Is the denervation or hyperinnervation of the cardiac sympathetic nerve in the subepicardium related to unexpected cardiac death?

BackgroundPast studies have reported that abnormal innervation of cardiac sympathetic nerve can cause sudden cardiac death through the arrythmogenesis; however, the severe cardiac sympathetic degeneration does not necessarily cause clinical problems. This study aimed to examine whether denervation or hyperinnervation of cardiac sympathetic nerves in the subepicardium is associated with unexpected cardiac death (UCD).MethodsCardiac tissues of 278 forensic autopsy cases within 48 h after death were analyzed by double-staining immunohistochemistry for tyrosine hydroxylase and neurofilament. The density of nerve fascicles and the degeneration rate in the subepicardium of the left ventricular anterior wall were compared between the UCD group and the non-UCD group.ResultsThe density of nerve fascicles was lower in the SCD group (median: 51.9/cm²) than in the non-SCD group (median: 58.9/cm²); however, the difference was not significant (P=.08). The degeneration rate was higher in the SCD group (median: 0.19) than in the non-SCD group (median: 0.17), but again, the difference was not significant (P=.43). The multiple logistic regression model did not show a significant association between the incidence of UCD and the density of nerve fascicles or the degeneration rate.ConclusionsIt cannot be concluded that the denervation or hyperinnervation of cardiac sympathetic nerves in the subepicardium is related to UCD. Abnormal innervation of cardiac sympathetic nerves in the subepicardium may not have a substantial effect on UCD, compared to other arrhythmogenic factors.     

Is cell death and replacement a factor in aging?

The central theme of the 3rd International Conference on Functional Genomics of Ageing was tissue regeneration as a remedial strategy to address age-related cellular damage and the pathology that ensues. The conference included sessions on maintaining genome integrity and the potential of stem cells to restore function to damaged tissues. In addition to several human syndromes that appear to reflect accelerated ageing, there are now a number of mouse models that prematurely display phenotypes associated with ageing. The intent of this summary presented at the end of the conference was to: (1) discuss various human syndromes and mouse models of accelerated ageing; (2) evaluate whether the phenotypes displayed might result from an elevated rate of cell death coupled with an inability to adequately maintain cell number in various tissues with increasing age; and (3) discuss whether similar events may be occurring during normal ageing, albeit much more slowly.     

AdCD40L--crossing the valley of death?

CD40-mediated cancer therapy has been under development since it became clear that CD40 plays a profound role in the stimulation of adaptive immune responses. Further, CD40 signaling on tumor cells may lead to growth arrest or even apoptosis that improves therapy outcome. The therapeutic window is appealing since the immune system is selective and normal cells do not apoptose upon CD40 signaling. AdCD40L is an adenoviral-based immunostimulatory gene therapy under evaluation for its efficacy to treat cancer. Because of its nature, the adenoviral backbone will stimulate TLRs while CD40L potentiates the shifts toward Th1 type of immunity. AdCD40L has shown efficacy in various murine models, and safety studies have been performed on dog patients and in human clinical trials. AdCD40L has been used for both ex vivo gene modification of tumor cell vaccines as well as for direct intratumoral injections. Lately, an oncolytic vector has been used to further increase the eradication of solid tumors that as a consequence further boosts the release of tumor antigens and creates danger signaling in the tumor micro milieu. This review discusses the currently unfolding mechanisms of action of AdCD40L gene therapy and its possibilities to reach clinical care.     

Is the renal space closed?

The aim of this study is to verify the aperture or the closure of the renal space. The study is undertaken on histological sections of fetuses in the horizontal and sagittal planes. On each side, the kidney and the suprarenal gland are disposed in a space that is closed on all sides. The anterior and posterior layers of the renal fascia fuse at the upper pole of the space to become continuous with the inferior fascia of the diaphragm. Likewise, they merge at the lower pole and at the lateral border of the space to become continuous with the fasciae of the parietal muscles. At the medial border of the space, the two layers merge to continue medially with the peri-aortocaval connective tissue; they penetrate the hilum and beneath it enclose the ureter.     

Is AI the Ultimate QA?

Journal of Digital Imaging - We are among the many that believe that artificial intelligence will not replace practitioners and is most valuable as an adjunct in diagnostic radiology. We suggest a...