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Lymphoid infiltration

The presence of interstitial histiomacrophage infiltration of interalveolar walls, pneumonia, acute bronchitis, congestion of vessels, hemorrhages, peribronchial and perivascular lymphoid infiltration, foci of emphysema and dystelectasis were eonsidered in the assessment of morphological changes in the lungs. [Pg.427]

Figure 10 shows the intensity of perivascular and peribronchial lymphoid infiltration which accompanies inflammatory process development in the lungs. The intensity of perivascular and peribronchial lymphoid infiltration varied throughout the experiment, depending on the date of observation and date of receiving the drug. [Pg.432]

The fluctuations in lymphoid infiltration volume in animals from both groups are wave-like. In group I, the lymphoid response on Days 1 and 3 was lower than in group II while on Days 5 and 7, the lymphoid... [Pg.432]

Fig. 10. The comparative analyses of perivascular and peribronchial lymphoid infiltration intensity in the lungs of animals from a group of control and the group that got MFPC Grinization . Fig. 10. The comparative analyses of perivascular and peribronchial lymphoid infiltration intensity in the lungs of animals from a group of control and the group that got MFPC Grinization .
Figure 12 shows dynamics of the changes in the quantitative characteristics of spleen megakaryocytes. It is obvious that their dynamics is the same as in perivascular and peribronchial lymphoid infiltration study. Hence, perivascular and peribronchial lymphoid infiltration condition reflects systemic reaction of the lymphoid tissue of mice to the maximum concentration of the virus in the lungs and bacterial flora activation in case of MFPC Grinization application which results in more adequate and concordant immune response in animals from group II. [Pg.434]

Microscopic investigation of the mice from group I revealed the presence of vessel congestion, small numerous intralobular and perivenular infiltrates, moderate focal protein-hydropic degeneration combined with polymorphism of hepatocyte nuclei and inconstant lymphoid infiltration of portal tracts. Marked activation of histiomacrophage elements — hepatic macrophages must be emphasized. Homotypic moderate inflammatory alterations remained in the liver on Days 3, 5, 7 and 10. The presence of inflammatory mononuclear infiltration in the walls of central veins, typical for a viral infection, reflects a massive lesion of the vascular... [Pg.435]

Benzene is metabolized primarily in the liver by the cytochrome P-450 system (Parke 1989). It appears that the metabolism of benzene by the hepatic cytochrome P-450 system plays an important role in its bioactivation and toxicity. Sammett et al. (1979) provided corroborative evidence of this by showing that partial hepatectomy of rats diminished both the rate of metabolism of benzene and its toxicity. An increase in altered hepatic foci has been shown in male rats after benzene exposure in conjunction with initiator and promotor administration (Dragan et al. 1993). A dose of 500 mg/kg of benzene administered subcutaneously once daily, 5 days a week for 26 weeks to Wistar rats resulted in focal fine droplet fatty metamorphosis with accompanying lymphoidal infiltration in the liver after 12 weeks (Bloch et al. 1990). In some cases a proliferated histocyte-like cells formed clusters in the vicinity of the periportal fields. After 26 weeks, more diffuse steatosis, feathery degeneration of hepatocytes, single necrotic cells were seen. [Pg.209]

Aluminium causes histological changes at injection sites, and these stain with hematoxylin and eosin (53). Of four patients studied, one had a sclerosing lipogranu-loma-hke reaction with unhned cystic spaces containing crystalline material. Another presented as a large symptomatic subcutaneous swelling, which microscopically showed diffuse and widespread involvement of the subcutaneous tissues by a lymphoid infiltrate with prominent lymphoid follicles. [Pg.100]

Heavy-Chain Disease. Rarely, unusual forms of IgG, IgA, or light chains polymerize and cause a similar syndrome with high blood viscosity. Heavy-chain diseases in which the paraprotein consists only of a heavy chain, usually incomplete, are rare conditions associated with lymphoid infiltration. The most common of these is a-chain disease, in which the intestine is infiltrated and severe malabsorption may be seen. [Pg.573]

There is a definite association between the size of a primary melanoma lesion and the likelihood of metastases. The prognostic factor originally used to determine survival was based on the cross-sectional profile of the primary tumor. The cross-sectional profile could be evaluated if the deepest invasive tumor cells lay above or below the sweat glands. This assessment was further clarified by Clark, who described the relationship of depth of invasion of the cancer cells to the standard anatomic landmarks of the skin (Table 133-3). Clark s classification is a practical approach for patients with more superficial tumors, because tumors classified as Clark levels I through III seldom metastasize. That classification system has been criticized because of problems associated with practical measurements. Melanoma lesions that occur in the presence of lymphoid infiltration, fibrosis, or even the cells of preexisting nevi are difficult to assess with classic reference landmarks. [Pg.2529]

Ill. Bani D, Giannotti B. Differentiation of interdigitating reticulum cells and Langerhans cells in the human skin with T-lymphoid infiltrate. An immunocytochemical and ultrastructural study. Arch Histol Cytol. 1989 52(4) 361-372. [Pg.188]

The majority of non-neoplastic and neoplastic lymphoid infiltrates in the lung are related to BALT. In neoplasia, BALT proliferations can explain most neoplastic pulmonary lymphoid diseases. As stated earlier in the chapter, pathologists may encounter difficulty in distinguishing between neoplastic and non-neoplastic lymphoid lesions. In many instances, molecular biology techniques such as flow cytometry are necessary to... [Pg.387]

FIGURE 12.18 Lymphomatoid granulomatosis is composed of a variegated lymphoid infiltrate. X 100. [Pg.391]

Thymomas may occur in the pleura and can be confused with mesothelioma. These neoplasms may be confused with a sarcomatoid mesothelioma with a heavy lymphoid infiltrate or with a lymphohistiocytoid mesothelioma. None of the cases presented by Moran and coworkers showed radiographic evidence of a mediastinal tumor, however 6 cases showed histologic features of a mixed (lymphocyte-epithelial) thymoma. The neoplastic thymic epithelial cells express keratin and CD5. [Pg.444]

Paraffin sections are also acceptable substrates for the immunohistologic separation of benign and malignant T-cell infiltrates of the skin. As alluded to earlier, the authors have found that CD4-predominant intraepider-mal lymphoid infiltrates, which also show concurrent negativity for CD3, CD5, CD7, CD43, or CD45RO, are... [Pg.476]

Deep Lymphoid Infiltrates Simulating Small Cell or Mixed B-Cell Lymphomas... [Pg.476]

The utility of another marker—the bcl-2 protein (BCLP)—has been analyzed in several studies of cutaneous lymphoid infiltrates. That moiety is an inhibitor of apoptosis, and it is overexpressed in malignant lymphoid cells that demonstrate a t(14 18) chromosomal translocation. The latter is most characteristically seen in follicular lymphomas (Fig. 13.20). However, it would appear that BCLP unexpectedly has limited differential diagnostic usefulness in the narrower context of cutaneous lymphoproliferations. Many examples of CLH, CTCL, and various B-cell lymphomas of the skin are BCLP positive, and one must restrict attention only to overtly follicular proliferations in order to realize any benefit from this marker. Follicular CLH is BCLP negative, but follicular lymphoma in the skin also shows inconsistent positivity for that marker. [Pg.477]

Rest EB, Horn TD. Immunophenotypic analysis of benign and malignant cutaneous lymphoid infiltrates. Clin Dermatol. 1991 9 261-272. [Pg.493]

Cerroni L, Smolle J, Soyer HP, et al. Immunophenotyping of cutaneous lymphoid infiltrates in frozen and paraffin-embedded tissue sections a comparative study. / Am Acad Dermatol. 1990 22 405-413. [Pg.493]

Fucich LF, Freeman SF, Boh EE, et al. Atypical cutaneous lymphoid infiltrates and a role for quantitative immunohis-tochemistry and gene rearrangement studies. Int J Dermatol. 1999 38 749-756. [Pg.494]

Rittet JH, Adesokan PN, Fitzgibbon JF, et al. Paraffin section immunohistochemistry as an adjrmct to morphologic analysis in the diagnosis of cutaneous lymphoid infiltrates. J Cutan Pathol. 1994 21 481-493. [Pg.494]

Burg G, Dtrmmer R, Haeffner A, et al. From inflammation to neoplasia mycosis fungoides evolves from reactive inflammatory conditions (lymphoid infiltrates) transforming into neoplastic plaques and mmors. Arch Dermatol. 2001 137 949-952. [Pg.494]

Ceballos KM, Gascoyne RD, Martinka M, et al. Heavy multinodular cutaneous lymphoid infiltrates clinicopathologic feamres and B-cell clonality. J Cutan Pathol. 2002 29 159-167. [Pg.494]

FIGURE 19.4 DCIS is heavily obscured with lymphocytes, but smooth-muscle myosin heavy chain clearly reflects the presence of myoepithelial cells (A). Another case in which myoepithelial cells are easy to see with p63 in spite of heavy lymphoid infiltrate on core biopsy, which confirms a lack of invasion (B). [Pg.765]


See other pages where Lymphoid infiltration is mentioned: [Pg.428]    [Pg.428]    [Pg.429]    [Pg.430]    [Pg.430]    [Pg.432]    [Pg.433]    [Pg.433]    [Pg.143]    [Pg.1554]    [Pg.555]    [Pg.573]    [Pg.407]    [Pg.2519]    [Pg.2532]    [Pg.178]    [Pg.388]    [Pg.388]    [Pg.388]    [Pg.388]    [Pg.389]    [Pg.391]    [Pg.476]    [Pg.766]    [Pg.804]   
See also in sourсe #XX -- [ Pg.433 ]




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