Gastric emptying in cats using foods varying in fiber content and kibble shapes.

The purpose of this study is to evaluate the influence of kibble shape and fiber content of commercial dry foods on gastric emptying in healthy cats. Eight healthy cats were used to evaluate four different diets which varied in shape of kibble (round versus triangle) or fiber content (low versus high). Diets were labeled with 99mTc-mebrofenin and gastric emptying was evaluated with nuclear scintigraphy. There was a significant difference between the kibble shapes at both T50 and T20. The triangle shaped kibble required significantly longer time than the round kibble to reach T50 (P = 0.02) and T20 (P = 0.001). Diet fiber content did not have a significant influence on T50, and T20. The influence of caloric and water intake was assessed with division of cats into high, medium, and low intake groups. The caloric intake had its main effect at T50 with the lowest quartile of caloric intake requiring significantly less time to reach T50 than the middle group and upper quartile (P = 0.05). Water intake did not have a significant effect on gastric emptying in this study. There was no relationship or correlation between the surface area of the food (cm2/kg) and T90, T50, and T20.

Carcinogenic effects of hyperthermia.

The purpose of this paper is to assess the evidence for and against the premise that hyperthermia is carcinogenic. The paper is one of several published in this issue of the International Journal of Hyperthermia on the subject of the health risks of hyperthermia. The motivation for this issue of the journal was the result of a World Health Organization workshop that dealt with this issue, as it relates to exposure of the population to RF fields. Since hyperthermia can be a natural consequence of such exposures, the health risks of hyperthermia are relevant in this context. Particularly in the case of carcinogenesis, it is necessary to provide a brief overview of the data that have been generated to examine the carcinogenic risks of RF exposure, so that these results can be compared with studies that have examined the carcinogenic risks of hyperthermia. For this reason, the paper is organized into three sections dealing with: (1) effects of heat on DNA damage/repair and mutations, (2) in vivo studies evaluating the carcinogenic potential of heat alone and combined with other carcinogens, and (3) in vivo studies involving RF exposures. The bulk of the data presented indicate that hyperthermia alone is not carcinogenic. If hyperthermia occurs in the presence of exposure to known carcinogens, such as radiation or chemical carcinogens there is the potential for modulation of carcinogenic effects of those agents. In some circumstances, hyperthermia can actually protect against tumour formation. In other instances, hyperthermia clearly increases incidence of tumour formation, but this occurs following thermal exposures (several degrees C temperature rise for up to 1 h or more) and radiation (therapeutic levels as for treatment of cancer) or chemical carcinogen doses higher than would be encountered by the general population. The extrapolation of these results to the general population, where radiation exposure levels would be at background and temperature rise from incidental RF exposure, such as cell phones (which are estimated to cause no more than 0.1 degrees C temperature rise) is not recommended. Current evidence indicates that the temperature elevations resulting from RF exposure are not carcinogenic. Caution should be used in situations where exposure to known carcinogens is combined with thermal exposures high enough to cause tissue damage. A summary of thermal thresholds for tissue damage from hyperthermia is presented in another paper in this special issue (Dewhirst et al.). No data exist that examine the carcinogenic risks of chronic thermal exposures below the threshold for detectable tissue damage, either alone or in combination with known carcinogens. This is an important goal for future research.

Basic principles of thermal dosimetry and thermal thresholds for tissue damage from hyperthermia.

This paper is one of several in this Special Issue of the International Journal of Hyperthermia that discusses the current state of knowledge about the human health risks of hyperthermia. This special issue emanated from a workshop sponsored by the World Health Organization in the Spring of 2002 on this topic. It is anticipated that these papers will help to establish guidelines for human exposure to conditions leading to hyperthermia. This comprehensive review of the literature makes it clear that much more work needs to be done to clarify what the thresholds for thermal damage are in humans. This review summarizes the basic principles that govern the relationships between thermal exposure (temperature and time of exposure) and thermal damage, with an emphasis on normal tissue effects. Methods for converting one time-temperature combination to a time at a standardized temperature are provided as well as a detailed discussion about the underlying assumptions that go into these calculations. There are few in vivo papers examining the type and extent of damage that occurs in the lower temperature range for hyperthermic exposures (e.g. 39-42 degrees C). Therefore, it is clear that estimation of thermal dose to effect at these thermal exposures is less precise in that temperature range. In addition, there are virtually no data that directly relate to the thermal sensitivity of human tissues. Thus, establishment of guidelines for human exposure based on the data provided must be done with significant caution. There is detailed review and presentation of thermal thresholds for tissue damage (based on what is detectable in vivo). The data are normalized using thermal dosimetric concepts. Tables are included in an Appendix Database which compile published data for thresholds of thermal damage in a variety of tissues and species. This database is available by request (contact MWD or PJH), but not included in this manuscript for brevity. All of the studies reported are for single acute thermal exposures. Except for brain function and physiology (as detailed in this issue by Sharma et al) one notes the critical lack of publications examining effects of chronic thermal exposures as might be encountered in occupational hazards. This review also does not include information on the embryo, which is covered in detail elsewhere in this volume (see article by Edwards et al.) as well as in a recent review on this subject, which focuses on thermal dose.

Quantitative and qualitative scintigraphic measurement of renal function in dogs exposed to toxic doses of Gentamicin.

Five, 3-month-old mongrel dogs weighing between 4.5 to 5.5 kg were studied to evaluate and compare the efficiency of 99mTc-DTPA, 99mTc-MAG3, and 99mTc-DMSA in detecting gentamicin-induced renal tubular injury. After baseline renograms using all three methods, all dogs received daily intramuscular injections of gentamicin at a dose of 30-45 mg/kg. Additional studies were obtained after a cumulative dose of 450, 1,575, and 2,250 mg of gentamicin was reached. Glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and percentage of total renal uptake measurements were calculated. Baseline and post-gentamicin injection blood urea nitrogen (BUN) and serum creatinine values were determined. A Duncan test revealed significant renal function impairment at 450 mgs of cumulated gentamicin with 99mTc-DMSA and at 1,575 mgs of cumulated gentamicin for 99mTc-DTPA and 99mTc-MAG3. There was no correlation between BUN and serum creatinine values when compared to gentamicin (p > 0.05). The images obtained with 99mTc-MAG3 were of better quality than those obtained with 99mTc-DTPA even under severe renal dysfunction. Percentage of 99mTc-DMSA uptake indicated renal damage, before than GFR and ERPF. BUN and serum creatinine measurements were poor indicators of gentamicin-induced renal failure.