Pathogenesis related proteins from grapes Pathogenesis-related (PR) proteins are typically acidic, of low molecular mass and highly resistant to proteolytic degradation. They accumulate in berries and leaves of grapevines (Figure 5) in response to pathogen attack and are thought to contribute in resistance (Xxxxxxxxx et al. 1998). The type of tissue, developmental stage, and type of infecting pathogen were observed to vary the pattern of PR-protein expression (Xxxxx et al. 1997; Xxxxxxx et al. 1999; Xxxxxx et al. 2002). In grape berries, PR-protein levels are also produced constitutively as a normal part of the ripening process (Xxxxxxxx et al. 1997; Xxxxxxxxxx et al. 1997) and this has been a prophylactic measure against environmental stress and pathogen attack (Xxxxxx and Xxxxxxxx 2000). Chitinase and thaumatin-like proteins represent the predominant PR-proteins in grape berries. These two protein families account for half of the soluble protein in ripe grapes (Xxxxxx et al. 1998). Xxxxxx et al. (2002) showed that grapevine leaves and berries expressed polygalacturonase inhibitor proteins (PGIPs) in response to infection by B. cinerea. PGIPs are thought to contribute to disease resistance by inhibiting the degradation of the plant cell wall by fungal polygalacturonases. PR proteins can also be induced in leaves and berries as part of a defensive response to the classical PR protein gene-inducers (wounding, chemical elicitors, pathogen attack, or abiotic stress) by the expression of specific PR genes (Xxxxxx et al. 1999; Xxxxxxxx and Xxxxx 2000). These processes modulate the levels and proportions of the PR proteins in grapes, apparently depending on the factors like cultivar, region, climate, and agricultural practices (Xxxxxxxx et al. 2003).
Pathogenesis. To investigate the pathogenesis of SLE and LN, we focused on DNA. First, we studied microchimerism (Mc), which is the presence of a small number of genetically distinct cells (of any type and originating from a different zygote) in an individual. Fetal Mc arises from fetal cells that enter the maternal circulation. We used differences in genetic polymorphisms between individuals to detect Mc. Second, we studied the contribution of known lupus susceptibility polymorphisms in familial lupus nephritis. Both of these approaches are discussed below. SLE
Pathogenesis. The prime target for inflammation in RA is the synovium, which when inflamed is termed synovitis. The synovium in a normal joint serves as an important source of nutrients for cartilage as cartilage itself has no blood supply. Another important function of the synovium is the production of hyaluronic acid, which acts as lubrication for the joint. Hyaluronic acid is present in small volumes in the normal joint and helps normal movement and function. The synovial cells also produce collagens and fibronectins which make up the structural framework of the synovial interstitium. In RA, the inflamed synovium produces larger quantities of synovial fluid, which clinically is seen as joint swelling or effusion and is one of the hallmarks of RA. The fluid is also less viscous than normal synovial fluid and contains high levels of inflammatory cells and other mediators of the inflammatory process. The lining of normal synovium is only a few cells thick (1-3), with few if any inflammatory cells, but in RA the lining becomes markedly hypertrophied, up to 8- 10 cells thick. Cells seen in the layer in RA are predominantly macrophages and fibroblasts. The layer below this, the subintimal layer, contains the blood vessels which supply the synovium and normally contains very few cells. However, in RA, this layer is heavily infiltrated with inflammatory cells, including T cells, B cells and macrophages. Accompanying this heavy infiltration is new blood vessel formation, called angiogenesis. The greatly hypertrophied synovium is also called pannus and it has almost tumour like qualities as it invades and erodes adjacent cartilage and bone, which leads to the erosions seen on x-ray. It is felt that T cells play a central role in the pathogenesis of RA, but other cells such as B cells, macrophages, fibroblasts and osteoclasts also play vital roles in the inflammatory process. [Xxxx et al. 2001] The first step in the inflammatory process in RA is the uptake of antigen by antigen presenting cells (APCs), which is then degraded into peptides which are inserted into the groove of HLA-DR molecules on the surface of the APCs and presented to CD4+ T cells. The antigens which trigger this process are unknown; they may be autoantigens, microbial antigens or other external antigens. The T cell receptor recognises the HLA-DR, antigenic peptide complex and through a series of molecular events and gene transcription the T cell becomes activated. [Xxxxxxx et al. 1993] In order for the T cell...
Pathogenesis. If PathoGenesis is responsible for causing any Non- ------------ conforming Finished Product, PathoGenesis will pay ALP the Processing Fees for both the Non-conforming Finished Product and the Finished Product.
Pathogenesis. During the Term and for five years thereafter, ------------ PathoGenesis will obtain and maintain comprehensive general liability insurance (including broad form general liability, completed operations and products liability, personal injury liability, blanket contractual liability and broad form property damage liability) with limits of not less than $5,000,000 combined single limit for bodily injury and property damage liability per occurrence and annual aggregate, containing a cross liability or severability of interests clause. During the Term, PathoGenesis will obtain and maintain worker's compensation insurance as required under applicable law and employer's liability insurance with a limit of not less than $1,000,000. With respect to such insurance coverage required under this section 10.5(b): (i) PathoGenesis will furnish ALP with certificates of insurance evidencing at least the required coverage as soon as practicable evidencing at least the required coverage as soon as practicable after the Effective Date and each anniversary of the Effective Date during the Term (and for five years thereafter if such coverage is then required hereunder); and (ii) all policies will include Provisions for at least 30 days prior written notice of any material change or cancellation (whether for non-payment or otherwise).
Pathogenesis. The pathogenesis and spectrum of disease in LF has developed in recent years. As a result of ultrasound studies, it is now understood that all patients have some underlying pathology [23], although not all will present with clinical pathology. The heterogeneity of pathology among patients is not well understood, although it is probably related to the immunology in each patient. Among asymptomatic microfilaria-positive individuals, hidden lymphatic damage has been found. As the microfilaremia levels decrease over time, patients transition to become acutely symptomatic experiencing acute adenolymphangitis (ADL) and acute filarial attacks (AFL). The interval between detective microfilaremia and symptoms is the clinical incubation period [24] which may vary between 2 and 10 years in an endemic community. Following the acute phase, many patients begin to show signs of chronic lymphedema, which may lead to advanced stages of elephantiasis. Tropical pulmonary eosinophilia is a rare outcome that involves paraoxysmal cough and wheezing, weight loss, low-grade fever, adenopathy, and pronounced blood eosinophilia (>3000 eosinophils (White blood cells)/μl) [2]. Tropical pulmonary eosinophilia is a result of intense immune response to circulating microfilaria. Persons with this outcome will have low mf levels, but will be antigen and antibody positive. In most cases, there are restrictive pulmonary function abnormalities. If not treated with DEC, the disease may progress to chronic restrictive lung disease with interstitial fibrosis.
Pathogenesis. The presence of placental vascular anastomoses is a conditio sine qua non for the development of TTTS. Injection studies of twin placentas have shown that such anastomoses are almost invariably present in monochorionic twins and extremely rare in dichorionic twins5. Three types of anastomoses have been documented: from artery to artery, from vein to vein and from artery to vein. Arterio-venous anastomoses are unidirectional and are referred to as “deep” anastomoses since they proceed through a shared placental cotyledon, whereas arterio-arterial and xxxx-venous anastomoses are bi-directional and are referred to as “superficial” since they lie on the chorionic plate (Figure 1). Injection studies of monochorionic placentas have demonstrated that arterio-arterial, arterio-venous and xxxx-venous anastomoses are present in 80%, 95% and 20% of monochorionic placentas, respectively 60-62. The presence of at least one arterio-venous anastomosis has been shown to be essential for the development of chronic TTTS26;61-63. According to the classic pathophysiological concept, chronic TTTS is caused by net imbalance of blood flow between the twins due to arterio-venous anastomoses7;8. Blood from one twin (the donor) is pumped through an artery into the shared placental cotyledon and then drained through a vein into the circulation of the other twin (the recipient). Unless blood is pumped back from the recipient to the donor through oppositely directed FIGURE 1 Placenta injection study with colored dye from a monochorionic twin gestation without chronic twin-to- twin transfusion syndrome delivered after 38 weeks of gestation. Arteries are injected with dark-blue dye and veins with orange dye. The arrow at the bottom of the picture indicates an arterio-arterial anastomosis. An arterio-venous anastomosis from twin 2 to twin 1 is pointed out in the center of the picture, whereas an arterio-venous anastomosis from twin 1 to twin 2 is indicated at the top of the picture. Twin 2 has a velamentous cord insertion. deep arterio-venous anastomoses or through superficial anastosmoses, an imbalance of blood volumes occurs, gradually leading to the development of chronic TTTS. The presence of arterio-arterial anastomoses in particular is thought to give some protection against the development of chronic TTTS by compensating for the circulatory imbalance caused by the uni-directional arterio-venous anastomoses7;8. Various studies have demonstrated that these bi-directional arterio-art...
