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Liu Y.,Hebei Medical University | Liu Y.,Key Orthopaedic Biomechanics Laboratory of Hebei Province | Peng M.,252 Hospital of Peoples Liberation Army | Lin L.,Second Hospital of Cangzhou City | And 3 more authors.
Osteoporosis International | Year: 2015

Summary: This study retrospectively reviewed 327 nonagenarians who underwent hip fracture surgery at six hospitals. Functional status, postoperative complications, and 1-year mortality were evaluated, and relationships between these factors and American Society of Anesthesiologists (ASA) grade were analyzed. ASA grade was significantly associated with postoperative complications and 1-year mortality.Introduction: Few previous studies have reported outcomes after hip fracture in nonagenarians, and these studies did not report significant associations between ASA grade and mortality. However, most of these studies included only a small number of patients from a single hospital. This study aimed to evaluate the relationships between ASA grade and functional status, postoperative complications, and mortality rate in nonagenarians undergoing hip fracture surgery.Methods: This study included 327 nonagenarians who underwent hip fracture surgery between January 2000 and December 2012. Patients with open fractures, subtrochanteric fractures, polytrauma, and pathological fractures were excluded. The medical records and X-rays were retrospectively reviewed. The relationships between ASA grade and functional status, postoperative complications, and 1-year mortality were analyzed.Results: There were significant associations between the ASA grade and the rates of postoperative complications and 1-year mortality (both p < 0.05). All pairwise comparisons showed significant differences in postoperative complication rates between ASA grades (all p < 0.05). All pairwise comparisons, except for grades I vs. II and grades II vs. III, also showed significant differences in mortality rates between ASA grades (all p < 0.05). There were significant associations between the preoperative ability to manage activities of daily living and the rates of postoperative complications and 1-year mortality (both p < 0.05).Conclusions: ASA grade was significantly associated with the rates of postoperative complications and 1-year mortality in nonagenarians undergoing hip fracture surgery. The preoperative functional status was also significantly associated with these outcomes. © 2014, International Osteoporosis Foundation and National Osteoporosis Foundation. Source


Liu L.,Hebei Medical University | Wei J.,Fifth Hospital of Shijiazhuang City | Huo X.,Third Hospital of Shijiazhuang City | Fang S.,Hebei Medical University | And 4 more authors.
Molecular Medicine Reports | Year: 2012

During the process of liver fibrosis, hepatic stellate cells (HSCs) play a critical role in the excessive production of extracellular matrix (ECM). Previous studies have indicated that the monomer IH764-3, one of the major bioactive components of Salvia miltiorrhiza, is able to inhibit HSC proliferation and induce the apoptosis of activated HSCs in vitro. In the current study, we used a rat model of liver fibrosis induced by bile duct ligation (BDL) to investigate the effect of the monomer IH764-3 on the induction of apoptosis in HSCs in vivo. The rat model of liver fibrosis was established by BDL. Immunohistochemical staining of α-smooth muscle actin (α-SMA) was performed to detect HSC activation and proliferation and HSC apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and α-SMA immunohistochemical double staining. In addition, the protein expression levels of focal adhesion kinase (FAK), p-FAK (Tyr397), extracellular signal-regulated kinase (ERK) and p-ERK and the mRNA expression levels of FAK and ERK were measured by western blotting and reverse transcription-polymerase chain reaction (RT-PCR), respectively. The monomer IH764-3 was associated with a significant decrease in intrahepatic fibrogenesis and collagen deposition and attenuated the liver fibrosis induced by BDL. Immunohistochemical staining revealed that the expression of α-SMA in the IH764-3 group was significantly decreased compared with that in the model group (12.92±2.45 vs. 22.65±2.16%, P<0.01). TUNEL and α-SMA immunohistochemical double staining also confirmed that IH764-3 increased the apoptotic rate of the activated HSCs (34.8±4.5 vs. 4.72±0.37%, P<0.01). Moreover, the results revealed that IH764-3 downregulated the expression levels of FAK, p-FAK (Tyr397), ERK and p-ERK in the liver tissue of rats with liver fibrosis. The monomer IH764-3 ameliorates experimental liver fibrosis by inhibiting HSC proliferation and inducing HSC apoptosis, warranting its use as a potential therapeutic agent in the treatment of liver fibrosis. Source


Zhang A.,Hebei Medical University | Yan X.,Hebei Medical University | Li H.,Hebei Medical University | Gu Z.,Third Hospital of Shijiazhuang City | And 4 more authors.
Experimental Lung Research | Year: 2014

Objective: To observe the expression of endogenous TMEM16A in rat alveolar type II epithelial cells (AT-II) and A549, and study the effect of TMEM16A on lipopolysaccharide (LPS)-induced proinflammatory cytokine secretion. Methods: Rat AT-II cells were isolated and TMEM16A protein expression in rat AT-II cells was measured by Western blot. TMEM16A mRNA and protein expressions in A549 were measured by real-time quantitative polymerase chain reaction (PCR) and Western blot, respectively. TMEM16A gene was transfected into A549 using Lipofectamine 2000. Transfected cells were selected in the presence of G418 to create a stable TMEM16A overexpression A549 cell line. The expression of TMEM16A in A549 was knocked down by lentiviral vector-mediated RNA interference. TNF-α and IL-8 levels were determined by enzyme-linked immunosorbent assay (ELISA). A dual-luciferase reporter assay system was used to measure the transcriptional activity of NF-κB. Results: (1) Endogenous TMEM16A was expressed in rat AT-II and A549. (2) TMEM16A expression in A549 significantly increased at 24 hours and 36 hours, and then decreased at 48 hours after LPS treatment. (3) TMEM16A mRNA and protein expressions were increased in the stable TMEM16A overexpression A549 cell line. (4) TMEM16A overexpression decreased the LPS-induced TNF-α and IL-8 secretions. (5) TMEM16A mRNA and protein expressions were knocked down in TMEM16A-siRNA lentivirus transfected A549. (6) TMEM16A knockdown increased the LPS-induced TNF-α and IL-8 secretions. (7) TMEM16A overexpression inhibited LPS-induced NF-κB activation. Conclusions: TMEM16A is expressed in AT-II. TMEM16A in A549 inhibits LPS-induced NF-κB activation and decreases proinflammatory cytokines release, protecting A549 from acute LPS-mediated damage. © 2014 Informa Healthcare USA, Inc. Source


Feng X.-J.,Hebei Medical University | Liu S.-X.,Hebei Medical University | Wu C.,Hebei Medical University | Kang P.-P.,Hebei Medical University | And 8 more authors.
American Journal of Physiology - Cell Physiology | Year: 2014

Our previous experiment confirmed that high-mobility group box chromosomal protein 1 (HMGB1) was involved in the pathogenesis of Lupus nephritis (LN) by upregulating the proliferation of the mouse mesangial cell line (MMC) through the cyclin D1/CDK4/p16 system, but the precise mechanism is still unknown. Therefore, in the present study, we demonstrated that HMGB1 induced the proliferation of MMC cells in a time- and concentration-dependent manner, downregulated phosphatase and tensin homolog deleted on chromosome ten (PTEN) expression, increased the level of Akt serine 473 phosphorylation, and induced p65 subunit nuclear translocation. The overexpression of PTEN prevented the upregulation of HMGB1-induced proliferation by blocking the activation of Akt. The knockdown of Akt by siRNA technology and blocking the nuclear factor-κB (NF-κB) pathway using pyrrolidine dithiocarbamate (PDTC) and SN50, inhibitors of NF-κB, both attenuated the HMGB1-induced proliferation by counteracting the activation of the cyclin D1. In addition, while sh-Akt partly blocked the nuclear translocation of the p65 subunit, PDTC did not affect the activation of the Akt induced by HMGB1 in MMC cells. These findings indicate that HMGB1 induced the proliferation of MMC cells by activating the PTEN/phosphoinositide-3-kinase (PI3K)/Akt/NF-κB signaling pathway. © 2014 the American Physiological Society. Source


Su Y.-H.,Hebei Medical University | Zhang S.-B.,Third Hospital of Shijiazhuang City | Cui H.-X.,Hebei Medical University | Kang L.,Hebei Medical University | And 3 more authors.
Acta Anatomica Sinica | Year: 2013

Objective: To examine the correlation of draxin expression and neural crest migration in chick embryonic spinal cord at different developmental stages. Methods: Ten chick embryos at different stages were used. In situ hybridization and immunohistochemistry were used to observe the localization of draxin expression, the migration pathway of neural crest cell-the spatial correlation of draxin expression and the neural crest migration. Living tissue incubation with draxin alkaline phosphatase (draxin-AP) recombinant protein was used to check the binding ability of migrating neural crest with draxin protein. Results: With development, the draxin expression and neural crest migration had a very similar anterior-posterior gradient in chick embryonic spinal cord. Draxin was expressed in the dorsal neural tube, roof plate and dorsal tip of dermomyotome which surrounded the migration pathway of neural crest cells. We also found that portion of migrating neural crest cells bound to draxin-AP protein directly. Conclusion: Draxin is expressed in the tissues surrounding the neural crest migration pathway and portion of migrating neural crest cells binds to draxin protein directly. We conclude therefore that draxin may be involved in the regulation of neural crest cell migration in chick embryonic spinal cord. Source

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