We undertook a prospective study comparing the unreamed interlocking nail to Hoffmann external skeletal fixation (ESF) in the treatment of 36 consecutive patients with open type IIIA and IIIB tibia fractures. The choice of interlocking nail or Hoffmann ESF was randomized, ultimately producing four different patient groups: group 1, type IIIA fractures treated by interlocking nail; group 2, type IIIA fractures treated by ESF; group 3, type IIIB fractures with interlocking nail; and group 4, type IIIB fractures with ESF. The average length of follow-up was 20.5 months. The infection rate was highest in group 3 (3 of 8). The malrotation, malunion, and nonunion rates were highest in group 4 and lowest in group 1. These results suggest the unreamed interlocking nail is a good choice for the treatment of open type IIIA tibia fractures, but not recommended for the treatment of open type IIIB tibia fractures because of the high infection rate.

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Iliac vein rupture is rare and primarily results from major trauma or occurs during pelvic surgery. Spontaneous nontraumatic rupture is even more unusual, with only 14 cases reported in the literature. We report an additional case, summarize all of the cases, and discuss the possible causes and treatment of iliac vein rupture and the role of anticoagulants in postoperative management.

Stress-induced cardiac hypertrophy leads to heart failure. Our previous studies demonstrate that insulin-like growth factor—II receptor (IGF-IIR) signaling is pivotal to hypertrophy regulation. In this study, we show a novel IGF-IIR alternative spliced transcript, IGF-IIRα (150 kDa) play a key role in high-salt induced hypertrophy mechanisms. Cardiac overexpression of IGF-IIRα and high-salt diet influenced cardiac dysfunction by increasing pathophysiological changes with up-regulation of hypertrophy markers, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). We found that, cardiac hypertrophy under high-salt conditions were amplified in the presence of IGF-IIRα overexpression. Importantly, high-salt induced angiotensin II type I receptor (AT1R) up regulation mediated IGF-IIR expressions via upstream mitogen activated protein kinase (MAPK)/silent mating type information regulation 2 homolog 1 (SIRT1)/heat shock factor 1 (HSF1) pathway. Further, G-coupled receptors (Gαq) activated calcineurin/nuclear factor of activated T-cells, cytoplasmic 3 (NFATc3)/protein kinase C (PKC) signaling was significantly up regulated under high-salt conditions. All these effects were observed to be dramatically over-regulated in IGF-IIRα transgenic rats fed with a high-salt diet. Altogether, from the findings, we demonstrate that IGF-IIRα plays a crucial role during high-salt conditions leading to synergistic cardiac hypertrophy.

Doxorubicin (DOX) is an anthracycline antibiotic commonly employed for the treatment of various cancers. However, its therapeutic uses are hampered by side effects associated with cumulative doses during the course of treatment. Whereas deregulation of autophagy in the myocardium has been involved in a variety of cardiovascular diseases, the role of autophagy in DOX-induced cardiomyopathy remains debated. Our earlier studies have shown that DOX treatment in a rat animal model leads to increased expression of the novel stress-inducible protein insulin-like growth factor II receptor-α (IGF-IIRα) in cardiac tissues, which exacerbated the cardiac injury by enhancing oxidative stress and p53-mediated mitochondria-dependent cardiac apoptosis. Through this study, we investigated the contribution of IGF-IIRα to dysregulation of autophagy in heart using both in vitro H9c2 cells (DOX treated, 1 µM) and in vivo transgenic rat models (DOX treated, 5 mg/kg ip for 6 wk) overexpressing IGF-IIRα specifically in the heart. We found that IGF-IIRα primarily localized to mitochondria, causing increased mitochondrial oxidative stress that was severely aggravated by DOX treatment. This was accompanied by a significant perturbation in mitochondrial membrane potential and increased leakage of cytochrome c, causing increased cleaved caspase-3 activity. There were significant alterations in phosphorylated AMP-activated protein kinase (p-AMPK), phosphorylated Unc-51 like kinase-1 (p-ULK1), PARKIN, PTEN-induced kinase 1 (PINK1), microtubule-associated protein 1 light chain 3 (LC3), and p62 proteins, which were more severely disrupted under the combined effect of IGF-IIRα overexpression plus DOX. Finally, LysoTracker Red staining showed that IGF-IIRα overexpression causes lysosomal impairment, which was rescued by rapamycin treatment. Taken together, we found that IGF-IIRα leads to mitochondrial oxidative stress, decreased antioxidant levels, disrupted mitochondrial membrane potential, and perturbed mitochondrial autophagy contributing to DOX-induced cardiomyopathy.

Nonoperative treatment significantly decreased the rate of nontherapeutic laparotomy but carried the risks of higher transfusion requirements and delaying operation. When surgery was indicated, the policy of minimal intervention positively affected the patients' outcomes. The goal of surgery should be hemorrhage control rather than resection of the injured liver tissues.

Heart failure (HF) and cardiac hypertrophy is an unfavorable outcome of pathological cardiac remodeling and represents the most important contributing factor for HF and cardiac hypertrophy. Amygdalin (AMG) is a cyanogenic glycoside derived from bitter almonds. Accumulating evidences have highlighted their pharmacological potentials against various diseases. However, there is no report delineating the potential of AMG against angiotensin (Ang II) induced cardiac injuries. Thus, the present study was performed to explore whether AMG could ameliorate Ang II induced cardiomyopathies and thereby ascertain the underlying mechanisms thereof. To this end, H9c2 cells were treated with Ang II and thereafter treated with various concentration of AMG and finally the cardio‐protective effects of AMG were analyzed through Western blotting, immunofluorescence, and insilico analysis. Our results showed that the cardiomyocyte cell size, inflammatory markers and cytokines(pNF‐κB, TNF‐α, iNOS and COX‐2) were markedly increased following Ang II treatment; nevertheless, treatment with AMG led to considerable decrement in the Ang II induced enlargement of the cardiomyocytes, and attenuate the expression of hypertrophic markers(ANP, BNP and MHC‐7), inflammatory markers and cytokines. Additionally, oxidative stress related proteins (Nrf2, catalase, SOD‐2, and GPX‐4) were markedly increased following AMG treatment. Molecular docking reveals the interaction of AMG with Nrf2 possessing good binding affinity. Cumulatively, our study highlights the cardio‐protective role of AMG against Ang II induced cardiomyopathies, including oxidative stress and inflammation effects. The intriguing in vitro results warrants the need of further animal studies to truly ascertain their potentialities.

This work presents a biomedical signal processor (BSP) with hybrid functional cores to optimize the power dissipation and system flexibility for mobile healthcare applications. Embedded with the biomedical core and a 32-bit RISC core, multi-features are extracted for classification and the abnormal data are compressed. In addition, the crypto core secures both the data and wireless link protocols to protect the user privacy. This BSP chip is fabricated in a 90nm standard CMOS technology with core area of 1.17mm 2 . To overcome the leakage in advanced technology, a duty-cycled clock generator minimizes the system active duty and the inactive functions are power gated. Operating at 25MHz frequency and 0.5V supply voltage, the energy of RISC core is down to 3.44pJ/cycle. Accompanied with dedicated biomedical and crypto cores, the average BSP power achieves 38µW at 25MHz and 0.5/1.0V when performing the ECG alarm application.