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Objective: To present the clinical signs and treatment methods for atypical tumor‐like meibomitis in two dogs. Animals Studied: A 4‐year‐old castrated‐male Coton de Tulear (Case 1) and a 6‐year‐old spayed‐female Maltese dog (Case 2). Procedure: Full ophthalmic examination revealed a well‐circumscribed, firm, and raised solitary mass on the upper eyelid of the left (Case 1) and right eye (Case 2). Case 1 showed a recurrent mass with a diameter of 2–3 mm, which was excised by the referring veterinarian. The possibility of meibomian gland involvement was suggested histopathologically. Case 2 had a history of blepharitis treated with systemic corticosteroids 4 years ago. Results: Topical and systemic antibiotics and anti‐inflammatory drugs were administered to reduce inflammation and prevent secondary infections. In Case 1, the mass appeared static at the beginning of medication; however, after stopping antibiotics while tapering steroids, the mass increased in size and was associated with suppurative discharge. In Case 2, the mass continued to grow despite treatment, showing a similar infection pattern. Cytological examination revealed neutrophilic inflammation with cocci infection, and bacterial culture confirmed the presence of Staphylococcus pseudintermedius in both cases. When steroid administration was stopped and antibiotic administration was initiated according to the results of the antibiotic susceptibility test, the mass rapidly decreased in size and completely disappeared. There was no recurrence on follow‐up. Conclusions: A unilateral antibiotic‐responsive tumor‐like solitary mass on the upper eyelid resolved without surgical treatment. Medical treatment must be considered when treating atypical eyelid masses, and the use of appropriate antibiotics through antibiotic susceptibility testing is important. [ABSTRACT FROM AUTHOR]

Background: Evaluating regeneration is essential for the classification and differential diagnosis of anemia in dogs. Early detection of regeneration is challenging in anemic dogs. Objectives: This study assessed the value of immature reticulocyte fraction (IRF) in differentiating preregenerative anemia (PRA) from nonregenerative anemia (NRA) in dogs. Animals: Ninety‐four dogs: 49 controls and 45 with anemia. Methods: Case‐control study. Fractions of low‐, medium‐ (MFR), and high‐fluorescence reticulocytes (HFR), were measured using the ADVIA 2120i hematology analyzer. The IRF was calculated as the sum of percentages of MFR and HFR. Data from dogs with regenerative anemia (RA, n = 19), PRA (n = 11), and NRA (n = 15) were retrospectively analyzed. The value of IRF was compared with reticulocyte production index (RPI) using the receiver operating characteristic (ROC) curve. Results: The median of IRF was significantly higher in dogs with RA (46.5%; range, 40.9‐53.6%; P <.001) and PRA (40.6%; range, 27.7‐47.1%; P =.01) than in controls (22.1%; range, 16.9‐29.3%). The IRF in dogs with PRA showed no difference compared to dogs with RA (P >.99) but was higher than dogs with NRA (18.7%; range, 8.8‐24%; P =.00). The area under the ROC curve of IRF was superior to that of RPI (0.897 vs 0.818, P =.00) in differentiating dogs with PRA from NRA. Conclusions and Clinical Importance: The IRF is a reliable variable for detecting early regeneration in anemic dogs without reticulocytosis. The study suggests that the measurement of IRF could be useful in classifying anemic dogs. [ABSTRACT FROM AUTHOR]

Background: Serum uromodulin concentration has been described as a novel biomarker of chronic kidney disease (CKD) in humans but not dogs. Objective: To evaluate the serum uromodulin concentration in dogs with CKD and assess its diagnostic performance in distinguishing dogs with CKD from healthy dogs. Animals: Forty‐nine dogs with CKD (International Renal Interest Society [IRIS] Stage 1, n = 23; Stage 2, n = 20; Stage 3‐4, n = 6) and 25 healthy controls. Methods: Prospective, observational study. Serum uromodulin concentration was measured using a canine‐specific enzyme‐linked immunosorbent assay (ELISA), and its correlation with conventional renal markers was analyzed. Results: Serum uromodulin concentrations were significantly lower in the CKD group than in the control group (P <.001), but no significant difference was observed among stages of CKD. A negative correlation was observed between serum uromodulin concentration and conventional renal markers (blood urea nitrogen concentration, r = −.60, P <.0001; serum creatinine concentration, r = −.46, P <.0001; serum symmetric dimethylarginine concentration [SDMA], r = −.65, P <.0001). In receiver operating characteristic analysis, the area under the curve (AUC) of uromodulin (AUC, 0.97; 95% confidence interval [CI], 0.94‐1.00) was higher than that of SDMA (AUC, 0.87; 95% CI, 0.79‐0.95) for CKD diagnosis (P =.01). The AUC of uromodulin (AUC, 0.95; 95% CI, 0.89‐1.00) also was higher than that of SDMA (AUC, 0.72; 95% CI, 0.58‐0.87) in distinguishing dogs with Stage 1 CKD from controls (P =.001). Conclusions and Clinical Importance: Serum uromodulin concentration is decreased in dogs with CKD. Thus, serum uromodulin may be a valuable diagnostic marker for CKD in dogs, particularly in identifying early‐stage CKD. [ABSTRACT FROM AUTHOR]

Metformin, a drug for type 2 diabetes mellitus, has shown therapeutic effects for various cancers. However, it had no beneficial effects on the survival rate of human malignant mesothelioma (HMM) patients. The present study was performed to elucidate the underlying mechanism of metformin resistance in HMM cells. Glucose‐starved HMM cells had enhanced resistance to metformin, demonstrated by decreased apoptosis and autophagy and increased cell survival. These cells showed abnormalities in mitochondria, such as decreased ATP synthesis, morphological elongation, altered mitochondrial permeability transition pore and hyperpolarization of mitochondrial membrane potential (MMP). Intriguingly, Mdr1 was significantly upregulated in mitochondria but not in cell membrane. The upregulated mitochondrial Mdr1 was reversed by treatment with carbonyl cyanide m‐chlorophenyl hydrazone, an MMP depolarization inducer. Furthermore, apoptosis and autophagy were increased in multidrug resistance protein 1 knockout HMM cells cultured under glucose starvation with metformin treatment. The data suggest that mitochondrial Mdr1 plays a critical role in the chemoresistance to metformin in HMM cells, which could be a potential target for improving its therapeutic efficacy. This study illustrated that glucose‐deficient conditions facilitated resistance to metformin in human malignant mesothelioma (HMM) cells through Mdr1 increasing in defected mitochondria. It also increased through mitochondrial membrane potential hyperpolarization and mitochondrial dysfunction rescued glucose‐starved HMM cells as a result of metformin treatment. [ABSTRACT FROM AUTHOR]