Complex regional pain syndrome

Complex regional pain syndrome known as reflex sympathetic dystrophy, describes an array of painful conditions that are characterized by a continuing regional pain, disproportionate in time or degree to the usual course of any known trauma or other lesion. Starting in a limb, it manifests as extreme pain, limited range of motion, changes to the skin and bones, it may affect one limb and spread throughout the body. Two subtypes exist. Having both types is possible; the classification system in use by the International Association for the Study of Pain divides CRPS into two types. It is recognised that people may exhibit both types of CRPS. Clinical features of CRPS have been found to be inflammation resulting from the release of certain proinflammatory chemical signals from the nerves, sensitized nerve receptors that send pain signals to the brain, dysfunction of the local blood vessels' ability to constrict and dilate appropriately, maladaptive neuroplasticity; the signs and symptoms of CRPS manifest near the injury site.

The most common symptoms are extreme pain, including burning, stabbing and throbbing. The pain is out of proportion to the severity of the initial injury. Moving or touching the limb is intolerable. With diagnosis of either CRPS types I or II, patients may develop burning allodynia. Both syndromes are characterized by autonomic dysfunction, which presents with localized temperature changes, and/or edema; the patient may experience localized swelling. Drop attacks fainting, fainting spells are infrequently reported, as are visual problems; the symptoms of CRPS vary in duration. One version of the McGill pain index, a scale for rating pain, ranks CRPS highest, above childbirth and cancer. Since CRPS is a systemic problem any organ can be affected. Symptoms may change over time, they can vary from person to person. Symptoms can change numerous times in a single day. CRPS was considered to have three stages however more recent studies suggest people affected by CRPS do not progress through sequential stages and the staging system is no longer in wide use.

Growing evidence instead points towards distinct sub-types of CRPS. Complex regional pain syndrome is uncommon, its cause is not understood. CRPS develops after an injury, heart attack, or stroke. Investigators estimate that 2–5% of those with peripheral nerve injury, 13-70% of those with hemiplegia will develop CRPS. In addition, some studies have indicated that cigarette smoking was strikingly present in patients and is statistically linked to RSD; this may be involved in its pathology by enhancing sympathetic activity, vasoconstriction, or by some other unknown neurotransmitter-related mechanism. This hypothesis was based on a retrospective analysis of 53 patients with RSD, which showed that 68% of patients and only 37% of controls were smokers; the results are limited by their retrospective nature. 7% of people who have CRPS in one limb develop it in another limb. Inflammation and alteration of pain perception in the central nervous system are proposed to play important roles; the persistent pain and the perception of nonpainful stimuli as painful are thought to be caused by inflammatory molecules and neuropeptides released from peripheral nerves.

This release may be caused by inappropriate cross-talk between sensory and motor fibers at the affected site. CRPS is not a psychological illness, yet pain can cause psychological problems, such as anxiety and depression. Impaired social and occupational function occur. Complex regional pain syndrome is a multifactorial disorder with clinical features of neurogenic inflammation, nociceptive sensitisation, vasomotor dysfunction and maladaptive neuroplasticity; the "underlying neuronal matrix" of CRPS is seen to involve cognitive and motor as well as nociceptive processing. In contrast to previous thoughts reflected in the name RSD, it appears that there is reduced sympathetic nervous system outflow, at least in the affected region. Wind-up (the increased se

1988 Japanese motorcycle Grand Prix

The 1988 Japanese motorcycle Grand Prix was the first round of the 1988 Grand Prix motorcycle racing season. It took place on the weekend of 25–27 March 1988 at the Suzuka Circuit. Tadahiko Taira was on pole of the 5-column grid. Wayne Rainey got the start and lead through the first turns, with Kevin Schwantz, Wayne Gardner and Christian Sarron behind. Schwantz took the inside of the hairpin. At the end of the 1st lap, it was Schwantz and Gardner a gap to Toshihiko Honma and Sarron. Gardner and Schwantz swapped the lead many times. Eddie Lawson and Niall Mackenzie moved through the field to 4th. Norihiko Fujiwara lowsided at the hairpin. On the last lap Gardner ran off the track and stayed on, but lost any chance of winning the race

Alfalfa mosaic virus

Alfalfa mosaic virus known as Lucerne mosaic virus or Potato calico virus, is a worldwide distributed phytopathogen that can lead to necrosis and yellow mosaics on a large variety of plant species, including commercially important crops. It is the only Alfamovirus of the Bromoviridae family. In 1931 Weimer J. L. was the first to report AMV in alfalfa. Transmission of the virus occurs by some aphids, by seeds or by pollen to the seed; the virion has a capsid but no envelope. The icosahedral symmetry of the capsid is round to elongated; the range for the length of the virion particle is about 30–57 nm. AMV is composed of 4 particles with a diameter of 18 nm; the genetic material of AMV consists of 3 linear single strands RNAs and a subgenomic RNA, obtained by transcription of the negative- sense strand of RNA 3. RNA 1 and 2 encode proteins needed for replication. RNA 3 is required for the synthesis of the protein responsible for cell-to-cell movement. RNA 4 encodes the capsid. Beside encapsidation and its role in movement the viral coat protein plays a role in the initiation of RNA replication.

This property is called genome activation and means that the genomic nucleic acid is not infectious without the capsid. Specific association of the coat protein with the RNA 3’- terminal sequences or with the subgenomic mRNA is required for the infection. Bacilliform particles contain separately encapsidated RNAs 1, 2 and 3. Spheroidal particles each have two copies of RNA 4; the nucleotide sequence of the complete genome has been determined and the length of the genome is 8274 nucleotides. RNA 1, 2, 3 and 4 are 3644, 2593, 2037 and 881 nucleotides long; the AMV cycle can be split up in 5 steps: 1st step: AMV enters the cell and the particles disassemble. The capsid protein remains attached to the coat protein binding site at the 3’- end of the RNAs; the initiation factors elF4A, elF4E and elF4G of the host bind to the cap. 2nd step: The coat protein interacts with an initiation factor. This triggers translation of RNA1 and 2 into replicase proteins P1 and P2; the complex P1/P2 binds to the RNA. 3rd step: Targeting of RNA to the tonoplast by P1/P2.

The capsid dissociates from CPB. CPB undergoes a conformational change into TLS. P1/P2 bind to the minus- strand promoter, made up of TLS and hairpin E. 4th step: Minus- strand RNAs are synthesized. 5th step: Plus- strand RNAs and viral proteins are synthesized. Virions assemble.. AMV infects over 600 plant species in 70 families; some hosts: potato, tobacco, bluebeard... Symptoms vary from wilting, white flecks, malformation like dwarfing, mottles, mosaics to necrosis depending on the virus strain, host variety, stage of growth at infection and environmental conditions. Signs of infection can disappear quickly; the virus can be detected in each part of the host plant. The virions are found in the cytoplasm of the infected plant. Inclusions of Alfalfa mosaic virus In vitro AMV has a longevity of 1–4 days. Temperature and light are the environmental factors that have the greatest influence on the multiplication and movement of AMV in the plant and thus indirectly on the symptoms. Under low temperature the appearance of necrosis for example is less than that for high temperature.

The virus reaches his inactivation temperature at 60–65 °C. Dark conditions slow down the virus multiplication. A hypothesis for this phenomenon is that shading causes a decrease in ATP production by photosynthesis; the optimum pH was found to be about pH 7–7.5 for AMV in sap. It has been proved that in the important forage grass alfalfa, the infection by AMV leads to a decrease of Cu, Fe, Mn, P and Zn quantities. On the other hand, an increase in N was observed. Infected alfalfa was not seen to be harmful for domestic animals. AMV is a variable plant virus and several strains with minor differences exist. Distinction is based on different symptoms in one or two chosen hosts and on, for example, differential physico-chemical properties; the vectors are insects of family Aphididae. AMV can be transmitted by seed, through mechanical inoculation of plant sap and by the parasitic plant dodder; the combination of seed-infected plants and spreading by aphids results in high levels of infection. The host range of the virus includes food and pasture crops.

Infection by AMV causes important yield losses, reduces winter survival and facilitates infection of the affected plant by other pathogens. Insecticides against aphids are not effective for controlling AMV. Recommendations are sowing healthy seed, managing weeds, avoiding growing crops adjacent to infected pasture and other cultural practices to minimize AMV. Work has been done on creating transgenic AMV resistant plants. For example, DNA derived from AMV encoding the gene for the capsid has been inserted into alfalfa plants; this reduced the susceptibility of the plants to infection by AMV and the plants would be