Taizhou Second Peoples Hospital

Taizhou, China

Taizhou Second Peoples Hospital

Taizhou, China
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Cheng Z.,Soochow University of China | Cheng Z.,Bengbu Medical College | Wang W.,Traditional Chinese Medicine Hospital of Kunshan | Han Y.,Soochow University of China | And 5 more authors.
British Journal of Neurosurgery | Year: 2017

Low pressure hydrocephalus (LPH) is a rare type of hydrocephalus with low intracranial pressure and ventriculomegaly. The recognition of LPH is important, and the treatment is difficult and very complicated. An understanding of how to drain cerebrospinal fluid when the intracranial pressure is lower than the opening pressure of the value represents a critical issue. Seven patients who suffered from the pain of hydrocephalus syndrome and were diagnosed with LPH were retrospectively reviewed. A ventricle peritoneal shunt was applied to all patients, and the valve system was adjusted to the lowest pressure; however, the clinical manifestations of hydrocephalus in five of seven patients did not improve over one week. Intermittent pressing of the valve in combination with the maintenance of a semi-reclined position were subsequently implemented. The symptoms of hydrocephalus began to improve from three days to two months following the initiation of intermittent valve pressing in combination with the maintenance of a semi-reclined position. At the twelve months follow up, six of seven patients (85.7%) showed good recovery to minimal disability. Intermittent valve pressing in combination with a semi-reclined position is an effective and easy method to drain cerebrospinal fluid when the intracranial pressure (ICP) is lower than the opening pressure of the value and improve hydrocephalus symptoms. © 2017 The Neurosurgical Foundation


PubMed | Jiangsu Traditional Chinese Medical Hospital and Taizhou Second Peoples Hospital
Type: | Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie | Year: 2016

Recent evidence suggests that CD200 fusion protein (CD200Fc), a CD200R1 agonist may attenuate inflammatory responses in autoimmune diseases and neuro-degeneration. While, little is known about the function of CD200Fc in cigarette smoke extract (CSE)-induced mouse Cardiac Microvascular Endothelial Cells (mCMECs). The present study was designed to elucidate the effects of CD200Fc on CSE-induced vascular endothelial barrier (VEB) dysfunction and inflammatory responses, which is a highly clinically relevant model of smoking related cardiovascular diseases.mCMECs were pre-treated with 1, 10 and 100g/ml CD200Fc for 24h respectively, and then treated with 250g/ml CSE for different times (24h or 120min). The transepithelial electrical resistance (TEER) and transport of fluorescent markers were used to measure VEB function in CSE-induced mCMECs. Western blot and immunofluorescent staining analysis were used to detect the expression of tight junction proteins, such as Zona Occludens-1 (ZO-1) and Claudin-1 in CSE-induced mCMECs. We measured the expression of pro-inflammatory cytokines in CSE-induced mCMECs by using ELISA and RT-PCR. In addition, the NF-B activity in CSE-induced mCMECs were investigated by using nuclear/cytosol fractionation and western blot analysis.In vitro treatment with CSE increased the transport of fluorescent markers and decreased TEER levels in mCMECs, respectively, which were attenuated by CD200Fc (10 and 100g/ml) pretreatment. The CSE-induced up-regulation of pro-inflammatory cytokines such as Cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), platelet endothelial cell adhesion molecule-1 (PECAM-1), vascular cell adhesion molecule-1 (ICAM-1), Prostaglandin E2 (PGE2), tumor necrosis factor- (TNF-), interleukin-6 (IL-6) and IL-8 in mCMECs was also abrogated by CD200Fc (10 and 100g/ml) pretreatment. CD200Fc also inhibited CSE-induced nuclear factor kappa-light-chain-enhancer of activated B cells (NF-B) activation in mCMECs, such as inhibition of its DNA binding activity, phosphorylated expression, and translocation to nucleus.Thus, CD200Fc exert anti-inflammatory effect and protect VEB function in CSE-induced mCMECs. The vasoprotective effects of CD200Fc may be specifically beneficial in pathophysiological conditions associated with smoking related cardiovascular diseases.


You J.,Taizhou Second Peoples Hospital | He X.,Taizhou Second Peoples Hospital | Ding H.,Taizhou Second Peoples Hospital | Zhang T.,Nanjing Southeast University
Cell Biochemistry and Biophysics | Year: 2014

Breast cancer metastasis suppressor 1 (BRMS1) was originally identified as a metastasis suppressor gene in human breast cancer. Previous studies have reported that loss of BRMS1 expression correlates with tumor progression, and poor prognosis in NSCLC. However, the role of BRMS1 in NSCLC is not fully understood. In this study, we found that expression of BRMS1 in A549 cells did not affect cell growth under normal culture conditions but sensitized cells to apoptosis induced by serum deprivation. Consistently, knockdown of endogenous BRMS1 expression in H1299 cells suppressed cell apoptosis. We identified that BRMS1 regulate apoptosis in NSCLC cells by modulating Stat3 activation. Taken together, our results show that BRMS1 sensitizes NSCLC cells to apoptosis through Stat3 signaling pathway, suggesting a potential role of BRMS1 in regulating NSCLC apoptosis and metastasis. © 2014 Springer Science+Business Media New York.


To examine the antiproliferative effect of the combination of docetaxel and sorafenib, applied to the representative non-small cell lung cancer cell line A549 cells either wild type or with acquired resistance to docetaxel (A549/D). The aim of this study is to evaluate the synergistic effect of combination treatment on cell growth inhibition and to elucidate the involved molecular mechanisms. A549 cells with acquired resistance to docetaxel were established by continuous exposure to docetaxel. We examined the effect of different combinatorial treatment on cell proliferation and cell cycle distribution. In addition, the effect of combinatorial treatments on proliferative and apoptotic signalling pathway were studied. Our results showed that the synergistic effect presented when A549 cells were treated with docetaxel followed by sorafenib or when A549/D cells were treated in reverse sequence. Furthermore, we suggested that synergistic effect in A549/D cells was caused by inhibiting P-gp function and altering in the balance of growth and apoptotic signalling pathways. Our data suggested a potential role of sorafenib in chemosensitizing docetaxel-resistant cancer cells. This study also provides molecular evidence for applying different therapeutic strategies for patients with different genetic and proteomic profile. © 2013 Springer Science+Business Media New York.


PubMed | Taizhou Second Peoples Hospital
Type: Journal Article | Journal: Cell biochemistry and biophysics | Year: 2015

Breast cancer metastasis suppressor 1 (BRMS1) was originally identified as a metastasis suppressor gene in human breast cancer. Previous studies have reported that loss of BRMS1 expression correlates with tumor progression, and poor prognosis in NSCLC. However, the role of BRMS1 in NSCLC is not fully understood. In this study, we found that expression of BRMS1 in A549 cells did not affect cell growth under normal culture conditions but sensitized cells to apoptosis induced by serum deprivation. Consistently, knockdown of endogenous BRMS1 expression in H1299 cells suppressed cell apoptosis. We identified that BRMS1 regulate apoptosis in NSCLC cells by modulating Stat3 activation. Taken together, our results show that BRMS1 sensitizes NSCLC cells to apoptosis through Stat3 signaling pathway, suggesting a potential role of BRMS1 in regulating NSCLC apoptosis and metastasis.

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