ABSTRACT
BACKGROUND@#Pathological cardiac hypertrophy is one of the main activators of heart failure. Currently, no drug can completely reverse or inhibit the development of pathological cardiac hypertrophy. To this end, we proposed a silicate ion therapy based on extract derived from calcium silicate (CS) bioceramics for the treatment of angiotensin II (Ang II) induced cardiac hypertrophy. @*METHODS@#In this study, the Ang II induced cardiac hypertrophy mouse model was established, and the silicate ion extract was injected to mice intravenously. The cardiac function was evaluated by using a high-resolution Vevo 3100 small animal ultrasound imaging system. Wheat germ Agglutinin, Fluo4-AM staining and immunofluorescent staining was conducted to assess the cardiac hypertrophy, intracellular calcium and angiogenesis of heart tissue, respectively. @*RESULTS@#The in vitro results showed that silicate ions could inhibit the cell size of cardiomyocytes, reduce cardiac hypertrophic gene expression, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and b-myosin heavy chain (b-MHC), decrease the content of intracellular calcium induced by Ang II. In vivo experiments in mice confirmed that intravenous injection of silicate ions could remarkably inhibit the cardiac hypertrophy and promote the formation of capillaries, further alleviating Ang II-induced cardiac function disorder. @*CONCLUSION@#This study demonstrated that the released silicate ions from CS possessed potential value as a novel therapeutic strategy of pathological cardiac hypertrophy, which provided a new insight for clinical trials.
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ObjectiveTo investigate the effects of dexmedetomidine on postoperative cognitive dysfunction (POCD) in the elderly patients undergoing laparoscopic radical trachelectomy.MethodsSixty ASA Ⅰ or Ⅱ patients (aged 65-80 yr and weighing 55-74 kg) undergoing elective laparoscopic radical trachelectomy were randomly divided into two groups:30 patients received intravenous injection of dexmedetomidine 0.2 μg · kg - 1 ·h- 1 ( group D EX) and 30 received same volume of normal saline (control group,group NS) after induction of anesthesia.Cognitive function was assessed at 1 day before operation and on the 7th day after operation using a battery of nine cognitive dysfunction tests.ResultsCompared with group NS,on the 7th postoperative day,the incidence of POCD was decreased in group DEX ( P ＜ 0.05 ).ConclusionDexmedetomidine can improve POCD in the elderly patients undergoing laparoscopic radicaltrachelectomy.
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Through Hydroxyl (-OH) reacting with isocyanate group (-NCO), 13 Wt% nano-hydroxyapatite (n-HA)/polyurethane (PU) composite guided bone regeneration membrane was synthesized by use of solvent evaporation method. Its surface character was analyzed by XRD, IR, TG, contact angle, water absorption, elongation and combustion test and SEM. The results indicate that nano-HA/PU has good homogeneity,the interface between the inorganic mineral and organic polymer is optimized to create proper combination; that n-HA crystals are similar to the apatite crystals in natural bone, HA/PU composite membrane has good hydrophilicity mechanical behavior; and that many pores are observed on the membrane which help cells' metabolism. So the HA/PU composite membrane, thus prepared, has the potential for use in guided bone regeneration and tissue engineering.
Subject(s)
Biocompatible Materials , Chemistry , Bone Regeneration , Durapatite , Chemistry , Guided Tissue Regeneration , Methods , Nanocomposites , Chemistry , Polyurethanes , Chemistry , Tissue Engineering , Methods , Tissue Scaffolds , ChemistryABSTRACT
In the present study, we have cloned the gene of human neurotrophin-3 (hNT-3) from the genomic DNA of white blood cells (WBC) by polymerase chain reaction (PCR). The amplification products were cloned into pUC19 and sequenced. Genomic sequence comparison of the cloned fragment and the reported hNT-3 (GenBank M61180) reveals 7 base differences: 1 in the signal peptide, 3 in the prepro peptide, and 3 in the mature hNT-3. Except the 2 varied bases (16th, T to G; 285th, A to C) in the signal peptide and pro-sequence resulted in the change of their encoded amino-acids (Tyr→Asp; Gln→His), the other varied bases have no influence on their respective encoded amino-acids, and all the changes have no influence on the open reading frame (ORF) of the hNT-3.
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AIM: To explore the expressive profile of nestin protein in the focal ischemic brain and to study the recovery mechanism of brain focal infarct . METHODS: Cellular morphology, time-course and distribution pattern of nestin positive response were immunohistochemically examined in different brain regions of 36 adult male SD rats. RESULTS: Nestin positive response of different brain regions in sham operated rats was present in small- and micro-vasculartures and the third ventricle bottom and ependyma. A large number of nestin positive cells were detected in ischemic brain, and were more remarkable in the cortical areas of parietal lobe and preoptic area as well as ischemic caudoputamen. Stellate nestin positive cells were located in the deep layer of ischemic cortex, but fibrillary cells were located in the shallow layer. Nestin positive cells in the ischemic caudoputamen showed the same changes of morphology as those cells in the deep layer of ischemic cortex. Morphological and number alterations of nestin positive cells were the most remarkable at 1 weeks post-ischemia, which showed more hypertrophy and proliferation in morphology, and a marked increase in number was present in the ischemic cerebral cortex and the ischemic caudoputamen. These alterations of nestin positive cells persisted up to 6 weeks post-ischemia, and then, the nestin positive response in the ischemic brain decreased gradually. CONCLUSION: Focal cerebral ischemia induces nestin re-expression on reactive astrocytes, which may be very important to the self-recovery of cerebral infarct.