Manipulating ruminal fermentation: a microbial ecological perspective

The essential role of ruminal microflora in ruminant nutrition provides the potential for improvement in animal production via altering the numbers or activities of specific classes of microorganisms. Successful alterations will be facilitated by an understanding of the microbial ecology of the rumen based on its mechanistic underpinnings. Demonstrated improvements in ruminal fermentation can be traced to their consonance with well-established principles of microbial ecology (niche occupancy, selective pressure, adaptation, and interactions) and the thermodynamics and kinetics of substrate utilization. Application of these principles to several proposed alterations of the ruminal bacterial population allows a prediction of their relative feasibility. Improving fiber digestion, decreasing protein degradation, and detoxifying feed components that are present in low concentrations will be difficult to achieve in the rumen and are best approached by altering the feed, either genetically or with postharvest treatment. By contrast, the detoxification of feed components present in high concentration, and redirection of electron disposal away from methanogenesis, are more productive targets for microbiological research.     

Primary extranodal non-Hodgkin lymphoma of the oral cavity. An analysis of 34 cases

A case of macroglossia and resulting apertognathia because of primary amyloidosis in a 65-year-old man with multiple myeloma is described. In addition, a retrospective study of the oral manifestations of primary amyloidosis and multiple myeloma in the last 15 years is reported.     

Chronic tonsillitis

1. Maintenance of phosphate homeostasis is essential for energy producing and oxygen delivery systems, particularly, when the energy requirements are increased in certain conditions, such as septicaemia. We investigated the phosphaturic response to parathyroid hormone (PTH) in endotoxin (ETx)-treated rats in order to clarify the renal regulation of phosphate excretion during endotoxaemia. 2. Wistar rats that had undergone thyroparathyroidectomy were challenged with either Escherichia coli ETx (n = 8) or saline vehicle (n = 9). Thirty-minute renal clearance tests were done before and after PTH infusion. Rats infused with saline instead of PTH served as time controls for the ETx- (n = 7) and saline-treated (n = 8) rats. 3. In time control rats, ETx administration enhanced phosphate excretion progressively and this was associated with an obvious increase in the level of kidney adenosine 3', 5'-cyclic mono-phosphate (P < 0.005) compared with levels following saline vehicle administration. However, this phosphaturia in late-phase endotoxaemia was not observed in rats infused with PTH; ETx, but not saline vehicle, blunted the PTH-mediated increase in phosphate excretion (P < 0.005). Increased urinary noradrenaline and constant dopamine excretion were observed in endotoxaemic rats. Endotoxin administration produced marked metabolic acidosis and hypocapnia in comparison with the administration of the saline vehicle. 4. To test whether renal tubular sensitivity to parathyroid hormone related-protein (PTHrP) was enhanced during endotoxaemia, phosphaturic response to PTHrP in ETx- (n = 7) and saline-treated rats (n = 7) was examined. Parathyroid hormone related-protein infusion produced phosphaturia in both groups. However, the severity of the phosphaturia after PTHrP infusion was less in ETx-than in saline-treated rats. 5. In summary, although ETx administration causes a progressive increase in phosphate excretion in the absence of PTH, this is overcome by the antiphosphaturic effect of ETx, attenuating PTH-mediated phosphaturia after PTH infusion.     

Corneal toxicity study of two perfluorocarbon liquids in rabbit eyes

Perfluorocarbon liquids are fully fluorinated, synthetic, transparent compounds with a high specific gravity. These compounds are being increasingly used as an intraoperative tool for repair of complicated retinal detachments. A potential complication of their use, however, is liquid entering the anterior chamber in aphakic patients. In the study described herein we evaluated the effects of two of these liquids when placed in the anterior chamber of the rabbit eye. Sixteen rabbit eyes underwent anterior chamber injection of 0.05 ml of either perfluoroctane, perfluoropolyether, or balanced salt solution (control eyes). Animals were monitored clinically by biomicroscopy and external photography for up to 14 days, after which they were sacrificed and the corneas processed for light and for scanning electron microscopy. The animals injected with perfluoropolyether showed more intense stromal inflammation and corneal vascularization (p less than 0.02) than did those that received perfluoroctane. However, the perfluoroctane group showed more of the "fish-egging" phenomenon (p less than 0.03). Loss of endothelial cells was similar in the two groups, as determined by light and scanning electron microscopy. These results suggest that the corneal toxicity of these two perfluorocarbon liquids is such that their use as vitreous substitutes should be limited to short-term replacement.     

Proliferation of gemistocytic cells and glial fibrillary acidic protein (GFAP)-positive oligodendroglial cells in gliomas: a MIB-1/GFAP double labeling study

Affinity chromatography using different lytic transglycosylases as a specific ligand revealed an interaction of both murein hydrolases and murein synthases. This interaction is taken as evidence for the assemblage into a multienzyme complex that could function as a murein replicase precisely copying the given three-dimensional structure of the murein sacculus. The sacculus of the mother cell would function as a template, which is identically replicated by copying the lengths of the existing glycan strands and the pattern of crosslinkages. A hypothetical enzyme complex specifically involved in cell division and a complex specifically involved in cell elongation are presented. It is postulated that PBPs 1a and/or 1b are present in both complexes, whereas the presence of PBP2 or PBP3 defines the specificity of the murein-synthesizing machinery as being involved in either cell elongation or septation. Moreover, the proposed "holoenzyme" suprastructure could explain why the specific inhibition of PBPs 1a/1b results in bacteriolysis and why inhibition of PBP2 and PBP3 causes the well-known morphological alterations, spherical growth, and filamentation, respectively.     

Carboxylic ester hydrolase and amylase in ischemic pancreatitis in the guinea pig

OBJECTIVES: To define the clinical, neuropsychological, and radiological features of bilateral parietal lobe atrophy. METHODS: Four patients underwent a comprehensive longitudinal neuropsychological assessment, as well as MRI and HMPAO-SPECT. RESULTS: The consistent findings in the patients were early visuospatial problems, agraphia of a predominantly peripheral (or apraxic) type, and difficulty with bimanual tasks, all of which outweighted deficits in memory and language until later in the course of the illness. As the disease progressed, impairments in the phonological aspects of language and in auditory-verbal short term memory were often striking, perhaps reflecting spread from the parietal lobe to perisylvian language areas. Three patients went on to develop a global dementia and fulfilled the criteria for a clinical diagnosis of probable Alzheimer's disease; the fourth patient has only recently been identified. Neuroimaging disclosed bilateral parietal lobe atrophy (MRI) and hypoperfusion (SPECT), which was out of proportion to that seen elsewhere in the brain. One patient has died and had pathologically confirmed Alzheimer's disease with particular concentration in both superior parietal lobes. CONCLUSIONS: Bilateral biparietal atrophy is a recognisable clinical syndrome which can be the presenting feature of Alzheimer's disease. Although the label "posterior cortical atrophy" has been applied to such cases, review of the medical literature suggests that this broad rubric actually consists of two main clinical syndromes with features reflecting involvement of the occipitotemporal (ventral) and biparietal (dorsal) cortical areas respectively.