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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
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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
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Categories: Stations of Keihan Electric Railway | Railway stations in Kyoto Prefecture | Kyoto Prefecture railway station stubs
Monday, May 10, 2010
Kowata Station
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
Sunday, May 9, 2010
Christofle
China Product
Christofle is a manufacturer of fine silver flatware and home accessories based in France since 1830. They are renowned for their sterling, silverplate and stainless flatware. Among Christofle's product lines are silver picture frames, crystal vases and glassware, porcelain dinnerware and silver jewelry. Christofle is also well known for their silver holloware.
Artists and designers such as Man Ray, Jean Cocteau, Gio Ponti, Andre Putman, Martin Szekely, Ito Morabito (Ora-to) and Richard Hutten are among those whose creations have been made by Christofle. freeze dried rose petals
The origins of Christofle date to 1830 when jeweler Charles Christofle assumed management of a jewelry workshops pertaining to his wife's family. Christofle today is under the control and ownership of the Christofle family, the current generation being represented by Maurizio Borletti. Christofle was publicly-traded until 1998, when Borletti and others took the firm private. glow cups
Christofle manufactures their products in France and in Brazil, and they are sold worldwide through 75 Pavillon Christofle retail stores and also through 400 department stores and specialty shops. lighted ice cubes
References
Style on a Silver Platter, India Today, 2/28/08
Christofle: A Legend Revisited, Diplomat, June 2006
External links
Wikimedia Commons has media related to: Christofle
Official website
Christofle Hotel Division, Table De France, North America
This French corporation or company article is a stub. You can help Wikipedia by expanding it.
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Categories: Companies established in 1830 | Companies of France | French silversmiths | French company stubs
Phone fraud
China Product
Types of frauds
Fraud against users
Frauds against users by phone companies mini tape dispenser
Cramming is the addition of charges to a subscriber's telephone bill for services which were neither ordered nor desired by the client, or for fees for calls or services that were not properly disclosed to the consumer. These charges are often assessed by dishonest third-party suppliers of data and communication service that phone companies are required, by law, to allow the third-party to place on the bill. heavy duty stapler
Slamming is any fraudulent, unauthorized change to the default long-distance/Local carrier or DSL internet service selection for a subscriber's line, most often made by dishonest vendors desirous to steal business from competing service providers. Main article: Telephone slamming. auto tape dispenser
Fraud against customers by third parties
PBX dial through (hi) can be used fraudulently by placing a call to a business and then requesting to be transferred to "9-0" or some other outside toll number. (9 is normally an outside line and 0 then connects to the utility's operator) The call appears to originate from the business (instead of the original fraudulent caller) and appears on the company's phone bill. Trickery (such as impersonation of installers and telco personnel "testing the system") or bribery and collusion with dishonest employees inside the firm may be used to gain access.
Autodialers may be used for a number of dishonest purposes, including telemarketing fraud or even as War dialing. War dialers take their name from a scene in the early-1980's movie WarGames in which a 'cracker' programs a home computer to dial every number in an exchange, searching for lines with auto-answer data modems. Sequential dialing is easy to detect, pseudo-random dialing is not. One more recent variant involves claiming to be a customer-owned coin-operated telephone (COCOT) vendor, connecting an autodialer to what should have been a payphone line, dialing an assorted series of toll-free "wrong numbers" (such as +1-800 in US, which effectively reverses the charges) and then demanding that the called parties reimburse the fraudulent COCOT provider for the cost of "calls received from a payphone".
Autodialers are also used to make many short duration calls, mainly to mobiles, leaving a missed call number which is either premium rate or contains advertising messages. Knowns as Wangiri from Japan where it originated.
Dialer programs containing malware or malicious code have been used to cause personal computers to disconnect from an existing legitimate local provider and instead dial into a premium (usually overseas) number. The first of these used a Moldovan phone number[citation needed].
Pre-pay telephone cards and "calling cards" are also very vulnerable to fraudulent use; these cards contain a number or passcode which can be dialed in order to bill worldwide toll calls to the card. Anyone who obtains the passcode can dishonestly misuse it to make or to resell toll calls.
809 scams take their name from the former +1 (809) area code which used to cover most of the Caribbean nations (it has since been split into multiple new area codes, adding to the confusion). The numbers *look* like Canadian or US telephone numbers but turn out to be costly, overpriced international calls. Entire Caribbean 'phone exchanges (such as +1-876-HOT-...) numbers in Jamaica, plus numbers in Antigua, Montserrat and a number of other Caribbean or overseas countries) are used to bypass consumer protection laws which govern premium numbers and phone sex operations such as +1-900 or 976 services in the victim's home country. Other variants on this scheme involve leaving messages on pagers or making bogus claims of being a relative in a family emergency to trick users into calling the foreign numbers, then attempting to keep the victim on the line as long as possible in order to incur the cost of an expensive foreign call.
The 10xxx or 1010xxx codes used to select an alternate long-distance carrier on a per-call basis were also widely misused by phone sex scammers and spammers in the early days of competitive long distance; the phone-sex operations would misrepresent themselves as alternate long-distance carriers to evade consumer protection measures which prevent US 'phone subscribers from losing local or long-distance service due to calls to +1-900 or 976 premium numbers. This practice has largely been replaced by the misuse of numbers in former +1-809 countries or other overseas numbers as cash-strapped governments in many poorer nations are willing to condone the practice.
Telemarketing fraud takes a number of forms; much like mail fraud, solicitations for the sale of goods or investments which are never delivered or worthless and requests for donations to bogus unregistered charities are not uncommon. Callers often prey upon sick and elderly persons; scams in which a caller attempts to obtain banking or credit card information also frequently occur. One other variant
involves calling a number of business offices, asking for model numbers of various pieces of office equipment in use (such as photocopiers) and then sending unsolicited shipments of supplies for the machines then billing the victims at artificially inflated prices.
Verizon, at the customer's request, will put a Cramming Block on the customer's account, that prevents third parties from adding charges. To obtain the free Cramming Block call Verizon customer service.
Fraud against phone companies
Fraud by phone companies against one another
Interconnect fraud involves the falsification of records by telephone carriers in order to deliberately miscalculate the money owed by one telephone network to another. This affects calls originating on one network but carried by another at some point between source and destination.
Refiling is a form of interconnect fraud in which one carrier tampers with CID (caller-ID) or ANI data to falsify the number from which a call originated before handing the call off to a competitor. Refiling and interconnect fraud briefly made headlines in the aftermath of the Worldcom financial troubles; the refiling scheme is based on a quirk in the system by which telcos bill each other - two calls to the same place may incur different costs because of differing displayed origin. A common calculation of payments between telcos calculates the percentage of the total distance over which each telco has carried one call to determine division of toll revenues for that call; refiling distorts data required to make these calculations.
Fraud against the phone company by users
Subscription fraud: for example, signing up with a bogus name, or no intention to pay
Frauds against the phone company by third parties
Phreaking involves obtaining knowledge of how the telephone network operates, which can be used (but isn't always) to place unauthorised calls. The history of phone phreaking shows that many 'phreaks' used their vast knowledge of the network to help telephone companies. There are, however, many phreaks that use their knowledge to exploit the network for personal gain, even today. In some cases social engineering has been used to trick telco employees into releasing technical information. Early examples of phreaking involved generation of various control tones, such as a 2600 hertz blue box tone to release a long-distance trunk for immediate re-use or the red box tones which simulate coins being inserted into a payphone. These exploits no longer work in many areas of the telephone network due to widespread use of digital switching systems and out-of-band signaling. There are, however, many areas of the world where these control tones are still used and this kind of fraud is still continuing to happen.
A more high-tech version of the above is switch reprogramming, where unauthorized "back door" access to the phone company's network or billing system is used to allow free telephony. This is then sometimes resold by the 'crackers' to other customers.
Payphones have also been misused to receive fraudulent collect calls; most carriers have turned off the feature of accepting incoming calls or have muted the payphones internal ringing mechanism for this very reason.
Cloning (telephony) has been used as a means of copying both the electronic serial number and the telephone number of another subscriber's 'phone to a second (cloned) 'phone. Airtime charges for outbound calls are then mis-billed to the victim's cellular 'phone account instead of the perpetrator's. Cordless phones are often even less secure than cellphones, though there are a number of security issues currently affecting cellular phones. There are a number of other privacy concerns with mobile and cordless 'phones; a scanner radio may intercept analogue conversations in progress.
Frauds against the phone company by phone company employees
This section requires expansion.
See also
Caller ID spoofing
Credit card fraud
Dial tapping
Internet fraud
Mail fraud
Mobile phone spam
Vishing
Wire fraud
External links
State-by-State Comparison of Cramming Laws plus recommended course of action for affected consumers
Find and Report Trouble callers
Billing World article: Telecom Fraud on the Rise
Lasar's Letter on the Federal Communications Commission: FCC slams 13 telcos for slamming--exonerates three
Identify Fraudulent Charges in Your Phone Bill guide from non-profit consumer group on identifying and disputing fraudulent charges
16 Ways You Can be Phone Scammed a list of the most popular phone scams.
OFCOM: Problems with your landline phone: slamming - advice from the British communications regulator
Daily Mail: Phone scam hits thousands
The Guardian: When slamming the phone prompts a row
The Guardian: Orange slammed as users see red - concerns over data protection by British mobile telecom suppliers
Bell Canada Fraud Control Centre
Categories: FraudHidden categories: Articles with limited geographic scope | USA-centric | All articles with unsourced statements | Articles with unsourced statements from February 2007 | Articles to be expanded from May 2008 | All articles to be expanded
Polyphenism
China Product
Definition
A polyphenism is a biological mechanism that causes a trait to be polyphenic. For example, crocodiles possess a sex-determining polyphenism, and therefore their gender is a polyphenic trait.
When polyphenic forms exist at the same time in the same panmictic (interbreeding) population they can be compared to genetic polymorphism. With polyphenism the switch between morphs is environmental, but with genetic polymorphism with the determination of morph is genetic. These two cases have in common that more than one morph is part of the population at any one time. This is rather different from cases where one morph predictably follows another during, for instance, the course of a year. In essence the latter is normal ontogeny where young forms can and do have different forms, colours and habits to adults. prescription swimming goggles
The discrete nature of polyphenic traits differentiates them from traits like weight and height, which are also dependent on environmental conditions but vary continuously across a spectrum. When a polyphenism is present, an environmental cue causes the organism to develop along a separate pathway, resulting in distinct morphologies; thus, the response to the environmental cue is ll or nothing. The nature of these environmental conditions varies greatly, and includes seasonal cues like temperature and moisture, pheromonal cues, kairomonal cues (signals released from one species that can be recognized by another), and nutritional cues. blade table tennis
Examples of Polyphenism table tennis paddle
Sex determination
Sex-determining polyphenisms allow a species to benefit from sexual reproduction while permitting gender ratios other than unity. This is beneficial to the species because a large female-to-male ratio maximizes reproductive capacity. However, temperature-dependent sex determination (as seen in crocodiles) limits the range in which a species can exist, and makes the species susceptible to endangerment by changes in weather pattern. Temperature-dependent sex determination has been proposed as an explanation for the extinction of the dinosaurs.
Population-dependent and reversible sex determination, found in animals such as the blue wrasse fish, have less potential for failure. In the blue wrasse, only one male is found in a given territory: larvae within the territory develop into females, and adult males will not enter the same territory. If a male dies, one of the females in his territory becomes male, replacing him. While this system ensures that there will always be a mating couple when two animals of the same species are present, it could potentially decrease genetic variance in a population, for example if the females remain in a single male's territory. Furthermore, this system is inherently unstable on a small scale because a single mutation causing a fish to remain permanently male would spread quickly through the population (due to high female availability) and might eventually cause loss of females in the species, and therefore extinction.
The caste system in insects
The caste system of insects enables eusociality, the division of labor between non-breeding and breeding individuals. A series of polyphenisms determines whether larvae develop into queens, workers, and in some cases soldiers. In the case of the ant, P. morrisi, an embryo must develop under certain temperature and photoperiod conditions in order to become a reproductively-active queen. This allows for control of the mating season, but like sex determination, limits the spread of the species into certain climates. In bees, royal jelly provided by worker bees causes a developing larva to become a queen. Royal jelly is only produced when the queen is aging or has died. This system is less subject to influence by environmental conditions, yet prevents unnecessary production of queens.
Seasonal pigmentation changes
Polyphenic pigmentation is adaptive for insect species that undergo multiple mating seasons each year. Different pigmentation patterns provide appropriate camouflage throughout the seasons, as well as alter heat retention as temperatures change. Because insects cease growth and development after eclosion, their pigment pattern is invariable in adulthood: thus, a polyphenic pigment adaptation would be less valuable for species whose adult form survives longer than one year. Birds and mammals, however, are capable of continued physiological changes in adulthood, and some display reversible seasonal polyphenisms, such as coat color in the Arctic fox.
Predator-Induced Polyphenisms
Predator-induced polyphenisms are advantageous because they allow the species to develop in a more reproductively-successful way in a predator absence, but to otherwise assume a more defensible morphology. However, this advantageous polyphenism can quickly become neutral or a disadvantage if the predator evolves to stop producing the kairomone to which the prey responds. For example, the fly larvae that feed on Daphnia cucullata (a water flea) release a kairomone that Daphnia can detect. When the fly larvae are present, Daphnia grow large helmets that protect them from being eaten. However when the predator is absent, Daphnia have smaller heads and are therefore more agile swimmers.
Cannibalistic Polyphenism
The spadefoot toad polyphenism maximizes its reproductive capacity in temporary desert ponds. While the water is at a safe level, the tadpoles develop slowly on a diet of other opportunistic pond inhabitants. However, when the water level is low and desiccation is imminent, the tadpoles develop a morphology (wide mouth, strong jaw) that permits them to cannibalize. Cannibalistic tadpoles receive better nutrition and thus metamorphose more quickly, avoiding death as the pond dries up.
Evolution of Polyphenisms
A mechanism has been proposed for the development of polyphenisms:
A mutation results in a novel, heritable trait.
The trait frequency expands in the population, creating a population on which selection can act.
Pre-existing (background) genetic variation in other genes results in phenotypic differences in expression of the new trait.
These phenotypic differences undergo selection; as genotypic differences narrow, the trait becomes:
Genetically fixed (non-responsive to environmental conditions)
Polyphenic (responsive to environmental conditions)
Evolution of novel polyphenisms through this mechanism has been demonstrated in the laboratory. Suzuki and Nijhout used an existing mutation (black) in a monophenic green hornworm (M. sexta) that causes a black phenotype. They found that if larvae from an existing population of black mutants were raised at 20C, then all the final instar larvae were black; but if the larvae were instead raised at 28C, the final instar larvae ranged in color from black to green. By selecting for larvae that were black if raised at 20C but green if raised at 28C, they produced a polyphenic strain after thirteen generations.
This fits the model described above because a new mutation (black) was required to reveal pre-existing genetic variation and to permit selection. Furthermore, the production of a polyphenic strain was only possible because of background variation within the species: two alleles, one temperature-sensitive and one stable, were present for a single gene upstream of black (in the pigment production pathway) before selection occurred. The temperature-sensitive allele was not observable because at high temperatures, it caused an increase in green pigment in hornworms that were already bright green. However, introduction of the black mutant caused the temperature-dependent changes in pigment production to become obvious. The researchers could then select for larvae with the temperature-sensitive allele, resulting in a polyphenism.
See also
Phenotypic switching
References
^ Noor MA, Parnell RS, Grant BS (2008). "A Reversible Color Polyphenism in American Peppered Moth (Biston betularia cognataria) Caterpillars". PLoS ONE 3 (9): e3142. doi:10.1371/journal.pone.0003142. PMID 18769543. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0003142.
^ Woodward, D.E. and Murray, J.D. (1993). On the effect of temperature-dependent sex determination on sex ratio and survivorship in crocodilians. Proc. R. Soc. Lond. [B] 252:149-155.
^ Ford E.B. 1975. Ecological genetics. 4th ed, Chapman & Hall, London
^ Woodward, D.E. and Murray, J.D. (1993). On the effect of temperature-dependent sex determination on sex ratio and survivorship in crocodilians. Proc. R. Soc. Lond. [B] 252:149-155.
^ Gilbert, S.F. (2003). Developmental Biology, 7 edn (Sunderland, Massachusetts, Sinauer Associates, Inc.). pp.731.
^ Gilbert, S.F. (2003). Developmental Biology, 7 edn (Sunderland, Massachusetts, Sinauer Associates, Inc.). pp.732
^ Abouheif, E., and Wray, G.A. (2002). Evolution of the gene network underlying wing polyphenism in ants. Science 297, 249-252.
^ Braendle, C., and Flatt, T. (2006). A role for genetic accommodation in evolution? Bioessays 28, 868-873.
^ Gilbert, S.F. (2003). Developmental Biology, 7 edn (Sunderland, Massachusetts, Sinauer Associates, Inc.). pp.727.
^ Gilbert, S.F. (2003). Developmental Biology, 7 edn (Sunderland, Massachusetts, Sinauer Associates, Inc.). pp.735.
^ Storz, B.L. (2004). Reassessment of the environmental mechanisms controlling developmental polyphenism in spadefoot toad tadpoles. Oecologia 141, 402-410.
^ Braendle, C., and Flatt, T. (2006). A role for genetic accommodation in evolution? Bioessays 28, 868-873.
^ Suzuki, Y., and Nijhout, H.F. (2006). Evolution of a polyphenism by genetic accommodation. Science 311, 650-652.
Note: The seventh edition of Gilbert's Developmental Biology is available online: DevBio.
Categories: Biology | Subfields and areas of study related to evolutionary biology | Evolutionarily significant biological phenomena | Population ecologyHidden categories: Unclassified articles missing geocoordinate data | All articles needing coordinates
Semiconductor device fabrication
China Product
History
When feature widths were far greater than about 10 micrometres, purity was not the issue that it is today in device manufacturing. As devices became more integrated, cleanrooms became even cleaner. Today, the fabs are pressurized with filtered air to remove even the smallest particles, which could come to rest on the wafers and contribute to defects. The workers in a semiconductor fabrication facility are required to wear cleanroom suits to protect the devices from human contamination.
In an effort to increase profits, semiconductor device manufacturing has spread from Texas and California in the 1960s to the rest of the world, such as Europe, Israel, and Asia. It is a global business today. solar blankets
The leading semiconductor manufacturers typically have facilities all over the world. Intel, the world's largest manufacturer, has facilities in Europe and Asia as well as the U.S. Other top manufacturers include STMicroelectronics (Europe), Analog Devices (US), Atmel (US/Europe), Freescale Semiconductor (US), Samsung (Korea), Texas Instruments (US), GlobalFoundries (Germany, Singapore, future New York fab in construction), Toshiba (Japan), NEC Electronics (Japan), Infineon (Europe), Renesas (Japan), Taiwan Semiconductor Manufacturing Company (Taiwan), Fujitsu(Japan/US), NXP Semiconductors (Europe), Micron Technology (US), Hynix (Korea) and SMIC (China). rockwool insulation
Wafers extruded polystyrene
Main article: wafer (semiconductor)
A typical wafer is made out of extremely pure silicon that is grown into mono-crystalline cylindrical ingots (boules) up to 300 mm (slightly less than 12 inches) in diameter using the Czochralski process. These ingots are then sliced into wafers about 0.75 mm thick and polished to obtain a very regular and flat surface.
Once the wafers are prepared, many process steps are necessary to produce the desired semiconductor integrated circuit. In general, the steps can be grouped into two areas:
Front-end processing
Back-end processing
Processing
In semiconductor device fabrication, the various processing steps fall into four general categories: deposition, removal, patterning, and modification of electrical properties.
Deposition is any process that grows, coats, or otherwise transfers a material onto the wafer. Available technologies consist of physical vapor deposition (PVD), chemical vapor deposition (CVD), electrochemical deposition (ECD), molecular beam epitaxy (MBE) and more recently, atomic layer deposition (ALD) among others.
Removal processes are any that remove material from the wafer either in bulk or selectively and consist primarily of etch processes, either wet etching or dry etching. Chemical-mechanical planarization (CMP) is also a removal process used between levels.
Patterning covers the series of processes that shape or alter the existing shape of the deposited materials and is generally referred to as lithography. For example, in conventional lithography, the wafer is coated with a chemical called a photoresist. The photoresist is exposed by a stepper, a machine that focuses, aligns, and moves the mask, exposing select portions of the wafer to short wavelength light. The unexposed regions are washed away by a developer solution. After etching or other processing, the remaining photoresist is removed by plasma ashing.
Modification of electrical properties has historically consisted of doping transistor sources and drains originally by diffusion furnaces and later by ion implantation. These doping processes are followed by furnace anneal or in advanced devices, by rapid thermal anneal (RTA) which serve to activate the implanted dopants. Modification of electrical properties now also extends to reduction of dielectric constant in low-k insulating materials via exposure to ultraviolet light in UV processing (UVP).
Many modern chips have eight or more levels produced in over 300 sequenced processing steps.
Front-end processing
Front-end processing refers to the formation of the transistors directly on the silicon. The raw wafer is engineered by the growth of an ultrapure, virtually defect-free silicon layer through epitaxy. In the most advanced logic devices, prior to the silicon epitaxy step, tricks are performed to improve the performance of the transistors to be built. One method involves introducing a straining step wherein a silicon variant such as silicon-germanium (SiGe) is deposited. Once the epitaxial silicon is deposited, the crystal lattice becomes stretched somewhat, resulting in improved electronic mobility. Another method, called silicon on insulator technology involves the insertion of an insulating layer between the raw silicon wafer and the thin layer of subsequent silicon epitaxy. This method results in the creation of transistors with reduced parasitic effects.
Gate oxide and implants
Front-end surface engineering is followed by: growth of the gate dielectric, traditionally silicon dioxide (SiO2), patterning of the gate, patterning of the source and drain regions, and subsequent implantation or diffusion of dopants to obtain the desired complementary electrical properties. In memory devices, storage cells, conventionally capacitors, are also fabricated at this time, either into the silicon surface or stacked above the transistor.
Back-end processing
Metal layers
Once the various semiconductor devices have been created they must be interconnected to form the desired electrical circuits. This back end of line (BEOL, the latter portion of the wafer fabrication, not to be confused with back end of chip fabrication which refers to the package and test stages) involves creating metal interconnecting wires that are isolated by insulating dielectrics. The insulating material was traditionally a form of SiO2 or a silicate glass, but recently new low dielectric constant materials are being used. These dielectrics presently take the form of SiOC and have dielectric constants around 2.7 (compared to 3.9 for SiO2), although materials with constants as low as 2.2 are being offered to chipmakers.
Interconnect
Synthetic detail of a standard cell through four layers of planarized copper interconnect, down to the polysilicon (pink), wells (greyish) and substrate (green).
Historically, the metal wires consisted of aluminium. In this approach to wiring often called subtractive aluminium, blanket films of aluminium are deposited first, patterned, and then etched, leaving isolated wires. Dielectric material is then deposited over the exposed wires. The various metal layers are interconnected by etching holes, called vias, in the insulating material and depositing tungsten in them with a CVD technique. This approach is still used in the fabrication of many memory chips such as dynamic random access memory (DRAM) as the number of interconnect levels is small, currently no more than four.
More recently, as the number of interconnect levels for logic has substantially increased due to the large number of transistors that are now interconnected in a modern microprocessor, the timing delay in the wiring has become significant prompting a change in wiring material from aluminium to copper and from the silicon dioxides to newer low-K material. This performance enhancement also comes at a reduced cost via damascene processing that eliminates processing steps. In damascene processing, in contrast to subtractive aluminium technology, the dielectric material is deposited first as a blanket film, and is patterned and etched leaving holes or trenches. In single damascene processing, copper is then deposited in the holes or trenches surrounded by a thin barrier film resulting in filled vias or wire lines respectively. In dual damascene technology, both the trench and via are fabricated before the deposition of copper resulting in formation of both the via and line simultaneously, further reducing the number of processing steps. The thin barrier film, called copper barrier seed (CBS), is necessary to prevent copper diffusion into the dielectric. The ideal barrier film is as thin as possible. As the presence of excessive barrier film competes with the available copper wire cross section, formation of the thinnest continuous barrier represents one of the greatest ongoing challenges in copper processing today.
As the number of interconnect levels increases, planarization of the previous layers is required to ensure a flat surface prior to subsequent lithography. Without it, the levels would become increasingly crooked and extend outside the depth of focus of available lithography, interfering with the ability to pattern. CMP (chemical mechanical planarization) is the primary processing method to achieve such planarization although dry etch back is still sometimes employed if the number of interconnect levels is no more than three.
Wafer test
The highly serialized nature of wafer processing has increased the demand for metrology in between the various processing steps. Wafer test metrology equipment is used to verify that the wafers haven't been damaged by previous processing steps up until testing. If the number of dieshe integrated circuits that will eventually become chips etched on a wafer exceeds a failure threshold (ie. too many failed dies on one wafer), the wafer is scrapped rather than investing in further processing.
Device test
Main article: wafer testing
Once the front-end process has been completed, the semiconductor devices are subjected to a variety of electrical tests to determine if they function properly. The proportion of devices on the wafer found to perform properly is referred to as the yield.
The fab tests the chips on the wafer with an electronic tester that presses tiny probes against the chip. The machine marks each bad chip with a drop of dye. The fab charges for test time; the prices are on the order of cents per second. Chips are often designed with estability features such as "built-in self-test" to speed testing, and reduce test costs.
Good designs try to test and statistically manage corners: extremes of silicon behavior caused by operating temperature combined with the extremes of fab processing steps. Most designs cope with more than 64 corners.
Die preparation
Main article: die preparation
Once tested, the wafer is scored and then broken into individual die -- wafer dicing. Only the good, unmarked chips go on to be packaged.
Packaging
Main article: integrated circuit packaging
Plastic or ceramic packaging involves mounting the die, connecting the die pads to the pins on the package, and sealing the die. Tiny wires are used to connect pads to the pins. In the old days, wires were attached by hand, but now purpose-built machines perform the task. Traditionally, the wires to the chips were gold, leading to a ead frame (pronounced eed frame) of copper, that had been plated with solder, a mixture of tin and lead. Lead is poisonous, so lead-free ead frames are now mandated by ROHS.
Chip-scale package (CSP) is another packaging technology. A plastic dual in-line package, like most packages, is many times larger than the actual die hidden inside, whereas CSP chips are nearly the size of the die. CSP can be constructed for each die before the wafer is diced.
The packaged chips are retested to ensure that they were not damaged during packaging and that the die-to-pin interconnect operation was performed correctly. A laser etches the chip name and numbers on the package.
List of steps
This is a list of processing techniques that are employed numerous times in a modern electronic device and do not necessarily imply a specific order.
Wafer processing
Wet cleans
Photolithography
Ion implantation (in which dopants are embedded in the wafer creating regions of increased (or decreased) conductivity)
Dry etching
Wet etching
Plasma ashing
Thermal treatments
Rapid thermal anneal
Furnace anneals
Thermal oxidation
Chemical vapor deposition (CVD)
Physical vapor deposition (PVD)
Molecular beam epitaxy (MBE)
Electrochemical Deposition (ECD). See Electroplating
Chemical-mechanical planarization (CMP)
Wafer testing (where the electrical performance is verified)
Wafer backgrinding (to reduce the thickness of the wafer so the resulting chip can be put into a thin device like a smartcard or PCMCIA card.)
Die preparation
Wafer mounting
Die cutting
IC packaging
Die attachment
IC Bonding
Wire bonding
Thermosonic Bonding
Flip chip
Tab bonding
IC encapsulation
Baking
Plating
Lasermarking
Trim and form
IC testing
Hazardous materials
Many toxic materials are used in the fabrication process. These include:
poisonous elemental dopants such as arsenic, antimony and phosphorus
poisonous compounds like arsine, phosphine and silane
highly reactive liquids, such as hydrogen peroxide, fuming nitric acid, sulfuric acid and hydrofluoric acid
It is vital that workers not be directly exposed to these dangerous substances. The high degree of automation common in the IC fabrication industry helps to reduce the risks of exposure of this sort. Most fabrication facilities employ exhaust management systems, such as wet scrubbers, combustors, heated absorber cartridges etc, to control the risk to workers and also the environment if these toxic materials are released into the atmosphere.
See also
Atomic layer deposition
Electronic design automation
Foundry (electronics)
GDS II
Health hazards in semiconductor manufacturing occupations
International Technology Roadmap for Semiconductors
Microfabrication
OASIS (Open Artwork System Interchange Standard)
Semiconductor Equipment and Materials International (SEMI) the semiconductor industry trade association
References
^ Zeno Gaburro (2004). "Optical Interconnect". in Lorenzo Pavesi and David J. Lockwood. Silicon Photonics. Springer. ISBN 3540210229.
^ http://www.uic.com/wcms/WCMS2.nsf/index/Resources_26.html
External links
Semiconductor glossary
BYU Cleanroom - semiconductor properties, calculators, processes, etc.
Categories: Semiconductor device fabricationHidden categories: Articles needing additional references from September 2008 | All articles needing additional references
