Stem cell therapy and tissue engineering represent a forefront of current research in the treatment of heart disease. With these technologies, advancements are being made into therapies for acute ischemic myocardial injury and chronic, otherwise nonreversible, myocardial failure. The current clinical management of cardiac ischemia deals with reestablishing perfusion to the heart but not dealing with the irreversible damage caused by the occlusion or stenosis of the supplying vessels. The applications of these new technologies are not yet fully established as part of the management of cardiac diseases but will become so in the near future. The discussion presented here reviews some of the pioneering works at this new frontier. Key results of allogeneic and autologous stem cell trials are presented, including the use of embryonic, bone marrow-derived, adipose-derived, and resident cardiac stem cells.
Introduction: Ureterocele is a rare urogenital malformation. The treatment is variable and complicated as it depends on several factors. The aim of this study was to evaluate the management and outcomes of children with ureterocele and to compare single system and duplex system ureteroceles. Materials and Methods: A retrospective study was conducted and all patients with ureterocele operated from January 1992 to December 2018 were included. The records of those included were assessed, and a detailed case record sheet was filled. The outcome parameters assessed were the persistence of symptoms and additional surgical procedure performed. Results: Forty-seven patients (28 boys and 19 girls) with a median age of presentation of 21 months were included. Four patients had bilateral ureterocele. Overall, 51 renal units with ureterocele were studied. Twenty renal units of the 31 renal units with duplex system underwent cystoscopic decompression, and of these, 8 (40%) needed a second procedure. Fourteen renal units of the remaining 20 renal units with single system underwent cystoscopy and decompression, and of these, 1 (7%) required another procedure (P = 0.024). Sixteen renal units had ectopic ureterocele, of which 9 (56%) underwent heminephrectomy/nephrectomy. Intravesical ureterocele was present in 35 renal units, of which only 2 (5.7%) underwent nephrectomy or heminephrectomy ( P < 0.001). Conclusion: Duplex system ureteroceles are more likely to require a second procedure following an endoscopic puncture. Units with ectopic ureterocele were more likely to need nephrectomy.
Background: Surgical drains of various types have been used, with the best intentions, in different surgeries for many years. It is often open question whether they achieve their intended purpose despite many years of surgery. There is paucity of evidence for the benefit of many types of surgical drainage and many surgeons still ‘follow their usual practice’. The dictum ‘when in doubt, drain’ from Lawson Tait, is well known to surgeons’. But many studies we find routine placement of drain has been shown to be ineffective or potentially harmful in various abdominal surgical procedure. We thus performed a systematic review of the studies of outcomes of with or without peritoneal drain in abdominal surgeries.Methods: A comparable study was conducted in between two groups with and without drain in patient belonging to all age undergoing small and large bowel surgeries. A random patient selection was done. Pooled estimates of mortality, morbidity, wound infection, blockage, pain, anastomotic leak, re-intervention and length of hospital stay were calculated.Results: With drain; duration of stay is more than without drain with p value found to be 0.0087. Drain is ineffective due to blockage in 38% patient. Wound infection is more with drain with p (0.003). Pain is more with drain with p (0.0001). There is no difference in anastomotic leak, distension, re-intervention and mortality with or without drain.Conclusions: After a century of scientific investigation and research, all surgeons should recall the words of Halstead ‘no drainage at all is better than ignorant employment of it’ rather than the advice of Lawson Tait ‘when in doubt, drain.
Activating mutations in PIK3CA are among the most significant oncogenic events across all cancers, making it an important target for drug development. Yet the application of PI3K inhibitors in the clinic has been limited by the difficulty of achieving an adequate therapeutic window, due to the critical role that PI3K signaling plays in normal physiologic processes, such as glucose homeostasis. In theory, the therapeutic window could be improved if it were possible to design mutant selective inhibitors, as has been demonstrated with other oncogenes such as EGFR. However, unlike EGFR, the most predominant PIK3CA activating mutations do not reside in the kinase active site, presenting a major challenge for rational structure-based design. Nevertheless, it was recently shown that the PI3K inhibitor taselisib is able to achieve modest levels of mutant selectivity both across cancer lines as well as in cell lines that were engineered to express mutant or wild-type PIK3CA. Taselisib was also shown to selectively induce degradation of mutant versus wild-type PIK3CA, leading to the speculation that this degradation may be responsible for the observed selectivity. In order to better understand the origins of mutant selectivity for taselisib and several other PIK3CA inhibitors, we assessed these inhibitors in a variety of biophysical and biochemical assays under conditions designed to mimic physiologic settings. In parallel, we also investigated the mechanistic basis of this selectivity in our engineered cell lines. Our results are consistent with the hypothesis that selective degradation of mutant PIK3CA is the predominant mechanism underlying mutant selectivity for this class of PIK3CA active site inhibitors. This abstract is also being presented as Poster B03. Citation Format: Lan Nguyen, Kyle Edgar, Kyung Song, Stephen Schmidt, Victorai Schutz, Noriko Ishisoko, Eric Torres, Akash Das, Divya Murali, Steve Sideris, Timothy Wendorff, Matt Saabye, Hans Purkey, Jawahar Sudhamsu, Steven Staben, Emily Hanan, Georgia Hatzivassiliou, Lori Friedman, Nicholas F. Endres. Selective degradation of mutant PIK3CA promotes increased mutant specificity in a subset of PI3K ATP-competitive inhibitors [abstract]. In: Proceedings of the AACR Special Conference on Targeting PI3K/mTOR Signaling; 2018 Nov 30-Dec 8; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Res 2020;18(10_Suppl):Abstract nr PR03.
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