Turk J Med Sci
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The success of treatment of bone fracture and defects are based on a proper contact and compression between the bone fracture fragments. Intraoperative manipulations such as bone compression or distractions are generally done in order to achieve this. However, none of the bone plates currently in routine use allow these manipulations after fixation to the bone, requiring refixation and repeated drilling, and screwing operations. Based on this shortcoming, we designed a novel adjustable bone plate (ABP) system which allows bone shortening and lengthening even after fixation to the bone surface. The aim of the paper is to clarify the unique properties of the novel bone plate. ⋯ The potential of the new generation ABP plate for use in bone compression, distraction, and the segmental bone transfer is a promising invention for clinical applications in the future.
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Ankaferd hemostat (ABS; Ankaferd Blood Stopper®, İstanbul, Turkey) is a hemostatic agent having an impact on red blood cell– fibrinogen interactions. The hemostatic effect of ABS depends upon the quick promotion of a protein network, particularly fibrinogen gamma, in relation to the erythrocyte aggregation. The entire physiological process involves ABS-induced formation of the protein network by vital erythrocyte aggregation. ⋯ The literature search on ABS was performed in PubMed, Web of Science (SCI expanded), and Scopus with particular focus on the studies of molecular basis of ABS, in vivo research, case series, and controlled randomized clinical studies. Current perspective for the utilization of ABS is to provide hemostasis with accelerating wound healing. Future controlled trials are needed to elucidate the pleiotropic clinical effects of ABS such as antineoplastic, antiinflammatory, antiinfective, antifungal, and antioxidative effects.
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Tuberous sclerosis complex (TSC) is an autosomal dominant, multisystem disorder that is characterized by cellular and tissue dysplasia in several organs. With the advent of genetic and molecular techniques, mutations in the TSC1 or TSC2 genes were discovered to be responsible for mTOR overactivation, which is the underlying mechanism of pathogenesis. TSC is a highly heterogenous clinical entity with variable presentations and severity of disease. ⋯ The TAND checklist is a useful tool for routine use in the clinical evaluation of TSC patients. A multidisciplinary treatment plan, based on the specific problems and needs of individuals, is the key to management of this genetic condition. Ongoing research studies have been providing promising leads for developing novel mechanistic strategies to address the pathophysiology of TSC.
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Preclinical animal models of breast cancer provide the opportunity to identify chemopreventive drugs with single-agent activity as well as effective multi-modality regimens for primary as well as secondary prevention in high-risk persons. Our group has used the 7,12-dimethylbenz(a)anthracene (DMBA) mouse model of carcinogen-induced breast cancer to explore the clinical potential of two tyrosine kinase inhibitors and a nucleoside analog as chemopreventive agents. ⋯ The tumors developing despite chemoprevention were not only small and grew slowly, but they also displayed a uniquely more pro-apoptotic protein expression profile. Hence, our experimental chemopreventive drugs were capable of preventing the development of aggressive mammary gland tumors with an apoptosis-resistant protein expression profile.
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Apart from its metabolic or physiological functions, melatonin has a potent cytoprotective activity in the physiological and pathological conditions. It is synthetized by the pineal gland and released into the blood circulation but particularly cerebrospinal fluid in a circadian manner. It can also easily diffuse through cellular membranes due its small size and lipophilic structure. ⋯ In this term, melatonin is a promising molecule for the treatment of neurodegenerative disorders, such as ischemic stroke, which melatonin reduces ischemic brain injury in animal models of ischemic stroke. It regulates also circadian rhythm proteins after ischemic stroke, playing roles in cellular survival. In this context, present article summarizes the possible role of melatonin in the pathophysiological events after ischemic stroke.