Effective long-term management of urolithiasis depends on identification and manipulation of factors contributing to initial stone formation; identification of these factors depends on accurate identification of the mineral composition of the urolith involved. The purpose of this study was to determine the chemical composition of uroliths obtained from the low urinary tract of dogs in Mexico City. One hundred and five cases of urolithiasis were studied in which stones were surgically obtained from the low urinary tracts of dogs treated in different hospitals. The chemical composition of the uroliths was quantitatively and qualitatively determined by stereoscopic microscopy, IR-spectroscopy, scanning electron microscopy and X-ray microanalysis. Age of animals ranged from 4 months to 14 years, with a median of 5 years. Composition and distribution of the uroliths were struvite 38.1%, calcium oxalate 26.7%, silica 13.3%, urate 7.6%, mixed 11.4%, compounds 1.9%, and cystine 1%. Most uroliths were found in pure breed dogs (75.2%); 23 different breeds were identified, and more than half of the submissions were from breeds of small size. In our study, the frequency of struvite, calcium oxalate, cystine, urates, mixed and compounds stones are in agreement with papers that report on dog populations in America and Europe, but a higher frequency of silica uroliths was observed in Mexico City dogs.

The unfolded protein response (UPR) in the hippocampal regions Cornu Ammonis 1 hippocampal region, Cornu Ammonis 3 hippocampal region, and dentate gyrus, as well as in the cerebral cortex of 3-month-old and 18-month-old rats were studied in a model of 15 min of global cerebral ischemia followed by 48 h of reperfusion. UPR was measured by quantifying the protein disulfide isomerase (PDI), C/EBPhomologous protein (CHOP), GRP78 and GRP94 transcripts using qPCR and the amounts of PDI and GRP78 by western blot. The study shows how the mRNA levels of these genes were similar in 3-month-old and 18-month-old sham-operated animals, but the ischemic insult elicited a noticeable increase in the expression of these genes in young animals that was scarcely appreciable in older animals. The striking increase in the mRNA levels of these genes in 3-month-old animals was abolished or even reverted by treatment with meloxicam, an anti-inflammatory agent. Western blot assays showed that the UPR was still detectable 48 h after ischemia in some of the studied areas, and provided evidence that the UPR is different between young and older animals. Western blot assays carried out in young animals also showed that meloxicam elicited different effects on the levels of PDI and GRP78 in the cerebral cortex and the hippocampus. We conclude that the UPR response to ischemic/reperfusion insult is age-and probably inflammation-dependent and could play an important role in ischemic vulnerability. The UPR appears to be strongly decreased in aged animals, suggesting a reduced ability for cell survival.

We conclude that OGD induces a rapid autophagic response in the cerebral cortex that plays a neuroprotective role. Polyubiquitination levels and control of the glutamate release appear to be involved in the neuroprotective role of autophagy.

Our data suggest that changes in the AMPAR isoforms could be associated with ageing in the different structures studied. Although GluR2 editing seems to be involved in age-dependent vulnerability to ischaemia supporting the 'GluR2 hypothesis', this alone does not explain the differential vulnerability in the different brain regions. Finally, inflammation could play a role in protection from I/R-induced injury.

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