Human Coronary Artery Remodeling, Beginning and End of the Atherosclerotic Process

BACKGROUND, AIMS OF THE STUDY: The objective of the study was to relate the progress of coronary artery remodeling to the earliest stages of the atherosclerotic process. For this purpose, a mathematical model for description of dimensional change of the coronary artery wall and its constituent components was developed and applied. MATERIALS AND METHODS: The study used coronary artery samples randomly taken from each of 83 consecutive, unselected postmortems. All samples were routinely fixed and processed to paraffin for the preparation of right-angled, 5-micron sections, routinely stained and mounted for subsequent analysis. Computer assisted image analysis, using 32 systematic random, radial sampling lines, was used for interactive measurements of distance from centre of lumen to points defining intima, media and adventitia thickness along the radial intercept, which were subsequently tabled for analysis of variance, calculations of (group –vessel) means, and related to stage of pathology. RESULTS: Pre-atherosclerotic changes, before any localised changes in especially intima dimensions, are found, consisting of a process of gradual vascular widening, associated with temporally at least partly dissociated increases in width, which as a fraction of total vessel radius show a phased process. In these, the intima first increases, subsequently remains stable, and finally reduces in width proportionally to the increasing diameter. The media shows a similar initial increase, on average stabilising in the third phase after reaching a plateau value in the second. The adventitia, already increasing in phase 1, continues to increase in phase 2, accelerating in phase 3. The complex process, as found, occurs systematically in all vessels, is distributed circumferentially, and precedes the development of localised lesions of the intima. CONCLUSIONS: The findings suggest the existence of a diffuse complex of changes, consisting of a gradual vascular widening followed by narrowing, with associated mural changes reflecting the atherosclerotic process

Valuta management en management control

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Figure 4

<p>Line diagram mean thickness- intima (Th-int), -media (Th-med), -adventitia (Th-adv) For Th-int/r-IEL (thickness intima/radius Internal Elastic Lamina) reference and stages.</p

Figure 2

<p>Line diagram relation mean radius lumen (r-lu) and thickness intima (Th-int) for 5% Th-int/r-IEL (thickness intima/radius Internal Elastic Lamina) intervals.</p

Figure 3

<p>Line diagram relation mean thickness media (Th-med) and thickness adventitia (Th-adv) For 5% Th-int/r-IEL (thickness intima/radius Internal Elastic Lamina) intervals.</p

Figure 1

<p>Number of measurements (percent) divided in to histological categories. N: normal coronary artery, AN: possibly abnormal artery-(circumferentially widened intima, width less than media-, A: abnormal artery-artery widened circumferentially, width more than media-, AE: abnormal artery- intima widened non-circumferentially, the remainder of the intima circumference is normal in width-, EN: abnormal artery-extensive, well developed plaque, the remaining circumference is normal in appearance-, EA: abnormal artery: extensive, well developed plaque, the remaining circumference shows pathologic changes-, EE: abnormal artery- circumferential atherosclerotic plaque. Th-int/r-IEL: ratio thickness intima/radius Internal Elastic Lamina.</p

Dodelijk verlopende levercelnecrose na gebruik van glafenine

The case is described of a patient with fulminant hepatic failure attributed to intake of glafenine 400 mg daily for 15 days. The first symptoms appeared two weeks after discontinuation of glafenine. Other causes of hepatic necrosis could be excluded. Approximately five weeks after the onset of symptoms the patient died of hepatic failure. At autopsy massive hepatic necrosis and massive pancreatic necrosis were demonstrated

Dodelijk verlopende levercelnecrose na gebruik van glafenine

The case is described of a patient with fulminant hepatic failure attributed to intake of glafenine 400 mg daily for 15 days. The first symptoms appeared two weeks after discontinuation of glafenine. Other causes of hepatic necrosis could be excluded. Approximately five weeks after the onset of symptoms the patient died of hepatic failure. At autopsy massive hepatic necrosis and massive pancreatic necrosis were demonstrated

Preclinical studies on toxicity, antitumour activity and pharmacokinetics of cisplatin and three recently developed derivatives

Preclinical studies were performed in mice, rats and dogs of cis-diamminedichloroplatinum(II) (CDDP) and its derivatives cis-l,l-di(aminomethyl) cyclohexane platinum(II) sulphate (TNO-6), cis-diammine-l,l-cyclobutanedicarboxylate platinum(II) (CBDCA) and cis-dichloro, trans-dihydroxybis-isopropylamine platinum(IV) (CHIP). In mice toxicity and antitumour activity were determined. All three derivatives were at least as toxic as CDDP for haemopoietic stem cells and were less active than CDDP against the mouse tumours leukaemia L1210 and osteosarcoma C22LR. Toxicology studies in rats revealed no renal toxicity after a single dose of TNO-6. Fractionated doses of TNO-6 and CBDCA did cause renal toxicity but less than CDDP. CHIP produced little or no kidney damage. In dogs, TNO-6 (1.5 mg/kg) produced more severe kidney damage-although this was reversible-than CDDP (2 mg/kg). Half-lives of distribution were 4.0-5.1 min for TNO-6 and 9.7 min for CDDP, while half-lives of elimination were 3.6-6.6 days and 5.9 days respectively. Plasma levels, normalized for the dose, were at least two times higher after TNO-6 than after CDDP. Twelve weeks after drug administration, plasma levels were undetectable, while tissue concentrations could still be measured. The platinum concentration in kidney cortex was higher after CDDP than after TNO-6. © 1984.SCOPUS: ar.jinfo:eu-repo/semantics/publishe