[Determination of pulegone in the essential oil of Mentha pulegium L. from Chile].
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Biomedical subjects
Publications and source records attributed to M Montes.
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Tissue temperature and impedance were measured in dog skin during freezing in situ. The previously frozen skin was removed by punch biopsies 3 days later to permit microscopic evaluation of the extent of necrosis. The histologic observations were related to the temperature and impedance measurements in an effort to determine the usefulness of the monitoring techniques in clinical cryosurgery. Tissue temperature and impedance have a definite relationship in tissue freezing, but the range of temperatures about any impedance values causes some concern. The tissue biopsies showed that an impedance value of at least 10 Mohms is not always associated with tissue death. In these experiments, there was the usual range of temperatures in relation to tissue death, but tissue temperatures of -30 degrees C and colder were always associated with complete necrosis. It is concluded that tissue temperatures are the more accurate and useful monitoring technique to supplement clinical judgment. However, impedance techniques may also be used to monitor therapy, especially if used primarily to monitor depth of therapy, and if controlled by clinical judgment wary of the inaccuracy of the technique.
Six different freezing/thawing programs, which varied freezing rate, duration of freezing, and thawing rates, were used to investigate the effect of these factors on cell destruction in dog skin. The range of tissue temperatures produced was from -15 to -50 degrees C. The extent of destruction was evaluated by skin biopsies 3 days after cold injury. In single, short freezing/thawing cycles, the temperature reached in the tissue was the prime factor in cell death. Longer freezing time and slow thawing were also important lethal factors which increased destruction of cells. Cooling rate, whether slow or fast, made little difference in the outcome. The experiments suggested that present-day, commonly employed cryosurgical techniques, which feature fast cooling, slow thawing, and repetition of the freeze/thaw cycle, should be modified by the use of maintenance of the tissue in the frozen state for several minutes and slow thawing. Thawing should be complete before freezing is repeated. These modifications in technique will maximize tissue destruction, an important consideration in cancer cryosurgery.
We previously found that a pulse dose of vitamin D3 increased [99mTc]PPi uptake by rat myocardial necrosis. Vitamin D3 raised serum and lesion [Ca] but not, we now report, lesion [Fe]. We now also report that D3 increased [99Tc]PPi uptake by myocardial infarcts (L) in dogs from 0.345 +/- 0.007% administered (kg) dose/g in controls to 0.703 +/- 0.089 in treated (p less than 0.025). Vitamin D3 decreased uptake by dog bone (B) as measured in rib and sternum, increasing L/B from 1.10 +/- 0.23 to 2.30 +/- 0.52 (p = 0.06) X (L) was positively, (p less than 0.005) and uptake by sternum was negatively (p less than 0.05) correlated with serum [Ca] and [P], respectively. Scintigrams graded by a "blinded" observer, showed 4+, 4+, and 3+ infarcts, respectively, in three D3-treated dogs, and 2+, 2+, and 1+, respectively, in three untreated. One untreated and one treated dog were negative; the latter showed the least response to D3 in serum [Ca] and [99mTc] in tissue samples. Vitamin D3 can increase L/B in dogs, enhancing scintigraphic images.
The effect of a pulse dose of Vitamin D3 on uptake of [99mTc]MDP by fractured and osteoporotic bone, respectively, was compared with D3's effect on uptake by normal bone in rats. At 4, 7, and 14 days, respectively, after femoral fracture, basal uptake was significantly (p less than 0.005) increased at the fracture site by 336.8, 276.1, and 183.5%, respectively, over the contralateral control site. D3-treated rats had lower uptakes than untreated controls at all three fracture sites and at 12 of 15 normal bone sites but analysis of variance showed the uptake differences were not significant. Cortisone-induced osteoporosis caused a significant (p less than 0.05) decrease in basal uptake. The decrease occurred in all nine bone areas studied. D3 caused a significant (p less than 0.05) increase (mean 16.2%) in uptake by these osteoporotic bones, but a significant (0.1 greater than p greater than 0.05) decrease (mean 13.0%) in uptake by the same bones in normal controls. Thus, D3 had an effect on uptake by the bone lesion, osteoporosis, that differed from D3's effect on uptake by fracture or normal bone.
A case of heterotopic gastric mucosa in discrete nodules of the duodenum is presented. Its radiographic and endoscopic appearance is described. The light and electron microscopic features are analyzed. Ultrastructural examination of its organization, cellular and subcellular components revealed similarities to normal fundic gastric mucosa. The histological and clinical differences between heterotopic gastric mucosa and duodenal metaplastic change are discussed.
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The most common marker autoantibody among patients with polymyositis is anti-Jo1. The patient (John P.) providing the prototype serum for this specificity had both interstitial lung disease and polymyositis. A preliminary survey by Ouchterlony analysis and counter immunoelectrophoresis of serum from 15 patients with idiopathic interstitial lung disease revealed no anti-Jo1 or other precipitating autoantibodies. This provides no evidence to suggest that anti-Jo1 has specificity for interstitial lung disease per se. However, this autoantibody may serve as a possible marker for some patients with overlap of polymyositis and interstitial lung disease. The several interesting features about this patient's diseases and course are discussed.
In order to evaluate alternate techniques of preparing veins for use as homografts, 102 femoral veins were harvested from adult mongrel dogs. The veins were treated in four different ways, then transplanted into recipient animals bypassing their ligated femoral arteries. Group I--24 veins (6 cm each) were harvested and immediately transplanted. Group II--24 veins were stored in 15% dimethyl sulfoxide (DMSO) solution at -120 C for 21 days prior to transplantation. Group III--26 veins were stored for 21 days in plasminate solution at -60 C prior to use as allografts. Group IV--28 veins were stored in 0.5% gluteraldehyde solution for 21 days prior to implantation. Animals were randomly sacrificed at 1-month, 2-month, 6-month, and 12-month intervals. Patency of the transplant was determined weekly by ultrasound. Specimens were sent for light and scanning electron microscopy at the time of harvest, prior to implantation, and at sacrifice. Endothelial damage was graded on a scale of 0-16. Veins in Group II had a significantly higher patency rate (68% at 1 year) than Group III (35%) and Group IV (11%) (p less than 0.05). The intimal layer of all patent vessels was replaced by an organized mural thrombus. Partial endothelialization of the luminal surface was most prevalent in Group II. Intimal damage related to storage technique was significant in Group III (p less than 0.01). At sacrifice, severe endothelial damage was present in all groups (p less than 0.01). In conclusion, veins stored in 15% dimethylsulphoxide (DMSO) solution at -120 C have immunologic and physical characteristics that yield patency rates acceptable for clinical use when autogenous tissue is not available.
Myocardial protection was evaluated in 2 groups of 5 infants each undergoing correction of either tetralogy of Fallot (TOF) or subcristal ventricular septal defect (VSD). In group A, profound hypothermia and total circulatory arrest (PHTCA) was utilized. In group B, profound hypothermia and total circulatory arrest combined with potassium cardioplegia (PHTCA + K) was the method of protection used. The analysis was carried out by sequential measurements of clinical, electrocardiographic, enzymatic (CK-MB) and ultrastructural parameters. There were no operative deaths. One infant had a second operation for recurrent VSD. The average anoxic time was 35.4 min in group A (PHTCA) and 32.6 min in group B (PHTCA + K). Analysis of our data demonstrated that when potassium cardioplegia was added to PHTCA, there was less intraoperative myocardial damage according to physiological, ultrastructural and biochemical parameters than when profound hypothermia and total circulatory arrest was applied alone.
D-Galactosamine is an amino sugar with unique hepatotoxic properties in animals. Although the mechanism of liver injury by galactosamine remains controversial, a role for bacterial endotoxin has been suggested. In the present study, using New Zealand rabbits, we show that the significant increase in serum glutamic oxaloacetic transaminase which followed the injection of 4.25 mmole/kg of D-galactosamine was completely prevented in animals subjected to resection of small bowel and colon. Using an immunoradiometric assay specific for E. coli 026 endotoxin we showed that after instillation of 50 mg of E. coli into the colon, serum levels of this endotoxin were higher in the animals injected with galactosamine than the controls injected with saline. However, the differences in endotoxin concentration between the two groups of animals was statistically significant only at 30 and 60 min. The role of endotoxin in the pathogenesis of galactosamine liver injury is reviewed and discussed.
The incidence of transient bacteremia following endoscopic injection sclerotherapy of esophageal varices was evaluated in 18 patients subjected to 40 sessions of injection sclerotherapy. Blood cultures were obtained before sclerotherapy and at five minutes, 30 minutes, and 24 hours after sclerotherapy. The injectors as well as the endoscope were cultured before and after the procedure. Blood cultures were positive in two patients after injection sclerotherapy (Enterobacter cloacae and Staphylococcus species, coagulase-negative, respectively) for an incidence of 5% of transient bacteremia. Pseudomonas aeruginosa was the most frequent bacteria isolated from the injector after sclerotherapy. We conclude that the incidence of transient bacteremia after sclerotherapy is no higher than routine upper-intestinal endoscopy.
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Although liver failure from sepsis is a frequent occurrence in serious ill, hospitalized patients, little information is available on the histologic changes of the liver. We examined the histopathology of the liver of 19 patients who died of clinical sepsis and attempted to relate certain features of the illness or treatment to the observed histopathologic changes. The most striking finding was midzonal and peripheral necrosis of a moderate to marked degree in 11 of 19 patients. Other important changes were acute inflammation and cholestasis. The severity of hepatocellular necrosis did not appear to be influenced by the premortem circulating pathogen, by the nutritional support administered or by the arterial blood pressure. It is suggested that hepatocellular necrosis is characteristic of sepsis and may be caused by loss of specific factors which normally maintain liver function and structure.
Radioactive imaging agents are chemically designed for selective distribution. Another approach to selectivity is to find stable compounds that favorably influence this distribution. Using a rat model of myocardial necrosis, we studied effects of various stable compounds (as a single, large dose or fractionated into short series) on the ratio, uptake of Tc-99m pyrophosphate (PPi) by the target lesion/uptake by the principal nontarget, bone (L/B). Vitamin D3s ability to increase L/B was mediated by the hypercalcemia and hyperphosphatemia that it caused. The hypercalcemia was accompanied by increased [Ca] in the lesion. In contrast, pulse doses of desoxycorticosterone acetate (DOCA) at 7 and 6 hr before killing increased uptake by lesion, increasing L/B from 0.19 +/- 0.03 to 0.45 +/- 0.08 (p less than 0.01), with no change in serum [Ca] and minimal changes in serum [P], [Na], and [K]. DOCA also increased the lesion-to-blood ratio from 6.5 +/- 0.07 to 15.4 +/- 3.9 (p less than 0.05). These results encourage further study of DOCA's effect and investigation of other stable drugs that may influence distribution of other imaging agents.
Metyrapone tartrate, 400 mg/kg i.p. raised the LD50 for acetaminophen from 340 mg/kg i.p. to 540 mg/kg i.p. in fasting male Swiss white mice. The minimum protective dose of metyrapone was 200 mg/kg. Metyrapone was effective in preventing death when given up to 2 h after acetaminophen administration. The LD50 for metyrapone tartrate was 760 mg/kg i.p. Metyrapone decreased or prevented acetaminophen induced hepatic damage measured either by histology or plasma glutamate pyruvate transaminase activity. Metyrapone tartrate, 400 mg/kg i.p., inhibited the severe liver glutathione depletion seen with acetaminophen alone. It is proposed that metyrapone protects mice from acetaminophen induced liver toxicity and death by inhibiting the oxidation of acetaminophen to a toxic intermediate.
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