Phosphorus in periphyton mats provides the best metric for detecting low-level P enrichment in an oligotrophic wetland.

Growing concern over the ecological consequence of phosphorus (P) enrichment in freshwater wetlands has elicited considerable debate over the concentration of water column P associated with eutrophication. In the oligotrophic Everglades, the displacement of native communities by enriched ones is widespread and has occurred at sites experiencing only minimal elevations in P input. To help define regulatory criteria for P inputs to the Everglades, we constructed an experiment that mimics P input to the natural system by continuously delivering P at concentrations elevated 5, 15 and 30 microgl(-1) above ambient to 100-m long flow-through channels. We compared patterns of P accumulation in the water, periphyton, detritus and soils among the channel treatments and also along a 16 km transect from an enriched canal that inflows to the interior of the same marsh. Water column TP and SRP were unrelated to input TP concentration in both the experiment and the marsh transect. However, concentrations of TP in periphyton mats were significantly elevated at all levels of experimental enrichment and as far as 2 km downstream from water inputs into the marsh. Elevated periphyton TP was associated with significant loss of periphyton biomass. In oligotrophic wetlands, traditional measures of water column SRP and TP will substantially underestimate P loading because biotically incorporated P is displaced from the water column to benthic surfaces. Using periphyton TP as a metric of P enrichment is uncomplicated and analogous to pelagic TP assessments in lakes where most P is sequestered in phytoplankton.

Testosterone acts as a coronary vasodilator by a calcium antagonistic action.

T acts as a vasodilator in vitro and in vivo. Supplemental T therapy in humans with angina improves symptoms and reduces objective measures of ischemia. In left anterior descending coronary arteries taken from adult male Wistar rats, T abolishes 100+/-4.2% of calcium-dependent contraction induced by potassium chloride, 82.3+/-6.1% of the mostly calcium-dependent contraction induced by prostaglandin-F-2-alpha, but only 45.3+/-3.4% of the contraction induced by phorbol-12,13-dibutyrate (PDBu) in the presence of extracellular calcium, and 54.5+/-4.5% of the contraction induced by PDBu in the absence of extracellular calcium. These findings suggest that T is primarily inhibiting the calcium-dependent elements of vascular contraction.

Electrophysiology and pathology evaluation of the Yucatan pig as a non-rodent animal model for regulatory and mechanistic toxicology studies.

Six male and six female Yucatan pigs were utilized to investigate the feasibility of this species as a non-rodent model for routine regulatory and mechanistic toxicology studies. This study evaluated disease surveillance and computerized electrophysiology, along with possible gross and micropathology changes. Two pigs were used as sentinel animals to evaluate the microbiological status of the vendor upon arrival; the other pigs were maintained as biomonitors and to provide baseline clinical chemistry, urinalysis, pathology and electrophysiology data. The electrophysiology tests conducted included electrocardiography (ECG), electroretinography (ERG) and quantitative electroencephalography (qEEG), which achieved consistent baseline values with acceptable intrasubject variation. Tissue cholinesterase and histochemical staining were done to determine their suitability for testing cholinesterase compounds. Evaluation of the serum chemistry profile demonstrated increased CPK and LDH, which was likely associated with slight haemolysis or minor subclinical muscle stress during handling. There were no additional clinical chemistry changes or findings in haematology, urinalysis parameters or gross pathology. Micropathology found an absence of background lesions which would interfere with routine toxicology studies, except for a mild rhinitis. The aetiological agent was identified by electron microscopy as being consistent with inclusion body rhinitis of swine, previously unreported in miniature swine. This would most notably interfere with inhalation studies. The anatomical and physiological similarities of the Yucatan pig, along with its ability to accept the performance of electrophysiology tests allow this species to be considered as a suitable model for organ system testing in toxicology studies.

Motor power pharmacodynamics of subarachnoid hyperbaric 5% lidocaine in the sitting position.

BACKGROUND: Repetitive dynamometric measurement using a plantar flexion power device (PFPD) provides detailed data describing the onset and offset of motor block following spinal administration of lidocaine. The aim of this study was to evaluate administration of two doses of spinal lidocaine in the sitting position to determine whether our dynamometric model produces data consistent with our current understanding of the pharmacokinetics of subarachnoid, hyperbaric, 5% lidocaine. METHODS: Twenty male patients (54 to 80 yr) undergoing cystoscopy received spinal anaesthesia with either 75 mg (n = 10) or 100 mg of hyperbaric lidocaine 5%, in the sitting position, under standardised conditions. Plantar flexion muscle power was recorded during onset and offset of anaesthesia using a load cell interfaced with a computer (PFPD). RESULTS: Onset of paralysis following spinal block in the sitting position was rapid and complete with motor power declining exponentially to 5% of preoperative values by 8.5 min in all patients. There was no difference in decay or recovery of plantar flexion motor power data between dosage groups in the sitting position. Measurement using the PFPD shows that onset of motor paralysis is described by an exponential decay and that motor recovery occurs at a fixed rate. Extent of block to cold and pinprick was similar in both dosage groups in the sitting position (median T4). CONCLUSION: This study shows that in the sitting position, doses less than 75 mg of 5% hyperbaric lidocaine are required to significantly improve ambulatory times.

Method for screening drug and chemical effects in laboratory rats using computerized quantitative electroencephalography.

A minimally-invasive method of quantitative electroencephalography (qEEG) that requires no anesthetics and parallels techniques of naturalistic stimulation was developed and validated for regulatory testing of drugs and chemicals in rats. Male and female Fischer 344 rats were utilized in a randomized-block design to measure qEEG target parameters associated with a range of cholinesterase inhibition. For this study, physostigmine was administered ip at doses of 0.05, 0.2 or 1.0 mg/kg, resulting in average cholinesterase inhibition in plasma (28, 38 and 70%), erythrocytes (19, 24 and 36%), and brain (2, 10 and 31%) which correlated well with increased total power and amplitude changes. Additional treatment-related effects consisted of decreased relative alpha and beta, increased relative delta, and a left-shift in the spectral-edge frequency. In a second study, male and female Sprague-Dawley rats were utilized in a treatment-by-subjects design to determine qEEG target parameter changes due to the M2 autoreceptor agonist oxotremorine. Repeated incremental doses (0.05, 0.1, 0.2 mg/kg; ip) of oxotremorine resulted in increased beta contribution, a right-shift in the spectral-edge frequency and decreased alpha contribution. These qEEG results with physostigmine and oxotremorine correlate well with receptor-specific and general muscarinic effects, making it a reliable contribution to analysis of agonist and antagonist effects of cholinergic compounds.

Method for screening drug and chemical effects in laboratory rats using computerized quantitative electroencephalography.

A minimally-invasive method of quantitative electroencephalography (qEEG) that requires no anesthetics and parallels techniques of naturalistic stimulation was developed and validated for regulatory testing of drugs and chemicals in rats. Male and female Fischer 344 rats were utilized in a randomized-block design to measure qEEG target parameters associated with a range of cholinesterase inhibition. For this study, physostigmine was administered ip at doses of 0.05, 0.2 or 1.0 mg/kg, resulting in average cholinesterase inhibition in plasma (28, 38 and 70%), erythrocytes (19, 24 and 36%), and brain (2, 10 and 31%) which correlated well with increased total power and amplitude changes. Additional treatment-related effects consisted of decreased relative alpha and beta, increased relative delta, and a left-shift in the spectral-edge frequency. In a second study, male and female Sprague-Dawley rats were utilized in a treatment-by-subjects design to determine qEEG target parameter changes due to the M2 autoreceptor agonist oxotremorine. Repeated incremental doses (0.05, 0.1, 0.2 mg/kg; ip) of oxotremorine resulted in increased beta contribution, a right-shift in the spectral-edge frequency and decreased alpha contribution. These qEEG results with physostigmine and oxotremorine correlate well with receptor-specific and general muscarinic effects, making it a reliable contribution to analysis of agonist and antagonist effects of cholinergic compounds.

Epidemiology of brain tumours in man and their relationship with chemical agents.

The 2000 or so deaths that result each year in England and Wales from brain tumours, as defined by ICD 191, represent approximately 0.3-0.4% of all deaths, with a slightly greater incidence in men than in women. Because of the low incidence of mortality from other causes in childhood, brain cancer accounts for 3.5% of all deaths in the 1-14-year age group. Mortality from brain cancer increased considerably between 1931 and 1961 but this is probably explained by changes in disease classification and improvements in diagnostic techniques. Because of the relatively low incidence of brain cancer in man, cohort studies need to be large in order to accrue sufficient cases for meaningful interpretation. Large cohort studies may run the risk of diluting a high-risk group of workers with lesser or non-exposed individuals. These considerations have encouraged the investigation of brain cancer by case-control studies and the interpretation of these must take into account possible sources of bias. At present the evidence for any chemical causation of brain cancer in man is inconclusive.

Breath methane excretion in patients with unresected colorectal cancer.

The objective of our study was to verify or refute the observation that patients with unresected colorectal cancer are more likely to be breath methane excretors than the general population. Intracolonic heme had no effect on breath methane excretion of 11 normal volunteers given oral hemoglobin. Laxative-enema colonoscopy preparation had a profound effect on the subsequent measurement of breath methane. Three of 4 volunteer methane excretors became nonexcretors, and 2 remained nonexcretors for 21 days and 7 months, respectively. No significant difference was found in the frequency and the amount of breath methane excretion in 55 patients with unresected colorectal cancer and in 99 control subjects. However, 13 patients with unresected descending or sigmoid colon cancers were almost twice as likely to be breath methane excretors as 38 patients with colorectal cancer at other sites.