Introduction and objectives: Chlamydia (C.) felis can cause infection which may be associated with conjunctivitis and/or respiratory tract disease, particularly in kittens, but could also be the cause of the disease in adult cats. Infection is more common in multi-cat environments. The...

Breast cancer (BC) treatment efficacy is often compromised by tumor cell plasticity and multidrug resistance of multi-factorial origin. Among emerging therapeutic agents, flavonoids - a structurally diverse group of naturally occurring polyphenols - have demonstrated a significant potential to modulate the Janus kinase/signal transducer and activator of transcription (JAK-STAT) signaling pathway, a key driver of oncogenic transformation, immune evasion, and therapeutic failure in BC. Notably, natural compounds, including but not restricted to apigenin, quercetin, naringenin, morin, luteolin, butein, xanthohumol, silibinin, baicalein, nobiletin, rosmanol, orientin, eriocitrin, breviscapine, 8-hydroxydaidzein, icariside I, cardamonin, epigallocatechin-3-gallate, fisetin, brutieridin, melitidin, isoliquiritigenin, and sophoraflavanone G, have been recognized as potent JAK-STAT modulators in BC models. Through targeted interference with this pathway, flavonoids exert pleiotropic antitumor effects - enhancing the efficacy of chemotherapeutic agents, suppressing cellular proliferation and invasion, and reducing tumor aggressiveness. Beyond JAK-STAT signaling, flavonoids also influence several additional therapy resistance-related mechanisms, including regulation of ATP-binding cassette (ABC) transporters, promotion of apoptosis, suppression of epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs), cell cycle arrest, mitochondrial autophagy and mitophagy modulation, as well as remodeling of the tumor microenvironment. This article provides a comprehensive overview of the molecular mechanisms by which flavonoids overcome therapeutic resistance in BC, focusing on JAK-STAT signaling modulation. The paper follows principles of Predictive, Preventive, and Personalized Medicine (3PM), promoting the paradigm shift from reactive to proactive medicine. Contextually, it underscores the importance of multidisciplinary research to elucidate flavonoid-specific mechanisms, identify predictive biomarker panels, and develop advanced delivery systems, integrates patient phenotyping, multi-level diagnostics, and AI-driven data interpretation to enable cost-effective primary and secondary prevention, and therapeutic algorithms tailored to personalised patient profiles improving therefore individual outcomes.

The aim of the study was to investigate the potential of cell-based regenerative therapy for elbow joints affected by osteoarthritis. Interest was focused on two intra-articular applications of amnion-derived mesenchymal stem cells (A-MSCs) to a group of different breeds of dogs with elbow osteoarthritis (13 joints). Two injections were performed 14 days apart. We evaluated synovial fluid biomarkers, such as IFN-γ, IL-6, IL-15, IL-10, MCP-1, TNF-α, and GM-CSF, by multiplex fluorescent micro-bead immunoassay in the treated group of elbows (n = 13) (day 0, day 14, and day 28) and in the control group of elbows (n = 9). Kinematic gait analysis determined the joint range of motion (ROM) before and after each A-MSCs application. Kinematic gait analysis was performed on day 0, day 14, and day 28. Kinematic gait analysis pointed out improvement in the average range of motion of elbow joints from day 0 (38.45 ± 5.74°), day 14 (41.7 ± 6.04°), and day 28 (44.78 ± 4.69°) with statistical significance (p < 0.05) in nine elbows. Correlation analyses proved statistical significance (p < 0.05) in associations between ROM (day 0, day 14, and day 28) and IFN-γ, IL-6, IL-15, MCP-1, TNF-α, and GM-CSF concentrations (day 0, day 14, and day 28). IFN-γ, IL-6, IL-15, MCP-1, GM-CSF, and TNF- α showed negative correlation with ROM at day 0, day 14, and day 28, while IL-10 demonstrated positive correlation with ROM. As a consequence of A-MSC application to the elbow joint, we detected a statistically significant (p < 0.05) decrease in concentration levels between day 0 and day 28 for IFN-γ, IL-6, and TNF-α and statistically significant increase for IL-10. Statistical significance (p < 0.05) was detected in TNF-α, IFN-γ, and GM-CSF concentrations between day 14 and the control group as well as at day 28 and the control group. IL-6 concentrations showed statistical significance (p < 0.05) between day 14 and the control group.

This study compared the effects of butorphanol-medetomidine and butorphanol-dexmedetomidine combinations on echocardiographic parameters during propofol anaesthesia in dogs. The dogs were randomly divided into two groups. In the butorphanol-medetomidine (BM) group, butorphanol (0.2 mg/kg) and medetomidine (15 μg/kg) were intravenously administered; in the butorphanol-dexmedetomidine (BD) group, butorphanol (0.2 mg/kg) and dexmedetomidine (7.5 μg/kg) was used. Anaesthesia was induced with propofol and maintained with a constant-rate infusion of propofol (0.2 mg/kg/min). The echocardiographic parameters were assessed in conscious dogs (T₀). Echocardiography was conducted again at 10 min post premedication (T₁), followed by assessments at 30 (T₂), 60 (T₃), and 90 (T₄) mins. The dogs were subjected to diagnostic procedures (radiography, computed tomography) under anaesthesia. A significant reduction in heart rate and cardiac output was noted in both groups at T₁. There was no significant difference in the stroke volume between the BM and BD groups. The application of butorphanol-dexmedetomidine caused a significant increase in the left ventricular internal diameter in diastole and the diameter of the left atrium compared to that caused by butorphanol-medetomidine. This study documented that butorphanol-medetomidine and butorphanol-dexmedetomidine combinations caused similar reductions in heart rate and cardiac output in both groups. ‘New´ valvular regurgitation occurred following their administration.

Dry eye disease (DED) is a chronic debilitating ophthalmological disease with the current therapeutic options focused on the suppression of the symptoms. Among the possibilities of how to improve DED therapy, polyphenols have shown an enormous capacity to counteract DED functional changes. The study aimed to specifically target pathophysiological mechanisms by the addition of fisetin to the cyclosporine treatment protocol. We examined dog patients with DED on cyclosporine treatment that were administered 0.1% fisetin or fisetin-free eye drops. For the assessment of fisetin effects, tear film production and matrix metalloproteinase 9 (MMP-9) were studied in the tear film. Tear production was not recovered after 7 or 14 days (9.40 mm ± 6.02 mm, p = 0.47; 9.80 mm ± 6.83 mm, p = 0.53, respectively). MMP-9 levels significantly increased after 7 days and then dropped after 14 days (775.44 ng/mL ± 527.52 ng/mL, p = 0.05; 328.49 ng/mL ± 376.29 ng/mL, p = 1.00, respectively). Fisetin addition to cyclosporine DED treatment was not able to restore tear fluid production but influenced molecular pathological events through MMP-9.

The purpose of the study was to evaluate the occurrence and range of refractive errors in dogs of different ages. A total of 99 clinically healthy, mixed-breed mesocephalic dogs were included in the study and divided into three different age groups according to the current human/pet analogy chart: 40 adults (23 males, 17 females, 1–8 years old, 3–70 kg), 21 seniors (14 males, 7 females, 6–11 years old, 7–42 kg), and 38 geriatrics (22 males, 16 females, 8–13 years old, 5–45 kg). All the dogs underwent an ophthalmic examination, including Schirmer tear test, tonometry, biomicroscopy, and ophthalmoscopy. Neither eye drops nor pharmacological sedatives were administered before the autorefractometry. The refractive states were assessed bilaterally using a hand-held Retinomax 3 (Righton) autorefractor. The results underwent statistical analysis using Statistica v12 software (ANOVA and t-test). A P-value < 0.05 was considered as significant. Emmetropia, defined as a refractive state > −0.5 D and < +0.5 D, was found in 36% of the adult, 43% of the senior, and 38% of the geriatric patients. Anisometropia was found in 1% of the adult, 9.5% of the senior and 5.5% of the geriatric dogs when the refractive power of the two eyes differed ≥ 1.0 myopia ≤ −0.5 D and hyperopia ≥ +0.5 D were found in 23% and 41% of the adult eye globes as well as 24% and 33% in the senior dogs and 15% and 47% in the geriatric dogs, respectively. The maximal values of the myopia in the adult and geriatric dogs were −2.5 D and −2.75 D, respectively. The maximal values of the hyperopia in the adult and geriatric dogs were 1.75 D and 2.5 D, respectively. No statistically significant correlation was found between the groups. Ametropia is a common refractive state for dogs of different ages. The most frequent refractive state in ametropic mixed-bed dogs in all age groups is hyperopia.