cglez/bert-base-uncased-ft-ohsumed
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Continuous, in vivo pulmonary venous admixture from fiberoptically measured hemoglobin saturations.
In six anesthetized swine, pulmonary venous admixture (Qsp/Qt) was calculated by four methods: a) Qsp/Qt 1, fiberoptically measured arterial and mixed venous Hgb saturation (SaO2 and SvO2), PaO2 and PvO2 derived from saturations; b) Qsp/Qt 2, fiberoptically measured SaO2 and SvO2, PaO2 and PvO2 measured by blood gas analysis; c) Qsp/Qt 3, PaO2 and PvO2 measured by blood gas analysis, SaO2 and SvO2 derived from tensions; d) Qsp/Qt 4, SaO2 and SvO2 measured by bench oximetry, PaO2 and PvO2 derived from saturations.
Input from the fiberoptic catheters was fed into a computer programmed to calculate Qsp/Qt 1 every 20 sec.
Fifty-eight of these values were compared with simultaneously calculated Qsp/Qt 2, 3, and 4.
There was no difference between fiberoptic and derived SaO2 or fiberoptic and cooximetric SvO2.
Correlations and slopes for Qsp/Qt 1 with Qsp/Qt 2, 3, and 4 were significant (p less than .05).
Comparing mean differences, Qsp/Qt 1 was significantly different only from Qsp/Qt 3 (p less than .01).
We conclude that dual oximetry reliably tracks Qsp/Qt.
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1
| 4,656
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Pichinde virus infection in strain 13 guniea pigs reduces intestinal protein reflection coefficient with compensation.
Pichinde virus inoculation into strain 13 guinea pigs is a model with features reputed to be similar to hemorrhagic fever in humans.
Although the infection is lethal by day 13-19, guinea pigs of approximately 600 g do not show edema or effusions.
This raises the questions of whether capillary damage is present in such infected animals and, if it is, why edema is absent.
The effects of Pichinide virus on protein transport across jejunal capillaries were examined in 38 normal and 7 infected strain 13 guinea pigs 12 days after inoculation.
The latter lost 20.3% body weight but maintained normal blood pressure, serum protein concentration, and jejunal lymph flow.
However, their protein solvent drag reflection coefficient (sigma) was reduced to .52 +/- .03 (mean +/- SE) from .73 +/- .02 (2P less than .001), while permeability-surface area product was not changed.
In the absence of gross edema or effusions, Pichinde virus-infected guinea pigs demonstrated a leaky gut capillary wall to protein compatible with an increase in pore size or large pore number less than sufficient to change permeability-surface area product.
Compensatory mechanisms that prevent edema at this stage are efficient and may include reduced capillary pressure or some degree of capillary flow stasis.
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2
| 3,932
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Marked improvement of glucose homeostasis in diabetic ob/ob mice given oral vanadate.
The trace element vanadium exerts insulinlike effects in vitro and decreases hyperglycemia in insulin-deficient animals.
This study examined whether vanadate can improve glucose homeostasis in genetically obese hyperglycemic insulin-resistant ob/ob mice, which present metabolic abnormalities similar to those of human non-insulin-dependent diabetes.
Sodium orthovanadate (0.3 mg/ml) was administered for 7 wk in H2O.
Vanadate treatment induced a fall in fed and fasted plasma glucose and insulin levels and improved tolerance to oral glucose; the stimulated glucose area was decreased by 65%, and an early peak of insulin secretion was restored.
During an intravenous glucose tolerance test, the glucose disappearance rate was twofold higher in vanadate-treated mice, and the reappearance of a significant insulin response was also observed.
Moreover, vanadate produced a twofold increase in hepatic glycogen content and prevented the exhaustion of pancreatic insulin stores.
The hypoglycemic response to exogenous insulin was similar in control and treated mice.
In vitro experiments showed that basal glucose oxidation by hemidiaphragms was 32% higher in vanadate-treated mice than in controls, although stimulation by insulin was similar in both groups.
In conclusion, oral vanadate caused a marked and sustained improvement of glucose homeostasis in diabetic insulin-resistant mice by exerting an insulinlike effect on peripheral tissues and apparently preventing the exhaustion of pancreatic insulin stores.
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3
| 5,446
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Ischemic brain damage in a model of acute subdural hematoma.
Ischemic brain damage is the most important neuropathological finding in humans who die after acute subdural hematoma; however, its causes are poorly understood.
We have produced acute subdural hematoma in the rat by injecting 400 microliters of autologous blood (approximately 20% of intracranial volume) into the subdural space.
Extensive areas of ischemic damage, involving 14 to 16% of the volume of the hemisphere, developed in this model at 4 and 24 hours after the lesion.
The hematomas were associated with a brief peak in intracranial pressure (51 mm Hg), which remained at three times normal levels (14 mm Hg) for 3 hours.
In this model, therefore, ischemic damage appears to be due to the local effects of blood overlying the cortex at 4 hours after the ictus, rather than to globally raised intracranial pressure.
The implications for the pathophysiology of acute subdural hematomas in humans are discussed.
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4
| 536
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Effect of cyclosporin on generalized Shwartzman reaction in diabetic rats.
The effect of cyclosporin (CsA) on the endotoxin-induced generalized Shwartzman reaction (GSR) was studied in diabetic and nondiabetic rats.
After 4.5 wk of diabetes, CsA (20 mg/kg) or intralipid as a control substance was given intraperitoneally daily for 10 days.
Next, diabetic rats were given either high-dose (2 mg/kg or low-dose (0.1 mg/kg) endotoxin (Escherichia coli 026:B6 lipopolysaccharide B) as a single injection.
The rats were killed at intervals of 1, 4, 8, and 24 h.
No significant glomerular thrombi were seen in the nondiabetic control animals, whereas the severity of glomerular thrombi in the diabetic animals was dependent on the presence or absence of CsA, endotoxin dose, and degree of glycemic control.
In the diabetic rats, glomerular thrombi occurred maximally at 4 h but were no longer present at 24 h.
The CsA/high-dose-endotoxin rats had fewer glomerular thrombi than rats receiving the intralipid/high-dose endotoxin, but this difference was not statistically significant.
The CsA/low-dose-endotoxin rats had increased glomerular thrombi compared with the intralipid/low-dose-endotoxin rats (P less than 0.01).
Insulin treatment reduced the glomerular capillary thrombi in the CsA/low-dose-endotoxin diabetic animals.
Thus, CsA aggravates the GSR with low-dose endotoxin but has no significant effect when high-dose endotoxin is given.
Improved glycemic control reduces the GSR in CsA-treated rats.
Thus, the interrelationships of diabetes, endotoxin, and CsA on the GSR are complex, and the pathogenesis of these events is unclear.
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5
| 7,218
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L-tryptophan implicated in human eosinophilia-myalgia syndrome causes fasciitis and perimyositis in the Lewis rat.
Tryptophan-associated eosinophilia-myalgia syndrome (L-TRP-EMS) is a newly described syndrome which occurred in epidemic fashion in the United States in the summer and fall of 1989.
Epidemiologic data has linked the syndrome to intake of L-tryptophan (L-TRP) from one specific manufacturer, but the precise etiologic compound(s) must be established by replication of the syndrome in an appropriate animal model.
In this study, implicated L-TRP, United States Pharmacopeia (USP) grade L-TRP, or vehicle was administered by gavage in a blinded fashion for 38 d to female Lewis rats at doses comparable with those ingested by patients who developed the eosinophilia-myalgia syndrome.
Animals receiving implicated L-TRP, but not those receiving USP grade L-TRP or vehicle, developed histologic signs consistent with fasciitis and perimyositis, specific pathologic features of human L-TRP-EMS.
Peripheral blood eosinophilia was not observed.
Hypothalamic corticotropin releasing hormone mRNA levels were lower and plasma corticosterone levels tended to be lower in the animals that received implicated L-TRP.
Plasma L-kynurenine was higher in both L-TRP-treated groups compared to the vehicle-treated animals.
The female Lewis rat is known to be susceptible to a wide variety of inflammatory diseases.
Identification of specific inflammatory changes in this rat following exposure to implicated L-TRP indicates that this animal model will be important in subsequent investigations into the etiology, pathogenesis, and treatment of human L-TRP-EMS.
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6
| 9,013
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Receptor changes in the spinal cord of sheep associated with exposure to chronic pain.
There is evidence that post-injury hypersensitivity is partly due to changes in the central nervous system.
Sheep with foot rot were used to investigate the effect of chronic pain on some receptors thought to be involved in spinal nociceptive processing systems (alpha 2 adrenoceptor and mu and delta opioid receptors).
Saturation binding studies showed a variable distribution of [3H] clonidine (alpha 2 adrenoceptor agonist) in the spinal cord of normal sheep.
The number of receptors (Bmax) present in areas thought to be involved in nociceptive processing, laminae I and II and lamina X, increased to 131% and 169% of control sheep values respectively in animals exposed to chronic pain.
The affinity of the receptors (KD), however, remained unchanged at approximately 2 nM.
There was less [3H]DAGO (mu opioid agonist) and [3H]DPDPE (delta opioid agonist) binding in the sheep spinal cord.
Both opioid receptor types being mainly located in the superficial dorsal horn.
The [3H]DPDPE binding was unchanged in the sheep with foot rot, whilst the number (Bmax), but not the affinity, of the [3H]DAGO binding sites increased in laminae I and II in lame animals to 130% of the control sheep values.
Hence, in animals in chronic pain, the number of alpha 2 adrenoceptors and mu opioid receptors increased mainly in areas of the sheep spinal cord associated with nociception.
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7
| 2,881
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SCH-39304 in prevention and treatment of disseminated candidiasis in persistently granulocytopenic rabbits.
To investigate the potential use of SCH-39304 for the prevention and treatment of disseminated candidiasis in granulocytopenic patients, we studied its in vivo antifungal activity as preventive, early, and late treatments in three models (acute, subacute, and chronic) of disseminated candidiasis in persistently granulocytopenic rabbits.
SCH-39304 was an effective as amphotericin B alone and fluconazole alone for the prevention of disseminated candidiasis.
SCH-39304 alone and fluconazole alone were as effective as amphotericin B plus flucytosine for early treatment of subacute disseminated candidiasis.
When treatment was delayed for 5 days to establish chronic disseminated candidiasis, SCH-39304 was less effective than amphotericin B plus flucytosine.
In comparison with different treatment regimens, SCH-39304 was more effective in early and preventive treatment.
Thus, SCH-39304 was comparable to treatment control regimens in prevention and early treatment of subacute disseminated candidiasis.
SCH-39304 also was most effective in granulocytopenic rabbits with disseminated candidiasis when used for prevention or early treatment.
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8
| 589
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In vivo assessment of shock-wave pressures. Implication for biliary lithotripsy.
During extracorporeal shock-wave lithotripsy, the pressure profile, which is generated by the lithotriptor, determines the risk of tissue damage.
In the present study, the pressure distribution of a lithotriptor (Lithostar; Siemens A.G., Erlangen, Federal Republic of Germany) was investigated in 10 pigs, five of which had gallstones surgically implanted into the gallbladder.
The in vivo values were compared with in vitro data.
Measurements were carried out along the shock-wave transmission path at the focus within the gallbladder, the adjacent liver, the diaphragmatic surface of the right lung, and the shock-wave exit site from the skin.
Interposition of ribs did not cause a significant decrease in focal positive pressure.
However, a gallstone positioned in the focus caused a 30%-65% reduction in pressure, recorded immediately behind the stone.
Pressures obtained in vivo were always 15%-25% lower than those measured in vitro.
The spatial distributions of the positive pressure in vivo and in vitro were almost identical.
There was a high correlation between the pressures in vitro and in vivo (r = 0.88; P less than or equal to 0.01).
This justifies assessment of shock-wave energies generated during biliary lithotripsy by extrapolation of in vitro data.
It is concluded that it is possible to characterize different lithotriptors by in vitro pressure profile measurements.
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9
| 3,148
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Calcium, parathyroid hormone, and vitamin D in the "prehypertensive" Dahl salt-sensitive rat.
The purpose of this study was to determine if alterations of calcium and calcium regulating hormones precede the onset of NaCl-induced hypertension in the Dahl salt-sensitive (S) rat.
After a 5-day balance study, serum ionized calcium, parathyroid hormone (PTH), and 1,25-dihydroxy vitamin D concentrations were measured in Dahl-S and salt-resistant (R) rats that had been maintained on a "normal" (1%) or high (7%) NaCl intake.
Blood pressure was higher in Dahl-S than Dahl-R (P less than .01), but was not affected by 5 days of high NaCl.
On both NaCl intakes, urine calcium excretion was increased, serum calcium was decreased, and serum PTH and 1,25 dihydroxy vitamin D were increased in Dahl-S compared to Dahl-R (P less than .01).
On the high NaCl intake, fecal calcium was greater in Dahl-S than in Dahl-R, and net 5-day calcium balance was less positive in Dahl-S (P less than .05).
Thus, alterations of calcium, PTH, and vitamin D precede NaCl-induced hypertension in Dahl-S.
These alterations may contribute to the development of hypertension in this animal model.
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10
| 3,898
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Experimental models of temporal lobe epilepsy: new insights from the study of kindling and synaptic reorganization.
Temporal lobe epilepsy is a common localization-related epileptic syndrome characterized by complex partial seizures, ictal and interictal epileptic discharges arising from limbic structures of the temporal lobe, and association with hippocampal sclerosis.
Temporal lobe epilepsy may follow perinatal injury and febrile convulsions, may be progressive, and frequently becomes refractory to standard antiepileptic therapy.
The neurobiology that underlies these features of temporal lobe epilepsy is not known.
Recent studies in experimental models have provided new insights that may help clarify the relationship of seizures, hippocampal sclerosis, and temporal lobe epilepsy.
Observations from the study of the hippocampus with kainic acid-induced lesions, the kindling model, and other experimental models of epilepsy have demonstrated that seizures induce structural and electrophysiologic alterations in hippocampal pathways that may lead to increased excitability and could play a role in the development and progression of temporal lobe epilepsy.
These alterations include mossy fiber synaptic reorganization, induction of NMDA-mediated synaptic transmission, and progressive hippocampal neuronal loss induced by brief kindled seizures.
Some of the structural alterations induced by kindling have also been observed in the human epileptic temporal lobe, raising the possibility that mechanisms operative in kindling may play a role in the pathogenesis of hippocampal sclerosis and in the syndrome of human temporal lobe epilepsy.
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11
| 6,283
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Chronic ethanol feeding and acute ethanol exposure in vitro: effect on intestinal transport of biotin.
This study examined the effects of chronic ethanol feeding and acute ethanol exposure in vitro on biotin transport in rat intestine.
Transport studies were performed with intestinal everted sacs.
Ethanol was fed to rats for 6-7 wk.
Compared with pair-fed controls, ethanol feeding significantly decreased plasma biotin concentrations and transport at physiological concentrations (0.01, 0.1, and 0.3 mumol/L) but not at pharmacological concentration (100 mumol/L).
When added to the incubation medium of everted jejunal sacs from dry-food-fed rats, ethanol (2% vol:vol) significantly inhibited the transport of biotin at a physiological concentration (0.1 mumol/L) but not at a pharmacological concentration (100 mumol/L).
The inhibitory effect of ethanol on the transport of 0.1 mumol biotin/L increased with increasing concentration of ethanol in the incubation medium [0.5% to 5% (vol:vol)].
Acetaldehyde, the major ethanol metabolite, also significantly inhibited biotin transport at 0.2% (vol:vol).
These data demonstrate that chronic ethanol feeding and acute ethanol exposure in vitro inhibit the intestinal transport of biotin by the carrier-mediated process.
Chronic ethanol feeding is also associated with a significant decrease in plasma biotin concentrations.
The ethanol-induced inhibition in intestinal transport of biotin may be a contributing factor in reducing plasma biotin concentrations.
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12
| 4,682
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Treatment evaluation of experimental staphylococcal infections: comparison of beta-lactam, lipopeptide, and glycopeptide antimicrobial therapy.
LY 146032, teicoplanin, vancomycin, oxacillin, cephalothin, cefamandole, ampicillin plus sulbactam, and cefoperazone plus sulbactam were studied against six isolates of staphylococci (including both Staphylococcus aureus and coagulase negative staphylococci) using in vivo and in vitro methods.
In vitro susceptibility measurements demonstrated that all six isolates were sensitive to LY 146032 and vancomycin and that five of six isolates were sensitive to tiecoplanin, cefamandole, ampicillin plus sulbactam, and cefoperazone plus sulbactam.
Comparison of antimicrobial therapy in an in vivo rabbit model demonstrated that cefoperazone plus sulbactam was active against the greatest number of isolates (five of six) based on a reduction of greater than or equal to 5.0 log10 colony forming units per milliliter (CFU/ml) from growth control at the end of the animal treatment study.
Vancomycin and oxacillin were equal in achieving reductions of greater than or equal to 5.0 log10 CFU/ml in four of the six isolates.
Comparing each isolate's in vivo outcome to in vitro data shows that in vitro susceptibility tests overpredict the sensitivity of these six isolates to LY 146032 and vancomycin, are variable for teicoplanin, cefamandole, ampicillin plus sulbactam, and cefoperazone plus sulbactam, and underpredict for oxacillin.
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13
| 5,970
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Increased activity of calcium leak channels in myotubes of Duchenne human and mdx mouse origin.
Elevated free Ca2+ concentrations found in adult dystrophic muscle fibers result in enhanced protein degradation.
Since the difference in concentrations may reflect differences in entry, Ca2+ leak channels in cultures of normal and Duchenne human myotubes, and normal and mdx murine myotubes, have been identified and characterized.
The open probability of leak channels is markedly increased in dystrophic myotubes.
Other channel properties, such as mean open times, single channel conductance, ion selectivity, and behavior in the presence of pharmacological agents, were similar among myotube types.
Compared to the Ca2+ concentrations in normal human and normal mouse myotubes, intracellular resting free Ca2+ concentrations ([Ca2+]i) in myotubes of Duchenne and mdx origin were significantly higher at a time when dystrophin is first expressed in normal tissue.
Taken together, these findings suggest that the increased open probability of Ca2+ leak channels contributes to the elevated free intracellular Ca2+ concentration in Duchenne human and mdx mouse myotubes.
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14
| 8,536
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Effects of exercise on myocardial catecholamine content and ischemic injury in dogs with gradual coronary occlusion.
The effects of exercise on catecholamine content and the extent of myocardial damage in dogs with Ameroid constrictor occlusion of the left circumflex coronary artery were determined.
Tissue samples from both the anterior and posterior walls of the left ventricle were obtained for determination of catecholamine content, and the rest of the ventricles were processed for histologic examination.
When subjected to treadmill exercise for 40 days after surgery, obstructed animals performed significantly less exercise than sham-operated animals and showed significantly higher percentages of ischemia and necrosis in the left ventricle than sedentary, obstructed, sham-operated, or control dogs.
Levels of norepinephrine and epinephrine in the posterior wall of the left ventricle were significantly lower than in the other groups.
Our data show that exercise in this well-known model of chronic coronary artery stenosis produced deleterious effects on the myocardium and suggest a marked heterogeneity of catecholamine stores in the myocardium that may have important functional and electrophysiologic consequences.
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15
| 2,592
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Lyme borreliosis in the severe combined immunodeficiency (scid) mouse manifests predominantly in the joints, heart, and liver.
The authors describe the histopathologic evolution of Lyme disease in severe combined immunodeficiency (scid) and normal C.B-17 and C57BL/6 mice inoculated with Borrelia burgdorferi.
Starting on day 7 after inoculation, all scid mice infected subcutaneously in the tail with a low-passage European tick isolate of B.
burgdorferi had clinical evidence of arthritis characterized by reddening and swelling of tibiotarsal joints.
Later on, other joints, ie, metatarsal and ulnacarpal joints were also affected.
The infection of scid mice resulted in a persistent spirochetemia and the development of a multisystem disease with chronic progressive inflammation of joints, heart, and liver.
Major histopathologic alterations included 1) severe joint lesions, characterized by the presence of hyperplastic inflamed synovial lining cells associated with the erosion and destruction of cartilage and/or bone; 2) pancarditis with infiltrations of mononuclear cells in the endocardium, myocardium, and pericardium; and 3) hepatitis with mononuclear cell infiltrations confined to the portal field and central vein, granulomatous reactions, and eventually the development of liver fibrosis.
In addition, smaller more confined lesions were found in kidneys, lung, brain, and striated muscle.
The inflammatory infiltrates in the various organs were associated mostly with Mac-1+ cells, largely monocytes and macrophages, as well as some polymorphonuclear leukocytes, but not B and T lymphocytes.
Infective spirochetes could be readily isolated from blood and joints and were found at the site of inoculum and the myocardium.
In contrast, subcutaneous inoculation of normal C.B-17 or C57BL/6 mice with spirochetes in general did not result in clinical signs of arthritis.
Only 10% to 20% of the C57BL/6 mice, but none of the C.B-17 mice, showed clinical evidence of oligoarthritis, which appeared not before day 36 after inoculation.
In general, the infection of normal mice resulted in minimal lesions in various organs, and no spirochetes could be visualized or reisolated from their tissues.
The data demonstrate that Lyme borreliosis may develop in mice in the absence of detectable specific B and T cells and thus suggest an immunologic control of the disease in this species.
The scid mouse model therefore can be used to define the components of the immune system responsible for the suppression and/or the progression of the disease.
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16
| 7,695
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Venous hemodynamics in a chronic venous valvular insufficiency model.
To develop a large-animal model of chronic venous valve incompetence, 13 greyhound dogs underwent unilateral hindlimb venous valve lysis with a valve cutter apparatus pulled retrograde through the iliac, femoral, and lateral saphenous veins.
Bilateral venous pressures in the lateral saphenous vein were recorded before valve lysis, immediately after valve lysis, and at intervals from 1 to 14 weeks after valve lysis, with the dogs in the supine position and elevated 80 degrees semierect, as well as after stimulated hindlimb muscle contraction to empty the hindlimb veins.
Passive venous filling time with elevation and 90% venous refilling time after muscle contraction were calculated.
From immediately after through 14 weeks after valve lysis, a shortened venous filling time and 90% venous refilling time as well as an elevated poststimulation venous pressure were noted.
This valve lysis method successfully produced a hemodynamically verified model of venous valvular insufficiency.
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17
| 5,637
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Case-control study of Cryptosporidium parvum infection in Peruvian children hospitalized for diarrhea: possible association with malnutrition and nosocomial infection.
A retrospective, hospital-based case-control study was used to investigate whether there were any clinical characteristics that could distinguish Cryptosporidium parvum-infected children with diarrhea from other non-C.
parvum-infected children with diarrhea.
Ten percent (24 of 248) of children admitted to a rehydration ward at Cayetano Heredia University Hospital, Lima, Peru, were infected with C.
parvum.
The 24 patients infected with C.
parvum (cases) were matched to an equal number of noninfected patients (controls).
C.
parvum-infected patients were more likely to be malnourished than were children without this infection (P less than 0.05).
Also nosocomial infection caused by C.
parvum occurred in three severely malnourished patients, two of whom died.
No other clinical or laboratory characteristics were found that would distinguish children with diarrhea caused by C.
parvum from other children with diarrhea.
In children hospitalized for diarrhea C.
parvum infection occurs most frequently in malnourished children.
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18
| 2,598
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Intraluminal fibrosis induced unilaterally by lobar instillation of CdCl2 into the rat lung.
Lung injury induced by intratracheal instillation of cadmium chloride (CdCl2) into the rat lung may serve as a model of human interstitial lung disease.
In this study, CdCl2 solutions were instilled through a lobar bronchus into the left lung of the rat.
Two doses (400 micrograms or 50 micrograms of CdCl2, each in 400 microliters of neutral saline) were used and the morphologic changes occurring during the first 7 days after a single exposure were documented by light and electron microscopy.
With the higher dose, inflammatory cells appeared in the alveolar interstitium 1 day after CdCl2 administration.
Edema and thickening of the alveolar walls were evident, as were damaged type I epithelial cells and denuded basement membranes.
Fibrin was found in the air spaces.
Within 2 days, inflammatory cells were seen in large numbers and fibroblasts were observed passing through gaps in the alveolar basement membranes into the air spaces.
By 4 and 7 days after CdCl2, various forms of intraluminal fibrosis, including intrabronchiolar budding, mural incorporation, and obliterative changes, were observed.
The contralateral lungs had normal-appearing architecture for all the time points investigated.
In the lower dose exposure, gradients of alveolar damage were observed in which normal lung, interstitial fibrosis, and/or intraluminal fibrosis were seen within treated lungs.
In the mildly damaged regions, interstitial fibrosis predominated, while in the more severely damaged regions, mural incorporation of the convoluted basement membranes was observed.
The pulmonary fibrosis that developed appeared to be similar to some human interstitial lung diseases and may offer a system in which to study the regulation of collagen deposition and fibrosis development in these pathologic conditions.
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19
| 8,473
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Evaluation of metastatic cardiac calcification in a model of chronic primary hyperparathyroidism.
Recent reports have fueled an interest in the prevalence and significance of metastatic calcium deposition in patients with chronic hyperparathyroidism.
Experimental data are limited by the lack of suitable in vivo animal models.
We have developed a model of marked hypercalcemia and overproduction of parathyroid hormone using somatic gene transfer.
Briefly, the process involves infection of cultured rodent fibroblasts (RAT-1 cells) with a retroviral expression vector that contains the gene encoding human parathyroid hormone.
Fibroblasts are grown to confluence on collagen-coated dextran microcarrier beads and are injected into the peritoneal cavities of syngeneic Fisher rats.
Human parathyroid hormone production in rat serum is quantified by an immunoradiometric assay for human parathyroid hormone (1-84), which does not recognize rat parathyroid hormone.
These rats consistently show production of human hormone within a week.
Levels increase progressively, often to 1 ng/ml within 60 days of injection.
Serum calcium showed a concomitant rise to an average of 15.5 mg/dl.
In this study, 13 rats that had been transplanted with parathyroid hormone-producing fibroblasts were killed 80 days after injection.
Examination of the skeleton revealed demineralization and histopathologic sequelae of parathyroid hormone excess with extensive osteoclastic bone resorption.
Examination of the hearts revealed calcification in five of 13 hearts.
There was no involvement of major coronary arteries or conducting systems, but there was calcification of cardiac myocytes, primarily in subepicardial region.
This model may permit an understanding of the mechanisms for sudden cardiac death in severe hypercalcemia.
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20
| 7,824
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Tissue changes around loose prostheses. A canine model to investigate the effects of an antiinflammatory agent.
The aseptically loosened prosthesis provided a means for investigating the in vivo and in vitro activity of the cells associated with the loosening process in seven dogs.
The cells were isolated and maintained in culture for sufficient periods of time so that their biologic activity could be studied as well as the effect of different agents added to the cells in vivo or in vitro.
The biologic response as determined by interleukin-1 and prostaglandin E2 activity paralleled the roentgenographic appearance of loosening and the technetium images and observations made at the time of revision surgery.
The correlation between clinical, roentgenographic, histologic, and biochemical loosening indicates that the canine model is suitable for investigating the mechanisms of prosthetic failure.
A canine model permits the study of possible nonsurgical therapeutic interventions with the ultimate hope of stopping or slowing the loosening process.
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21
| 7,976
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Nephropathy in model combining genetic hypertension with experimental diabetes. Enalapril versus hydralazine and metoprolol therapy.
We compared the effects of the angiotensin-converting enzyme inhibitor enalapril and a conventional antihypertensive regimen (hydralazine and metoprolol) on kidney function, albuminuria, and glomerular ultrastructure in hypertensive diabetic and nondiabetic rats.
Diabetes was induced with streptozocin at 8 wk of age in spontaneously hypertensive (SHR) rats.
Antihypertensive drugs were administered in drinking water from the time of induction of diabetes in all groups.
Blood pressure reduction was equal in the diabetic and nondiabetic SHR rats receiving either enalapril or hydralazine plus metoprolol.
In diabetic SHR rats, there was a rise in serum creatinine after 32 wk, which did not occur in diabetic rats treated with either antihypertensive regimen or in nondiabetic rats.
Both drug regimens reduced albuminuria in diabetic and nondiabetic SHR rats to a similar degree.
Enalapril and the combination of hydralazine and metoprolol were associated with decreased glomerular basement membrane thickness and glomerular volume in diabetic and nondiabetic SHR rats without significant effect on fractional mesangial volume.
Thus, antihypertensive therapy retards the development of albuminuria, glomerular basement membrane thickening, and glomerular hypertrophy in the rat in the presence or absence of diabetes.
No specific benefit of angiotensin-converting enzyme inhibition was observed in these hypertensive models of nephropathy.
Human studies comparing the effects of different classes of antihypertensive drugs on kidney function, proteinuria, and glomerular morphology are warranted.
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22
| 6,476
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Development of multiple necrotizing enteritis induced by a tumor necrosis factor-like cytokine from lipopolysaccharide-stimulated peritoneal macrophages in rats.
We report the development of an animal model of multiple necrotizing enteritis (MNE) in rats.
When rats were injected directly with a culture supernatant of lipopolysaccharide (LPS)-stimulated rat peritoneal macrophages into the abdominal aorta, the overt pathologic lesions of MNE developed within 30 minutes after injection.
The rats showed an elevated level of blood fibrinogen degradation product content even 30 minutes after injection.
Furthermore the rats that were pretreated intravenously with heparin sulfate did not develop MNE, indicating the acute disturbances of blood microcirculation in the intestine.
Multiple necrotizing enteritis was developed also by the injection with recombinant tumor necrosis factor (rTNF) but rarely was observed with even a high dose of recombinant interleukin-1 (rIL-1) or platelet-activating factor (PAF).
The supernatant was cytotoxic in vitro to TNF-susceptible LM and many other cells but was less cytotoxic to the TNF-resistant LR line.
Partial purification of the supernatant suggested that the supernatant contained a cytokine that has biochemical features of TNF.
Furthermore polyclonal anti-TNF antibody could inhibit not only the cytotoxicity in vitro but also MNE development in vivo by this factor.
These data strongly indicate that MNE possibly could be caused by a TNF-like cytokine produced by macrophages that are stimulated by the endotoxin.
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23
| 7,385
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Scatter photocoagulation restores tissue hypoxia in experimental vasoproliferative microangiopathy in miniature pigs.
Experimental retinal branch vein occlusion using argon laser photocoagulation in miniature pigs induced the development of ischemic retinal territories associated with preretinal neovascularization.
Preretinal partial pressure of oxygen (PO2) measurements on the ischemic territories, using O2-sensitive microelectrodes, established that the ischemic retinal areas were hypoxic.
Scatter photocoagulation of these ischemic hypoxic territories restores the local PO2 to the normal values within 2 weeks.
Hence, the reported inhibitory effect of photocoagulation on the development of retinal neovascularization could be due to a reversal effect on tissue hypoxia.
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24
| 372
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Kinin/prostaglandin system: its therapeutic value in surgical stress.
Multiple system organ failure as a consequence of injury or sepsis remains the major reason for death in critically ill patients.
One of the treatment concepts that has recently attracted clinical attention is the administration of kinins and prostaglandins (PGs).
On the basis of experimental data, there is reason to believe that these compounds may have the potential to manipulate favorably certain processes and mechanisms (such as inflammatory or ischemic reactions) thought to be important in the pathophysiology of surgical stress.
However, thus far, information on those effects in humans is still scarce.
On the other hand, administration of kinins and PGs is technically possible and can be performed safely, even in intensive care patients.
Therefore, different techniques, effects, and side-effects of kinin/PG therapy deserve clinical testing.
It remains to be seen whether this concept will be useful in the treatment of critically ill surgical patients.
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25
| 8,202
|
Glutathione S-transferase. Novel vaccine against Fasciola hepatica infection in sheep.
The potential of GST as a vaccine candidate against liver fluke infection in ruminants was studied by vaccinating sheep (n = 9) with GST purified from adult worms of Fasciola hepatica and challenging with 500 F.
hepatica metacercariae.
The immunization induced a high antibody response to GST in contrast to the poor or undetectable response to this Ag observed in naturally infected sheep.
Throughout the trial, the progress of the fluke infection was monitored by measuring RBC hemoglobin levels, the extent of liver damage and the fecal egg output in the sheep.
This analysis indicated that a subpopulation (n = 4) of the GST vaccinated animals exhibited no anemia, reduced liver damage and a lower mean fecal egg count relative to the infected control group suggesting a lower fluke burden in these animals.
Worm burdens in the livers of the GST vaccine group (107 +/- 22) were 57% lower than in the infected control group (250 +/- 25).
The subpopulation of the GST vaccine group demonstrated a 78% reduction in mean worm burdens relative to the control group.
These results show that GST of adult F.
hepatica is a novel Ag that can significantly protect sheep against liver fluke infection.
The results suggest that the immune response to GST is directed to the juvenile worm reducing the number of worms that can establish in the liver of the vaccinated animals.
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26
| 7,528
|
Regional ischemia in cerebral venous hypertension due to embolic occlusion of the superior sagittal sinus in the rat.
To determine the pathophysiological changes in brain tissue that characterize damage following cerebral venous hypertension, a model of cerebral venous hypertension in the rat was devised.
This experimental model has the advantage of simultaneously measuring the regional changes in cerebral blood flow as well as the metabolism.
The ischemic area demonstrated by the accumulation of NADH is confined to the cerebral cortex and becomes enlarged in proportion to the increase in venous pressure.
This metabolic disturbance appears even in the very early period following cerebral venous hypertension.
These pathophysiological features are different from those observed in the case of intracranial hypertension.
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27
| 2,639
|
Isolation of Tete serogroup bunyaviruses from Ceratopogonidae collected in Colorado.
Two viruses were isolated from ceratopogonid midges collected in northern Colorado.
Electron microscopy indicated that both isolates were bunyavirus-like.
Indirect fluorescent antibody and serum dilution-plaque reduction neutralization tests showed that these isolates were members of the Tete serogroup, most closely related antigenically to Tete and Batama viruses but distinguishable from both and from each other.
We suggest the name Weldona virus for these isolates.
Antibody in both waterfowl and passerine birds in northern Colorado indicates the enzootic presence of these viruses in northern Colorado and raises unanswered questions about the introduction and establishment of Tete serogroup viruses in the Americas.
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28
| 2,128
|
Effect of diltiazem and thromboxane A2 synthetase inhibitor (OKY-046) on vessels following experimental subarachnoid hemorrhage.
In order to examine the functional changes in the vascular smooth muscle, the effects of a thromboxane A2 synthetase inhibitor (OKY-046) and a calcium channel blocker (diltiazem) on vessels following subarachnoid hemorrhage, and the contractile activity of cerebral vessels with various vasoactive agents, were investigated by studying isometric tension recordings in rings of cat basilar artery.
The maximum contractile activities of the vessels in response to noradrenalin and adrenaline during the course of subarachnoid hemorrhage were significantly less than those in the control group.
On the other hand, the maximum contractile activity of the vessels in response to prostaglandin F2 alpha on the seventh day following subarachnoid hemorrhage was significantly augmented compared with that in the control group.
A significant decline in the relaxation of responsiveness to diltiazem during the course of subarachnoid hemorrhage was observed compared with that of diltiazem in the control group.
This responsiveness to vasoactive agents was not influenced by the application of OKY-046.
The present study reveals functional changes in vascular smooth muscle exposed to subarachnoid hemorrhage in response to vasoactive agents and a calcium entry blocker.
Thromboxane A2 may not be a significantly influential factor in the present results.
It is suggested that cerebral vasospasm may well be related to functional changes of the arterial wall, which appear to be associated with derangement of the mechanisms of smooth muscle constriction and dilatation based on organic changes.
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29
| 8,283
|
Laparoscopic tubal sterilization. The potential for thermal bowel injury.
One of the most severe complications of laparoscopic tubal sterilization is bowel burns, although they often go undetected at the time of laparoscopy.
Controversy remains over whether these injuries are caused directly by operator error or indirectly from a hot oviduct's or instrument's inadvertently touching and burning the intestine.
A study was performed to determine the potential for direct or indirect bowel burns using bipolar electrocoagulation in rabbits.
The results indicate that neither a hot tube nor hot (recently used) forceps could cause injuries to the serosal surface of the intestine.
That was true both of immediate injury and after one to five days of recovery.
It was observed that the hot uterine tube caused significant bowel adhesions by five days after the procedure.
Direct electrocoagulation of the bowel using 40 W for three seconds caused a minor, noticeable blanch on the bowel that was not detectable with gross or histologic means after one day of recovery.
A direct bowel injury did result when 80 W was used for three seconds; the bowel became perforated after one day.
These findings indicate that it is unlikely that one can produce a bowel burn indirectly from a hot uterine tube or instrument and that only a direct insult to the bowel appears to cause an injury.
However, adhesions could be a complication of the procedure and should be considered.
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30
| 6,660
|
Hemodynamic determinants of subdiaphragmatic venous return during closed-chest CPR in a canine cardiac arrest model.
OBJECTIVE: To assess the hemodynamic determinates of peripheral subdiaphragmatic venous-to-right-heart return during closed-chest CPR.
MODEL: Seven anesthetized dogs subjected to electrically induced ventricular fibrillation for five minutes.
INTERVENTIONS: Conventional closed-chest CPR and closed-chest CPR with continuous abdominal binding at a chest compression rate of 60 per minute, a compression-to-relaxation ratio of 50:50, and a ventilation-to-compression ratio of 1:5.
METHODS: Solid-state catheters were positioned in the ascending aorta, right atrium (RA), and inferior vena cava (IVC).
Cannulating electromagnetic flow probes were inserted into the IVC and a carotid artery.
Analog-to-digital conversion was performed electronically.
Five minutes after ventricular fibrillation was induced, interventions were performed in an alternating sequence.
Systolic, diastolic, and mean pressures and flows were measured and compared.
STATISTICAL METHODS: Two-tailed, unpaired t test applied to equal sample size, linear regression analysis, and multiple regression analysis.
RESULTS: Abdominal binding during CPR significantly increased (P less than .05) all measured systolic and diastolic CPR intravascular pressures compared with CPR without abdominal binding but did not affect IVC-to-right-heart venous return.
During conventional CPR without abdominal binding, venous return was dependent on the diastolic IVC pressure (r = .86, P = .014), mean IVC pressure (r = .80, P = .03), and carotid blood flow (r = .99, P = .001) but not on the IVC-to-RA pressure gradient.
With abdominal binding, venous return was not correlated with any study hemodynamic variable, including the peripheral venous-to-RA pressure gradient.
CONCLUSION: Venous return from the subdiaphragmatic venous bed during CPR is dependent on venous pressure, not on the peripheral venous-to-right-heart pressure gradient.
Abdominal binding during CPR does not affect venous return.
Venous return during CPR diastole is highly dependent on central venous capacitance (left heart outflow during CPR systole).
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31
| 9,983
|
The effect of chronic renal insufficiency on cyclosporine nephrotoxicity.
Despite cyclosporine's efficacy in preventing rejection, its use has been hampered by nephrotoxicity.
Questions remain concerning its application in patients with decreased renal function.
The purpose of this study was to 1) establish a reliable animal model with chronic renal insufficiency (CRI) to study cyclosporine (CyA) nephrotoxicity, and 2) compare the long-term (50 day) severity of CyA nephrotoxicity in CRI versus normal animals.
Fischer 344 rats were divided into six groups (15 to 22 each).
In three groups, CRI was induced by a 5/6th nephrectomy (three groups were sham operated).
After three wks., daily i.p.
injections of olive oil, CyA at five mg./kg., or CyA at 30 mg./kg.
daily were administered.
Serum and urine were collected at 10 day intervals for the determination of biochemical indices of renal function.
Animals were sacrificed after 50 days of treatment and renal histology was evaluated by light and electron microscopy.
Chronic CyA treatment was well tolerated by both intact and CRI rats, suggesting that this is a reliable model for long-term CyA toxicity studies.
CyA decreased renal function at day 50 in both CRI and intact animals.
CRI of mild to moderate degree had little effect on the biochemical and histological indices of CyA induced nephrotoxicity.
CRI does appear to potentiate the metabolic toxicity that occurs after chronic treatment with high dose CyA.
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32
| 5,464
|
Spinal cord thromboplastin-induced coagulopathy in a rabbit model.
Coagulopathy results from many diverse events, including several neurogenic causes.
Using a rabbit model, we produced coagulopathy by injecting autologous spinal cord and extracted thromboplastin intravenously.
Serial coagulation panels were performed to evaluate the activation of the thrombotic and fibrinolytic pathways.
Group 1 animals (n = 4) received intravenous injections of homogenized spinal cord tissue.
Coagulopathy was not produced with 36 mg of homogenized spinal cord tissue, but 50 mg or more resulted in death.
Group 2 animals (n = 12) received intravenous injections of extracted rabbit cord thromboplastin, which contained approximately 60% activity of a commercially purified rabbit brain thromboplastin.
Five animals receiving 2.5 to 5.5 mg of thromboplastin per kilogram of body weight survived with evidence of coagulopathy.
Seven animals receiving 2.5 to 100 mg of thromboplastin per kilogram of body weight died.
Group 3 (4 control animals) received normal saline injections without changes in clinical or laboratory status.
The thrombotic pathway was activated in all animals as evidenced by decreased platelet counts and fibrinogen levels.
Activation of the fibrinolytic system was demonstrated by increased concentrations of protamine sulfate and abnormal euglobulin clot lysis times.
The most sensitive parameters were the platelet count, protamine sulfate concentration, and white cell count (margination), which became abnormal within 15 minutes after the injections and returned to normal within 1 hour.
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33
| 571
|
Prevention of necrotizing enterocolitis in the rat with prenatal cortisone.
Cortisone acetate is known to accelerate maturation of the immature intestine.
The effect of prenatal administration of cortisone acetate on the morbidity and mortality of necrotizing enterocolitis was examined in a rat pup model.
Pregnant rats were administered cortisone acetate, 20 mg/100 g of body weight, or normal saline by daily IP injection from day 18-21 of gestation.
Rat pups were taken from the mothers before suckling was initiated, fed a simulated rat milk formula, and subjected to daily ischemic insults to produce an animal model of necrotizing enterocolitis.
Both morbidity and the mortality rates were significantly improved with prenatal cortisone treatment.
Maturation of the intestinal mucosal barrier was accelerated with the cortisone treatment as measured by decreased serum concentrations of a fed antigen, ovalbumin.
Aerobic bacterial colonization of the small intestine and translocation of bacteria to the liver were decreased in the pups pretreated with steroids.
These changes observed in a rat model of necrotizing enterocolitis may explain the decreased incidence of necrotizing enterocolitis in human infants born to mothers who received corticosteroids late in gestation.
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34
| 7,267
|
The HIV cytopathic effect: potential target for therapy?
HIV kills activated infected CD4+ T cells after a burst of replication and the release of large numbers of virions.
From a review of the literature on HIV regulatory genes and from preliminary mathematical models of HIV dynamics at four levels (host population epidemiology, the immune system, gene regulation within infected cells, and selection of mutants) we have arrived at the theory that in the etiology of HIV the HIV cytopathic effect may actively be caused by a viral regulatory gene product.
The most likely candidate is the rev regulatory protein.
Rev and the analogous rex protein from HTLV-I (human T cell leukemia virus) both have two active sites with similar function: one site locates the protein in the nucleus/nucleolus, and the other site interacts with viral mRNAs, facilitating their export from the nucleus to the cytoplasm.
Rev seems to have a third functional site near the 3' end.
We conjecture that this site may be responsible for the cytopathic effect.
We think that rev acts on cellular genes that normally induce senescence and cell death during development, or T-cell maturation, or on terminal differentiation.
We propose that mathematical and computer models of the immune system could be used to explore whether suppression of the cytopathic action of the rev protein could be of therapeutic benefit in restoring the ability of the immune system to clear HIV or at least to extend latency.
We also suggest how immune deficiency disease might be created as laboratory artifact in animal populations.
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35
| 7,148
|
Restenosis after balloon angioplasty. A practical proliferative model in porcine coronary arteries.
A model of proliferative human restenosis was developed in domestic pigs by using deep injury to the coronary arterial media.
Metal wire coils were delivered percutaneously to the coronary arteries of 11 pigs with an oversized, high-pressure (14 atm) balloon and were left in place for times ranging from 28 to 70 days.
During placement, the balloon expanded the coils and delivered them securely within the arterial lumen.
Light microscopic examination of the vessels confirmed fracture of the internal elastic lamina by the coil.
An extensive proliferative response occurred in 10 of the 11 pigs and was associated with a luminal area narrowing of at least 50% in all but one pig.
The histopathologic features of the proliferative response were identical to those observed in human cases of restenosis after angioplasty.
Immunohistochemical studies confirmed the prominence of smooth muscle cells in the proliferative tissue.
A similar response was obtained in two of five porcine coronary arteries in which balloon inflation only was performed, without coil implant.
This model is practical and inexpensive and closely mimics the proliferative portion of human restenosis both grossly and microscopically.
Thus, it may be useful for understanding human restenosis and for testing therapies aimed at preventing restenosis after balloon angioplasty or other coronary interventional procedures.
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36
| 2,635
|
A comparison of host responses of the Mongolian jird to infections of Brugia malayi and B. pahangi.
Host responses of jirds receiving a single subcutaneous inoculation of subperiodic Brugia malayi were compared with those of jirds similarly infected with B.
pahangi.
Parasite burdens, lymphatic lesion severity, granulomatous reactivity, antibody responses to parasite antigens, and complete blood cell counts were assessed at 60 and 150 days post-inoculation.
At 60 days post-inoculation, percentages of adults recovered at necropsy and lymphatic lesion severity were greater in B.
pahangi-infected jirds.
At 150 days post-inoculation, lesion severity and percentages of worms recovered were similar in both infections.
No significant differences were noted in either infection in reactivity to homologous or heterologous parasite antigens in any parameter measured.
Similarities in the kinetics of the inflammatory reactivities of the 2 infections suggest that previous observations made in the jird-B.
pahangi model could be utilized in designing studies using B.
malayi.
Further, the more marked lesion severity observed in B.
pahangi-infected jirds and the relative ease of maintaining B.
pahangi in the laboratory support the continued use of this system as a conceptual model for the study of lymphatic lesion pathogenesis.
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37
| 9,710
|
Modulation of fluid absorption and the secretory response of rat jejunum to cholera toxin by dietary fat.
To study the effects of dietary fat on jejunal water and ion absorption and on cholera toxin-induced secretion, 3 week old Sprague Dawley rats were fed isocaloric diets.
Forty per cent of the total calories were given as fat, as butter (high saturated fat), olive oil (high monounsaturated fat), or corn oil (high polyunsaturated fat), with one group on low fat (10% of calories) standard laboratory diet as controls.
During in vivo jejunal perfusion studies we found that (i) a polyunsaturated fat (corn oil) supplemented diet improves jejunal absorption of water and electrolytes and these changes are independent of the observed concentrations of luminal prostaglandins; (ii) high dietary fat appreciably reduced the secretory response to cholera toxin, probably without fundamentally changing the mechanism by which cholera toxin induces secretion.
We conclude that dietary fat composition altered the permeability and transport characteristics of the small intestine.
This observation might have relevance to some human diarrhoeal disorders.
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38
| 570
|
A comparison in vitro of human and rabbit distal colonic muscle responses to inflammatory mediators.
The present study compared in vitro the motor responses of human and rabbit distal colonic longitudinal and circular muscle to acetylcholine, histamine, leukotrienes B4 and D4, and prostaglandins E2 and F2 alpha.
The active and passive mechanical properties of these muscles were also evaluated.
All muscle types were contracted by acetylcholine and histamine.
Longitudinal muscle from both species was contracted by prostaglandin E2 and prostaglandin F2 alpha, although rabbit muscle was more sensitive.
Prostaglandin E2 relaxed the majority of both human and rabbit circular muscle preparations that were studied.
Prostaglandin F2 alpha first relaxed and then contracted circular muscle from both species.
Leukotriene B4 had no effect on any tissue studied.
Leukotriene D4 caused transient relaxations in a proportion of all muscle types, but the relaxations were not concentration-related.
Contractile responses did not differ under isotonic recording conditions, but relaxations were much more clearly defined.
Based on experiments using atropine, phentolamine and propranolol, and pyrilamine or tetrodotoxin, it was concluded that the responses of both human and rabbit distal colonic muscles to these inflammatory mediators have a similar pharmacological basis.
All muscle types exhibited low passive tension and developed active tension in the range 0.8-1.2 Lo.
These data strongly support the belief that after the onset of an induced colitis, the rabbit colon has value as a predictive model for the study of inflammatory mediator-induced colonic motility changes in humans.
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39
| 5,634
|
An epidemic outbreak of cryptosporidiosis: a prospective community study from Guinea Bissau.
In the first year of a prospective community study of childhood diarrhea conducted in a semiurban area in the capital of Guinea Bissau, Cryptosporidium sp.
was found in 73 (6.0%) of 1216 episodes of diarrhea.
The parasite was the second most prevalent intestinal parasite, and the only one significantly associated with diarrhea (OR = 2.79, P = 0.0006).
The seasonal distribution was striking, with a peak prevalence in the beginning of the rainy season (May 17.6%) when an epidemic outbreak of diarrhea started.
The prevalence was highest in children younger than 18 months, an age at which prevalences of other intestinal parasites were low.
This reverse age pattern may possibly be explained by the small infective dose needed to create severe infections, by air-borne transmission and by the development of protective immunity.
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40
| 3,074
|
Imbalance between the mechanisms of activation and inhibition of metalloproteases in the early lesions of experimental osteoarthritis.
Levels of tissue inhibitor of metalloproteases (TIMP) and plasminogen activator (PA)/plasmin were measured and the distribution of PA was studied by immunohistochemical techniques in cartilage and synovium samples from dogs subjected to sectioning of the anterior cruciate ligament of their right knees and sham operation of their left knees (controls).
Twenty-three animals were divided into 3 groups and killed at 2, 4, or 8 weeks after surgery.
The levels of PA and plasmin were found to be significantly elevated in the osteoarthritic (OA) knee cartilage and synovium at all times after surgery, except for levels of PA in the OA cartilage at 2 weeks.
There was a positive correlation between the levels of PA and plasmin in the synovial membrane (r = 0.64, P less than 0.001).
In OA knees, the presence of high levels of total and active collagenase was detected in cartilage and in synovium.
The levels of these 2 forms of collagenase showed a positive correlation both in cartilage (r = 0.65, P less than 0.001) and in synovium (r = 0.77, P less than 0.001).
The levels of TIMP in cartilage from OA and sham operated knees were similar.
Although the TIMP level was increased in the OA synovium, it was found only in trace amounts in cartilage.
Immunohistochemical studies revealed that both forms of PA, urokinase-type PA and tissue-type PA, and TIMP were present in OA tissues.
In the synovium, they were found mainly in monocyte/macrophages, synovial lining cells, and blood vessel cells.
In OA cartilage, PA was present only at the superficial level in chondrocytes and in cartilage matrix, whereas TIMP was present in chondrocyte lacunae throughout the full thickness of the cartilage.
TIMP was also detected in the superficial level of cartilage from sham operated knees.
The results of this study indicate that in OA tissues, there are conditions that favor the synthesis and activation of metalloproteases.
PA and plasmin are likely to play an important role in the physiologic activation of metalloproteases, although they are probably not the only system involved in this process.
The lack of increased TIMP levels in the OA cartilage, in the presence of increased metalloprotease activity, is also a possible contributing factor in the enzymatic degradation of this tissue.
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41
| 6,090
|
Moderate hypothermia after cardiac arrest of 17 minutes in dogs. Effect on cerebral and cardiac outcome.
Moderate hypothermia (30 degrees C) induced before circulatory arrest is known to improve neurologic outcome.
We explored, for the first time in a reproducible dog outcome model, moderate hypothermia induced during reperfusion after cardiac arrest (resuscitation).
In three groups of six dogs each (N = 18), normothermic ventricular fibrillation cardiac arrest (no blood flow) of 17 minutes was reversed by cardiopulmonary bypass--normothermic in control group I (37.5 degrees C) and hypothermic to 3 hours in groups II (32 degrees C) and III (28 degrees C).
Defibrillation was achieved in less than or equal to 5 minutes and partial bypass was continued to 4 hours, controlled ventilation to 20 hours, and intensive care to 96 hours.
All 18 dogs survived.
Electroencephalographic activity returned significantly earlier in groups II and III.
Mean +/- SD best neurologic deficit between 48 and 96 hours was 44 +/- 8% in group I, 38 +/- 12% in group II, and 35 +/- 7% in group III (differences not significant).
Best overall performance category 2 (good outcome) between 48 and 96 hours was achieved in none of the six dogs in group I and in four of the 12 dogs in the combined hypothermic groups II and III (difference not significant).
Mean +/- SD brain total histologic damage score was 130 +/- 22 in group I, 93 +/- 28 in group II (p = 0.05), and 80 +/- 26 in group III (p = 0.03).
Gross myocardial damage was greater in groups II and III than in group I--numerically higher overall and significantly higher in group III for the right ventricle alone (p = 0.02).
Moderate hypothermia after prolonged cardiac arrest may or may not improve cerebral outcome slightly and can worsen myocardial damage.
|
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|
42
| 5,472
|
Effect of dosage and timing of administration of naloxone on outcome in the rat ventral compression model of spinal cord injury.
The effect of the dosage and timing of administration of naloxone after spinal cord injury in rats via the ventral compression technique is presented.
The rat ventral compression technique allows for a ventral compression of the spinal cord without the requirement of a previous laminectomy.
It therefore facilitates the creation of an experimental lesion that is similar to that observed in the human clinicopathological situation.
The first part of the two-part study presented herein involved the determination of the optimal dose of naloxone, administered intraperitoneally 45 minutes after the creation of the lesion.
Of the groups studied (control group through 10.0 mg/kg group), 2.0 mg/kg of naloxone proved to be superior to both lesser and greater dosages.
The second part of the study involved the administration of a 2.0 mg/kg dose of naloxone at varying intervals ranging from 10 minutes before lesioning to 24 hours after lesioning.
A multiphasic response was again demonstrated, with an optimal time of administration occurring 45 minutes after the creation of the lesion.
A significant effect was offered by a midrange dose of naloxone (2.0 mg/kg), administered at 45 minutes after injury (P less than 0.02 by analysis of variance and Duncan's multiple range test).
These findings are discussed with respect to recent evidence regarding the effects of narcotic antagonists on both mu and kappa narcotic receptors.
Past and future experiments must account for these responses to multiphasic dosage and timing of administration.
Failure to do so may lead to erroneous conclusions.
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43
| 933
|
Heart rate variability before and after myocardial infarction in conscious dogs at high and low risk of sudden death.
Heart rate variability has been demonstrated both experimentally and clinically to be of prognostic importance in determining mortality after myocardial infarction.
However, no paired studies have been reported to examine heart rate variability before and after myocardial infarction.
The hypothesis was tested that low values of heart rate variability provided risk assessment both before and after myocardial infarction with use of an established canine model of sudden cardiac death.
Risk for sudden death was assessed 1 month after myocardial infarction by a protocol in which exercise and myocardial ischemia were combined; dogs that developed ventricular fibrillation were classified at high risk for sudden death (susceptible) and the survivors were considered low risk (resistant).
In resistant dogs, myocardial infarction did not affect any measure of heart rate variability: 1) mean RR interval, 2) standard deviation of the mean RR interval, and 3) the coefficient of variance (standard deviation/RR interval).
By contrast, after myocardial infarction, susceptible dogs showed significant decrease in all measures of heart rate variability.
Before myocardial infarction, no differences were seen between susceptible and resistant dogs.
However, 30 days after infarction, epidemiologic analysis of the coefficient of variance showed high sensitivity and specificity (88% and 80%, respectively), predicting susceptibility.
Therefore, results of analysis of 30 min of beat to beat heart period at rest 30 days after myocardial infarction are highly predictive for increased risk of sudden death.
|
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|
44
| 3,220
|
Critical volume for pulmonary acid aspiration: reappraisal in a primate model.
We have studied, in the monkey, the critical volume for the production of severe pneumonitis following pulmonary aspiration of gastric contents.
Aspiration of 0.4 ml kg-1 and 0.6 ml kg-1 at pH1 produced mild to moderate clinical and radiological changes, but no deaths.
Aspiration of 0.8 ml kg-1 and 1.0 ml kg-1 at pH1 was associated with an increasingly severe pneumonitis.
At 1.0 ml kg-1, 50% of the animals died--a mortality rate considerably less than that reported previously in animal studies.
If these results were to be extrapolated to humans, the critical volume for severe aspiration could be increased from 25 ml to 50 ml (0.8 ml kg-1), considerably reducing the percentage of patients perceived to be "at risk".
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|
45
| 6,661
|
Manual translaryngeal jet ventilation and the risk of aspiration in a canine model.
STUDY OBJECTIVES: Manual translaryngeal jet ventilation (TLJV) is a safe and effective method of maintaining normal ventilation in apneic subjects.
Little data exist on the amount of airway protection afforded with this technique of airway management.
We sought to evaluate the risk of aspiration during manual TLJV.
SETTING: Data were collected in a laboratory animal model.
DESIGN: A prospective, nonrandomized, controlled trial was performed.
PARTICIPANTS: Seventeen adult apneic mongrel dogs were enrolled.
INTERVENTIONS: Intratracheal Gastrograffin was instilled and radiographic changes assessed during ventilation using a 0 to 3 scale (none to severe).
Thirty-six trials were performed, with equal numbers at both 30 degrees and 45 degrees head elevation.
The three groups studied were animals without airway protection (control), animals with a cuffed endotracheal tube (tube), and animals with a percutaneous TLJV cannula and a 50-psi oxygen source ventilated at a rate of 20 breaths per minute (jet).
MEASUREMENTS AND MAIN RESULTS: Significantly less radiographic evidence of aspiration was noted in the jet and tube groups at 30 degrees and 45 degrees compared with control animals (P = .002 each).
At 45 degrees head elevation a trend toward increased aspiration scores in the jet group compared with the tube group (P = .065) was observed.
CONCLUSION: In our model, manual TLJV at 20 breaths per minute and an I:E ratio of 1:2 provided protection from aspiration comparable to that observed with a cuffed endotracheal tube at 30 degrees head elevation.
At 45 degrees elevation, this protection was diminished.
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46
| 7,384
|
Experimental retinal branch vein occlusion in miniature pigs induces local tissue hypoxia and vasoproliferative microangiopathy.
In miniature pigs, retinal veins were experimentally occluded using argon laser coagulation.
Microvascular modifications leading to retinal hemorrhages and retinal edema were observed some hours after the occlusion.
These lesions resolved progressively within 3 weeks after the occlusion, but in most cases ischemic retinal territories persisted.
Preretinal partial pressure of oxygen (PO2) measurements, using double barrelled O2-sensitive microelectrodes, showed that all the ischemic areas were indeed hypoxic.
In half of the experiments, preretinal and intravitreal new vessels grew on the ischemic territories.
Tissue hypoxia appears to be a key step in triggering neovascularization.
However, the critical level of hypoxia was not determined.
|
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47
| 2,032
|
Protection from chemotherapy-induced alopecia in a rat model.
Alopecia (hair loss) is among the most distressing side effects of cancer chemotherapy.
Little progress has been made, however, in its prevention or treatment, partly because of the lack of suitable experimental model.
In recent work on the treatment of myelogenous leukemia in the rat, the following observations were made: (i) treatment of 8-day-old rats with cytosine arabinoside consistently produced alopecia, and (ii) ImuVert, a biologic response modifier derived from the bacterium Serratia marcescens, uniformly produced complete protection against the alopecia.
In subsequent experiments, both cyclophosphamide and doxorubicin also produced alopecia in this model, and the doxorubicin-induced alopecia was prevented by treatment with ImuVert.
The potential relevance of these observations to chemotherapy-induced alopecia in the clinical setting should be examined.
|
C22
|
48
| 3,106
|
Bretylium tosylate versus lidocaine in experimental cardiac arrest
Bretylium tosylate has been shown effective in the treatment of ventricular fibrillation and in the prevention of its recurrence.
However, lidocaine is generally preferred because bretylium could have adverse hemodynamic effects related to its antiadrenergic action.
To explore further the differences between these two antiarrhythmic agents, the authors compared the effects of bretylium, lidocaine, and saline on a standardized dog model of ventricular fibrillation followed by electromechanical dissociation (EMD).
The protocol included three successive episodes of cardiac arrest in each animal.
Three minutes before each episode of ventricular fibrillation, 5 mg/kg of bretylium tosylate (n = 11), 1 mg/kg of lidocaine (n = 9) or saline (n = 12) were administered blindly.
There was no difference in the duration of cardiac arrest (bretylium, 8 min 18 sec; lidocaine, 7 min 54 sec; saline, 8 min 20 sec) or the total doses of epinephrine required to resuscitate the animals.
Both bretylium and lidocaine appeared to preserve cardiac function 5 minutes after recovery, as stroke volume increased from 17.8 +/- 6.7 to 18.7 +/- 6.7 mL (NS) after bretylium and from 17.7 +/- 7.7 to 19.0 +/- 7.0 mL (NS) after lidocaine, but decreased from 19.0 +/- 5.3 to 14.6 +/- 6.0 mL (P less than .05) after saline.
During the first 10 minutes of EMD, ventricular fibrillation or ventricular tachycardia recurred in 4 dogs treated with lidocaine, 3 dogs treated with saline, but no dog treated with bretylium (P less than .05 between bretylium and saline).
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49
| 90
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Reproduction of transfusion-related acute lung injury in an ex vivo lung model
Leukoagglutinins are implicated in transfusion-related acute lung injury (TRALI).
In the present study, severe lung vascular leakage was reproduced by application of a leukoagglutinating antibody of anti-5b specificity in an ex vivo lung model.
The antibody originated from a multiparous donor-plasma, observed to cause noncardiogenic edema during transfusion therapy.
Heated full plasma (anti-5b-titer 1/128) or purified immunoglobulin G fraction was used for the studies.
Ex vivo isolated rabbit lungs were perfused with albumin buffer, and human granulocytes (PMN) were admixed to the recirculating perfusate.
In presence of anti-5b antibody plus 5b-positive PMN plus rabbit plasma as complement-source, severe lung edema occurred after a latent period of 3 to 6 hours.
Pulmonary artery pressure was only transiently and moderately increased, and the leakage reaction could be traced back to a several-fold increase in lung vascular permeability.
In contrast, no vascular leakage was noted in lungs perfused in the absence of anti-5b antibody, PMN, or rabbit plasma.
Moreover, no permeability increase occurred on use of 5b-negative PMN.
This reproduction of TRALI in an ex vivo lung model corroborates the role of leukoagglutinating antibodies in initiating PMN-dependent respiratory distress and suggests a contribution of concomitant complement activation.
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50
| 3,940
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Inhibition of hepatic glucose production by SDZ 51641.
The new oral hypoglycemic agent SDZ 51641 was evaluated in nondiabetic rats and a rat model of human non-insulin-dependent diabetes mellitus.
Diabetes was induced with a single injection of 37.5 mg/kg streptozocin, and the rats exhibited hyperglycemia in the fed state with normal insulin levels.
Treatment of nondiabetic animals with 100 mg/kg SDZ 51641 given orally significantly decreased serum glucose and ketone levels within 4 h without affecting insulin levels.
Nonesterified fatty acids increased more than twofold during the same period.
Its effect on ketone and fatty acid levels suggests that SDZ 51641 acts as an inhibitor of fatty acid oxidation.
Diabetic rats treated with SDZ 51641 exhibited a significant acute hypoglycemic response, which was more pronounced after 3 days of treatment.
The compound also significantly decreased serum cholesterol and triglyceride levels 27 and 53%, respectively.
When endogenous hepatic glucose production was assessed in nondiabetic and diabetic animals via continuous infusion of [3-3H]glucose, we found that hepatic glucose production was elevated 43% in diabetic compared with control animals.
When diabetic rats were treated with 100 mg/kg SDZ 51641, hepatic glucose production decreased to normal levels within 6 h.
Hyperinsulinemic-euglycemic clamp studies indicated that SDZ 51641 had no effect on insulin-stimulated glucose utilization.
Measurement of [1-14C]oleate oxidation in isolated hepatocytes demonstrated that SDZ 51641 inhibited long-chain fatty acid oxidation in a concentration-dependent manner.
The compound was ineffective at inhibiting long-chain fatty acid oxidation in epitrochlearis or soleus muscles.
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51
| 7,502
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A borna virus cDNA encoding a protein recognized by antibodies in humans with behavioral diseases.
Borna disease virus (BDV) causes a rare neurological disease in horses and sheep.
The virus has not been classified because neither an infectious particle nor a specific nucleic acid had been identified.
To identify the genome of BDV, a subtractive complementary DNA expression library was constructed with polyadenylate-selected RNA from a BDV-infected MDCK cell line.
A clone (B8) was isolated that specifically hybridized to RNA isolated from BDV-infected brain tissue and BDV-infected cell lines.
This clone hybridized to four BDV-specific positive strand RNAs (10.5, 3.6, 2.1, and 0.85 kilobases) and one negative strand RNA (10.5 kilobases) in BDV-infected rat brain.
Nucleotide sequence analysis of the clone suggested that it represented a full-length messenger RNA which contained several open reading frames.
In vitro transcription and translation of the clone resulted in the synthesis of the 14- and 24-kilodalton BDV-specific proteins.
The 24-kilodalton protein, when translated in vitro from the clone, was recognized by antibodies in the sera of patients (three of seven) with behavioral disorders.
This BDV-specific clone will provide the means to isolate the other BDV-specific nucleic acids and to identify the virus responsible for Borna disease.
In addition, the significance of BDV or a BDV-related virus as a human pathogen can now be more directly examined.
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52
| 5,985
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A mouse model of the aniridia-Wilms tumor deletion syndrome.
Deletion of chromosome 11p13 in humans produces the WAGR syndrome, consisting of aniridia (an absence or malformation of the iris), Wilms tumor (nephroblastoma), genitourinary malformations, and mental retardation.
An interspecies backcross between Mus musculus/domesticus and Mus spretus was made in order to map the homologous chromosomal region in the mouse genome and to define an animal model of this syndrome.
Nine evolutionarily conserved DNA clones from proximal human 11p were localized on mouse chromosome 2 near Small-eyes (Sey), a semidominant mutation that is phenotypically similar to aniridia.
Analysis of Dickie's Small-eye (SeyDey), a poorly viable allele that has pleiotropic effects, revealed the deletion of three clones, f3, f8, and k13, which encompass the aniridia (AN2) and Wilms tumor susceptibility genes in man.
Unlike their human counterparts, SeyDey/+ mice do not develop nephroblastomas.
These findings suggest that the Small-eye defect is genetically equivalent to human aniridia, but that loss of the murine homolog of the Wilms tumor gene is not sufficient for tumor initiation.
A comparison among Sey alleles suggests that the AN2 gene product is required for induction of the lens and nasal placodes.
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53
| 795
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Synergism between hepatic injuries and a nonhepatotropic reovirus in mice. Enhanced hepatic infection and death.
Reovirus type 1, after intravenous inoculation in the adult mouse, is secreted via bile into the intestine in an infectious form.
Although reovirus type 1 is rapidly removed from systemic circulation by the liver and the lung, very few hepatocytes express reovirus antigen during infection.
In intestinal cells, reovirus replicates selectively in the crypts.
This site preference may be due to active cell proliferation in the crypts.
We hypothesized that the state of the cell may affect virus replication and tested this hypothesis by using chemical and surgical means to increase hepatic mitotic activity.
Adult mice were treated with carbon tetrachloride or surgical trauma, inoculated with reovirus type 1 intravenously, and subsequently killed.
Virus antigen was identified using a highly specific immunohistochemical technique.
Liver sections were stained using immunoperoxidase with specific rabbit antireovirus antibody.
Hepatotoxin and surgical trauma increase reovirus antigen detection in both Kupffer cells and hepatocytes.
Only the sequential administration of CCl4 and virus caused mortality at doses sublethal for each alone.
These data demonstrate a synergism between hepatic injury and reovirus which results in a significant increase in the magnitude of viral infection and contributes to mortality.
Such synergism may be important in idiopathic liver disease.
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54
| 2,631
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Endemic Cryptosporidium and Giardia lamblia infections in a Thai orphanage.
We conducted a point prevalence survey for enteric protozoa in 205 institutionalized orphans 1-61 months of age in Bangkok, Thailand.
Cryptosporidium was identified in 17 children (8%), Giardia lamblia in 42 (20%), and 3 children (1%) had both parasites.
At the time of diagnosis, diarrheal symptoms were present in a minority of subjects: 36% of children with Cryptosporidium alone, 10% with G.
lamblia alone, and in 20% of those with neither parasite.
Although chronic nutritional status (height/age) was similar in all groups, acute nutritional status (weight/height) was lower only in children with Cryptosporidium (Z score = -1.39 +/- 0.13) compared with children with G.
lamblia (mean Z score +/- SEM = -0.56 +/- 0.26) or neither parasite (Z score = -0.78 +/- 0.13; P = 0.05).
Detectable levels of Cryptosporidium-specific IgG antibodies by ELISA were identified in 15 of 16 Thai children with Cryptosporidium and in 17 of 19 Thai children without Cryptosporidium (mean OD +/- SEM = 1.27 +/- 0.18 vs.
1.06 +/- 0.13, respectively), but in only 1 of 18 sera from toddlers in day-care centers in Denver, CO (OD = 0.128 +/- 0.03).
Although neither infection with Cryptosporidium nor G.
lamblia was consistently associated with acute diarrheal symptoms, Cryptosporidium was more often associated with depressed acute nutritional status than G.
lamblia.
The high prevalence of specific antibodies to Cryptosporidium in Thai orphans suggests an association between high rates of exposure with asymptomatic excretion of the parasites.
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55
| 368
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Peripheral venous monitoring with acute blood volume alteration: cuff-occluded rate of rise of peripheral venous pressure.
We investigated the use of a new peripheral hemodynamic monitoring technique, the cuff-occluded rate of rise of peripheral venous pressure (CORRP), in the assessment of volume status in fluid overload.
Seven adult mongrel dogs were given a general anesthetic, and monitoring lines were inserted.
The animals were then subjected to an incremental volume overload of approximately 13% of estimated initial blood volume at 5-min intervals until a total volume infusion nearly equal to the animal's initial blood volume was reached.
Comparison of the various monitoring techniques (e.g., cardiac output, CVP, systemic BP, pulmonary wedge pressure) demonstrated that the peripheral measurement of CORRP had better correlation with known administered volume (r = .96) than any of the other variables.
The sensitivity of each of the variables in assessing small amounts of volume overload was also studied.
The volume of crystalloid infusion necessary to cause a clinically significant change (defined as greater than 2 SD above the baseline mean) was compared for each of the monitoring variables.
CORRP was equivalent to the other variables in sensing early volume overload.
In summary, in the anesthetized animal model CORRP appears to be a sensitive, minimally invasive method of assessing volume status in acute volume overload.
The efficacy of CORRP in a canine hemorrhagic shock and reperfusion model had previously been demonstrated.
This technique could be clinically applicable in situations such as trauma with hemorrhagic shock, intraoperative volume changes, and in the assessment of intravascular volume after resuscitation.
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56
| 4,611
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Targeting gene expression to the epidermis of transgenic mice: potential applications to genetic skin disorders.
The ability to specifically target gene expression to the epidermis of transgenic mice offers the exciting possibility of creating animal models of certain skin disorders that are inherited in man.
It may be possible to produce mouse models of dominantly inherited keratinization disorders by targeting the expression of mutant genes encoding the major differentiation products of the epidermis, such as the differentiation specific keratins, filaggrin and cell envelope proteins.
Mouse models for other skin disorders associated with abnormal regulation of growth, such as psoriasis, may be generated by targeting the overexpression of cytokines and growth factors, which are thought to play important roles in the pathogenesis of this disease.
The development of currently unavailable animal models for certain inherited human skin diseases would not only contribute to our understanding of the pathogenesis of these diseases at the molecular level, but also provide interesting models for therapeutic intervention.
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57
| 6,119
|
Focal ischemic damage is reduced by CPP-ene studies in two animal models.
We have studied a new high-affinity competitive N-methyl-D-aspartate antagonist, D-CPP-ene (SDZ-EAA 494), in two models of focal cerebral ischemia.
In the cat middle cerebral artery occlusion model (6 hours' survival), pretreatment with D-CPP-ene reduced infarct size by 64% (15 mg/kg dose) and 60% (4.5 mg/kg dose).
There was no reduction in infarct size at a dose of 1.5 mg/kg.
Treatment 1 hour after the occlusion reduced infarct size slightly, but not significantly.
In a new model of subdural hematoma in the rat, the zone of cortical ischemic damage beneath the blood clot was reduced by 54% with D-CPP-ene pretreatment.
Neuroprotective efficacy in a gyrencephalic species comparable to that of noncompetitive antagonists thus can be achieved with this agent.
These experiments also indicate that competitive N-methyl-D-aspartate antagonists may be clinically useful after traumatic intracranial hematomas.
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58
| 344
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Studies on the contact sensitizing activity of dithranol (anthralin) and 10-butyryl dithranol (butantrone).
The contact sensitizing activity of dithranol and butantrone (10-butyryl dithranol) was studied in 3 animal models: the guinea pig maximization test (GPMT), the closed patch test (CPT), and the mouse ear swelling test (MEST) in 2 different mouse strains.
In the GPMT, both dithranol and, to a greater extent, butantrone showed sensitizing potential.
Because butantrone was less irritant, the concentrations used were 10x higher than those of dithranol.
In the CPT, only butantrone was slightly positive.
In the MEST, with both CF-1 and Balb/c mice, dithranol caused less swelling of the test ear after challenge than butantrone.
According to the evaluation criteria of the MEST, only butantrone caused sensitization in 50% of the CF-1 mice and in 40% of the Balb/c mice.
Thus, the GPMT was the only test which indicated the minor contact sensitizing potential of dithranol.
On the other hand, the 10-butyryl analogue of dithranol showed undoubtedly stronger contact sensitizing potential than the parent compound in all tests.
Therefore, as compared to dithranol, an increased risk of sensitization should be considered.
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59
| 5,432
|
A rat femoral artery model for vasospasm.
A new animal model for vasospasm using rat femoral artery has been developed.
Whole blood, washed erythrocytes, or leukocytes in platelet-rich plasma were selectively applied to the adventitial surface of the femoral artery for 7 days in 15 rats, after which the vessels were perfusion-fixed and examined by light and transmission electron microscopy and immunohistochemistry.
As compared with matched control arteries, there was a prominent reduction in luminal cross-sectional area after 7 days in vessels exposed to whole blood or washed erythrocytes, but not in those exposed to leukocytes in platelet-rich plasma.
In arteries with luminal narrowing, light and transmission electron microscopy demonstrated marked morphological changes throughout the vessel wall similar to those seen in cerebral vasospasm after subarachnoid hemorrhage.
Immunohistochemistry disclosed a prominent loss of immunoreactive actin in smooth muscle cells of arteries exposed to whole blood or erythrocytes.
To assess the time course of arterial narrowing in this model, whole blood was selectively applied to the adventitial surface of femoral arteries in 23 rats for periods from 2 to 20 days.
As compared with control arteries, arterial narrowing was variably present at 2 days, progressively increased by 5 days, was maximal at 7 to 10 days, and returned to near control levels by 20 days.
The presence and severity of ultrastructural changes in vessel wall corresponded to the degree of arterial narrowing over time.
These results suggest that chronic narrowing in rat femoral artery exposed to periadventitial blood is analogous to that observed in cerebral arterial vasospasm after subarachnoid hemorrhage.
This new model represents a simple and reliable means to investigate pathogenic mechanisms and potential therapies for vasospasm.
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60
| 8,080
|
Experimental cardiac tamponade: correlation of pressure, flow velocity, and echocardiographic changes.
Seven episodes of experimental cardiac tamponade were induced in five anesthetized closed-chest dogs.
Simultaneous pericardial and intracavitary pressures were synchronized with superior vena caval and transvalvular pulsed-Doppler flow tracings.
The earliest indication of tamponade was the development of a negative transmural right atrial pressure that occurred during early ventricular diastole and was associated with echocardiographic evidence of right atrial collapse.
This was also associated with reversal of diastolic flow in the superior vena cava and with diminished early diastolic flow velocity across the tricuspid as well as the mitral valve.
During more advanced cardiac tamponade, the transmural right atrial pressure became negative during both early and late ventricular diastole as well as during isovolumic ventricular systole.
This was associated with a disappearance of early diastolic ventricular filling and right ventricular diastolic collapse as observed on two-dimensional echocardiography.
In hypotensive cardiac tamponade (cardiac output diminished by 70%), the decreased transmural right atrial pressure that developed during ventricular systole was accompanied by diminished antegrade flow in the superior vena cava.
In advanced and hypotensive tamponade, ventricular filling occurred mainly during atrial contraction.
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61
| 4,687
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Exacerbation of acute platelet thrombus formation in stenosed dog coronary arteries with smoke from a non-tobacco-burning cigarette.
The tobacco industry proposes to release a "new" cigarette with a burning charcoal tip, which heats the tobacco as air is drawn through it and into the lungs of the smoker.
It is claimed to be safer because the tobacco does not burn.
Using our established canine model of coronary artery stenosis with moderate intimal damage, we compared this new cigarette (0.4 mg nicotine) with a regular cigarette by ventilating dogs (n = 10) with room air and then either new or regular smoke (two cigarettes over about 10 minutes).
In our dog model, periodic acute platelet thrombus formation followed by embolization produced cyclical flow reductions in coronary blood flow where the rate of flow decline was proportional to the degree of in vivo platelet-vessel wall interaction.
The rate of flow decline increased from -4.81 +/- 1.29 ml/min2 to -9.60 +/- 2.29 ml/min2 after ventilation with the new-type smoke (p less than 0.01).
Similarly, the rate of flow decline increased from -5.43 +/- 1.28 ml/min2 to -9.28 +/- 2.31 ml/min2 after ventilation with regular cigarette smoke (p less than 0.01).
Despite the lack of a clear causal link between cigarette smoking and the acute manifestations of cardiovascular disease, the data presented here indicate that the new cigarette is just as potent as regular cigarettes at increasing in vivo platelet activity and exacerbating acute platelet thrombus formation in the dog.
We conclude that the new proposed non-tobacco-burning cigarette has deleterious effects similar to those of conventional cigarettes, and thus does not eliminate smoking as a risk factor in cardiovascular disease in human beings.
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62
| 8,727
|
Immunobiological studies on the alopecic (DEBR) rat.
The Dundee experimental bald rat (DEBR) has been proposed as an animal model of human alopecia areata, which is suspected of being an autoimmune disease.
This study was carried out to establish whether the immunological changes observed in the lesional DEBR rat correlated with studies of human alopecia areata.
The immune infiltrate was characterized using immunoperoxidase techniques on cryostat sections of vibrissa follicles.
Indirect immunofluorescence was used to quantify the peripheral blood leucocytes.
Some parallels were observed in the infiltration of human and DEBR rat follicles by T lymphocytes.
In contrast, pre-lesional DEBR rat follicles, which are not available for investigation in human alopecia areata, were not penetrated by leucocytes and MHC class II antigens were expressed in the precortical region of the epidermal component of these follicles.
Quantification of peripheral blood leucocytes showed significant increases in both T-lymphocyte subsets during lesional expression.
We consider that the pre-lesional form of the rat may provide important information as a model for the pre-lesional and uninvestigated form of alopecia areata in man.
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63
| 7,863
|
Platelet-activating factor: evidence against a role in hypoxic pulmonary vasoconstriction.
The mechanism of hypoxic pulmonary vasoconstriction (HPV) remains unknown.
The platelet-activating factor (PAF) antagonist WEB 2086 attenuated HPV in the isolated lung model of the rat.
We evaluated the effect of WEB 2086 on HPV in an intact animal.
Pigs were anesthetized, mechanically ventilated, and had their hemodynamic variables monitored with a pulmonary artery catheter and arterial line.
Cardiac output was measured by thermodilution.
Initial studies determined that PAF (0.03 to 1.0 micrograms) injected iv dose-dependently increased pulmonary vascular resistance (PVR) with a 262 +/- 58% increase in PVR 5 min after a dose of 1.0 microgram.
WEB 2086 (25 mg/kg iv) completely blocked the increase in PVR caused by iv PAF.
Additionally, indomethacin (2 mg/kg followed by 2 mg/kg.h iv) treatment of the animals attenuated the PAF-induced increase in PVR.
To evaluate the effect of WEB 2086 on HPV, animals were alternately ventilated with 21% oxygen and 10-min periods of 10% oxygen to induce HPV.
After three initial control episodes of hypoxic ventilation, WEB 2086 (25 mg/kg) was injected iv and two more episodes of ventilation with 10% oxygen were given.
During the three control HPV episodes the increases in PVR were 80 +/- 10%, 108 +/- 10%, and 107 +/- 22% (n = 5).
After WEB 2086, the increase in PVR during two episodes of hypoxia were 96 +/- 28% and 99 +/- 19%, respectively, which was not significantly different from the control response to hypoxia.
We conclude that iv PAF dose dependently increases PVR in pigs, and can be blocked by WEB 2086, that its effect is partially mediated through cyclooxygenase products, and that PAF does not appear to mediate HPV in this species.
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64
| 6,122
|
Comparison of phenytoin with noncompetitive N-methyl-D-aspartate antagonists in a model of focal brain ischemia in rat.
Recent in vitro and in vivo experiments have suggested that excitatory amino acid antagonists, particularly those active at the N-methyl-D-aspartate receptor subtype, are effective in ameliorating ischemic injury due to their antiexcitotoxic activity.
However, these drugs are also potent and effective in vivo anticonvulsants.
The present experiments compared the noncompetitive N-methyl-D-aspartate antagonists phencyclidine and MK-801 with the anticonvulsant phenytoin in a model of focal brain ischemia.
Fisher F-344 rats were subjected to tandem occlusion of the middle cerebral and ipsilateral common carotid arteries under halothane anesthesia.
Compounds were administered intravenously 30 minutes and 24 hours after arterial occlusion; infarct size was assessed at 48 hours after occlusion.
Phencyclidine had no effect on infarct volume at 1 mg/kg, significantly reduced (by 36%) infarct volume at 3 mg/kg, and produced a nonsignificant 26% decrease at 10 mg/kg.
The more potent and selective noncompetitive antagonist MK-801 reduced (by 32%) infarct volume significantly at 0.1 mg/kg, produced a nonsignificant 23% decrease at 0.3 mg/kg, and had no effect at 0.5 mg/kg.
Phenytoin, which is not a glutamate antagonist, reduced the infarct volume by 45% at 28 mg/kg.
A single dose of phenytoin (28 mg/kg) administered 30 minutes after occlusion was neuroprotective, but delaying drug administration for more than 2 hours was ineffective.
These data suggest that blockade of the N-methyl-D-aspartate receptor is effective in reducing the infarct size after focal cerebral ischemia.
The neuroprotective activity of phenytoin suggests that this may be related to the common anticonvulsant action.
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65
| 2,747
|
Effects of a 2.15-micron laser on human atherosclerotic xenografts in vivo.
The thulium-holmium-chromium:yttrium-aluminum-garnet (THC:YAG) laser has a tissue effect similar to that of the CO2 laser, with the advantage of transmissibility through flexible fibers.
The authors used a human-rabbit xenograft model to evaluate the thrombotic and healing responses of atherosclerotic vessels subjected to laser energy.
Occluded atherosclerotic human coronary artery segments were recanalized in vitro by use of the THC:YAG laser.
Destruction of plaque by the laser was achieved with minimal collateral thermal damage.
These vascular segments were then transplanted into the rabbit abdominal aorta.
The authors observed that the luminal surface of the lased vessels was more thrombogenic than that of the nonlased control vessels.
However, occlusion of the lased vessels did not occur.
Repair of laser-treated tissue progressed until a mature, nonthrombogenic fibrin-platelet aggregate was adherent to the luminal wall.
Overall, the lased vessels behaved in a fashion similar to the nonlased control vessels.
On the basis of these results, the authors believe that the THC:YAG laser may have use in human angioplasty.
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66
| 349
|
Low allergenicity of clonidine impedes studies of sensitization mechanisms in guinea pig models.
During clinical trials, a clonidine transdermal device has been found to induce clonidine-specific allergic contact dermatitis in up to 25% of patients during a treatment period of 1 year.
Using 3 different guinea pig strains, development was attempted of an experimental guinea pig model that would allow for in-depth studies into the mechanism of sensitization, and a possible role of transdermal device components.
Transient low-level clonidine allergy could be obtained only in a minority of animals, with severe sensitization procedures departing from epicutaneous applications, combined with intradermal (adjuvant) FCA injections.
Sensitization was not potentiated by additional booster procedures, including cyclophosphamide pretreatment, nor any of the putative cofactors (UV-treatments, C.
parvum or acetaldehyde involvement) studied.
These results suggest that the persistent skin contacts in man, with transdermal devices for sustained drug delivery, generate unique conditions favouring the development of allergic contact dermatitis, which are difficult to mimic in experimental animal models.
Thus, clinical allergy may develop even to extremely weak sensitizing drugs that can be safely used orally, and escape most currently available predictive contact allergy animal models.
Clinical studies remain unavoidable for studying factors that may reduce sensitization rates to more acceptable levels.
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67
| 4,626
|
Properties of strains of Escherichia coli O26:H11 in relation to their enteropathogenic or enterohemorrhagic classification.
Thirty-seven strains of Escherichia coli O26:H11 from infants and calves with diarrhea were examined for properties associated with enteropathogenic (EPEC) or enterohemorrhagic E.
coli (EHEC).
Strains were heterogeneous with respect to Vero cytotoxin (VT) production and hybridization with the EHEC plasmid-specific (CVD419) probe; 26 strains produced VT1; 1 produced VT2.
Twenty-four of 27 VT+ strains and 5 of 10 VT- strains hybridized with the CVD419 probe and produced enterohemolysin; these properties are characteristic of EHEC.
The strains did not hybridize with the EPEC adherence factor probe, a property characteristic of some EPEC.
Nevertheless, 36 strains adhered to HEp-2 cells in a localized manner and were positive by the fluorescence actin staining (FAS) test that is considered to correlate with the ability to cause attaching and effacing lesions in vivo.
EPEC and EHEC cause these lesions.
Although the FAS test appeared to be the most general pathogenicity test for the O26:H11 strains, it could not be used to assign strains specifically to EPEC or EHEC groups.
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68
| 9,078
|
Evidence against a requisite role for defective virus in the establishment of persistent hepadnavirus infections.
The factors involved in the establishment of persistent hepadnavirus infection are poorly understood.
Recent findings demonstrate that the sequence of the genome of hepatitis B virus (HBV) is variable in infected individuals and that, in some cases, virus mutants predominate.
Our objectives in the present study were to analyze the variability of woodchuck hepatitis virus (WHV) genomes in an infected animal and to determine whether sequence heterogeneity played a critical role in the ability of WHV to induce chronic infection.
We cloned and determined the complete nucleotide sequence of three supercoiled genomes from an animal that became infected after inoculation with a standardized WHV serum pool (i.e., the WHV7 virus pool).
We found that there were four nucleotide substitutions among the three genome sequences as well as a 73-nucleotide deletion in one of the recombinants.
DNA transfection experiments revealed that only one of the three recombinants was capable of independent replication.
These data suggest that a significant proportion of replicative templates in woodchucks that are infected with WHV are defective virus genomes.
Next, we compared the outcome of acute infection after inoculation with a serum pool containing a uniform population of replication competent virus (i.e., the WHV7R pool) with a serum pool composed of WHV genomes of variable sequence.
The WHV7R serum pool originated from a woodchuck that became a chronic carrier after in vivo transfection of the liver with the infectious WHV7 recombinant.
Neonatal woodchucks were inoculated with 5 x 10(6) WHV genome equivalents of either the WHV7 pool or the WHV7R pool.
All animals in the study became acutely infected with WHV.
Of the animals infected with the WHV7 serum pool, 65% became chronic carriers, while 80% of the animals infected with the WHV7R serum pool developed chronic infection.
Thus, infection of woodchucks with a serum pool containing defective virus resulted in a rate of chronic WHV infection that was similar to, or even lower than, a rate from a pool containing only wild-type virus.
This suggests that the presence of defective virus in the inoculum is not a prerequisite for the establishment of persistent hepadnavirus infections.
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69
| 569
|
A small animal model of human Helicobacter pylori active chronic gastritis.
Isolation of a spiral-shaped bacterium closely related to Helicobacter pylori from the cat stomach made it possible to investigate new small animal models of gastric infection.
Pure cultures of this bacterium, provisionally named "Helicobacter felis," were fed to germ-free mice.
The organism colonized the stomach in large numbers in mucus and deep in the gastric pits and showed the same gastric trophism found with H.
pylori.
Significant histopathology was seen in all H.
felis-infected mice.
At 2 weeks postinfection, an acute inflammatory response was seen composed primarily of eosinophils and neutrophils.
At 3 weeks, the polymorphonuclear response was more pronounced with large numbers of neutrophils in some areas forming small microabscesses.
Lymphocytes also increased in number.
By 8 weeks, several relatively large lymphoid nodules were present in the submucosa.
Multiple small microabscesses were still present in the pyloric mucosa.
This is the first animal model of bacterial gastritis to be described that shows progression from acute inflammation to persistent acute on chronic inflammation (active chronic) as is seen in human infection with H.
pylori.
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70
| 2,188
|
Evidence for platelet-activating factor as a novel mediator in experimental stroke in rabbits.
Platelet-activating factor is a potent mediator of inflammation, which has untoward effects on cerebrovascular and neural elements.
While several investigators have reported attenuation of ischemic damage after treatment with antagonists of platelet-activating factor, no study has proved endogenous production of platelet-activating factor in ischemia of the central nervous system.
We hypothesized that endogenous production of platelet-activating factor participates in the early pathologic manifestations of deteriorating stroke.
In 12 rabbits, we found tissue levels of platelet-activating factor measured by the release of serotonin from washed platelets to be elevated by approximately 20-fold in spinal cord injured by 25 minutes of ischemia and 2 hours of reperfusion (2.80 +/- 0.98 ng/g) compared with that in normal spinal cord (0.15 +/- 0.06 ng/g, p less than 0.01).
Given during ischemia to seven rabbits, 10 mg/kg i.p.
of a highly selective and potent antagonist of platelet-activating factor (BN 50739) accentuated the early postischemic hyperemia and prevented the delayed hypoperfusion measured by on-line laser-Doppler flowmetry (-35 +/- 7% of baseline [n = 7] without versus 33 +/- 14% with treatment, p less than 0.01) and the edema formation measured as the increase in tissue water content (4.4 +/- 0.7% without [n = 6] versus 2.1 +/- 0.6% with [n = 7]treatment, p less than 0.05) after 2 hours of reperfusion.
This neurochemical and pharmacologic evidence emphasizes a new perspective of ischemia-induced phospholipid degradation and suggests an important role for platelet-activating factor in the early manifestations of stroke.
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71
| 6,399
|
A simplified technique for the production of heart failure in the dog by rapid ventricular pacing.
Prolonged rapid ventricular pacing (VP) in dogs produces low output heart failure (HF) characterized by cardiomegaly, ascites, and elevated plasma renin and norepinephrine levels.
Commercially available pacemaker generators have a protective circuit that prevents pacing at rapid rates.
Previously, investigators have had to use either external temporary pacemakers or customized generators to pace at rates greater than 130 beats per minute (bpm).
The authors have developed a simple method to perform rapid VP by gluing magnets on Medtronic VVI generators, which allows programming in a temporary mode to sustain rates up to 400 bpm.
Our results using 10 generators in 55 dogs demonstrates that HF is produced in all dogs when VP is maintained at 250 bpm for an average of 28 days.
Technical difficulties during our early experience with this technique included magnets becoming unglued, loss of capture, and wound complications requiring generator removal.
Thus, our method reuses commercially available generators to rapidly pace the ventricles and induce HF.
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C22
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72
| 7,701
|
The natural history of intimal flaps in a canine model.
The natural history of arterial intimal flaps has not been well defined.
This study characterizes the natural history of unrepaired intimal flaps.
Thirty-nine 1-, 2-, and 3-mm hemispheric, distally based intimal flaps were made in 4- to 5-mm diameter canine femoral and carotid arteries.
Twenty arteries had 2- and 3-mm intimal flaps and were monitored for short-term arterial thrombosis and flap extension.
Nineteen had 1- and 2-mm intimal flaps and were monitored for thrombosis, long-term development of neointimal hyperplasia, arterial stenosis, and persistence of the flap.
While 40% of the arteries with 3-mm intimal flaps developed thrombosis in 3 to 5 days, only 3% of the arteries with 1- or 2-mm intimal flaps developed thrombosis.
Most 1- to 2-mm intimal flaps resolved and the subsequent development of neointimal hyperplasia or arterial stenosis was minimal.
Arteries with hemodynamically significant stenoses from intimal flaps warrant repair, while arteries with smaller intimal flaps may not require repair.
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C22
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73
| 2,593
|
Viral bronchiolitis during early life induces increased numbers of bronchiolar mast cells and airway hyperresponsiveness.
The objectives of this study were to determine the kinetics of Sendai virus-induced increases in bronchiolar mast cells and to determine whether virus-induced increases in bronchiolar mast cells were associated with increased airway responsiveness to methacholine and with altered allergic inflammatory responses to antigen stimulation.
Mast cell density in intrapulmonary airways was measured in outbred CD (Crl:CDBR) rats by use of morphometric techniques at 7, 15, 30, 60, and 90 days after viral or sham inoculation.
Density of bronchiolar mast cells was higher in virus-inoculated rats than in control rats at 30, 60, and 90 days after inoculation (P less than 0.01), but not at 7 or 15 days after inoculation.
Total pulmonary mast cell numbers were increased in virus-inoculated rats at 30 days after inoculation.
Rats at 42 days after viral inoculation had over a threefold increase in sensitivity to the concentration of nebulized metbacholine that would stimulate a 50% increase in respiratory resistance.
Virus-inoculated rats sensitized to ovalbumin had over a 10-fold increase (P less than 0.02) in pulmonary neutrophils that were recovered by bronchoalveolar lavage at 4 hours after ovalbumin aerosol challenge.
Virus-inoculated rats at this time also had higher densities of neutrophils in bronchiolar walls than allergen-exposed control rats.
The results indicate that Sendai virus induces increases in numbers of bronchiolar mast cells at times from 30 to 90 days after inoculation, and that mast cell increases are associated with airway hyperresponsiveness to methacholine and heightened allergic airway inflammatory reactions.
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C22
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74
| 9,349
|
Overestimation of myocardial infarct size by histologic measurement in a model of occlusion followed by reperfusion.
We studied 32 transverse left ventricular slices of myocardium from 16 pigs after 45 to 100 minutes of coronary artery occlusion followed by 180 minutes of reperfusion.
Infarct area for each slice was determined as follows: (1) grossly, by triphenyl tetrazolium chloride staining of each slice, and (2) microscopically, by complete histologic sectioning of the triphenyl tetrazolium chloride-stained surface of each slice.
Planimetry of necrotic and nonnecrotic areas was performed from tracings and photographs of triphenyl tetrazolium chloride-stained slices and from actual histologic sections.
When triphenyl tetrazolium chloride and histologic measurements were compared, necrotic tissue area had decreased 11.4% +/- 15.0% (2.59 +/- 1.04 vs 2.09 +/- 0.86 cm2).
Nonnecrotic tissue area decreased 20.6% +/- 24.0% (8.31 +/- 3.79 vs 5.16 +/- 2.73 cm2).
In this model of ischemia followed by reperfusion, with fixation and processing, viable tissue shrank almost twice as much as necrotic tissue.
This differential shrinkage introduces an error resulting in overestimation of infarct size by histologic quantitation.
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C22
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75
| 7,526
|
Magnetic resonance imaging of experimental rat brain tumors: histopathological evaluation.
Using RG-C6 glioma-transplanted rats, we studied precontrast and postcontrast magnetic resonance imaging, extravasation of Evans blue, and histology.
In all rats, tumor was enhanced with gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA).
The necrotic portion in the tumor, however, was not enhanced.
Hemorrhage and hydrocephalus were clearly visualized on both the precontrast and postcontrast images.
Blood-brain barrier-disrupted areas stained with Evans blue and areas enhanced with Gd-DTPA on magnetic resonance imaging were nearly consistent.
It is suggested that the mechanism of brain tumor enhancement with Gd-DTPA on magnetic resonance imaging is simply related to the degree of alteration of the blood-brain barrier.
The Gd-DTPA-enhanced magnetic resonance imaging, even with low magnetic field, is useful for the evaluation of size, shape, and location of experimental rat brain tumors.
|
C22
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76
| 6,077
|
Adoptive immunotherapy of human pancreatic cancer with lymphokine-activated killer cells and interleukin-2 in a nude mouse model.
A pancreatic cancer cell line was grown in orthotopic and heterotopic positions in young Swiss/NIH nude mice, which were tested with adoptive immunotherapy.
Mice were injected with 1 x 10(7) human cancer cells in the subcutaneous tissue and duodenal lobe of the pancreas.
The mice were randomly divided into four groups: group IA (LAK + IL-2) (N = 25) received 2 X 10(7) human lymphokine-activated killer (LAK) cells from normal donors by tail vein injection followed by 10,000 units of human recombinant interleukin-2 (IL-2) given intraperitoneally every 12 hours for 28 days; group IB (IL-2) (N = 27) was given the same dose of IL-2 alone; group IC (RPMI-1640) (N = 18) received a placebo consisting of 1 ml of RPMI-1640 intraperitoneally every 12 hours; and group ID (LAK) (N = 14) received 2 X 10(7) LAK cells but no IL-2.
Toxicity was significantly higher in group IB, with a mortality rate of 45.5% (10/22 animals) versus a 0% mortality (0/25) in group IA.
None of the group IA or IB animals died of pancreatic cancer during the experiment.
The animals that did not receive IL-2 died before 28 days in 14.2% of group IC and in 16.7% of group ID.
The area under the growth curve of subcutaneous tumors during the course of treatment and the pancreatic tumor weight at the end of treatment were compared in each group.
Subcutaneous tumors had a reduced rate of growth in group IA animals compared to all the other treatments.
Pancreatic tumor growth was slowed in group IA.
The animals treated with IL-2 alone (group IB) showed some slowing of tumor growth that was intermediate between group IA, group IC, and group ID.
A similar experiment was done with irradiated (375 rad) mice.
Nine nude mice with tumors were treated with LAK + IL-2 (group IIA), eight received IL-2 alone (group IIB), and seven received placebo (group IIC).
The antitumor effect of IL-2 alone was not present in the irradiated mice.
A highly significant difference persisted between group IIA and all other groups.
There was no difference in the histologic characteristics of tumors in control mice and in mice with inhibited tumor growth treated with IL-2 or IL-2 and human LAK cells.
These results show that adoptive immunotherapy with human LAK cells and human recombinant IL-2 is effective against human pancreatic cancer growing in nude mice.
This effect is independent from antitumor activity from IL-2 administrations alone.
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C22
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77
| 8,116
|
Cytomegalovirus infection promotes bacterial translocation in thermally injured mice.
Thermally injured mice that were given intraperitoneal injections of murine cytomegalovirus (MCMV) appeared to be clinically septic and to have increased mortality rates.
To evaluate the possible role of MCMV infection in promoting bacterial translocation in burned mice, mesenteric lymph nodes were cultured from two strains of mice (BALB/c and CBA) that were given thermal injuries alone, MCMV alone, or both.
BALB/c mice injected with 5 X 10(5) plaque-forming units MCMV following a 15% to 16% total body surface area scald injury had increased incidence of positive mesenteric lymph node cultures compared with other groups.
No intestinal mucosal histologies, mucosal dry weights, or wet-to-dry weight ratios in any animals were abnormal.
Differences in cecal bacterial concentrations were not observed.
Murine cytomegalovirus infection appears to enhance bacterial translocation in this model.
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C22
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78
| 365
|
Role of prostaglandin E1 in reducing pulmonary vascular resistance in an experimental model of acute lung injury.
To determine the role and efficacy of prostaglandin E1 (PGE1) on the cardiopulmonary derangements induced by glass bead embolism, two studies were performed.
In the first study, a dose response of PGE1 was tested in six animals that were first embolized with sufficient glass beads to double the pulmonary artery pressure (PAP).
This study demonstrated that PGE1 reduced PAP and cardiac output by a preload-mediated mechanism, as evidenced by a reduction in the right ventricular (RV) end-diastolic segment length, at doses of 15 and 30 ng/kg.min.
The second study was performed in two groups of animals, the control group (n = 6), and the treated group (n = 6), which were given PGE1 at 15 ng/kg.min after the PAP had been doubled by glass bead embolism.
RV preload was kept constant.
This study demonstrated that there was no difference in pulmonary vascular resistance between either the treated group or the control group.
There were no other significant differences between the two groups.
The results of both of these studies suggest that there is little afterload reducing effect of PGE1 in this model and at these dose ranges.
Part of the mechanism of PGE1 that improves pulmonary edema and gas exchange may be the reduction of filtration surface area and hydrostatic pressures in the lungs.
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C22
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79
| 8,833
|
Metabolic regulation of renal gluconeogenesis in response to sepsis in the rat.
1.
The regulation of renal gluconeogenesis was studied in rats made septic by a caecal ligation and puncture technique.
2.
Blood glucose concentrations were not markedly different in septic rats, but lactate, pyruvate and alanine concentrations were markedly increased, compared with sham-operated rats.
Conversely, blood ketone body concentrations were significantly decreased in septic rats.
Both plasma insulin and glucagon concentrations were markedly elevated in response to sepsis.
3.
The maximal activities of glucose-6-phosphatase (EC 3.1.3.9), fructose-1,6-bisphosphatase (EC 3.1.3.11), pyruvate carboxylase (EC 6.4.1.1) and phosphoenolpyruvate carboxykinase (EC 4.1.1.49) were markedly decreased in kidneys obtained from septic rats, suggesting diminished renal gluconeogenesis.
4.
Renal concentrations of lactate, pyruvate and other gluconeogenetic intermediates were markedly elevated in septic rats, whereas those of acetyl-CoA and fructose 2,6-bisphosphate were decreased and unchanged, respectively.
5.
The rate of gluconeogenesis from added lactate, pyruvate and glycerol was decreased in isolated incubated renal tubules from septic rats.
6.
Sepsis decreased the arteriovenous concentration difference for glucose, lactate, and alanine.
Septic rats showed decreased net rates of glucose production and net rates of removal of lactate and alanine as compared with sham-operated controls.
7.
It is concluded that the diminished capacity for renal gluconeogenesis in septic rats could be the result of changes in the maximal activities or regulation of key non-equilibrium gluconeogenic enzymes or both, but the effect of other factors (e.g.
toxins) has not been excluded.
|
C22
|
80
| 3,325
|
Effect of bladder outflow obstruction on the innervation of the rabbit urinary bladder.
The effects of bladder outflow obstruction on the innervation of the bladder were studied using a rabbit animal model.
Partial occlusion of the bladder neck was obtained by the placement of a silk ligature at that level; control animals underwent a sham procedure.
After a 3-month period, the presence of outflow tract obstruction was confirmed using urodynamic studies.
The animals were then killed and pharmacological assessments of the bladder innervation undertaken.
Detrusor muscle strip studies provided evidence of damage to the cholinergic innervation of the detrusor.
Also, muscle strips from obstructed animals showed reduced inhibitory responses to beta-adrenergic stimulation with isoprenaline.
In addition to these muscle strip studies, the bladder content of the neuropeptide substance P was assayed, but no significant change was observed in response to obstruction.
This finding suggests that substance P-containing sensory nerves may be spared from the denervating effect of bladder outflow obstruction.
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C22
|
81
| 2,869
|
In vitro cultivation of Cryptosporidium parvum and screening for anticryptosporidial drugs.
Sporozoites of Cryptosporidium parvum which were excysted in vitro from oocysts isolated from calves or patients with acquired immune deficiency syndrome underwent development in monolayers of the mouse fibroblast cell line L929.
Asexual multiplication occurred, with the maximum numbers of parasites usually being observed between 24 and 48 h after infection.
Gametocytes were also found, but their numbers were relatively small compared with those of the asexual stages.
A study was made of the effect on parasite development of 20 antimicrobial agents, most of which were anticoccidial or antimalarial agents.
The majority of the drugs had a limited inhibitory effect on parasite development, but usually only at high concentrations.
The two most active drugs were monensin and halofuginone, which reduced parasite multiplication by more than 90% at high concentrations.
In the case of monensin, however, inhibition of parasite development at higher concentrations was due, at least in part, to a toxic effect of the drug on the host cells.
|
C22
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82
| 4,986
|
Effect of endotoxin and a burn injury on lung and liver lipid peroxidation and catalase activity.
Both endotoxin and a burn alone produce oxidant-induced tissue lipid peroxidation.
The endotoxin response is due in large part to hydrogen peroxide.
The combination of endotoxin after a burn results in an increased liver, but not lung, oxidant injury.
Our purpose was to determine whether the burn oxidant injury inactivated endogenous liver tissue catalase, thereby amplifying a subsequent H2O2 insult.
Twenty-six adult sheep were studied.
Twelve sheep had a 15% TBS burn.
Tissue catalase activity, measured in lung and liver 3 days postburn, was significantly decreased from a control of 3.58 +/- 1.8 and 193 +/- 63, respectively, to 1.72 +/- 0.63 and 148 +/- 33 k(sec-1)/0.5 gram tissue.
The addition of endotoxin 3 days postburn resulted in an increase in liver malondialdehyde, MDA, a measure of lipid peroxidation, from a control of 110 +/- 80 to 450 +/- 54 nmol/gram tissue.
This value was significantly greater than the 210 +/- 80 nmol/gram tissue seen after endotoxin alone.
Lung tissue MDA with burn and endotoxin was 65 +/- 8 compared to 42 +/- 7 for control and 80 +/- 6 nmol/gram for endotoxin alone.
We conclude that a decrease in liver catalase activity occurs after a burn.
The decrease corresponds to an accentuated oxidant-induced lipid peroxidation after an added endotoxin insult where H2O2 is known to be an etiologic agent.
The catalase activity also decreases in postburn lung, but accentuated lung damage was not seen, indicating a variable tissue response from the burn-induced decrease in antioxidant activity.
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C22
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83
| 3,960
|
Inducement by fat feeding of basal hyperglycemia in rats with abnormal beta-cell function. Model for study of etiology and pathogenesis of NIDDM.
Non-insulin-dependent diabetes mellitus (NIDDM) is a heterogenous disorder characterized by defects in insulin action and secretion.
This study was aimed at developing a rat model in which these pathogenic factors might be studied.
Male Wistar rats were injected at 2 days of age with 45 or 30 mg/kg streptozocin (STZ) or vehicle (control).
Fasting plasma glucose and insulin levels were not significantly different between the two groups between 5 and 8 wk of age.
At 8 wk, half of each group was randomly assigned to isocaloric diets high in either fat (59% of calories) or starch (70% of calories).
After 1 wk on the diets, 45-mg/kg-STZ-administered fat-fed animals displayed significant fasting hyperglycemia (8.6 +/- 0.2 mM; P less than 0.01), which was exacerbated by the stress of anesthesia and/or cannulation, whereas no changes were observed in any of the other groups before (STZ starch fed, 6.7 +/- 0.1 mM; control fat fed, 6.8 +/- 0.1 mM; control starch fed; 6.4 +/- 0.1 mM) or after anesthesia and/or cannulation.
In the 30-mg/kg-STZ animals, fat feeding did not significantly elevate plasma glucose concentration, but a significant hyperglycemic response was seen with anesthesia and/or cannulation.
In all STZ groups, substantial impairment of glucose-induced insulin secretion was observed, particularly early-phase insulin secretion.
Further studies indicated that STZ animals on a diet conferring normal insulin sensitivity (starch) maintained basal normoglycemia and mildly impaired (i.v.) glucose tolerance despite this gross insulin secretory defect.
|
C22
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84
| 7,333
|
One hundred percent oxygen reverses muscle hypoxia in a rat hindlimb model of acute arterial occlusion.
Significant morbidity results from extremity ischemia after acute arterial occlusion.
Reestablishment of arterial flow is considered to be the ideal treatment, yet substantial tissue loss can occur before this is accomplished.
Using a rat hindlimb model we investigated whether the administration of 100% oxygen would decrease tissue hypoxia from acute arterial occlusion.
Adult male Sprague-Dawley rats were used, and Po2 recordings were taken from the gastrocnemius muscle by use of an oxygen electrode.
Baseline muscle Po2 was recorded, and then the femoral artery was occluded.
Repeat recordings were made after 20 minutes of ventilation with room air and after an additional 20 minutes of ventilation with 100% oxygen (N = 10).
Control groups consisted of animals undergoing occlusion but continued on room air (N = 3) and animals undergoing sham occlusion but receiving the period of 100% oxygen ventilation (N = 3).
Femoral artery occlusion produced a reduction in muscle Po2 from 28.0 +/- 1.4 to 6.1 +/- 2.0 (mean +/- SEM, p less than 0.001).
Ventilation with 100% oxygen reversed the tissue hypoxia produced by occlusion (27.3 +/- 2.0, p less than 0.001).
The administration of 100% oxygen without femoral artery occlusion resulted in a higher tissue Po2 than the occluded + oxygen group (94 +/- 12 vs 27.3 +/- 2.0, p less than 0.001).
Mean arterial blood pressure increased in the experimental group concomitant with the administration of 100% oxygen, but there was no correlation between final blood pressure and final tissue oxygen tension.
|
C22
|
85
| 3,368
|
Risk of occupational exposure to Herpesvirus simiae (B virus) in Quebec.
Herpesvirus simiae (B virus) causes a mild infection in macaques.
Transmission to humans may result in life-threatening encephalomyelitis.
To evaluate the risk of occupational exposure to B virus we surveyed the directors of 11 biomedical laboratories in Quebec that use monkeys.
Information was obtained on the monkey population and on the use of infection control measures recommended by the US Centers for Disease Control (CDC), Atlanta.
Of the 519 monkeys belonging to susceptible species the serologic status was positive in 264 (51%), all captured in the wilds, and it was unknown in 24 (5%).
All of the monkeys were caged individually, and newly acquired ones were quarantined for 2 to 8 weeks.
Of the 84 workers 52 (62%) handled monkeys whose serologic status was either positive or unknown.
Only five laboratories (representing 61% of the workers) complied fully with the CDC guidelines.
Nine of the laboratories had a wound management protocol, but only six had a designated specialist for consultation and prophylaxis.
Although no cases of B virus infection have been reported from Quebec the severity of human illness necessitates strict adherence to infection control measures and expert management of occupational exposure to susceptible monkeys.
|
C22
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86
| 4,615
|
Inherited mouse mutations as models of human adnexal, cornification, and papulosquamous dermatoses.
Nearly 100 mouse mutations have been described as causing some type of abnormality of the skin or hair.
As only a few of these mutations have been studied in detail, they remain an untapped resource for furthering knowledge of basic cutaneous physiology and understanding the pathophysiology of analogous diseases in humans.
Several diverse murine mutations are discussed.
These include "asebia," a mildly hyperkeratotoic disorder with sebaceous gland hypoplasia; "ichthyosis," an example of abnormal hair growth associated with hyperkeratosis; "rhino" and "hairless," two related examples of congenital follicular malformations; and "flaky skin", a potential animal model of eruptive psoriasis.
|
C22
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87
| 4,302
|
Use of immunoelectron microscopy to show Ebola virus during the 1989 United States epizootic.
A filovirus, serologically related to Ebola virus, was detected by "post-embedment" immunoelectron microscopical examination of MA-104 cells.
These had been infected by inoculation with serum samples obtained during the 1989 epizootic in cynomolgus monkeys (Macaca fascicularis), imported from the Philippines and maintained at Reston, Virginia, USA, a primate holding facility.
The immunoelectron microscopy method, when used in conjunction with standard transmission electron microscopy (TEM) of infected cells, provided consistent results and was simple to perform in this epizootic.
It is concluded that immunoelectron microscopy is potentially useful in the direct immunological diagnosis of Ebola and related filoviral infections (such as Marburg) in clinical samples obtained from those with acute infection.
|
C22
|
88
| 3,070
|
Systemic amiloride inhibits experimentally induced neovascularization.
Amiloride is an inhibitor of urokinase-type plasminogen activator, and might therefore have an inhibitory effect on neovascularization.
Neovascularization was induced in rabbit corneas via local implantation of prostaglandin E1 pellets prepared in a slow-release polymer.
Animals received daily intraperitoneal injections of 30 mg of amiloride, or an equivalent volume of saline solution for 5 days; both were well tolerated without severe untoward effect.
Neovascular response, as documented by corneal photographs, was evaluated after 5 days of injections.
The area of induced corneal neovascularization was decreased by 55% in animals receiving amiloride when compared with controls.
Thus, amiloride and similar compounds may prove useful in the study and management of neovascularization.
|
C22
|
89
| 325
|
Animal models of chronic inflammatory arthritis.
The use of animals has been indispensable to the investigation of the etiology, pathophysiology, and treatment of juvenile arthritis.
Because of ethical concerns about studying children, the difficulty of obtaining tissue, and the heterogeneous manifestations and protean course of chronic arthritis in childhood, the scope of potential research has been severely limited.
This brief review summarizes a few of the animal models most commonly used in chronic inflammatory arthritis research: subcutaneous air pouch, antigen-induced (including arthritogenic infectious agent), and spontaneous models.
In the spontaneous and antigen-induced animal models of arthritis, local and systemic immunoregulatory abnormalities clearly play a major role in the pathogenesis of arthritis.
By elucidating the immune response to those antigens, as well as the role of genetics and environment, the pathogenesis of juvenile rheumatoid arthritis may be better understood.
At the present time, however, the complexity of these models precludes more definitive interpretation and extrapolation to human diseases.
|
C22
|
90
| 7,117
|
Pathophysiological insights into the cardiomyopathy of Chagas' disease.
The evidence gained from both human and animal studies of chronic chagasic cardiomyopathy suggests that the disease occurs as a consequence of several discrete and progressive pathophysiological processes occurring after infection, the ultimate expression of which depends on a host of unidentified factors.
Collectively, the infection-associated events compromise microvasculature function and result in hypoperfusion, with consequences indistinguishable from those observed in other, nonparasitological cardiomyopathic diseases secondary to hypoperfusion.
Therefore, chronic chagasic cardiomyopathy may share similar pathophysiological abnormalities with other chronic congestive cardiomyopathic states.
|
C22
|
91
| 2,126
|
Experimental isobaric subarachnoid hemorrhage: regional mitochondrial function during the acute and late phase.
Patients treated for aneurysmal subarachnoid hemorrhage show, in the long-term follow up, an elevated rate of cognitive disturbances that are mainly related to the impact of the initial bleeding: the neurotoxic effects of blood deposition in subarachnoidal spaces may result in a diffuse encephalopathy, but the intrinsic mechanism and the biochemical correlates are not known.
In the present study we have evaluated mitochondrial function after experimental induction of subarachnoid hemorrhage.
Mitochondrial function was evaluated in four different rat brain areas (frontal cortex, occipital cortex, hippocampus, and brain stem) after experimental isobaric subarachnoid hemorrhage in rats.
Subarachnoid hemorrhage was induced by injecting 0.07 mL of arterial autologous blood into the cisterna magna.
Intracranial pressure did not significantly increase.
The nonsynaptic mitochondrial fraction was isolated from different rat brain areas, and the maximal rate of enzymatic reactions of some key enzymatic activities related to the Krebs cycle [nicotinamide adenine dinucleotide (oxidized form) (NAD+)-isocitrate dehydrogenase, citrate synthase, and succinate dehydrogenase] and of the electron transfer chain (cytochrome oxidase) were evaluated.
The nonsynaptic mitochondrial fraction was utilized also to check parameters related to the mitochondrial respiration: state 3, state 4, uncoupled state, respiratory control ratio, and adenosine 5'-diphosphate/oxygen ratio.
The biochemical parameters were measured at 1 and 72 hours after the subarachnoidal injection of blood.
Subarachnoid hemorrhage did not affect the mitochondrial enzymatic activities both at 1 and 72 hours, while the mitochondrial enzymatic activities parameters were significantly affected: in particular, a significant decrease of respiratory control ratio in all tested brain areas was demonstrated.
The increased mitochondrial vulnerability in the delayed phases could be one of the biochemical correlates of post-hemorrhagic encephalopathy.
|
C22
|
92
| 8,845
|
Causes, diagnosis, and treatment of pharyngitis.
Pharyngitis is a common disease of the respiratory tract that can be caused by several different viruses and bacterial organisms.
Clinically speaking, the most important causative agent is group A streptococcus (Streptococcus pyogenes).
Although rare, postpharyngitis complications arise as a result of disease caused almost exclusively by group A streptococcus.
Because group A streptococcal pharyngitis usually responds well to antimicrobial treatment, it is important to diagnose it.
Penicillin, erythromycin, and peroral first-generation cephalosporins have been documented to be effective.
In addition to group A streptococcus, C.
pneumoniae and M.
pneumoniae have also been detected in patients with pharyngitis.
The possibility of diagnosing these organisms is limited at the present.
Clinical surveys are still needed, moreover, to evaluate the effect of antimicrobial treatment on the disease caused by these organisms.
Although routine viral diagnostic methods do not help primary care physicians in treating patients with pharyngitis, information on bacteria and viruses in the immediate environment could prove to be of great help in daily clinical work.
|
C02
|
93
| 2,060
|
Assessing the risk of occupational acquisition of the human immunodeficiency virus: implications for hospital policy.
In determining infection control policy, it is essential to quantitatively assess the risk of transmission of human immunodeficiency virus (HIV) to health care workers and their families.
The risk should be placed in perspective by comparing it with other occupational hazards.
The risk of seroconversion from a needlestick injury can be calculated from the probability of a needlestick occurrence, the probability that the source patient is infected, and the probability of seroconversion, given an exposure.
The risk of seroconversion due to drawing 1000 blood specimens from seropositive patients is between 86 and 470 in 100,000.
The risk to surgeons from performing 25 operations on infected patients is approximately 272 in 100,000.
The risk of fatal injury in the course of one year's work on a Louisiana oil rig is between 188 and 283 per 100,000.
|
C02
|
94
| 5,602
|
Diagnosis of oral hairy leukoplakia by ultrastructural examination of exfoliative cytologic specimens.
Lingual exfoliative cytologic specimens (scrapings) were obtained from 18 patients positive for human immunodeficiency virus with clinical oral hairy leukoplakia.
Buccal mucosal scrapings were obtained from 12 of these patients.
The specimens were processed for examination by transmission electron microscopy (TEM).
Sixteen (89%) of the lingual specimens revealed infection of keratinocytes by herpes-type virus.
There was no evidence of virus infection in the 12 buccal mucosal scrapings.
Fungal hyphae were seen by TEM in 14 (78%) of the lingual scrapings and two (17%) of the buccal scrapings.
One exfoliative specimen and two biopsy specimens were stained for Epstein-Barr virus DNA with a DNA probe.
The demonstration of herpes-type virions by TEM in keratinocytes from a lesion clinically suspected to be hairy leukoplakia provides direct, objective diagnosis.
Furthermore, use of exfoliative cytologic specimens provides a clinically simple, noninvasive technique.
|
C02
|
95
| 8,503
|
Granulomatous Pneumocystis carinii pneumonia in a patient with the acquired immunodeficiency syndrome.
A patient with an unusual granulomatous response to infection with Pneumocystis carinii is described.
The diagnosis was made by open lung biopsy after two negative bronchoalveolar lavages.
|
C02
|
96
| 4,650
|
Distribution and specific identification of papillomavirus major capsid protein epitopes by immunocytochemistry and epitope scanning of synthetic peptides.
Monoclonal (MAbs) and polyclonal antibodies were produced against the major capsid protein of detergent-disrupted, purified bovine papillomavirus type 1 (BPV-1).
The precise locations of the corresponding epitopes were identified by the reactivity of MAbs and selected polyclonal antibodies with synthetic, overlapping, hexameric peptides corresponding with 95% of the BPV-1 major capsid protein.
The topography of these epitopes was determined by reactivity of antibodies with intact (conformational and nonconformational surface epitopes) and disrupted (external or internal nonconformational epitopes) BPV-1 virions.
The distribution of epitopes in various papillomaviruses of 13 different species was determined by reactivity of the MAbs and polyclonal sera with productively infected, formalin-fixed papillomas, fibropapillomas, and fibromas.
Epitope scanning, using MAbs and polyclonal antisera, resulted in the precise location of BPV-1 hexameric epitopes that could be correlated with their topography on the capsid and distribution in papillomatous lesions of various species.
|
C02
|
97
| 4,656
|
Pichinde virus infection in strain 13 guniea pigs reduces intestinal protein reflection coefficient with compensation.
Pichinde virus inoculation into strain 13 guinea pigs is a model with features reputed to be similar to hemorrhagic fever in humans.
Although the infection is lethal by day 13-19, guinea pigs of approximately 600 g do not show edema or effusions.
This raises the questions of whether capillary damage is present in such infected animals and, if it is, why edema is absent.
The effects of Pichinide virus on protein transport across jejunal capillaries were examined in 38 normal and 7 infected strain 13 guinea pigs 12 days after inoculation.
The latter lost 20.3% body weight but maintained normal blood pressure, serum protein concentration, and jejunal lymph flow.
However, their protein solvent drag reflection coefficient (sigma) was reduced to .52 +/- .03 (mean +/- SE) from .73 +/- .02 (2P less than .001), while permeability-surface area product was not changed.
In the absence of gross edema or effusions, Pichinde virus-infected guinea pigs demonstrated a leaky gut capillary wall to protein compatible with an increase in pore size or large pore number less than sufficient to change permeability-surface area product.
Compensatory mechanisms that prevent edema at this stage are efficient and may include reduced capillary pressure or some degree of capillary flow stasis.
|
C02
|
98
| 8,313
|
The emergence of hepatitis B as a sexually transmitted disease.
In the United States, approximately 300,000 cases of hepatitis B virus infection occur annually, and heterosexual activity is one of the most commonly reported risk factors for acquiring disease.
Until the number of infections transmitted through heterosexual contact can be reduced through hepatitis B vaccination, there is little chance of controlling this infection.
|
C02
|
99
| 7,381
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Acute syphilitic posterior placoid chorioretinitis.
Six patients with evidence of secondary syphilis presented with visual loss in both eyes caused by large, placoid, yellowish lesions with faded centers at the level of the pigment epithelium in the macula and juxtapapillary areas.
All eyes had vitreitis.
All of the lesions showed a similar fluorescein angiographic pattern of early hypofluorescence and late staining.
Five patients had mucocutaneous lesions typical of secondary syphilis.
All five patients treated with antibiotics had prompt improvement in visual function and resolution of the fundus lesions.
The ophthalmoscopic and angiographic appearance of these posterior fundus lesions was sufficiently characteristic to suggest a diagnosis of secondary syphilis.
Modification of the host response to syphilis by human immune deficiency virus (HIV) infection may be partly responsible for this peculiar fundus picture.
Three of the four patients tested positive for HIV.
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C02
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Dataset Card for Ohsumed
Ohsumed collection (available at ftp://medir.ohsu.edu/pub/ohsumed): it includes medical abstracts from the MeSH categories of the year 1991. In [Joachims, 1997] were used the first 20,000 documents divided in 10,000 for training and 10,000 for testing. The specific task was to categorize the 23 cardiovascular diseases categories. After selecting such category subset, the unique abstract number becomes 13,929 (6,286 for training and 7,643 for testing). As current computers can easily manage larger number of documents we make available all 34,389 cardiovascular diseases abstracts out of 50,216 medical abstracts contained in the year 1991.
Download Here:
- Cardiovascular diseases abstracts (in the first 20,000 abstracts of the year 1991)
Citation Information
Hersh WR, Buckley C, Leone TJ, Hickam DH, OHSUMED: An interactive retrieval evaluation and new large test collection for research, Proceedings of the 17th Annual ACM SIGIR Conference, 1994, 192-201.
Hersh WR, Hickam DH, Use of a multi-application computer workstation in a clinical setting, Bulletin of the Medical Library Association, 1994, 82: 382-389.
Alessandro Moschitti, A study on optimal parameter tuning for Rocchio text classifier. In proceedings of the 25th European Conference on Information Retrieval Research (ECIR 2003), Pisa, Italy, April, 2003.
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23,166
Models trained or fine-tuned on cglez/ohsumed