Cangzhou City Central Hospital

Cangzhou, China

Cangzhou City Central Hospital

Cangzhou, China
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Yang M.,Cangzhou City Central Hospital | Xiao L.-B.,Cangzhou City Central Hospital | Gao Z.-S.,Cangzhou City Central Hospital | Zhou J.-W.,Cangzhou City Central Hospital
Medical Science Monitor | Year: 2017

Background: Coronary artery bypass grafting (CABG) is a common procedure to circumvent the obstruction of coronary arteries when stents are unsuitable. CABG is a very traumatic surgery that requires redirecting blood flow to an external pump. Thus, this procedure has many risks during and after surgery, and minimizing these risks would greatly benefit the patients. Material/Methods: We selected 126 patients with coronary artery syndrome and who were unsuitable for stent percutaneous coronary intervention. The observation group received minimally invasive direct coronary artery bypass (MIDCAB), while the control group was treated with off-pump CABG. Results: Blood markers and echocardiography before and after treatment improved equally in both groups. Neither group exhibited obvious adverse reactions, or liver and kidney function damage. However, surgical bleeding and postoperative observation days were significantly reduced in the MIDCAB group. Death and cardiac shock at the end of follow-up were significantly lower in the MIDCAB group. Conclusions: Overall, the clinical benefits of MIDCAB and OP-CABG were similar, but MIDCAB significantly reduced postoperative hospital stay and intraoperative blood transfusion, and improved clinical prognosis. © Med Sci Monit.


Gao S.,Cangzhou City Central Hospital | Sun H.,Cangzhou City Central Hospital | Cheng C.,Cangzhou City Central Hospital | Wang G.,Cangzhou City Central Hospital
DNA and Cell Biology | Year: 2017

BRCA1-associated protein-1 (BAP1) is an important nuclear-localized deubiquitinating enzyme. Dysregulation of BAP1 has been reported in many types of cancers. However, there are few articles on the role of BAP1 in osteosarcoma (OS) and the molecular mechanisms of BAP1 in OS remain largely unknown. In this study, we examined the expression of BAP1 in the tissue sample from OS patients and healthy control subjects, and then investigated the biological function and molecular mechanisms of BAP1 in OS. We found that BAP1 was significantly reduced in OS patients and OS cell lines. Then we found that BAP1 has a key role in OS cell proliferation, apoptosis, migration, and invasion. Furthermore, we found that BAP1 exerted its influence on the PI3K/Akt signaling pathway and there was physical association between BAP1 and miR-125. In conclusion, our data highlight the important roles of BAP1 in the survival of OS. It may be a potential therapy for OS. © Copyright 2017, Mary Ann Liebert, Inc. 2017.


Dong X.,Cangzhou City Central Hospital | Shi D.,Cangzhou City Central Hospital
Reproductive Sciences | Year: 2017

Preeclampsia (PE) is a pregnancy-specific condition characterized by new-onset hypertension. There is evidence suggesting that imbalances of angiogenic factors, oxidative stress, and inflammation may be central to the pathogenesis of PE. We sought to investigate whether simvastatin would reduce mean arterial pressure, restore the angiogenic balance, and ameliorate inflammation and oxidative stress in a nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME)-induced rat model of PE. We found that blood pressure was significantly increased in the l-NAME group compared to normal pregnant dams (P <.01), and simvastatin reduced this difference. In addition, dams from the l-NAME group showed lower vascular endothelial growth factor (VEGF) and interleukin (IL) 10 levels and higher plasma-soluble FMS-like tyrosine kinase 1 (sFlt-1), tumor necrosis factor α (TNF-α), and oxidative stress marker malondialdehyde (MDA) levels as compared to control dams (P <.01, for all). Interestingly, simvastatin treatment significantly increased VEGF and IL-10 levels while decreased sFlt-1, TNF-α, and MDA levels compared to the untreated l-NAME group. Moreover, simvastatin treatment significantly upregulated protein expression of placental p-extracellular signal-regulated kinase (ERK1), p-p38 mitogen-activated protein kinase (MAPK), p-c-Jun N-terminal kinase, and p-protein kinase B compared to untreated l-NAME control. These results suggest that simvastatin treatment restores angiogenic balance and ameliorates inflammation and oxidative stress in a rat model of PE involving ERK/MAPK pathway. © Society for Gynecologic Investigation.


Yang L.,Cangzhou City Central Hospital Brain Campus | Dong X.,Cangzhou City Central Hospital
Environmental Toxicology and Pharmacology | Year: 2017

We aimed to evaluate the effect of natural antioxidant crocin in alleviating hemorrhagic shock (HS)-induced organ damages. HS rats were treated with crocin during resuscitation. Mortality at 12 h and 24 h post resuscitation was documented. HS and resuscitation induced organ injuries, as characterized by elevated wet/dry ratio, quantitative assessment ratio, blood urea nitrogen, creatinine, aspartate aminotransferase and alanine aminotransferase, whereas rats received crocin treatment demonstrated improvements in all the above characteristics. This protective effect coincided with reduced malondialdehyde and increased glutathione in both serum and lung tissues, indicating attenuated oxidative stress in crocin-treated rats. Myeloperoxide levels in lung, kidney and liver were also reduced. Crocin can potentially be used to protect organs from HS-induced damages during resuscitation due to its anti-oxidative role. © 2017 Elsevier B.V.


Yang L.,Cangzhou City Central Hospital Brain Campus | Dong X.,Cangzhou City Central Hospital
Journal of Interferon and Cytokine Research | Year: 2017

Hemorrhagic shock (HS) is associated with an excessive activation of inflammation, contributing to multiple organ failure in numerous medical or surgical conditions. To explore the therapeutic potential of crocin, a natural compound with anti-inflammatory properties, we administered crocin to rats during resuscitation following HS induced by withdrawing blood. Compared with control animals which were sham-treated, HS-operated rats showed organ damages as manifested by enhanced markers of multiple organ dysfunctions. Crocin treatment substantially reduced these parameters in rats subjected to HS, suggesting an alleviation of tissue injuries such as in the kidney, liver, pancreas, and muscle. The activation of NF-κB (nuclear factor κB) pathway in lung tissue by HS, as shown by increased nuclear translocation of p65 and IκBα phosphorylation, was diminished by crocin treatment. The crocin administration also significantly decreased the serum levels of proinflammatory cytokine TNF-α (tumor necrosis factor-α) and interleukin (IL)-6, whereas increased the level of anti-inflammatory cytokine IL-10 in HS-operated rats. These studies indicate that crocin administration may reduce inflammation-driven tissue damage in patients with HS. © Mary Ann Liebert, Inc. 2017.


Xing B.-H.,Hebei Medical University | Yang F.-Z.,Cangzhou City Central Hospital | Wu X.-H.,Hebei Medical University
Journal of Pharmacological Sciences | Year: 2016

Gestational diabetes mellitus (GDM) is a disease commonly occurs during mid to late pregnancy with pathologies such as hyperglycemia, hyperinsulinemia and mal-development of fetus. We have previously demonstrated that pancreatic endoderm (PE) derived from human embryonic stem cells (hESCs) effectively alleviated diabetic symptoms in a mouse model of GDM, although the clinical efficacy was limited due to oxidative stress. In this study, using the anti-oxidant agent naringenin, we aimed to further enhance the efficacy of hESC-derived PE transplant. Insulin-secreting PE was differentiated from hESCs, which were then transplanted into GDM mice. Naringenin was administered to mice receiving the PE transplant, with sham operated mice serving as negative control, to assess its effect on alleviation of GDM symptoms. We found that naringenin supplement further improved insulin response, glucose metabolism and reproductive outcome of the PE-transplanted female mice. Our new findings further potentiates the feasibility of using differentiated hESCs to treat GDM, in which anti-oxidative agent such as naringenin could greatly enhance the clinical efficacy of stem cell based therapies. © 2016 The Authors.


PubMed | Cangzhou City Central Hospital and Hebei Medical University
Type: Journal Article | Journal: Journal of pharmacological sciences | Year: 2016

Gestational diabetes mellitus (GDM) is a disease commonly occurs during mid to late pregnancy with pathologies such as hyperglycemia, hyperinsulinemia and mal-development of fetus. We have previously demonstrated that pancreatic endoderm (PE) derived from human embryonic stem cells (hESCs) effectively alleviated diabetic symptoms in a mouse model of GDM, although the clinical efficacy was limited due to oxidative stress. In this study, using the anti-oxidant agent naringenin, we aimed to further enhance the efficacy of hESC-derived PE transplant. Insulin-secreting PE was differentiated from hESCs, which were then transplanted into GDM mice. Naringenin was administered to mice receiving the PE transplant, with sham operated mice serving as negative control, to assess its effect on alleviation of GDM symptoms. We found that naringenin supplement further improved insulin response, glucose metabolism and reproductive outcome of the PE-transplanted female mice. Our new findings further potentiates the feasibility of using differentiated hESCs to treat GDM, in which anti-oxidative agent such as naringenin could greatly enhance the clinical efficacy of stem cell based therapies.


PubMed | Cangzhou City Peoples Hospital, Cangzhou City Central Hospital and Bethune International Peace Hospital
Type: Evaluation Studies | Journal: Nutrition research (New York, N.Y.) | Year: 2015

Gestational diabetes mellitus is a condition commonly encountered during mid to late pregnancy with pathologic manifestations including hyperglycemia, hyperinsulinemia, insulin resistance, and fetal maldevelopment. The cause of gestational diabetes mellitus can be attributed to both genetic and environmental factors, hence complicating its diagnosis and treatment. Pancreatic progenitors derived from human embryonic stem cells were shown to be able to effectively treat diabetes in mice. In this study, we have developed a system of treating diabetes using human embryonic stem cell-derived pancreatic endoderm in a mouse model of gestational diabetes mellitus. Human embryonic stem cells were differentiated in vitro into pancreatic endoderm, which were then transplanted into db/+ mice suffering from gestational diabetes mellitus. The transplant greatly improved glucose metabolism and reproductive outcome of the females compared with the control groups. Our findings support the feasibility of using differentiated human embryonic stem cells for treating gestational diabetes mellitus patients.


PubMed | Cangzhou City Peoples Hospital, Cangzhou City Central Hospital and Bethune International Peace Hospital
Type: Journal Article | Journal: Journal of physiology and biochemistry | Year: 2015

Gestational diabetes mellitus (GDM) has emerged as an epidemic disease during the last decade, affecting about 2 to 5% pregnant women. Even among women who have gestational hyperglycemia may also be positively related to adverse outcomes as GDM. Since heat shock protein (Hsp) 70 has been reported to be associated with diabetes and insulin resistance and its expression was reported to be negatively regulated by the membrane-permeable Hsp70 inhibitor MAL3-101 while positively regulated by the Hsp70 activator BGP-15, we investigated whether Hsp70 played a role in a gestational hyperglycemia mouse model. Mice were divided into non-pregnant and pregnant groups, and each comprised three subgroups: control, high-fat diet (HFD) + MAL3-101, and HFD + BGP-15. We examined the serum levels of triglycerides, total cholesterol, glucose, and insulin, as well as conducted thermal detection of brown adipose tissue (BAT). The role of Hsp70 in BAT apoptosis was also investigated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and caspase-3 staining. Higher serum level of Hsp70 was associated with increased bodyweight gain after pregnancy in mice fed HFD. Circulating Hsp70 was elevated in control pregnant mice compared to control non-pregnant mice. BGP-induced serum Hsp70 expression reduced triglycerides, total cholesterol, glucose, and insulin levels in the serum. Additionally, thermal detection of BAT, TUNEL, and caspase-3 staining revealed relationship correlation between Hsp70 and BAT functions. Hsp70 level is associated with hyperglycemia during pregnancy. Our results support the role of Hsp70 in facilitating BAT activities and protecting BAT cells from apoptosis via caspase-3 pathway.


PubMed | Cangzhou City Central Hospital
Type: | Journal: Reproductive sciences (Thousand Oaks, Calif.) | Year: 2016

Preeclampsia (PE) is a pregnancy-specific condition characterized by new-onset hypertension. There is evidence suggesting that imbalances of angiogenic factors, oxidative stress, and inflammation may be central to the pathogenesis of PE. We sought to investigate whether simvastatin would reduce mean arterial pressure, restore the angiogenic balance, and ameliorate inflammation and oxidative stress in a nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME)-induced rat model of PE. We found that blood pressure was significantly increased in the l-NAME group compared to normal pregnant dams (P < .01), and simvastatin reduced this difference. In addition, dams from the l-NAME group showed lower vascular endothelial growth factor (VEGF) and interleukin (IL) 10 levels and higher plasma-soluble FMS-like tyrosine kinase 1 (sFlt-1), tumor necrosis factor (TNF-), and oxidative stress marker malondialdehyde (MDA) levels as compared to control dams (P < .01, for all). Interestingly, simvastatin treatment significantly increased VEGF and IL-10 levels while decreased sFlt-1, TNF-, and MDA levels compared to the untreated l-NAME group. Moreover, simvastatin treatment significantly upregulated protein expression of placental p-extracellular signal-regulated kinase (ERK1), p-p38 mitogen-activated protein kinase (MAPK), p-c-Jun N-terminal kinase, and p-protein kinase B compared to untreated l-NAME control. These results suggest that simvastatin treatment restores angiogenic balance and ameliorates inflammation and oxidative stress in a rat model of PE involving ERK/MAPK pathway.

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