Inflammatory white cells

Hydrocortisone microspheres (108,109) and films (110) based on poly(lactic acid) have been investigated. A cage implant technique was used to study the performance of monolithic poly (DL-lactide) films loaded with hydrocortisone acetate (110). Films 1.5 x 0.6 cm were inserted into titanium wire-mesh cages 3.5 x 1.0 cm. The cages were implanted in the backs of rats and the inflammatory exudate was sampled periodically. The white cell concentration in the samples was lower than that of controls at all times during the 21-day test. 

Elevated ET-1 in SCA patients, even in the steady state, may play an important role in the dehydration of sickle erythrocytes and the resulting enhanced intra-erythrocytic HbS polymerization. Indeed, it has been shown that ET-1 activates Ca2+- gated K+ channels in mouse erythrocytes [34]. ET-1, as a pro-inflammatory agonist, has been shown to induce the production of inflammatory cytokines by monocytes. One of the cytokines, namely TNFa enhances the adherence of sickle erythrocytes to vascular endothelium [35]. In addition, endothehns upregulate the expression of endothelial adhesion molecules such as ICAM-l, VCAM-1 and E-se-lectin, which participate in the recruitment of white cells to the site of inflammation. The overall conclusions that can be drawn from these data is that ET-1 plays a critical role in the vasospasm and inflammation that result in VOC. The major effect of HU in ameliorating the clinical symptoms of SCA likely results from its ability to inhibit the chronically activated ET-1 expression in SCA patients. 

The polymorph is the dominant white cell in the blood stream and, like the macrophage, shares a common hemopoietic stem cell precursor with the other formed elements of the blood. It has no mitochondria, but utilizes its abundant cytoplasmic glycogen stores for its energy requirements thus, glycolysis enables these cells to function under anaerobic conditions such as those in an inflammatory focus. It is a nondividing, short-lived cell with a segmented nucleus. 

Length and size of CNTs seriously affect their cytotoxicities (Sato et al., 2005 Cui et al., 2007). CNTs of 825 nm in length caused stronger inflammation in human acute monocytic leukemia cell line THP-1 than CNTs of 220 nm in length, as shown in Fig. 9.5. However, histological observation as shown in Fig. 9.6, showed that no severe inflammatory response such as necrosis, white cells aggregates, etc. This result indirectly shows that CNTs can cause noninflammatory damage to local tissues. 

Substance P and the related tachykinins neurokinin A and neurokinin B are mainly found in neurons, particularly unmyelinated sensory somatic and visceral fibres, in enteric sensory neurons and in a number of pathways within the brain. The release of tachykinins from the peripheral ends of these neurons may play an important role in the neurogenic inflammatory responses to local injury and inflammation by promoting the release of histamine from mast cell degranulation, and the release of cytokines from invading white cells, as well as acting directly upon blood vessels to produce vasodilation and plasma extravasation. Neurogenic inflammation within... 

All patients with anterior uveitis should undergo dilated funduscopy. Such examination should be attempted on the initial visit, although it may be difficult because of patient discomfort and/or posterior synechia. In such cases, ophthalmoscopy on the first follow-up visit may yield more useful information. Without adequate careful examination of the peripheral fundus and posterior pole, one cannot rule out the possibility of posterior involvement or masquerade syndromes. Masquerade syndromes are disorders that present as uveitis but do not have an inflammatory etiology. Such diseases either cause a secondary uveitis or are mistaken for a primary uveitis, because of the presence of white cells, red blood cells, pigment, or tumor cells. Examples of masquerade syndromes may include lymphoma, leukemia, retinoblastoma, malignant choroidal melanoma, retinal detachment, and intraocular foreign body. 

Synovial flnid nsnally is mrbid hecanse of the large number of leukocytes in inflammatory fluid. White cell counts of 5000 to 50,000/mm are not uncommon in inflamed joints. The fluid is usually less viscous than that in normal joints or in fluid associated with osteoarthritis. Glucose concentrations of joint fluid are normal or low compared with those in serum drawn at the same time as synovial aspirates. The decrease is not as profound as the decrease associated with joint infection or systemic lupus erythematosus. 

White cells are physiologically and pathologically important as mediators of the inflammatory response (reviewed in [288]). Neutrophils are the first of the inflammatory cells to arrive at sites of injury. The neutrophils phagocytic capabilities and the release of proteinases and oxidants are important for fighting bacterial infections as well as clearing dead cell... 

Fig. 6.16a-d. Crohn s disease of the colon, a Indium labelled white cell scan in active disease with widespread involvement of the caecum, transverse and descending colon, b Barium follow through demonstrating stricture formation of the ascending colon with displaced adjacent bowel consistent with an inflammatory mass, c Ultrasound of the descending colon in a patient with active disease. Note the thickened bowel wall and the obliterated bowel lumen, d Coronal MRI showing marked wall thickening of the caecal pole with a narrowed lumen... 

In the rabbit cornea bioassay, no evidence of inflammatory response was observed with any of the implants at any time. On an average, the bulk of the polymers disappeared completely between 7 and 14 days after the implantation [66]. In similar animal experiments in which polyanhydride matrices containing tumor angiogenic factor (TAF) were implanted in rabbit cornea, a significant vascularization response was observed without edema or white cells. Moreover, and most importantly from the biocompatibiUty standpoint, polymer matrices without incorporated TAF showed no adverse vascular response [67,68]. 

An 80-year-old woman with acromegaly developed extensive fat necrosis in both buttocks after three deep subcutaneous doses of lameo-tide 60 mg extended release. The lesions first became apparent about 4 months after the first injection and developed over several months. There was central necrosis with surrounding inflammatory tissue. The CRP concentration and white cell count were normal and bacterial cultures were negative. Once the lesions were clearly demarcated they were excised. 

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