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At least 19 recordsLinked to original sources
PubMed1985

Bilateral and massive lipoidal infiltration of the cornea (secondary lipoidal degeneration).

A 41-year-old white man presented with bilateral white infiltration of the cornea from limbus to limbus. Extensive examination revealed no manifestations of disorders of lipid metabolism and the patient gave no history of previous ocular disease. VDRL and other serological tests were negative. The corneal button removed by penetrating keratoplasty from the right eye was studied by light microscopy, histochemistry and electron microscopy. The light microscopic appearance was consistent with lipoidal degeneration of the cornea associated with stromal vascularization and chronic keratitis, more likely a secondary lipoidal degeneration. Cholesterol clefts were seen in all levels of the stroma focally surrounded by a foreign body giant cell reaction. Lipid vacuoles were observed in extracellular and intracellular locations within histiocytes and fibroblasts in vascularized and inflammed areas. Lipid stains disclosed cholesterol crystals, neutral fats, and phospholipids.

Adult↗
PubMed1979

[Lipoid A, a factor in the pathogenesis of chronic pyelonephritis. Experimental and clinical studies of a lipoid A dependent pathological immune reaction].

Lipid A injected into the temporarily occluded renal pelvis of adult dogs, persisted in the kidney tissue and induced an abacterial interstitial nephritis with positive anti-lipid A titers. This reaction was increased by a single dose of lipid A vaccine, reduced by four consecutive immunisations prior to the lipid A injection and absent in puppies. The presence of IgG, IgM and complement complexes in the kidney was demonstrated by immunofluoroscopy. Lipid A antibody titers were measured by the passive hemolysis test in 349 humans. In two out of 20 healthy adults and 16 out of 18 children with recurrent urinary tract infection anti-lipid A antibodies were present. In contrast, no titers were found in 23 newborn babies. In a group of 156 patients with acute urinary tract infection, 28% revealed positive titers, whereas in a group of 132 patients with recurrent urinary tract infection titers occurred in 81%. Selected from this group of 132 patients 61 suffered from an acute infection of the upper tract. 59 oft these (96%) showed definite titers. There was no difference in the development of anti-lipid A antibodies between men and women and the height of the titers did not correlate with the clinical picture of the disease (acute or chronic). The combination of proteinuria and anti-lipid A antibodies indicates the pressure of reccurrent urinary tract infection or chronic pyelonephritis with about 90% accuracy. The titers are caused by immunogenically active lipid A in the body. Since lipid A has the ability to remain in the renal tissue for a long period of time and thereby to maintain the inflammatory response, long-term antimicrobial prophylaxis (six months) should be given to patients with a high risk of recurrent urinary tract infection.

Animals↗
PubMed1998

Lipoid pneumonia in lung cancer: radiographic and pathological features.

BACKGROUND: Obstructive pneumonia, a synonym for endogenous lipoid pneumonia, is often seen in patients with lung cancer, but details of this condition are still uncertain. METHODS: To elucidate the features of obstructive pneumonia, we radiopathologically studied 147 patients with lung cancer that had been resected. RESULTS: Gross inspection of the resected materials revealed evidence of endogenous lipoid pneumonia in 33 of the 147 patients with radiography that corresponded to obstructive pneumonia. We classified the 33 cases into three types as follows: (1) type I lipoid pneumonia, localized to the lung parenchyma distal to an airway obstructed by a tumor (23 cases); (2) type II lipoid pneumonia, features of type I lipoid pneumonia and consecutively spreading to the adjacent segment whose airway was not affected (five cases); (3) type III lipoid pneumonia, features of type II lipoid pneumonia and spreading to the isolated segments (five cases). Lipoid pneumonia was found in 16 of 89 (18%) adenocarcinoma cases and in 17 of 55 (31%) squamous cell carcinoma cases. In type I lipoid pneumonia, squamous cell carcinoma cases were predominant over adenocarcinoma cases (14 vs nine cases), but in type III lipoid pneumonia, adenocarcinoma cases predominated (four vs one case). Further, in cases of type III lipoid pneumonia, radiographs frequently revealed that lung cancers were cavitated. CONCLUSION: Lipoid pneumonia in lung cancer may be associated with factors that play a larger role than the cancer alone. It can be speculated that transbronchial dissemination of breakdown products of adenocarcinoma cells, including mucin, may contribute to the spread of the non-obstructive component of lipoid pneumonia, because the local physical effect of obstructed bronchus does not affect the non-obstructive component.

Adenocarcinoma↗
PubMed2004

[Comparative study of binding power of polymyxin B and its simulating peptide to lipopolysaccharides lipoid A].

OBJECTIVE: To observe the binding power of polymyxin B (PMB) and its simulation peptide to lipopolysaccharide (LPS) and lipoid A. METHODS: LPS and lipoid A were separately coated on biosensor. 5 microl of PMB (0.01 microg/L) 5 microl of its simulating peptide 1 (PMBSP1 0.01 microg/L) and 5 microl of its simulating peptide 2 (PMBSP2, 0.01 microg/L) were respectively added into the hydrophobic sample pool. The combining power of PMB and its simulating peptides PMBSP1 and PMBSP2 to LPS and lipoid A was compared. RESULTS (1) PMBSP1 almost did not bind LPS and lipoid A, while PMB and PMBSP2 possessed high affinity with LPS and lipoid A. (2) The peak value (98.41 +/- 7.31) rad/s of PMBSP2 binding LPS was much higher than that (83.58 +/- 5.42) rad/s of PMB in binding LPS (P < 0.05). While the peak value of PMB in binding lipoid A was similar to that of PMBSP2. (3) The peak value of PMB binding LPS was significantly lower than that of PMB in binding lipoid A (P < 0.05). But there was no difference between the peak value of PMBSP2 in binding LPS and that of PMBSP2 in binding lipoid A. (4) PMBSP2 could bind to LPS and lipoid A in a shorter time to reach peak levels. CONCLUSION: Compared with PMB, the PMBSP2 could bind to LPS and lipoid A in a shorter time. In addition, PMBSP2 exhibited similar affinity to LPS and lipoid A. This indicated that PMBSP might possess better anti-LPS activity due to its lack of space steric hindrance when PMBSP binding the lipoid A of LPS.

Cell Wall↗