. In vivo, ShK-186 paralyzes effector-memory T cells at the sites of inflammation and prevent their reactivation in inflamed tissues. In contrast, ShK-186 does not affect the homing to and motility within lymph nodes of naive and central memory T cells, most likely because these cells express the KCa3.1 channel and are therefore protected from the effect of Kv1.3 blockade. In proof-of-concept studies, ShK and its analogs have prevented and treated disease in rat models of multiple sclerosis, rheumatoid arthritis, and delayed type hypersensitivity.

As ShK toxin binds to the synaptosomal membranes, it facilitates an acetylcholine release at avian neuromuscular junctions while the Kv3.2 channels are expressed in neurons that fire at a high frequency (such as cortical GABAergic interneurons), due to their fast activation and deactivation rates. By blocking Kv3.2, ShK toxin depolarises the cortical GABAergic interneurons. Kv3.2 is also expressed in pancreatic beta cells. These cells are thought to play a role in their delayed-rectifier current, which regulates glucose-dependent firing. Therefore, ShK, as a Kv3.2 blocker, might be useful in the treatment of type-2 diabetes, although inhibition of the delayed-rectifier current has not yet been observed in human cells even when very high ShK concentrations were used.

Toxicity

Toxicity of ShK toxin in mice is quite low. The median paralytic dose is about 25 mg/kg bodyweight (which translates to 0.5 mg per 20 g mouse). In rats the therapeutic safety index was greater than 75-fold.

ShK-Dap22 is less toxic, even a dose of 1.0 mg dose did not cause hyperactivity, seizures or mortality. The median paralytic dose was 200 mg/kg body weight.

ShK-170 [a.k.a. ShK(L5)] does not cause significant toxicity in vitro. The peptide was not toxic to human and rat lymphoid cells incubated for 48 h with 100 nM of ShK-170 (>1200 times greater than the Kv1.3 half-blocking dose). The same high concentration of ShK-170 was negative in the Ames test on tester strain TA97A, suggesting that it is not a mutagen. ShK-170 had no effect on heart rate or heart rate variability parameters in either the time or the frequency domain in rats. It does not block the hERG (Kv11.1) channel that is associated with drug-associated cardiac arrhythmias. Repeated daily administration of the peptide by subcutaneous injection (10 g/kg/day) for 2 weeks to rats does not cause any changes in blood counts, blood chemistry or in the proportion of thymocyte or lymphocyte subsets. Furthermore, the rats administered the peptide gain weight normally.

ShK-186 [a.k.a. SL5] is also safe. Repeated daily administration by subcutaneous injection of ShK-186 (100 g/kg/day) for 4 weeks to rats does not cause any changes in blood counts, blood chemistry or histopathology. Furthermore, ShK-186 did not compromise the protective immune response to acute influenza viral infection or acute bacterial (Chlamydia) infection at concentrations that were effective in ameliorating autoimmune diseases in rat models. Interestingly, rats repeatedly administered ShK-186 for a month by subcutaneous injection (500 g/kg/day) did not develop anti-ShK antibodies. The reason for the low immunogenicity of the peptide is not well understood.

Many groups are developing Kv1.3 blockers for the treatment of autoimmune diseases.

Use

Because ShK toxin is a specific inhibitor of Kv1.1, Kv1.3, Kv1.6, Kv3.2 and KCa3.1, it may serve as a useful pharmacological tool for studying these channels. The Kv1.3 specific ShK analogs, ShK-170, ShK-186 and ShK-192, have been demonstrated to be effective in rat models of autoimmune diseases, and these or related analogs might have use as therapeutics for human autoimmune diseases.

Kv1.3 is also considered a therapeutic target for the treatment of obesity, for enhancing peripheral insulin sensitivity in patients with type-2 diabetes mellitus, and for preventing bone resorption in periodontal disease. Furthermore, because pancreatic beta cells, which have Kv3.2 channels, are thought to play a role in glucose-dependent firing, ShK, as a Kv3.2 blocker, might be useful in the treatment of type-2 diabetes, although inhibition of the delayed-rectifier current has not yet been observed in human cells even when very high ShK concentrations were used.

References

^ a b PDB 1ROO; Tudor JE, Pallaghy PK, Pennington MW, Norton RS (April 1996). "Solution structure of ShK toxin, a novel potassium channel inhibitor from a sea anemone". Nat. Struct. Biol. 3 (4): 31720. PMID 8599755. 

^ a b Norton RS, Pennington MW, Wulff H (December 2004). "Potassium channel blockade by the sea anemone toxin ShK for the treatment of multiple sclerosis and othfer autoimmune diseases". Curr. Med. Chem. 11 (23): 304152. PMID 15578998. http://www.bentham-direct.org/pages/content.php?CMC/2004/00000011/00000023/0003C.SGM. 

^ a b Castaeda O, Sotolongo V, Amor AM, Stcklin R, Anderson AJ, Harvey AL, Engstrm A, Wernstedt C, Karlsson E (May 1995). "Characterization of a potassium channel toxin from the Caribbean Sea anemone Stichodactyla helianthus". Toxicon 33 (5): 60313. doi:10.1016/0041-0101(95)00013-C. PMID 7660365. 

^ Pennington MW, Mahnir VM, Khaytin I, Zaydenberg I, Byrnes ME, Kem WR (December 1996). "An essential binding surface for ShK toxin interaction with rat brain potassium channels". Biochemistry 35 (51): 1640711. doi:10.1021/bi962463g. PMID 8987971. 

^ Pennington MW, Lanigan MD, Kalman K, Mahnir VM, Rauer H, McVaugh CT, Behm D, Donaldson D, Chandy KG, Kem WR, Norton RS (November 1999). "Role of disulfide bonds in the structure and potassium channel blocking activity of ShK toxin". Biochemistry 38 (44): 1454958. doi:10.1021/bi991282m. PMID 10545177. 

^ Pohl J, Hubalek F, Byrnes ME, Nielsen KR, Woods A and Pennington MW (1995), "Assignment of the three disulfide bonds in ShK toxin: A potent potassium channel inhibitor from the sea anemone Stichodactyla helianthus", Letters in Peptide Science 1 (6): 291297, doi:10.1007/BF00119770, http://www.springerlink.com/index/G14PL15184041U2L.pdf 

^ Wang F, Li H, Liu MN, Song H, Han HM, Wang QL, Yin CC, Zhou YC, Qi Z, Shu YY, Lin ZJ, Jiang T (December 2006). "Structural and functional analysis of natrin, a venom protein that targets various ion channels". Biochem. Biophys. Res. Commun. 351 (2): 4438. doi:10.1016/j.bbrc.2006.10.067. PMID 17070778. 

^ Shikamoto Y, Suto K, Yamazaki Y, Morita T, Mizuno H (July 2005). "Crystal structure of a CRISP family Ca2+ -channel blocker derived from snake venom". J. Mol. Biol. 350 (4): 73543. doi:10.1016/j.jmb.2005.05.020. PMID 15953617. 

^ Guo M, Teng M, Niu L, Liu Q, Huang Q, Hao Q (April 2005). "Crystal structure of the cysteine-rich secretory protein stecrisp reveals that the cysteine-rich domain has a K+ channel inhibitor-like fold". J. Biol. Chem. 280 (13): 1240512. doi:10.1074/jbc.M413566200. PMID 15596436. 

^ Gibbs GM, Scanlon MJ, Swarbrick J, Curtis S, Gallant E, Dulhunty AF, O'Bryan MK (February 2006). "The cysteine-rich secretory protein domain of Tpx-1 is related to ion channel toxins and regulates ryanodine receptor Ca2+ signaling". J. Biol. Chem. 281 (7): 415663. doi:10.1074/jbc.M506849200. PMID 16339766. 

^ Loukas A, Hintz M, Linder D, Mullin NP, Parkinson J, Tetteh KK, Maizels RM (December 2000). "A family of secreted mucins from the parasitic nematode Toxocara canis bears diverse mucin domains but shares similar flanking six-cysteine repeat motifs". J. Biol. Chem. 275 (50): 396007. doi:10.1074/jbc.M005632200. PMID 10950959. 

^ a b c d e f Kalman K, Pennington MW, Lanigan MD, Nguyen A, Rauer H, Mahnir V, Paschetto K, Kem WR, Grissmer S, Gutman GA, Christian EP, Cahalan MD, Norton RS, Chandy KG (December 1998). "ShK-Dap22, a potent Kv1.3-specific immunosuppressive polypeptide". J. Biol. Chem. 273 (49): 32697707. doi:10.1074/jbc.273.49.32697. PMID 9830012. 

^ a b c d Rauer H, Pennington M, Cahalan M, Chandy KG (July 1999). "Structural conservation of the pores of calcium-activated and voltage-gated potassium channels determined by a sea anemone toxin". J. Biol. Chem. 274 (31): 2188592. doi:10.1074/jbc.274.31.21885. PMID 10419508. 

^ Middleton RE, Sanchez M, Linde AR, Bugianesi RM, Dai G, Felix JP, Koprak SL, Staruch MJ, Bruguera M, Cox R, Ghosh A, Hwang J, Jones S, Kohler M, Slaughter RS, McManus OB, Kaczorowski GJ, Garcia ML (November 2003). "Substitution of a single residue in Stichodactyla helianthus peptide, ShK-Dap22, reveals a novel pharmacological profile". Biochemistry 42 (46): 13698707. doi:10.1021/bi035209e. PMID 14622016. 

^ a b c d e f Beeton C, Pennington MW, Wulff H, Singh S, Nugent D, Crossley G, Khaytin I, Calabresi PA, Chen CY, Gutman GA, Chandy KG (April 2005). "Targeting effector memory T cells with a selective peptide inhibitor of Kv1.3 channels for therapy of autoimmune diseases". Mol. Pharmacol. 67 (4): 136981. doi:10.1124/mol.104.008193. PMID 15665253. 

^ a b c d e Yan L, Herrington J, Goldberg E, Dulski PM, Bugianesi RM, Slaughter RS, Banerjee P, Brochu RM, Priest BT, Kaczorowski GJ, Rudy B, Garcia ML (May 2005). "Stichodactyla helianthus peptide, a pharmacological tool for studying Kv3.2 channels". Mol. Pharmacol. 67 (5): 151321. doi:10.1124/mol.105.011064. PMID 15709110. 

^ Lanigan MD, Kalman K, Lefievre Y, Pennington MW, Chandy KG, Norton RS (October 2002). "Mutating a critical lysine in ShK toxin alters its binding configuration in the pore-vestibule region of the voltage-gated potassium channel, Kv1.3". Biochemistry 41 (40): 1196371. doi:10.1021/bi026400b. PMID 12356296. 

^ a b c Chandy KG, Wulff H, Beeton C, Pennington M, Gutman GA, Cahalan MD (May 2004). "K+ channels as targets for specific immunomodulation". Trends Pharmacol. Sci. 25 (5): 2809. doi:10.1016/j.tips.2004.03.010. PMID 15120495. 

^ a b c d Beeton C, Wulff H, Singh S, Botsko S, Crossley G, Gutman GA, Cahalan MD, Pennington M, Chandy KG (March 2003). "A novel fluorescent toxin to detect and investigate Kv1.3 channel up-regulation in chronically activated T lymphocytes". J. Biol. Chem. 278 (11): 992837. doi:10.1074/jbc.M212868200. PMID 12511563. 

^ a b c d Beeton C, Wulff H, Standifer NE, Azam P, Mullen KM, Pennington MW, Kolski-Andreaco A, Wei E, Grino A, Counts DR, Wang PH, LeeHealey CJ, S Andrews B, Sankaranarayanan A, Homerick D, Roeck WW, Tehranzadeh J, Stanhope KL, Zimin P, Havel PJ, Griffey S, Knaus HG, Nepom GT, Gutman GA, Calabresi PA, Chandy KG (November 2006). "Kv1.3 channels are a therapeutic target for T cell-mediated autoimmune diseases". Proc. Natl. Acad. Sci. U.S.A. 103 (46): 174149. doi:10.1073/pnas.0605136103. PMID 17088564. 

^ a b c Pennington MW, Beeton C, Galea CA, Smith BJ, Chi V, Monaghan KP, Garcia A, Rangaraju S, Giuffrida A, Plank D, Crossley G, Nugent D, Khaytin I, Lefievre Y, Peshenko I, Dixon C, Chauhan S, Orzel A, Inoue T, Hu X, Moore RV, Norton RS, Chandy KG (January 2009). "Engineering a stable and selective peptide blocker of the Kv1.3 channel in T lymphocytes". Mol. Pharmacol.. doi:10.1124/mol.108.052704. PMID 19122005. 

^ Beeton C, Smith BJ, Sabo JK, Crossley G, Nugent D, Khaytin I, Chi V, Chandy KG, Pennington MW, Norton RS (January 2008). "The D-diastereomer of ShK toxin selectively blocks voltage-gated K+ channels and inhibits T lymphocyte proliferation". J. Biol. Chem. 283 (2): 98897. doi:10.1074/jbc.M706008200. PMID 17984097. 

^ Wulff H, Calabresi PA, Allie R, Yun S, Pennington M, Beeton C, Chandy KG (June 2003). "The voltage-gated Kv1.3 K+ channel in effector memory T cells as new target for MS". J. Clin. Invest. 111 (11): 170313. doi:10.1172/JCI16921. PMID 12782673. 

^ a b c Matheu MP, Beeton C, Garcia A, Chi V, Rangaraju S, Safrina O, Monaghan K, Uemura MI, Li D, Pal S, de la Maza LM, Monuki E, Flgel A, Pennington MW, Parker I, Chandy KG, Cahalan MD (October 2008). "Imaging of effector memory T cells during a delayed-type hypersensitivity reaction and suppression by Kv1.3 channel block". Immunity 29 (4): 60214. doi:10.1016/j.immuni.2008.07.015. PMID 18835197. 

^ a b c Beeton C, Wulff H, Barbaria J, Clot-Faybesse O, Pennington M, Bernard D, Cahalan MD, Chandy KG, Braud E (November 2001). "Selective blockade of T lymphocyte K+ channels ameliorates experimental autoimmune encephalomyelitis, a model for multiple sclerosis". Proc. Natl. Acad. Sci. U.S.A. 98 (24): 139427. doi:10.1073/pnas.241497298. PMID 11717451. 

^ Wulff H, Beeton C, Chandy KG (September 2003). "Potassium channels as therapeutic targets for autoimmune disorders". Curr Opin Drug Discov Devel 6 (5): 6407. PMID 14579513. 

^ Tucker K, Overton JM, Fadool DA (August 2008). "Kv1.3 gene-targeted deletion alters longevity and reduces adiposity by increasing locomotion and metabolism in melanocortin-4 receptor-null mice". Int J Obes (Lond) 32 (8): 122232. doi:10.1038/ijo.2008.77. PMID 18542083. 

^ Xu J, Koni PA, Wang P, Li G, Kaczmarek L, Wu Y, Li Y, Flavell RA, Desir GV (March 2003). "The voltage-gated potassium channel Kv1.3 regulates energy homeostasis and body weight". Hum. Mol. Genet. 12 (5): 5519. doi:10.1093/hmg/ddg049. PMID 12588802. 

^ Xu J, Wang P, Li Y, Li G, Kaczmarek LK, Wu Y, Koni PA, Flavell RA, Desir GV (March 2004). "The voltage-gated potassium channel Kv1.3 regulates peripheral insulin sensitivity". Proc. Natl. Acad. Sci. U.S.A. 101 (9): 31127. doi:10.1073/pnas.0308450100. PMID 14981264. 

^ Valverde P, Kawai T, Taubman MA (June 2005). "Potassium channel-blockers as therapeutic agents to interfere with bone resorption of periodontal disease". J. Dent. Res. 84 (6): 48899. doi:10.1177/154405910508400603. PMID 15914584. 

Categories: Ion channel toxins | Neurotoxins

Management of chronic headaches

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Treatments

Medicinal treatments

Analgesic and abortive medications carbide scrap

The most common chronic treatment method is the use of medicine. Many people try to seek pain relief from analgesic medicines (commonly termed pain killers), such as aspirin, acetaminophen, aspirin compounds, ibuprofen, and narcotics. Also, abortive medications can be used to top a headache once it has begun; such drugs include ergotamine (Cafergot), triptans (Imitrex), and prednisone (Deltasone). However, medical professionals advise that abuse of analgesics and abortive medications can actually lead to an increase in headaches. The painkiller medicines help headaches temporarily, but as the uick fix wears off, headaches become more re-current and grow in intensity. These ebound headaches can actually make the body less responsive to preventive medication. Therefore, analgesic and abortive medications are often advised for headaches that are not chronic in nature. catalytic converters scrap

Prophylactic (preventative) medications scrap catalytic converters

The most common medicines used to treat chronic (daily) headaches are called prophylactic medicines, which are used to prevent headaches. Such preventative medication is taken on a daily basis, even when a person may not have a headache. Prophylactic medicines are recommended for chronic headache patients because varied experiments prove that the medications educe the frequency, severity, and disability associated with daily headaches.14] A majority of the prophylactic medications work by inhibiting or increasing neurotransmissions in the brain, often preventing the brain from interpreting pain signals.

Preventative medicines include gabapentin (Neurontin), tizanidine (Zanaflex), fluoxetine (Prozac), amitriptyline (Elavil), and topiramate (Topamax). In testing, gabapentin was found to reduce the number of headache days a month by 9.1%. Tizanidine was found to decrease the average frequency of headaches per week, the headache intensity, and the mean headache duration. Through studies, Fluoxetine resulted in better mood ratings and ignificant increases in headache-free days.17] Despite being associated with depression, antidepressants, such as amitriptyline, have been found to effectively treat ear-daily headaches and numerous chronic pain conditions as well as improving mood and sleep two possible triggers for chronic headache sufferers. One study found that the headache frequency over a 28-day period lowered for chronic headache patients on topiramate. Another medication to prevent headaches is botulinum toxin type A (BoNTA or BOTOX), which is given by injection instead of being taken orally. In a clinical study of botulinum toxin type A, patients participating in the 9-month treatment period with three treatments experienced headache frequency decreases up to 50%. As with all medications, the preventative medications may have side effects. Since different people respond to drugs differently, chronic headache sufferers may have to go through a rial-and-error period to find the right medications. The previously mentioned medicines can improve headaches, but physicians recommend multiple forms of treatments.

Non-medicinal treatments

Physical therapy

In addition to medicines, physical therapy is a treatment to help improve chronic headaches. In physical therapy, a patient works together with a therapist to help identify and change physical habits or conditions that affect chronic headaches. Physical therapy for chronic daily headaches focuses on the upper body, including the upper back, neck, and face. Therapists assess and improve the patient body posture, which can aggravate headaches. During office sessions, therapists use manual therapy, such as a massage, stretching, or joint movement to release muscle tension. Other methods to relax muscles include heat packs, ice packs, and lectrical stimulation.26] Therapists also teach chronic headache sufferers at-home exercises to strengthen and stretch muscles that may be triggering headaches. In physical therapy, the patient must take an active role to practice exercises and make changes to his or her lifestyle for there to be improvement.

Acupuncture

Another non-medicinal treatment, which doesn require at-home exercises, is acupuncture. Acupuncture involves a certified acupuncturist picking particular points on the body to insert acupuncture needles; these points may differ on an individual basis. With chronic headache patients, the acupuncturist may needle ender points at or near the site of maximal headache pain.30] A study conducted by the University of North Carolina School of Medicine found that compared to medicinal treatment alone, medicinal treatment plus acupuncture resulted in more improvement for chronic daily headache patients. Another acupuncture study in Germany found that 52.6% of patients reported a decrease in headache frequency In both studies, acupuncture was not the only treatment. Trials show that acupuncture can cause elevant improvements for people with chronic headaches.

Relaxation training

Relaxation training is another form of non-pharmacological treatment for chronic headache. Relaxation training helps to reduce internal tension, allowing a person to control headaches triggered by stress. The different relaxation methods are normally taught by a psychologist or a therapist. Relaxation training works as people become in tune with their own body, allowing them to realize when it is necessary to decrease tension before a headache occurs. The point of relaxation training is to teach people n attitude of consciously setting out to relax but not trying too hard, enabling people to relax in everyday situations. Relaxation training includes two different types of methods: physical and mental.

Physical methods

Physical relaxation methods involve actual body movement or action. One physical method for releasing tension involves urposefully tensing and then relaxing groups of muscles in a definite sequence, which is named accordingly progressive muscle relaxation. Another physical method of relaxation is deep breathing. Deep breathing is done by breathing from the bottom of the lungs up, which is characterized by the rise and fall of the stomach, not the chest. These are the two most common physical methods of relaxation for chronic headache sufferers.

Mental methods

Also, relaxation therapy can involve mental techniques to decrease body tension. The first is called ocused imagery.41] Focused imagery involves concentration on relaxed body parts, followed by focus on tense muscles and imagining that the tense areas are being worked on or relaxed. The next mental technique involves focus on the whole body, instead of its individual parts. In eepening imagery, a person imagines the body tension as a meter of high to low, and works to reduce tension mentally. An additional mental strategy involves creating and experiencing a location of relaxation in the mind. The last mental strategy involves the chronic headache patient visualizing a place of stress in his or her life and imagining a relaxed response. Meditation in a relaxing environment is also suggested to prevent headaches. Meditation often involves repeating a one syllable sound or staring at a visual object to help focus attention. Relaxation helps the body to unwind, preventing the formation of headaches.

Biofeedback

Biofeedback is often used to evaluate the effectiveness of relaxation training, because it feeds back information to the chronic headache sufferer about the ody (biological) current state.49] One of the most common biofeedback tests is the Electromyograph (EMG), which evaluates the lectrical activity produced by muscles. Biofeedback also can measure electrical brain activity through a test called the Electroencephalograph (EEG). Another test, called the thermograph, measures skin temperature, because when a person is relaxed they have increased blood flow and a higher temperature. Another method is BVP biofeedback training, which improves chronic headaches by teaching a patient how to regulate and decrease arterial pulse amplitudes by restricting the arteries. When tense, a person sweat gland activity increases, which is measured by electrodermograph testing of the hands. Biofeedback methods have been proven to work. A study involving fifteen treatment sessions found that biofeedback was uccessful in reducing both frequency and severity of headache at discharge and over time.55] Biofeedback allows headache sufferers to identify problems and then seek to reduce them.

Changes in diet

Many physicians also recommend changes in diet to treat chronic headaches. Many chronic headache sufferers fail to recognize foods or beverages as headache factors, because the consumption may not consistently cause headaches or the headaches may be delayed. Many of the chemicals in certain foods can cause chronic headaches, including caffeine, monosodium glutamate (MSG), nitrites, nitrates, tyramine, and alcohols. Some of the foods and beverages that chronic headache sufferers are advised to avoid include caffeinated beverages, chocolate, processed meats, cheese and fermented dairy products, fresh yeast-risen baked goods, nuts, and alcohol as well as certain fruits and vegetables. Additionally, people may have differing dietary triggers on an individualized basis, because not all foods affect people the same way. Different medical professionals suggest different ways of testing or changing diets. Some may suggest eliminating a few of the potentially headache-causing foods at a time for a short period of time, while others suggest removing all the threatening foods from a person diet and slowly adding a couple back at a time. Yet, others may not suggest diet modification at all. The treatment of chronic headaches through changes in diet is based on personal opinion, and, therefore, controversial.

Behavioral therapy and psychological therapy

Also, behavioral therapy and psychological therapy are suggested treatments to reduce chronic headaches. Behavioral therapy and psychological therapy relate closely in their treatment methods, which include a combination of identifying headache stressors, biofeedback, relaxation training, and cognitive-behavioral therapy. Cognitive-behavioral therapy purpose s to identify and resolve the sources of recurrent stress.62] In treatment studies, patients with medication plus cognitive-behavioral therapy groups did better than groups with medication alone or cognitive-behavioral therapy alone. Psychological and behavioral therapies identify stressful situations and teach chronic headache patients to react differently, change their behavior, or adjust attitudes to reduce tension that leads to headaches. Treatments especially focus on motional, mental, behavioral, and social factors as they impact headaches. Patients are advised to simply avoid stressors when plausible or share their burdens with others. In this way, studies have found that patients with multimodal treatment in a group setting fare better than patients who follow multimodal treatment alone. Another behavioral study, which included multimodal treatment, showed that the requency of severe headaches was reduced by a clinically significant amount for 75% of the patients.68] Behavioral and psychological therapies work to identify and eliminate or reduce stressful situations that lead to chronic headaches.

Beyond behavioral modification, psychological therapy has a few distinct characteristics of its own. It is important to look at the psychological status of a chronic headache sufferer to dentify conditions that might interfere with headaches and treatments, such as depression. Also, psychological therapy suggests training in self-hypnosis. While hypnotized, patients are given suggestions to relax and use visual imagery to control headache mechanisms, which is very similar to relaxation therapy. Psychological therapists also analyze personal issues that may interfere in a chronic headache patient life, making him or her unable to make changes in lifestyle to improve headaches. Psychologist or psychiatric help for chronic headache patients is controversial, as a patient must be open to possible psychological factors in relation to headaches.

References

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 6

^ Mathew, Ninan T. "The Prophylactic Treatment of Chronic Daily Headache" p. 1552

^ Mathew, Ninan T. "The Prophylactic Treatment of Chronic Daily Headache" p. 1552

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 136

^ Harpole, Linda H., et al. "Headache Management Program Improves Outcome for Chronic Heachache" p. 716

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 40, "Success with Biofeedback found in Chronic Headache Treatment", Andrasik, F. "Behavioral Treatment Approaches to Chronic Headache" p. S81

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 88, 95

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 89, 94

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 24

^ Buchholz, David. Heal Your Headache: The 1-2-3 Program for Taking Charge of Your Headaches p. 46

^ Buchholz, David. Heal Your Headache: The 1-2-3 Program for Taking Charge of Your Headaches p. 50

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 95

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 95

^ a b c Mathew, Ninan T. "The Prophylactic Treatment of Chronic Daily Headache" p. 1553

^ Mathew, Ninan T. "The Prophylactic Treatment of Chronic Daily Headache" p. 1553-1560

^ Mathew, Ninan T. "The Prophylactic Treatment of Chronic Daily Headache" p. 1554

^ Mathew, Ninan T. "The Prophylactic Treatment of Chronic Daily Headache" p. 1557

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 99

^ Mathew, Ninan T. "The Prophylactic Treatment of Chronic Daily Headache" p. 1558

^ Mathew, Ninan T. "The Prophylactic Treatment of Chronic Daily Headache" p. 1553-1558

^ Mathew, Ninan T. "The Prophylactic Treatment of Chronic Daily Headache" p. 1559

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 91

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 109

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 111

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 113

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 113

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 113

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 113

^ Coeytaux, Remy R., et al. "A Randomized, Controlled Trial of Acupuncture for Chronic Daily Headache" p. 1115

^ Coeytaux, Remy R., et al. "A Randomized, Controlled Trial of Acupuncture for Chronic Daily Headache" p. 1115

^ Coeytaux, Remy R., et al. "A Randomized, Controlled Trial of Acupuncture for Chronic Daily Headache" p. 1121

^ Melchart, Dieter, et al. "Acupuncture for Chronic Headaches--an Epidemiological Study" p. 636

^ Melchart, Dieter, et al. "Acupuncture for Chronic Headaches--an Epidemiological Study" p. 632

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 117

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 122

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 122

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 123

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 124

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 125

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 125-126

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 128

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 128

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 128

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 128

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 129

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 129

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 130

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 130

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 133

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 134

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 134

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 134

^ Martin, Paul R. Psychological Management of Chronic Headaches p. 78

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 135

^ "Success with Biofeedback found in Chronic Headache Treatment"

^ Buchholz, David. Heal Your Headache: The 1-2-3 Program for Taking Charge of Your Headaches p. 65

^ Buchholz, David. Heal Your Headache: The 1-2-3 Program for Taking Charge of Your Headaches p. 76

^ Buchholz, David. Heal Your Headache: The 1-2-3 Program for Taking Charge of Your Headaches p. 74-75

^ Buchholz, David. Heal Your Headache: The 1-2-3 Program for Taking Charge of Your Headaches p. 88

^ Buchholz, David. Heal Your Headache: The 1-2-3 Program for Taking Charge of Your Headaches p. 71-72

^ Martin, Paul R. Psychological Management of Chronic Headaches p. 70-85, Andrasik, F. "Behavioral Treatment Approaches to Chronic Headache" p. S80

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 141

^ Andrasik, F. "Behavioral Treatment Approaches to Chronic Headache" p. S83

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 142-145

^ Andrasik, F. "Behavioral Treatment Approaches to Chronic Headache" p. S80

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 143-144

^ Harpole, Linda H., et al. "Headache Management Program Improves Outcome for Chronic Heachache" p. 722

^ Andrasik, F. "Behavioral Treatment Approaches to Chronic Headache" p. S82

^ Andrasik, F. "Behavioral Treatment Approaches to Chronic Headache" p. S83

^ Martin, Paul R. Psychological Management of Chronic Headaches p. 83

^ Martin, Paul R. Psychological Management of Chronic Headaches p. 83

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 146-147

^ Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need p. 146-147

Sources

Andrasik, F. "Behavioral Treatment Approaches to Chronic Headache." Neurological Sciences: Official Journal of the Italian Neurological Society and of the Italian Society Of Clinical Neurophysiology 24 Suppl 2 (2003): S80-5.

Buchholz, David. Heal Your Headache: The 1-2-3 Program for Taking Charge of Your Headaches. New York: Workman, 2002.

Coeytaux, Remy R., et al. "A Randomized, Controlled Trial of Acupuncture for Chronic Daily Headache." Headache 45.9 (2005): 1113-23.

Duckro, Paul N. Taking Control of Your Headaches: How to Get the Treatment You Need. rev ed. New York: Guilford Press, 1999.

Harpole, Linda H., et al. "Headache Management Program Improves Outcome for Chronic Headache." Headache 43.7 (2003): 715-24.

Martin, Paul R. Psychological Management of Chronic Headaches. New York: Guilford Press, 1993.

Mathew, Ninan T. "The Prophylactic Treatment of Chronic Daily Headache." Headache 46.10 (2006): 1552-64.

Melchart, Dieter, et al. "Acupuncture for Chronic Headaches--an Epidemiological Study." Headache 46.4 (2006): 632-41.

"Success with Biofeedback found in Chronic Headache Treatment." Journal of Chiropractic Technique 2.4; 4 (1990): 204.

v  d  e

Antimigraine preparations (N02C)

Analgesic/abortive

Serotonin modulators

Ergot alkaloids

Dihydroergotamine  Ergotamine  Methysergide  Lisuride

5-HT1 agonists

Triptans (Almotriptan, Avitriptan, Eletriptan, Frovatriptan, Naratriptan, Rizatriptan, Sumatriptan, Zolmitriptan) Alniditan

Other

Dotarizine

Other

Paracetamol#  Amidrine

Prevention of migraines

beta blocker (Propranolol#)  calcium channel blocker (Verapamil)  corticosteroid (Flumedroxone)  monosaccharide (Topiramate)  adrenergic agonist (Clonidine)

Ungrouped

piperidine (Pizotifen)  adrenochrome (Iprazochrome)  phenothiazine (Dimetotiazine)  benzoxepin (Oxetorone)  piperazine (Lomerizine)  azepine (Telcagepant)

#WHO-EM. Withdrawn from market. CLINICAL TRIALS: hase III. Never to phase III

Categories: Headaches | Chronic pain syndromesHidden categories: Articles needing additional references from August 2009 | All articles needing additional references