Movie Trailer The Founder1 Hindi, Bollywood Radio Station . 1 Hindi, Bollywood Radio Station. New Grain Trailers built by farmers for farmers: craftsmanship in every New Hopper Bottom Grain Trailer. The trailer for season 9 of 'The Real Housewives of Atlanta' has arrived ahead of its November debut. Design & Thinking is a documentary exploring the idea of Design Thinking. Laminitis is a disease that affects the feet of hooved animals and it is found mostly in horses and cattle. Clinical signs include foot tenderness progressing to. Laminitis - Wikipedia. Radiograph of a horse hoof showing rotation of the coffin bone and evidence of sinking, a condition often associated with laminitis. The annotation P2 stands for the middle phalanx, or pastern bone, and P3 denotes the distal phalanx, or coffin bone. The yellow lines mark the distance between the top and bottom part of the coffin bone relative to the hoof wall, showing the distal (bottom) of the coffin bone is rotated away from the hoof wall. Laminitis is a disease that affects the feet of hooved animals (ungulates) and it is found mostly in horses and cattle. Clinical signs include foot tenderness progressing to inability to walk, increased digital pulses, and increased temperature in the hooves. Severe cases with outwardly visible clinical signs are known by the colloquial term founder, and progression of the disease may lead to perforation of the coffin bone through the sole of the hoof, requiring aggressive treatment or euthanasia. Http:// - THE FOUNDER Official Trailer (2016) Michael Keaton McDonald's Franchise Movie HD The story of McDonald's founder, Ray Kroc. Spring Founder Prevention. We're coming to that time of year again when so many horse owners feel pressure to have their vets out to do spring shots, tube worming. Laminae. In horses, there are about 5. The basement membrane is then attached to the coffin bone via the connective tissue of the dermis. When severe enough, this results in displacement of the coffin bone within the hoof capsule. Three conditions are thought to cause secondary laminitis: Inflammation. Inflammatory events that are associated with laminitis include sepsis, endotoxemia, retained placenta, carbohydrate overload (excessive grain or pasture), enterocolitis, pleuropneumonia, and contact with black walnut shavings. Mechanical laminitis can occur when a horse habitually paws, is ridden or driven on hard surfaces (. Support limb laminitis is most common in horses suffering from severe injury to one limb, such as fracture, resulting in a non- weight bearing state that forces them to take excessive load on the opposing limb. This causes decreased blood flow to the cells, decreasing oxygen and nutrient delivery, and thus altering their metabolism which results in laminitis. Metalloproteinases are enzymes that can degrade collagen, growth factors, and cytokines to remodel the extracellular matrix of tissues. To prevent tissue damage, they are regulated by tissue inhibitors of metalloproteinases (TIMPs). In cases of laminitis, an underlying cause is thought to cause an imbalance of MMPs and TIMPs, favoring MMPs, so that they may cleave substances within the extracellular matrix and therefore break down the basement membrane. These include: Enzymatic and inflammatory theories: The enzymatic theory postulates that increased blood flow to the foot brings in inflammatory cytokines or other substances to the hoof, where they increase production of MMPs, which subsequently break down the basement membrane. The inflammatory theory states that inflammatory mediators produce inflammation, but recognizes that MMP production occurs later. Therefore, this is possibly a 2- step process, beginning with inflammation and leading to MMP production and subsequent laminitis. The end- result would be ischemia, leading to cellular death and breakdown between the lamellae. Subsequently, increased vascular permeability leads to edema within the hoof, compression of small vessels, and ischemia. Vasoactive amines may be partially to blame for changes in hoof blood flow. Change in insulin regulation may lead to laminitis. A single severe laminitic episode or repeated, less severe episodes can, depending upon the degree of separation of dermal and epidermal laminae, lead to either rotation or sinking of the pedal bone, both of which result in anatomical changes in the position of the coffin bone with visible separation of the laminae, colloquially known as founder. Rotation and distal displacement may occur in the same horse. Penetration of the sole is not inherently fatal; many horses have been returned to service by aggressive treatment by a veterinarian and farrier, but the treatment is time- consuming, difficult and expensive. Rotation is the most common form of displacement, and, in this case, the tip of the coffin bone rotates downward. A combination of forces (e. Also, ligaments attaching the collateral cartilages to the digit, primarily in the palmar portion of the foot, possibly contribute to a difference in support from front to back. The body weight of the animal probably contributes to rotation of the coffin bone. Rotation results in an obvious misalignment between PII (the short pastern bone) and PIII (the coffin bone). If rotation of the third phalanx continues, its tip can eventually penetrate the sole of the foot. Sinking is less common and much more severe. It results when a significant failure of the interdigitation between the sensitive and insensitive laminae around a significant portion of the hoof occurs. The destruction of the sensitive laminae results in the hoof wall becoming separated from the rest of the hoof, so that it drops within the hoof capsule. Sinking may be symmetrical, i. In extreme cases, this event allows the tip to eventually penetrate the sole of the foot. It generally lasts 2. Clinical laminitis may be prevented if cryotherapy (icing) is initiated during the developmental phase. Treatment response during this time determines if the horse will go into the subacute phase or chronic phase. Clinical signs at this time include bounding digital pulses, lameness, heat, and possibly response to hoof testing. Clinical signs seen in the acute phase resolve, and the horse becomes sound. The horse never shows radiographic changes, and there is no injury to the coffin bone. Severe P3 rotation and penetration into the sole. A lamellar wedge is evident. The chronic phase occurs if damage to the lamellae is not controlled early in the process, so that the coffin bone displaces. Changes that may occur include separation of the dermal and epidermal lamellae, lengthening of the dermal lamellae, and compression of the coronary and solar dermis. If laminitis is allowed to continue, long- term changes such as remodeling of the apex and distal border of the coffin bone (so that a . Compensated cases will have altered hoof structure, including founder rings, wide white lines, and decreased concavity to the sole. Horses will be relatively sound. On radiographs, remodeling of the coffin bone and in cases of rotational displacement, the distal hoof wall will be thicker than that proximally. Venograms will have relatively normal contrast distribution, including to the apex and distal border of the coffin bone, and the coronary band, but . This will lead to irregular horn growth and chronic lameness, and horses will suffer from laminitis . The solar dermis is often compressed enough to inhibit growth, leading to a soft, thin sole (< 1. In severe cases where collapse of the suspensory apparatus of P3 has occurred, the solar dermis or the tip of P3 may penetrate the sole. The horse will also be prone to recurrent abscessation within the hoof capsule. These causes can be grouped into broad categories. Endotoxins. The excess then moves on to the hindgut and ferments in the cecum. The presence of this fermenting carbohydrate in the cecum causes proliferation of lactic acid bacteria and an increase in acidity. This process kills beneficial bacteria, which ferment fiber. The endotoxins and exotoxins may then be absorbed into the bloodstream, due to increased gut permeability, caused by irritation of the gut lining by increased acidity. The result is body- wide inflammation, but particularly in the laminae of the feet, where swelling tissues have no place to expand without injury to other structures. This results in laminitis. Nitrogen compound overload: Herbivores are equipped to deal with a normal level of potentially toxic nonprotein nitrogen compounds in their forage. If, for any reason, rapid increases in levels of these compounds occur, for instance in lush spring growth on fertilized lowland pasture, the natural metabolic processes can become overloaded, resulting in liver disturbance and toxic imbalance. For this reason, many avoid using synthetic nitrogen fertilizer on horse pasture. If clover (or any legume) is allowed to dominate the pasture, this may also allow excess nitrogen to accumulate in forage, under stressful conditions such as frost or drought. Many weeds eaten by horses are nitrate accumulators. Direct ingestion of nitrate fertilizer material can also trigger laminitis, by a similar mechanism. Colic: Laminitis can sometimes develop after a serious case of colic, due to the release of endotoxins into the blood stream. Lush pastures: When releasing horses back into a pasture after being kept inside (typically during the transition from winter stabling to spring outdoor keeping), the excess fructan of fresh spring grass can lead to a bout of laminitis. Ponies and other easy keepers are much more susceptible to this form of laminitis than are larger horses. Frosted grass: Freezing temperatures in the fall also coincide with outbreaks of laminitis in horses at pasture. Cold temperatures cause growth to cease, so sugar in pasture grasses cannot be used by the plant as fast as it is produced, thus they accumulate in the forage. Cool- season grasses form fructan, and warm season grasses form starch. Fructan is theorized to cause laminitis by causing an imbalance of the normal bowel flora leading to endotoxin production. These endotoxins may exacerbate insulin resistance, or the damage to the lining of the gut may release other as yet unidentified trigger factors into the blood stream. For horses prone to laminitis, restrict or avoid grazing when night temperatures are below 4. When growth resumes during warmer weather, sugar will be used to form protein and fiber and will not accumulate. Untreated infections: Systemic infections, particularly those caused by bacteria, can cause release of endotoxins into the blood stream. A retained placenta in a mare (see below) is a notorious cause of laminitis and founder. Insulin resistance: Laminitis can also be caused by insulin resistance in the horse.
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