Prostate cancer is the second most common cancer globally in men, and in some countries is now the most diagnosed form of cancer. It is necessary to differentiate between benign and malignant prostate conditions to give accurate diagnoses. We aim to demonstrate the use of a 3D Mueller matrix method to allow quick and easy clinical differentiation between prostate adenoma and carcinoma tissues with different grades and Gleason scores. Histological sections of benign and malignant prostate tumours, obtained by radical prostatectomy, were investigated. We map the degree of depolarisation in the different prostate tumour tissues using a Mueller matrix polarimeter set-up, based on the superposition of a reference laser beam with the interference pattern of the sample in the image plane. The depolarisation distributions can be directly related to the morphology of the biological tissues. The dependences of the magnitude of the 1st to 4th order statistical moments of the depolarisation distribution are determined, which characterise the distributions of the depolarisation values. To determine the diagnostic potential of the method three groups of histological sections of prostate tumour biopsies were formed. The first group contained 36 adenoma tissue samples, while the second contained 36 carcinoma tissue samples of a high grade (grade 4: poorly differentiated—4 + 4 Gleason score), and the third group contained 36 carcinoma tissue samples of a low grade (grade 1: moderately differentiated—3 + 3 Gleason score). Using the calculated values of the statistical moments, tumour tissues are categorised as either adenoma or carcinoma. A high level (> 90%) accuracy of differentiation between adenoma and carcinoma samples was achieved for each group. Differentiation between the high-grade and low-grade carcinoma samples was achieved with an accuracy of 87.5%. The results demonstrate that Mueller matrix mapping of the depolarisation distribution of prostate tumour tissues can accurately differentiate between adenoma and carcinoma, and between different grades of carcinoma. This represents a first step towards the implementation of 3D Mueller matrix mapping for clinical analysis and diagnosis of prostate tumours.

Abdominal aortic aneurysm (AAA) is a potentially life-threatening disorder with a mostly asymptomatic course where the abdominal aorta is weakened and bulged. Cytokines play especially important roles (both positive and negative) among the molecular actors of AAA development. All the inflammatory cascades, extracellular matrix degradation and vascular smooth muscle cell apoptosis are driven by cytokines. Previous studies emphasize an altered expression and a changed epigenetic regulation of key cytokines in AAA tissue samples. Such cytokines as IL-6, IL-10, IL-12, IL-17, IL-33, IL-1β, TGF-β, TNF-α, IFN-γ, and CXCL10 seem to be crucial in AAA pathogenesis. Some data obtained in animal studies show a protective function of IL-10, IL-33, and canonical TGF-β signaling, as well as a dual role of IL-4, IFN-γ and CXCL10, while TNF-α, IL-1β, IL-6, IL-12/IL-23, IL-17, CCR2, CXCR2, CXCR4 and the TGF-β noncanonical pathway are believed to aggravate the disease. Altogether data highlight significance of cytokines as informative markers and predictors of AAA. Pathologic serum/plasma concentrations of IL-1β, IL-2, IL-6, TNF-α, IL-10, IL-8, IL-17, IFN-γ, and PDGF have been already found in AAA patients. Some of the changes correlate with the size of aneurysms. Moreover, the risk of AAA is associated with polymorphic variants of genes encoding cytokines and their receptors: CCR2 (rs1799864), CCR5 (Delta-32), IL6 (rs1800796 and rs1800795), IL6R (rs12133641), IL10 (rs1800896), TGFB1 (rs1800469), TGFBR1 (rs1626340), TGFBR2 (rs1036095, rs4522809, rs1078985), and TNFA (rs1800629). Finally, 5 single-nucleotide polymorphisms in gene coding latent TGF-β-binding protein ( LTBP4) and an allelic variant of TGFB3 are related to a significantly slower AAA annual growth rate.

The impairments of cerebral blood flow microcirculation brought on by cardiac and respiratory arrest were assessed with multi‐modal diagnostic facilities, utilising laser speckle contrast imaging, fluorescence spectroscopy and diffuse reflectance spectroscopy. The results of laser speckle contrast imaging show a notable reduction of cerebral blood flow in small and medium size vessels during a few minutes of respiratory arrest, while the same effect was observed in large sinuses and their branches during the circulatory cessation. Concurrently, the redox ratio assessed with fluorescence spectroscopy indicates progressing hypoxia, NADH accumulation and increase of FAD consumption. The results of diffuse reflectance spectra measurements display a more rapid grow of the perfusion of deoxygenated blood in case of circulatory impairment. In addition, consequent histopathological analysis performed by using new tissue staining procedure developed in‐house. It shows notably higher reduction of size of the neurons due to their wrinkling within brain tissues influenced by circulation impair. Whereas, the brain tissues altered with the respiratory arrest demonstrate focal perivascular oedema and mild hypoxic changes of neuronal morphology. Thus, the study suggests that consequences of a cessation of cerebral blood flow become more dramatic and dangerous compare to respiratory arrest.