Pathogenesis Clause Samples

Pathogenesis related proteins from grapes
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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 ▇▇▇▇-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 ▇▇▇▇-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 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-arterial anastomoses occur more frequently in monochorionic placentas of twins without chronic TTTS compared to placentas of twins with chronic TTTS around 80% and 25%, respectively 26;64-67. The antenatal detection of an arterio-arterial anastomosis with color Doppler ultrasound examination is associated with a 9-fold reduction in likelihood ratio of developing chronic TTTS68. This protective role of arterio-arterial anastomoses which was already proposed by ▇▇▇▇▇▇ in the 19th century7, has recently also been demonstrated in a mathematical computer model of chr...
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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. [▇▇▇▇ 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. [▇▇▇▇▇▇▇ et al. 1993] In order for the T cell...
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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).
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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.
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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.
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Pathogenesis. The pathogenesis and spectrum of disease in LF has developed in recent years.
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Related to Pathogenesis

  • Influenza Vaccine Upon recommendation of the Medical Officer of Health, all employees shall be required, on an annual basis to be vaccinated and or to take antiviral medication for influenza. If the costs of such medication are not covered by some other sources, the Employer will pay the cost for such medication. If the employee fails to take the required medication, she may be placed on an unpaid leave of absence during any influenza outbreak in the home until such time as the employee has been cleared by the public health or the Employer to return to the work environment. The only exception to this would be employees for whom taking the medication will result in the employee being physically ill to the extent that she cannot attend work. Upon written direction from the employee’s physician of such medical condition in consultation with the Employer’s physician, (if requested), the employee will be permitted to access their sick bank, if any, during any outbreak period. If there is a dispute between the physicians, the employee will be placed on unpaid leave. If the employee gets sick as a reaction to the drug and applies for WSIB the Employer will not oppose the application. If an employee is pregnant and her physician believes the pregnancy could be in jeopardy as a result of the influenza inoculation and/or the antiviral medication she shall be eligible for sick leave in circumstances where she is not allowed to attend at work as a result of an outbreak. This clause shall be interpreted in a manner consistent with the Ontario Human Rights Code.

  • Hepatitis B Vaccine Where the Hospital identifies high risk areas where employees are exposed to Hepatitis B, the Hospital will provide, at no cost to the employees, a Hepatitis B vaccine.

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