BackgroundAlthough there is serologic evidence of exposure of cats to Leptospira spp., clinical disease is rarely reported in cats.ObjectiveTo compare the seropositivity and urinary polymerase chain reaction (PCR) status for Leptospira spp. between healthy (H) cats and cats with kidney disease (KD), to investigate the serovars potentially involved, and to evaluate potential risk factors.AnimalsTwo hundred and forty client‐owned cats.MethodsCats were prospectively recruited and classified based on physical examination, complete blood count, serum biochemistry profile, and urinalysis (125 H and 115 KD cats). Leptospira spp. serology (titers ≥1 : 100 considered positive) and urinary PCR were performed in all cats. Data assessing risk factors, obtained from a questionnaire, were evaluated using logistic regression models.ResultsSeropositivity for Leptospira spp. was statistically different between groups: 7.2% (9/125) and 14.9% (17/114) in the H and KD, respectively (P = .05). The proportion of PCR‐positive cats was not. The most common serovars detected serologically were Pomona (n = 16) and Bratislava (n = 8). Risk factors for seropositivity included outdoor and hunting lifestyles (P = .03 and P < .001, respectively), the presence of another cat in the household (P < .01), and the sampling period, with the greatest number of cases identified between June and August (P =.02).ConclusionsSeropositivity was significantly greater in KD cats, suggesting that the role of Leptospira spp. in KD in cats should be further investigated. The detection of urinary shedding of leptospires in several cats identifies a potential role in the transmission of the organism.

Background:The spinocerebellar ataxia type 1 (SCA1) gene encoding ataxin-1 (ATXN1) contains an alternative open reading frame overlapping the ATXN1 coding sequence. Results: The alternative ATXN1 protein is constitutively co-expressed and interacts with ATXN1 N terminus. Alternative ATXN1 is also an RNA binding protein. Conclusion:ATXN1 is a genuine dual coding gene. Significance: Alternative ATXN1 may regulate the function of ATXN1 in physiological and pathological conditions.

Highlights d The cen and ik2 cis-NAT mRNAs co-localize to centrosomes in Drosophila embryos d Loss of cen disrupts ik2 centrosomal localization, revealing a targeting co-dependency d Centrosomal co-localization requires interactions between the 3 0 UTRs of cen and ik2 d Subcellular fractionation data reveal that cis-NATs often localize to similar sites

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Background: Hyperthyroid cats are at risk of developing azotemic chronic kidney disease (CKD) and diagnostic tools currently used to screen for CKD in hyperthyroid cats are either unreliable or impractical.Hypothesis: Urine N-acetyl-b-D-glucosaminidase index (NAG i ) is a good biomarker for azotemic CKD in hyperthyroid cats.Animals: Twenty-four newly diagnosed nonazotemic hyperthyroid cats and 10 healthy cats. Methods: All cats were evaluated for hyperthyroidism at baseline. Hyperthyroid cats were treated with methimazole and reevaluated once euthyroid. At the end of the study, cats were divided into 3 groups: healthy cats, nonazotemic, and azotemic euthyroid cats. Baseline group characteristics were compared to predict azotemic CKD. The influence of treatment on NAG i was evaluated.Results: Baseline NAG i was significantly different among groups (P 5 .004). Azotemic cats had a higher median value (13.12 U/g) when compared with healthy cats (1.38 U/g). With NAG i 42.76 U/g, negative and positive predictive values for development of azotemia were 77.7 and 50%, whereas the combination of a urine specific gravity (USG) 1.035 and T 4 47.80 mg/dL enhanced predictive values to 88.9 and 83.3%, respectively. NAG i values decreased significantly over time in treated nonazotemic cats.Conclusions and Clinical Relevance: Baseline NAG i did not differentiate azotemic from nonazotemic euthyroid cats. NAG i could be used to assess renal function during medical therapy allowing the clinician to adjust methimazole dosage accordingly. The combination of USG and T 4 could optimize identification of appropriate candidates for permanent treatment of hyperthyroidism.

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Experimental autoimmune encephalomyelitis (EAE) is a mouse model that reproduces cardinal signs of clinical, histopathological, and immunological features found in Multiple Sclerosis (MS). Mast cells are suggested to be involved in the main inflammatory phases occurring during EAE development, possibly by secreting several autacoids and proteases. Among the latter, the chymase mouse mast cell protease 4 (mMCP-4) can contribute to the inflammatory response by producing endothelin-1 (ET-1). The aim of this study was to determine the impact of mMCP-4 on acute inflammatory stages in EAE. C57BL/6 wild type (WT) or mMCP-4 knockout (KO) mice were immunized with MOG35–55 plus complete Freund's adjuvant followed by pertussis toxin. Immunized WT mice presented an initial acute phase characterized by progressive increases in clinical score, which were significantly reduced in mMCP-4 KO mice. In addition, higher levels of spinal myelin were found in mMCP-4 KO as compared with WT mice. Finally, whereas EAE triggered significant increases in brain levels of mMCP-4 mRNA and immunoreactive ET-1 in WT mice, the latter peptide was reduced to basal levels in mMCP-4 KO congeners. Together, the present study supports a role for mMCP-4 in the early inflammatory phases of the disease in a mouse model of MS.

Background Lymphedema is due to dysfunction of the lymphatic system. It can be primary or secondary. Pediatric lymphedema is more often primary and is a chronic disease with a heavy burden on quality of life. Methods Medical records of patients under 18 years of age referred between 1996 and 2021 to the specialized lymphedema clinic at the Sainte-Justine University Hospital Center were reviewed. Demographic data, sex, age at presentation, location of the lymphedema, clinical features, genetic testing, symptoms, complications, investigations, and treatment were collected. Results Of 180 referred patients, lymphedema was confirmed in 151, and 137 were primary lymphedema. Median age of apparition of primary lymphedema was 7.00 years and was significantly lower in boys than in girls. Primary congenital lymphedema was more frequent in boys (51.0%, 27.3% in girls, P = .007), and onset of primary lymphedema during adolescence was more frequent in girls (53.4%, 25.0% in boys, P = .001). Lower limbs were the most impacted (88.3%). Sixty patients had genetic testing, and 38 (63.3%) of them were discovered to have a pertinent genetic mutation. The most common mutated gene was the FLT4 gene (in 9 patients). Seven patients (5.1%) had associated extensive/central lymphatic malformation and 24 (17.6%) had a polymalformative syndrome/syndromic lymphedema. Conclusions Pediatric lymphedema is more frequent in girls, usually involves lower limb, and is most often sporadic, but often associated with a genetic mutation, and genetic testing should be performed.