Background Approaches to the evaluation of pulmonary arterial hypertension (PAH) in premature calves by using lung-specific epithelial and endothelial biomarkers are needed. Objective To investigate the evaluation of PAH in premature calves with and without respiratory distress syndrome (RDS) by using lung-specific epithelial and endothelial biomarkers and determine the prognostic value of these markers in premature calves. Animals Fifty premature calves with RDS, 20 non-RDS premature calves, and 10 healthy term calves. Methods Hypoxia, hypercapnia, and tachypnea were considered criteria for RDS. Arterial blood gases (PaO₂, PaCO₂, oxygen saturation [SO₂], base excess [BE], and serum lactate concentration) were measured to assess hypoxia. Serum concentrations of lung-specific growth differentiation factor-15 (GDF-15), asymmetric dimethylarginine (ADMA), endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), and surfactant protein D (SP-D) were measured to assess PAH. Results Arterial blood pH, PaO₂, SO₂, and BE of premature calves with RDS were significantly lower and PaCO₂ and lactate concentrations higher compared to non-RDS premature and healthy calves. The ADMA and SP-D concentrations of premature calves with RDS were lower and serum ET-1 concentrations higher than those of non-RDS premature and healthy calves. No statistical differences for GDF-15 and VEGF were found among groups. Conclusions and Clinical Importance Significant increases in serum ET-1 concentrations and decreases in ADMA and SP-D concentrations highlight the utility of these markers in the diagnosis of PAH in premature calves with RDS. Also, we found that ET-1 was a reliable diagnostic and prognostic biomarker for PAH and predicting mortality in premature calves.

Canine parvoviral enteritis (PVE) is one of the most common diseases in young dogs. A range of diseases and inflammatory conditions can cause endothelial glycocalyx (eGCX) disruption, therefore, this study aimed to determine the presence of eGCX damage in dogs with PVE using serum biomarkers of eGCX, and to evaluate their prognostic importance among survivor and non-survivor dogs. Twenty dogs diagnosed with PVE and 10 healthy dogs of both sexes, mixed-breed, and under 6 months of age were included in the study. Clinical examination, blood gas analysis, and complete blood cell counts of the dogs were performed. To detect the eGCX injury, serum endothelial cell-specific molecule-1 (ESM-1), syndecan-1 (SDC-1), angiopoietin-2 (Ang-2), and heparan sulfate (HS) levels were measured. Results showed that at the time of admission serum levels of ESM-1 were higher in dogs with PVE compared to that of the healthy dogs. Dogs with PVE were further assigned into two groups: survivors (n:10) and non-survivors (n:10). The ESM-1 had high sensitivity and specificity to differentiate between survivor and non-survivor dogs with values of 100% and 67%, respectively, with at an optimum cut-off point of ≥460 pg/mL. We concluded that higher levels of ESM-1 in dogs with PVE may indicate eGCX injury when compared to healthy dogs. Also, the high levels of serum ESM-1 in non-survivor dogs suggest that serum ESM-1 may carry some prognostic usefulness for predicting mortality in dogs with PVE.

In this study, it was aimed to evaluate hematology, some clinical and biochemical parameters, as well as mineral levels in calves with neonatal sepsis caused by diarrhea. In this study, 30 calves that were 0-10 days old, who did not receive any treatment and who met the criteria for diarrhea and sepsis within 24 hours at the latest, constitute the sepsis group, and 20 healthy calves in the same age group constitute the control group. Venous blood samples were taken from calves with sepsis before treatment and once from healthy calves. The mean heart rate per minute and respiratory rate were determined higher in the group with sepsis than in the control group. In addition, neutrophil counts were found to be higher in the sepsis group compared to the control group. Erythrocyte count and mean erythrocyte volume were found to be low. While the levels of alanine aminotransferase, aspartate aminotransferase, urea and creatinine were statistically significantly higher in the group with sepsis compared to the control group, magnesium concentrations were lower (p

The purpose of the present study was to determine hypoxic brain damage in calves with perinatal asphyxia using brain-specific damage biomarkers. Ten healthy and 25 calves with perinatal asphyxia were enrolled in the study. Clinical examination, neurological status score, and laboratory analysis were performed at admission, 24, 48, and 72 h. Serum concentrations of ubiquitin carboxy-terminal hydrolysis 1 (UCHL1), calcium-binding protein B (S100B), adrenomodullin (ADM), activitin A (ACTA), neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP) and creatine kinase-brain (CK-B) were measured. Histopathological and immunohistochemical examinations of the brain tissue were performed in 13 nonsurvivor calves. The neurological status score of the calves with asphyxia was significantly (p < 0.05) lower. Mix metabolic-respiratory acidosis and hypoxemia were detected in calves with asphyxia. Serum UCHL1 and S100B were significantly (p < 0.05) increased, and NSE, ACTA, ADM, and CK-B were decreased (p < 0.05) in calves with asphyxia. Histopathological and immunohistochemical examinations confirmed the development of mild to severe hypoxic-ischemic encephalopathy. In conclusion, asphyxia and hypoxemia caused hypoxic-ischemic encephalopathy in perinatal calves. UCHL1 and S100B concentrations were found to be useful markers for the determination of hypoxic-ischemic encephalopathy in calves with perinatal asphyxia. Neurological status scores and some blood gas parameters were helpful in mortality prediction.