Stimulated Raman Histology Interpretation by Artificial Intelligence Provides Near-Real-Time Pathologic Feedback for Unprocessed Prostate Biopsies.

PURPOSE: Stimulated Raman histology is an innovative technology that generates real-time, high-resolution microscopic images of unprocessed tissue, significantly reducing prostate biopsy interpretation time. This study aims to evaluate the ability for an artificial intelligence convolutional neural network to interpretate prostate biopsy histologic images created with stimulated Raman histology. MATERIALS AND METHODS: Unprocessed, unlabeled prostate biopsies were prospectively imaged using a stimulated Raman histology microscope. Following stimulated Raman histology creation, the cores underwent standard pathological processing and interpretation by at least 2 genitourinary pathologists to establish a ground truth assessment. A network, trained on 303 prostate biopsies from 100 participants, was used to measure the accuracy, sensitivity, and specificity of detecting prostate cancer on stimulated Raman histology relative to conventional pathology. The performance of the artificial intelligence was evaluated on an independent 113-biopsy test set. RESULTS: Prostate biopsy images obtained through stimulated Raman histology can be generated within a time frame of 2 to 2.75 minutes. The artificial intelligence system achieved a rapid classification of prostate biopsies with cancer, with a potential identification time of approximately 1 minute. The artificial intelligence demonstrated an impressive accuracy of 96.5% in detecting prostate cancer. Moreover, the artificial intelligence exhibited a sensitivity of 96.3% and a specificity of 96.6%. CONCLUSIONS: Stimulated Raman histology generates microscopic images capable of accurately identifying prostate cancer in real time, without the need for sectioning or tissue processing. These images can be interpreted by artificial intelligence, providing physicians with near-real-time pathological feedback during the diagnosis or treatment of prostate cancer.

Impact of non-Legionella bacteria on the uptake and intracellular replication of Legionella pneumophila in Acanthamoeba castellanii and Naegleria lovaniensis.

In aquatic environments, Legionella pneumophila survives, in association with other bacteria, within biofilms by multiplying in free-living amoebae. The precise mechanisms underlying several aspects of the uptake and intracellular replication of L. pneumophila in amoebae, especially in the presence of other bacteria, remain unknown. In the present study, we examined the competitive effect of selected non-Legionella bacteria (Escherichia coli, Aeromonas hydrophila, Flavobacterium breve, and Pseudomonas aeruginosa) on the uptake of L. pneumophila serogroup 1 by the amoebae Acanthamoeba castellanii and Naegleria lovaniensis. We also investigated their possible influence on the intracellular replication of L. pneumophila in both amoeba species. Our results showed that the non-Legionella bacteria did not compete with L. pneumophila for uptake, suggesting that the amoeba hosts took in L. pneumophila through a specific and presumably highly efficient uptake mechanism. Living and heat-inactivated P. aeruginosa best supported the replication of L. pneumophila in N. lovaniensis and A. castellanii, respectively, whereas for both amoeba species, E. coli yielded the lowest number of replicated L. pneumophila. Furthermore, microscopic examination showed that 100% of the A. castellanii and only 2% of the N. lovaniensis population were infected with L. pneumophila at the end of the experiment. This study clearly shows the influence of some non-Legionella bacteria on the intracellular replication of L. pneumophila in A. castellanii and N. lovaniensis. It also demonstrates the different abilities of the two tested amoeba species to serve as a proper host for the replication and distribution of the human pathogen in man-made aquatic environments such as cooling towers, shower heads, and air conditioning systems with potential serious consequences for human health.

D-myo-inositol derivatives alter liposomal membrane fluidity.

We investigated the effect on membrane fluidity induced by D-myo-inositol derivatives (IP3, IP4, IP5, IP6). Fluidity was determined as the anisotropy of fluorescence polarisation from liposome model membranes labelled with DPH (1,6-diphenyl-1,3,5 hexatriene). IP3 (10(-10) to 10(-5) M) increased the membrane fluidity with a maximum effect at 10(-5) M. For IP4, IP5 and IP6, at concentrations less than 10(-6) M these derivatives increased the membrane viscosity (i.e. reduced fluidity). This effect was enhanced when the derivatives were incorporated in the vesicles, rather than added to the vesicle suspension. In this case IP5 and IP6 increased viscosity over the reference values. We conclude that inositol derivatives directly modified membrane fluidity which could play a role in their effects in biological systems, beside the one mediated by binding to specific receptors.

Angiotensin II and related peptides alter liposomal membrane fluidity.

We investigated the effects of angiotensinogen (Ang), angiotensin I (Ang I), and angiotensin II (Ang II) on the fluidity of phosphatidylcholine vesicles. Changes in fluidity were assessed by changes in anisotropy values calculated from fluorescence polarization measurements. All three compounds produced an increase in membrane fluidity when localized inside the phosphatidylcholine vesicles. When placed outside the vesicles, Ang II increased bilayer rigidity (decreased fluidity), whereas Ang and Ang I produced no effect. These results suggest the possibility that these peptides may alter the fluidity of cell membranes by a direct action on the phospholipid bilayer, which may in turn interfere with receptor-mediated effects.

TLC characterization of liposomes containing angiotensinogen, angiotensine I, angiotensine II and saralazin.

Recent studies have described intracellular binding sites for angiotensine II. In vascular smooth muscle it was found that intracellular injection of angiotensin II increases the Ca2+ level. An alternative method for intracellular delivery of drugs is represented by using liposomes. Thus, the aim of this study was to characterize liposomes filled with angiotensinogen, angiotensine I (Ang I), angiotensine II (Ang II), and saralasin by a TLC method and examine the physiological effects of these on rat vascular smooth muscle. Ang II (for all concentrations tested in the aqueous phase) and Ang I (for concentrations less than 10(-4)M) did not affect the thin-layer chromatography migration of this type of vesicle, suggesting that dose-dependent effects on physio-pharmacological experiments could be studied. On the other hand, this type of experiment could not be performed for salarasin- or angiotensinogen-filled liposomes. Administration of liposomes containing Ang II (10(-6)M), Ang I (10(-6)M), angiotensinogen (10(-6)M) and saralasine (10(-6)M) caused the contraction to isolated rat aorta smooth muscle, suggesting the presence of active intracellular binding sites.

[Ultrastructural aspects in the development of the human heart. I. The cytoskeleton and motility of human embryonic myocardiocytes]. / Aspects ultrastructuraux dans le developpement du coeur humain. Note I: Le cytosquelette et la motilité des myocardocytes embrionaires humaines.

Electron microscopic investigations performed on heart tissue fragments from 12 human embryos. 8 to 15 weeks of age, showed that at the age of 8 weeks the myocardiocytes are poorly differentiated cells: they contain microfilaments of actin and myosin inserted on the cytoplasmic aspect of plasmalemma, a smooth endoplasmic reticulin and mitochondria, accounting for the early contraction. Gap junctions appear among myocardiocytes, confirming the myogenic theory of heart contractions. Within 10 to 15 weeks, actin and myosin myofilaments organize in sarcomeres. Eberth disks appear and numerous mitoses are to be seen.