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Lilies are considered nephrotoxic only to domestic cats, which belong to the family Felidae of the suborder Feliformia. However, a 7-month-old female meerkat, belonging to the family Herpestidae of the suborder Feliformia, presented with oliguria, seizure, tachypnea, self-biting and nystagmus after it ingested lilies. The meerkat died approximately 40 hr after lily ingestion. Gross and histopathologic lesions consistent with acute renal failure were conspicuous in the animal. The renal lesions were acute tubular necrosis, corresponding to the typical pathological changes of lily toxicosis in cats. In addition, massive hepatocyte necrosis and pulmonary congestion/edema were observed. These findings suggest that lily toxicosis in meerkats is characterized by pulmonary and hepatic failure, in addition to the renal failure observed in domestic cats. [ABSTRACT FROM AUTHOR]

The article investigates the cause of severe diabetic peripheral motor neuropathy in spontaneously Wistar Bonn Kobori (WBN/Kob) rats. Topics discussed include the epidemiology of human diabetic peripheral neuropathy, the results of various test performed on the subject like motor nerve conduction velocity (MNCV) and morphological analysis, and the discovery of a significant amelioration of MNCV by insulin treatment through electrophysiological analysis.

Background: Atopic dermatitis (AD) is a common skin disease characterized by chronic recurrent eczematous lesions, but its exact etiology and mechanism are unclear. We found that beige rats (DAbg/bg), a mutant model of Chediak-Higashi syndrome, develop skin lesions characterized by pruritus, excoriation, erosion and alopecia. We describe the beige rat and examine its possible usefulness as an AD model. Methods: Beige rats of 4, 8, 13, 16, 26 and 52 weeks were used. Histological analysis of the skin was performed. Plasma IgE and cytokines were measured. Th1 and Th2 cytokines and RANTES mRNA expression of skin and lymph nodes were evaluated. Passive cutaneous anaphylaxis (PCA) reactions were examined, and maximization tests were conducted. Results: Skin lesions begin to develop with increases in serum IgE levels and the expression of IL-4 mRNA in the lymph node and skin. Histologically, skin lesions are characterized by acanthosis, ulceration and inflammatory cell infiltration in the dermis. Inflammatory cells consist of CD3+, CD4+, ED1+, ED2+ and I-A+ mononuclear cells, eosinophils, degranulated mast cells and neutrophils accompanying interleukin (IL)-4, interferon (IFN)-γ and RANTES mRNA expressions of the skin. Inflammatory cells are reduced during chronification with decreased expressions of IL-4, IFN-γ and RANTES mRNA. In addition, the rats show a high sensitivity to PCA reactions and maximization tests. Conclusions: Our results show that some of the skin lesions of beige rats are morphologically similar to human AD, being characterized by inflammatory cell composition in the acute phase, and increased IgE and RANTES levels. However, the inflammatory process and cytokine expression pattern are different from those in human AD. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Clinical and experimental research have suggested that dyslipidemia aggravates diabetic peripheral neuropathy (DPN). However, whether dyslipidemia is a risk factor for DPN remains unclear. To investigate the effect of dyslipidemia on DPN, morphological features of peripheral nerves were analyzed in diabetic rats treated with a high-fat diet (HFD). Male rats were divided into four groups: nondiabetic rats (N), alloxan-induced diabetic rats (AL), diabetic rats treated with an HFD (AH), and nondiabetic rats treated with an HFD (HF). Combined hyperglycemia and dyslipidemia (AH group) induced a significant increase in plasma triglyceride and cholesterol levels. In addition, the combined effects contributed to a reduction in myelin size and a reduction in myelin thickness as indicated on sensory sural nerve histograms. There was also a reduction in the size of motor nerve axons when compared with the effects of hyperglycemia or dyslipidemia alone. However, the sensory nerve conduction velocity in the AH group was slightly but not significantly lower than those in the HF and AL groups. These results suggest that combined hyperglycemia and dyslipidemia induced mild peripheral motor and sensory nerve lesions, without significantly affecting sensory nerve conduction velocity. [ABSTRACT FROM AUTHOR]

The relationship between hypertension and diabetic peripheral neuropathy (DPN) has recently been reported in clinical research, but it remains unclear whether hypertension is a risk factor for DPN. To investigate the effects of hypertension on DPN, we analyzed morphological features of peripheral nerves in diabetic rats with hypertension. Male WBN/Kob rats were divided into 2 groups: alloxan-induced diabetic rats with deoxycorticosterone acetate-salt (DOCA-salt) treatment (ADN group) and nondiabetic rats with DOCA-salt treatment (DN group). Sciatic, tibial (motor) and sural (sensory) nerves were subjected to qualitative and quantitative histomorphological analysis. Systolic blood pressure in the two groups exhibited a higher value (>140 mmHg), but there was no significant difference between the two groups. Endoneurial blood vessels in both groups presented endothelial hypertrophy and narrowing of the vascular lumen. Electron microscopically, duplication of basal lamina surrounding the endothelium and pericyte of the endoneurial vessels was observed, and this lesion appeared to be more frequent and severe in the ADN group than the DN group. Many nerve fibers of the ADN and DN groups showed an almost normal appearance, whereas morphometrical analysis of the tibial nerve showed a significant shift to smaller fiber and myelin sizes in the ADN group compared with DN group. In sural nerve, the fiber and axon-size significantly shifted to a smaller size in ADN group compared with the DN group. These results suggest that combined diabetes and hypertension could induce mild peripheral nerve lesions with vascular changes. [ABSTRACT FROM AUTHOR]