Despite the advancement of clinical and preclinical research on PCa, which resulted in the last five years in a decrement of disease incidence by 3-4%, it remains the most frequent cancer in men and the second for mortality rate. Based on this evidence we present a brief dissertation on numerous preclinical models, comparing their advantages and disadvantages; among this we report the PDX mouse models that show greater fidelity to the disease, in terms of histopathologic features of implanted tumor, gene and miRNA expression, and metastatic pattern, well describing all tumor progression stages; this characteristic encourages the translation of preclinical results. These models become particularly useful in meeting the need of new treatments identification that eradicate PCa bone metastases growing, clarifying pathway of angiogenesis, identifying castration-resistant stem-like cells, and studying the antiandrogen therapies. Also of considerable interest are the studies of 3D cell cultures derived from PDX, which have the ability to maintain PDX cell viability with continued native androgen receptor expression, also showing a differential sensitivity to drugs. 3D PDX PCa may represent a diagnostic platform for the rapid assessment of drugs and push personalized medicine. Today the development of preclinical models in vitro and in vivo is necessary in order to obtain increasingly reliable answers before reaching phase III of the drug discovery.

Coxiella burnetii is an obligate intracellular pathogen and the cause of Q fever in many animal species and humans. Several studies have reported the association between C. burnetii and abortion, premature delivery, stillbirth, and weak offspring. However, no solid evidence indicates that C. burnetii causes endometritis, subfertility, and retained fetal membranes. For this study, histopathological and PCR evaluation were performed on 40 uterine biopsies from dairy cattle with poor fertility. Uterine swabs were concurrently tested with microbiology assays. The endometrial biopsies of 30 cows did not have any significant lesions, and no pathogens were identified by aerobic bacterial culture and PCR. Ten cows were PCR-positive for C. burnetii and negative for other pathogens by aerobic bacterial culture and PCR. These 10 cases revealed a mild to severe chronic endometritis admixed with perivascular and periglandular fibrosis. Immunohistochemical evaluation of C. burnetii PCR-positive biopsies identified, for the first time, the presence of intralesional and intracytoplasmic C. burnetii in macrophages in the endometrium of cattle.

Recent evidence highlights Parkinson’s disease (PD) initiation in the gut as the prodromal phase of neurodegeneration. Gut impairment due to microbial dysbiosis could affect PD pathogenesis and progression. Here, we propose a two-hit model of PD through ceftriaxone (CFX)-induced dysbiosis and gut inflammation before the 6-hydroxydopamine (6-OHDA) intrastriatal injection to mimic dysfunctional gut-associated mechanisms preceding PD onset. Therefore, we showed that dysbiosis and gut damage amplified PD progression, worsening motor deficits induced by 6-OHDA up to 14 days post intrastriatal injection. This effect was accompanied by a significant increase in neuronal dopaminergic loss (reduced tyrosine hydroxylase expression and increased Bcl-2/Bax ratio). Notably, CFX pretreatment also enhanced systemic and colon inflammation of dual-hit subjected mice. The exacerbated inflammatory response ran in tandem with a worsening of colonic architecture and gut microbiota perturbation. Finally, we demonstrated the beneficial effect of post-biotic sodium butyrate in limiting at once motor deficits, neuroinflammation, and colon damage and re-shaping microbiota composition in this novel dual-hit model of PD. Taken together, the bidirectional communication of the microbiota–gut–brain axis and the recapitulation of PD prodromal/pathogenic features make this new paradigm a useful tool for testing or repurposing new multi-target compounds in the treatment of PD.

The detection of diatoms into the organs is considered an important “biological marker” for the diagnosis of drowning in human pathology, but it still has a high possibility for false positive results. The aims of this study were: (1) to evaluate the contribution of pathological examination in drowning cases and (2) to investigate the differences in the number and location of diatoms between animals who died in drowning and non-drowning conditions. For these purposes, 30 dead adult dogs were selected for the study and subdivided into five groups. The group A comprised six cadavers dead for drowning; the group B comprised six control animals; the groups C, D, and E comprised six animals dead for causes other than drowning and subsequently immersed in water for 24, 48, and 72 h, respectively. On each animal, a complete macroscopic and histological examination and diatom test were performed. Diatoms test and quantification were also performed on drowning mediums. Pathological findings of the animals in the group A showed pulmonary congestion, oedema, and hemorrages in the lung. However, similar injuries were also observed in control and experimentally submerged cadavers. In contrast, we observed a statistically differences between drowning animals and all experimentally submerged groups and control animals regarding diatom numbers recovered from organ tissue samples (p < 0.05). Therefore, these findings suggest that the number of diatoms may be used as a valid tool to differentiate animals who died in drowning and non-drowning conditions, even if the latter were found in an aquatic environment.

White striping (WS) is an emerging myopathy of broiler chickens characterized by white striation of muscle. Despite the recent advances, the pathomechanism underlying the WS remains elusive. The aim of this study was to characterize morphological and molecular features of WS in broiler chickens. 50 pectoralis muscles were collected from 55 days old ROSS 308 broiler chickens with a mean weight of 3.5 kg. Samples were snap frozen and analyzed by histopathology, immunohistochemistry, and immunofluorescence. Real-time-PCR was used to evaluate the expression of different cytokines. Histological lesions were observed in all examined animals, both with and without macroscopic evidence of WS. WS muscles showed endomysial and perivascular inflammatory infiltrates of macrophages and cluster of differentiation (CD)8-positive T lymphocytes with severe myofiber atrophy, necrosis, fibrosis and replacement by adipose tissue. There was diffuse sarcoplasmic and sarcolemmal overexpression of the major histocompatibility complex class I (MHC I). The severity of the histologic lesions was positively correlated with the macroscopic degree of white striations. IL-6, IL-17 and lipopolysaccharide-induced TNF-α factor (LITAF) were overexpressed in severe lesions of WS. The presence of the CD8/MHC I complexes, together with the higher expression of IL-6, IL-17 and LITAF in severe degree of WS, suggest that the immune response may be involved in the progression of this myopathy and can be consistent with a hypoxia-induced inflammatory myopathy. These results help to understand the pathomechanism of WS contributing to the reduction of economic losses and improving poultry welfare.