Chronic necrotizing

Based on the different histological criteria, chronic hepatitis was subdivided in 1968 into (i.) chronic persistent hepatitis (CPH) (a term coined by H. F. Smetana as early as 1954) and (2.) chronic active hepatitis (CAH) (E. G. Saint et al., 1953) with a mild (type A) and a severe (type B) course. (7) In this context so-called chronic necrotizing hepatitis can be integrated. (24) (s. fig. 34.6) (s. tab. 34.1) This classification was further refined by the additional... 

Fig. 34.6 Chronic necrotizing hepatitis B marked postnecrotic cleft formation in the area of the left lobe of liver (10 months after severe, acute necrotic hepatitis). Brownish to brick-red colouring of the liver with a flat, undulatory surface, scarry indentations and proliferation of connective tissue as well as spots of capsular fibrosis. Fine hypervascular arteries, pronounced venous contours and isolated lymph vessel congestion...

Bronchiectasis is defined pathologically as an abnormal permanent dilation of bronchi and bronchioles due to chronic necrotizing infection of these airways (Robbins et al. 1999). Based on gross morphologic appearance, Reid (1950) classified bronchiectasis into cyhn-drical, varicose, or cystic type. With the exception of infectious diseases, cystic fibrosis is probably the most common cause of cHnically important bronchiectasis in the Caucasian population (Cartier et al. 1999). Bron-... 

Antibiotic LL-E19020a and LL-E19020P are described as useful agents for the treatment of chronic respiratory disease, fowl cholera, and necrotic enteritis in birds (76) and as anthelmintics in monogastric and mminant animals (28). 

Historically, osteomyelitis has been classified as acute or chronic based on duration of disease (Fig. 78-2).2,4 However, there are no established definitions for acute and chronic infections.2-4 Acute infection has been defined as first episode or recent onset of symptoms (less than 1 week).2,3 Chronic osteomyelitis is generally defined as relapse of the disease or symptoms persisting beyond 4 weeks.2,3 Others describe chronic osteomyelitis as the presence of necrotic bone.3 ... 

In the chronic inhalation bioassay of 1,2-dibromoethane conducted by NTP (1982) (discussed in Section 2.2.1.8), increased incidence of focal and centrilobular hepatocellular necrosis occurred in male and female F344 rats exposed to the highest dose (40 ppm) of 1,2-dibromoethane. Compound-related degenerative or necrotizing hepatocellular lesions did not occur in B6C3Fi mice following exposure to any concentration used. Liver lesions were not reported in rats after chronic inhalation exposure to 20 ppm 1,2-dibromoethane with or without 0.05% disulfiram in the diet however, hepatocellular tumors (not otherwise classified) were induced in exposed rats fed dietary disulfiram (Wong et al. 1982). Also see Section 2.2.1.8. 

In aminoglycoside-treated animals, the cells can be led to canonical apop-totic death through activation of caspases. Caspase-9 forms an apoptosome complex with cytochrome c and APAF-1 and leads to apoptosis through activation of caspase-3. Aminoglycosides activate caspases in auditory structures conversely, inhibition of caspase activity successfully blocks neomycin-induced vestibulotoxicity. In contrast, apoptotic markers were essentially absent in a mouse model of chronic kanamycin ototoxicity where death of auditory sensory cells ensued via cathepsins. The activation of cathepsin D was accompanied by the nuclear translocation of endonuclease G, necrotic cleavage of PARP, and activation of p,-calpain, all facets of necrotic cell death. 

CMME is a mucous membrane and respiratory irritant in both humans and animals. Acute exposure of rats and hamsters resulted in pulmonary edema and hemorrhage and necrotizing bronchitis. Human exposure to CMME has been reported to cause breathing difficulties, sore throat, fever, and chills. An increased frequency of chronic cough and low-end expiratory flow rates has been observed in a dose-related fashion with exposure to CMME and BCME. ... 

For debridement of necrotic tissue and liquefication of slough in acute and chronic lesions such as pressure ulcers, varicose, diabetic, and decubitus ulcers, burns, postoperative wounds, pilonidal cyst wounds, carbuncles, and miscellaneous traumatic or infected wounds. Also stimulates vascular bed activity to improve epithelization. 

It is doubtful whether the insect uses pederin for defensive purposes, because it acts on the skin of animals only when it is crushed and not through mere contact with the insect, even if prolonged. It also has neither insecticidal nor repellent properties (92). However, it causes epidermic necrotization as acute pederosis and desquamation as chronic pederosis on human skin. On the other hand, it stimulates bedsore cicatrization in lower doses and leads to complete healing. Application to mouse skin produces dermatitis with necrosis or huge edema, and the damaged tissue is reconstituted with a permanent loss of hair. 

The atherosclerotic lesions develop in a complex, chronic process. The first detectable lesion is the so-called fatty streak, an aggregation of lipid-laden macrophage foam cells. The next stage of development is the formation of plaques consisting of a core of lipid and necrotic cell debris covered by a layer of connective tissue and smooth muscle cells. These plaques hinder arterial blood flow and may precipitate clinical events by plaque rupture and thrombus formation. Platelets from the thrombi, activated macrophages, and smooth muscle cells release growth factors and cytokines resulting in an inflammatory-fibroproliferative response that leads to the advanced lesions of atherosclerosis. 

Besides the paranoid psychosis associated with chronic use of amphetamines, a specific lesion associated with chronic amphetamine use is necrotizing arteritis, which may involve many small and medium-sized arteries and lead to fatal brain hemorrhage or renal failure. Overdoses of amphetamines are rarely fatal they can usually be managed by sedating the patient with benzodiazepines. 

Treatment consisted of repeated removal of destroyed bone tissue and teeth, draining of abscesses, and reconstructive surgery. In severe cases, extensive removal of necrotic bone tissue led to permanent disfigurement. However, exposure levels of white phosphorus were not reported (Ward 1928). Case reports of development of phossy jaw following intermediate or chronic occupational exposure to unreported levels of white phosphorus and phosphorus compounds describe a similar progression of symptoms, with similar results even in cases... 

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