Predicting pre-Columbian anthropogenic soils in Amazonia.

The extent and intensity of pre-Columbian impacts on lowland Amazonia have remained uncertain and controversial. Various indicators can be used to gauge the impact of pre-Columbian societies, but the formation of nutrient-enriched terra preta soils has been widely accepted as an indication of long-term settlement and site fidelity. Using known and newly discovered terra preta sites and maximum entropy algorithms (Maxent), we determined the influence of regional environmental conditions on the likelihood that terra pretas would have been formed at any given location in lowland Amazonia. Terra pretas were most frequently found in central and eastern Amazonia along the lower courses of the major Amazonian rivers. Terrain, hydrologic and soil characteristics were more important predictors of terra preta distributions than climatic conditions. Our modelling efforts indicated that terra pretas are likely to be found throughout ca 154 063 km(2) or 3.2% of the forest. We also predict that terra preta formation was limited in most of western Amazonia. Model results suggested that the distribution of terra preta was highly predictable based on environmental parameters. We provided targets for future archaeological surveys under the vast forest canopy and also highlighted how few of the long-term forest inventory sites in Amazonia are able to capture the effects of historical disturbance.

Proximal Versus Distal Splenic Artery Embolisation for Blunt Splenic Trauma: What is the Impact on Splenic Immune Function?

PURPOSE: To compare the impact of proximal or distal splenic artery embolisation versus that of splenectomy on splenic immune function as measured by IgM memory B cell levels. MATERIALS AND METHODS: Patients with splenic trauma who were treated by splenic artery embolisation (SAE) were enrolled. After 6 months splenic volume was assessed by CT, and IgM memory B cells in peripheral blood were measured and compared to a local normal reference population and to a post-splenectomy population. RESULTS: Of the 71 patients who underwent embolisation, 38 underwent proximal embolisation, 11 underwent distal embolisation, 22 patients were excluded, 1 had both proximal and distal embolisation, 5 did not survive and 16 did not return for evaluation. There was a significant difference between splenectomy and proximal or distal embolisation and a trend towards greater preservation of IgM memory B cell number in those with distal embolisation-a difference that could not be attributed to differences in age, grade of injury or residual splenic volume. CONCLUSION: IgM memory B cell levels are significantly higher in those treated with SAE compared to splenectomy. Our data provide evidence that splenic embolisation should reduce immunological complications of spleen trauma and suggest that distal embolisation may maintain better function.

A student-run Geriatric Home Health Care Program.

This paper describes how medical students developed, maintained, and received curriculum credit for a home health care program for senior citizens, and how both patients and students have benefited from the program.

Influence of exogenous T4 on body weight, feed consumption, T4 levels, and myocardial glycogen in furazolidone-fed turkey poults.

Ten turkey poults each were placed in one of four groups: control, thyroxine (T4), furazolidone (FZ), and FZ + T4. Thyroxine (T4), at a concentration of 1 ppm, was included in the ration of poults fed T4 and FZ + T4, and furazolidone (FZ), at a concentration of 700 ppm, was included in the ration of poults fed FZ and FZ + T4 from 2 to 5 weeks of age. Levels of plasma T4 decreased significantly (P less than or equal to 0.05) between 2 and 5 weeks in control and FZ poults. At 5 weeks, plasma T4 levels were significantly (P less than or equal to 0.05) lower in FZ poults than in control poults and significantly (P less than or equal to 0.05) lower in the FZ + T4 poults than in the T4 poults. Exogenous administration of T4 had no effect on development of the round heart syndrome or on body weight, but significantly increased feed consumption in FZ-fed poults during weeks 4 (P less than or equal to 0.05) and 5 (P less than or equal to 0.01). Inclusion of T4 in the ration increased plasma levels of the hormone 12x in both T4 and FZ + T4 poults and significantly (P less than or equal to 0.05) increased myocardial glycogen content in T4 poults but not in FZ + T4 poults.

Furazolidone toxicity in neomycin-treated turkey poults.

Furazolidone (FZ) toxicity was evaluated in turkey poults treated with neomycin at a dose of 20 mg/kg body weight for 5, 10, or 26 days. Neomycin treatment had no effect on FZ-induced anorexia, delayed the onset of altered electrocardiographic patterns by approximately 1 week, and did not significantly affect the development of FZ-induced cardiomyopathy. Data indicated that FZ toxicity is not significantly altered by the gut microflora.

Effect of furazolidone on heart weights and myocardial moisture content in turkey poults.

Furazolidone (FZ) at 700 ppm in feed mixtures fed turkey poults from 2 to 5 weeks posthatching significantly increased the ratio of heart weight to body weight (p less than 0.001) and myocardial moisture content (p less than 0.05). The increase in myocardial moisture content is believed to be related to increased glycogen deposition under the influence of FZ since FZ removal from the diet decreased myocardial glycogen levels and moisture content to normal levels.

A morphometric study of myocardial mitochondria and myofibrils in turkey poults during development of furazolidone-induced cardiomyopathy.

Furazolidone (FZ) at a dose of 700 ppm was fed to turkey poults 2-5 weeks posthatching. At 3, 4, and 5 weeks of age, six poults each were sacrificed from control and FZ-fed groups. Samples of tissue from the outer free walls of the ventricles and the interventricular septum were removed and processed for electron microscopy. Volumetric density of mitochondria and myofibrils was determined by the point-counting technique. Significant reductions (p less than or equal to .05) in the volumetric density of mitochondria were observed at 5 weeks of age in the ventricular free walls of round-heart poults, and at 4 and 5 weeks of age in the interventricular septum. Significant reductions (p less than or equal to .05) in the volumetric density of myofibrils were noted at 4 weeks of age in the left ventricular free wall of FZ-fed normal poults and in the interventricular septum of round-heart poults. At 5 weeks of age, a significant increase (p less than or equal to .05) in myofibrils was observed in the left ventricular free wall of FZ-fed normal poults. Data confirms that the volumetric densities of mitochondria and myofibrils are significantly altered during development of FZ-induced hypertrophy.

The production of cardiomyopathy in turkey poults by the oral administration of furazolidone.

Furazolidone (FZ) was given to turkey poults two weeks post-hatching by stomach tube in doses of 60 and 80 mg/kg per day, and via the feed at a concentration of 700 ppm. Oral doses were given either as one dose at 8 a.m. or as two equal doses given at 8 a.m. and 4 p.m. Electrocardiographic (ECG) recordings were used to monitor the development of round-heart disease (RHD) and necropsies were performed on all poults to corroborate the ECG findings. All poults receiving FZ gained significantly less weight (p less than or equal to .05) than control poults. At oral doses of 80 mg/kg per day, the apparent acute toxicity of FZ resulted in high mortality during the first week of the experiment. At necropsy there were no signs of RHD in these poults. Most of the poults given FZ orally in doses of 60 mg/kg per day or at 700 ppm in the feed survived to the termination of the experiments. The majority of these poults showed ECG patterns that are typical of RHD. Myocardial lesions indicative of RHD were present at necropsy.

Blood glucose and tissue glycogen levels in turkey poults with spontaneous round heart disease and furazolidone-induced cardiomyopathy.

Furazolidone (FZ) at 700 ppm was added to feed mixtures fed turkey poults two weeks posthatching to induce acute experimental cardiomyopathy. Poults in the control pen received the same ration but without FZ. Four of the control poults developed spontaneous round heart disease. From EKG data and blood samples obtained at weekly intervals, poults were selected for sacrifice at 5 weeks of age. Tissue samples from the left myocardial wall, liver, and pectoralis major and tibialis anterior muscles were analyzed for glycogen by biochemical assay. Blood glucose was determined with the Technicon autoanalyzer. Deposition of glycogen increased significantly (p less than 0.05) in the myocardium of all affected poults and in the liver of all FZ-treated poults. Glycogen levels of the pectoralis major and tibialis anterior muscles were not affected by FZ, but a significant increase (p less than 0.05) was apparent in the pectoralis major muscle of spontaneous round heart poults. It was concluded that FZ influences glycogen metabolism, probably by enzyme inhibition, and that it tends to magnify effects seen in the spontaneous round heart syndrome. Glycogen infiltration of tissues such as the heart and white skeletal muscle suggests that the round heart syndrome may be a manifestation of the glycogen storage disease, idiopathic generalized glycogenosis. Lack of significant differences in the blood serum glucose levels of all poults indicates that these levels are not a reliable clinical parameter for monitoring development of the round heart syndrome.

Quantitation of cardiac gross morphology during the development of FZ-induced cardiomyopathy in turkey poults.

Furazolidone (FZ) at a dose of 700 ppm was fed to turkey poults 2-5 weeks posthatch. At 3, 4, and 5 weeks of age, seven poults each were sacrificed from control and FZ-fed groups. A section of ventricular tissue 1 mm thick was excised from the heart distal to the base at a level one-fourth of the distance between the base and apex. Parameters estimated from tracings of each section were area and circumference of both right and left ventricular lumen profile, area and circumference of entire heart profile, area of right ventricular free wall profile, area of left ventricular and septal wall profile, and area of entire heart muscle profile. A major finding was a sequential increase in the area of the ventricular lumina in the FZ-fed poults. Differences between the control and FZ-fed poults were statistically significant for the right lumen profile at 3 and 5 weeks of age and for the left lumen profile at 4 and 5 weeks of age. The area of the heart muscle profile was decreased in FZ-fed poults, but this difference was statistically significant only at 4 weeks of age. Data suggest that the pathogenesis of FZ-induced cardiomyopathy involves a dilation of ventricular lumina resulting in increased intraventricular blood volume and altered ECG patterns. Relationships between gross morphology and ECGs may be seen only in terminal cases of several weeks duration. This explains the inability to correlate ECGs with gross morphologic changes in all poults observed at necropsy.

Delayed T-cell maturation and suppression of mitogen-induced blastogenesis in turkey poults fed cortisone acetate and furazolidone.

The effect of cortisone acetate (CA) on the immune response of control and furazolidone (FZ)-fed turkey poults was investigated. CA, fed at a dose of 500 mg/kg of ration beginning at 1 week of age, decreased mortality but had little effect on the development of FZ-induced cardiomyopathy. When poults were 2 weeks of age, the in vitro stimulation of lymphocytes by phytohemagglutinin (PHA) and concanavalin A (Con A) was significantly depressed (P less than or equal to 0.001 and P less than or equal to 0.05, respectively) in cortisone-treated poults. The time of the peak response of lymphocytes from poults 2-5 weeks of age to in vitro stimulation by PHA was significantly delayed (P less than or equal to 0.01) and the magnitude of the response was significantly depressed (P less than or equal to 0.001) in cortisone-treated poults compared with control poults. Cortisone treatment had no effect on time of peak response to Con A stimulation but significantly depressed (P less than or equal to 0.05) the magnitude of the response. Poults receiving FZ administered by gastric tube showed a peak response to PHA stimulation significantly (P less than or equal to 0.05) earlier and significantly (P less than or equal to 0.05) greater than did control poults.

Quantitative morphological alterations during the development of furazolidone-induced cardiomyopathy in turkeys.

Cardiac structures were measured to determine the sequence of alterations during the development of spontaneous and furazolidone-induced cardiomyopathy in turkey poults 20 to 31 days after hatching. Samples of tissue from the free walls of the ventricles were removed and processed for electron microscopy. Volumetric density of cardiac structures was determined by the point-counting technique. The results indicate that the sequence of myocardial alterations is similar in both spontaneous and furazolidone-induced cardiomyopathy, but that these changes are more pronounced in the latter condition. Major changes include an early diminution in myofibrillar density, accompanied by a small reduction in mitochondrial density. This is followed by dilatation of the ventricular lumina and a decrease in the volume fraction of Z-bands. The increase in mass of the free walls of the ventricles in affected poults is due primarily to an increase in extracellular components and sarcoplasm devoid of organelles. The results suggest that the development of this myopathy is initiated by damage to the myofibrils of the cardiocytes.

Changes in myocardial ultrastructure during development of furazolidone-induced cardiomyopathy in turkeys.

Ultrastructural alterations were studied in spontaneous round heart and furazolidone (FZ)-induced cardiomyopathy in turkey poults 20 to 31 days after hatching. The two most consistent morphological changes were abnormal accumulation of cytoplasmic glycogen and myofibrillar lysis. These alterations were more extensive in the drug-induced condition, which suggests that more myocytes are affected than in the spontaneous form of the disease. Data indicate that the myocyte contractile proteins sustain the major injury while other organelles appear to be involved only in an incidental manner. These findings corroborate previous suppositions which pointed toward a metabolic defect as the basic mechanism underlying the development of both spontaneous round heart and FZ-induced cardiomyopathy in turkey poults.

Influence of thiamin supplements on furazolidone-induced cardiomyopathy in turkey poults.

Furazolidone (700 ppm) was fed to turkey poults from 2 to 5 weeks of age. The drug produced a cardiomyopathy and reduced the feed intake and growth of the birds. Thiamin was concurrently injected into the furazolidone-fed poults to determine whether the vitamin would prevent or reduce the severity of the cardiotoxic effect of the drug. Supplemental injections of thiamin had no significant effect on feed consumption or growth of the birds nor did they protect the heart against the cardiotoxicity. The conclusion is that furazolidone-induced cardiomyopathy is not caused by a thiamin deficiency.

Effect of including lasalocid or monensin singly or in combination with furazolidone on the growth and feed consumption of turkey poults.

Lasalocid and monensin are widely used to control coccidiosis in broilers, but not in turkey poults. Four feeding trials were conducted to determine the performance of turkey poults when these compounds were used singly or in combination with 100 ppm of furazolidone. Bodyweights and feed consumption were significantly depressed for five weeks after hatching by 150 ppm of lasalocid. Combining furazolidone with lasalocid ameliorated the toxic effect of lasalocid. Bodyweights were significantly depressed by 150 ppm of monensin in the fifth week after hatching, but there was no significant depression in feed consumption. Furazolidone exacerbated any toxic effects of monensin. Data indicate that monensin may be used safely at dosages greater than the recommended level of 60 to 99 ppm, but should not be used in combination with furazolidone.

Effects of furazolidone in the early chick embryo.

Effects of furazolidone in early chick embryos were investigated in order to determine the feasibility of using this biological system as a model for studying the mechanism(s) of furazolidone toxicity. Double and triple injections of varying dosages of furazolidone were administered via the yolk sac at early stages of incubation. Toxic levels of the drug affecting both growth and levels of glycogen were dosage-dependent and time-dependent. Double injections of furazolidone at a dose as little as 60 microgram/egg administered at 40 and 72 hr of incubation significantly retarded growth (P less than .001) and increased glycogen levels (P less than .05) in the embryo and yolk sac. Mortality was high in embryos receiving toxic levels of furazolidone, but no gross abnormalities were observed.

Distribution of myocardial glycogen in turkey poults during development of furazolidone-induced cardiomyopathy.

Furazolidone (FZ) at 700 ppm was added to feed mixtures fed turkey poults two weeks posthatching to induce experimental cardiomyopathy. Poults in the control pen received the same ration but without FZ. From ECG data obtained at weekly intervals, poults were selected for sacrifice at 3, 4, and 5 weeks of age. Myocardial samples from the right and left ventricular free walls were analyzed for glycogen by biochemical assay technics. Levels of glycogen were significantly (p less than .01) elevated in the FZ-treated poults at 3, 4, and 5 weeks of age. At all ages, the increase occurred in both the acid-soluble (TCA) and acid-insoluble (KOH) fractions with a proportionately greater increase in the TCA fraction. Results suggest that the effect of FZ on myocardial glycogen metabolism occurs very early and is more pronounced in the right ventricle than in the left ventricle even though both chambers may exhibit similar gross changes.

Electrocardiographic technic for identifying developing cardiomyopathies in young turkey poults.

A modification of the technic for the utilization of electrocardiographic (ECG) data to identify round heart poults was used to screen poults with questionable ECG recordings and to diagnose poults with early cardiomyopathies. In two experimental trials, using a voltage greater than .1 mV (NH) in the R wave of Lead I as a criterion, it was possible trom 20 to 24%. At subsequent periodic data gathering, 37% of the poults in Trial I and 27% of the poults in Trial II exhibited NH before developing the typical normal transitional to round heart (NT leads to R) ECG pattern of the round heart syndrome. Necropsy findings confirmed myocardial alterations in a majority of the poults with NH whether or not the typical round heart ECG pattern ensued. Application of this finding is discussed.

Activity of alpha-1, 4-glucosidase in furazolidone-induced glycogenosis.

Furazolidone (FZ) at 700 and 800 p.p.m. was added to feed mixtures fed turkey poults two and three weeks posthatching, respectively, to induce acute experimental cardiomyopathy. Poults in the control pen received the same ration but without FZ. From EKG data obtained at 2, 4, and 5 weeks of age, control unaffected and experimental affected poults were selected for sacrifice. Poults were sacrificed by cervical dislocation and appropriate samples of hepatic tissue were removed for assays of activity of alpha-1, 4-glucosidase. Results indicate that enzyme activity in affected FZ-treated poults is similar to that in unaffected control poults. Lack of significant differences in activity of this lysosomal enzyme suggests that FZ-induced glycogenosis may be related to the adult form of idiopathic generalized glucogenosis, the etiology of which remains unidentified.