Fermentation characteristics in stirred-tank reactor of exopolysaccharides with hypolipidemic activity produced by Pleurotus geesteranus 5#

In this study, the hypolipidemic effect of exopolysaccharides (EPS) from Pleurotus geesteranus 5# fermenting liquor by the optimal culture conditions in a 5-L stirred-tank reactor was investigated. The hypolipidemic effect of the polysaccharide, investigated in streptozotocin induced diabetic mice, decreased plasma glucose, total cholesterol and triacylglycerol concentrations by 17.1 %, 18.8 % and 12.0 %, respectively. The results of the present investigation strongly demonstrate the potential of this polysaccharide to prevent hyperglycemia in the experimental animals. Under optimal culture conditions, the maximum concentrations of mycelial and EPS were 22.63 g/L after 7 d cultivation and 11.09 g/L after 10 d, respectively. Furthermore, the morphological parameters (i.e. mean diameter, circularity, roughness and compactness) of the pellets and the broth viscosity were characterized. It was proved that compactness of the pellet morphology (R2=0.963, p<0.01) was significantly and positively determined with mycelial biomass. Moreover, mean diameter (R2=93.3, p<0.01) and broth viscosity (R2=0.950, p<0.01) were significantly and positively determined with EPS content

Astaxanthin ameliorates dopaminergic neuron damage in paraquat-induced SH-SY5Y cells and mouse models of Parkinson's disease

Parkinson’s disease (PD) is the second largest neurodegenerative disorder caused by the decreased number of dopaminergic (DAc) neurons in the substantia nigra pars compacta (SNpc). There is evidence that oxidative stress can contribute degeneration of DAc neurons in SNpc which is mainly caused by apoptotic cell death. Thus, suppressing oxidative stress and apoptosis of DAc neurons is an effective strategy to mitigate the progress of PD. Astaxanthin (AST) is a carotenoid, which mainly exists in marine organisms and is a powerful biological antioxidant. In this study, we aimed to determine the neuroprotective effect of AST on paraquat (PQ) -induced models of PD in vitro and in vivo. Here, we showed that AST significantly enhanced cell survival of SH-SY5Y cells against PQ toxicity by suppressing apoptotic cell death and oxidative stress. Moreover, we found that AST significantly ameliorated PQ-induced behavioral disorders associated with PD in C57BL/6 J mice and the damage to DAc neurons in the SNpc of mice. Lastly, we found that the neuroprotective effects of AST were conducted through inhibiting PQ-induced activation of MAPK signaling. In conclusion, our study indicates that AST had a strong protective effect on PQ-induced oxidative stress and antagonized apoptotic cell death in SH-SY5Y cells and PQ-induced mice PD model, which might provide new insights of AST for PD treatment

Incidence of Inadvertent Intraoperative Hypothermia and Its Risk Factors in Patients Undergoing General Anesthesia in Beijing: A Prospective Regional Survey.

Inadvertent intraoperative hypothermia (core temperature 2 h (OR = 3.44, 95% CI 1.90-6.22,), and intravenous un-warmed fluid (OR = 2.45, 95% CI 1.45-4.12) significantly increased the risk of hypothermia.The incidence of inadvertent intraoperative hypothermia in Beijing is high, and the rate of active warming of patients during operation is low. Concern for the development of intraoperative hypothermia should be especially high in patients undergoing major operations, requiring long periods of anesthesia, and receiving un-warmed intravenous fluids

Risk factors associated with intraoperative hypothermia, Beijing, China (N = 830).

<p>OR, Odds Ratio, Significant level indicates as P<0.05.</p><p>¹ adjusted OR were presented after adjusting all the variables in above table.</p><p>² patients receiving unwarmed IV fluid only</p><p>Risk factors associated with intraoperative hypothermia, Beijing, China (N = 830).</p

Change of intraoperative core temperature during operations.

<p>Patients’ core temperature was measured at the tympanic membrane beginning every 15 minutes after the induction of anesthesia and until the end of the operation. A total of 830 subjects were enrolled in the study; 89 (10.7%) received active warming, and 741(89.3%) received no warming.</p

Patient Demographics and Anesthesia/Surgery Data, Beijing, China (N = 830).

<p>¹ Magnitude of surgery as below: minor surgery: excision of lesion of skin; drainage of breast abscess, etc. Intermediate surgery: primary repair of inguinal hernia; excision of varicose vein(s) of leg; tonsillectomy/adenotonsillectomy; knee arthroscopy, etc. major surgery: total abdominal hysterectomy; endoscopic resection of prostate; lumbar discectomy; thyroidectomy, etc. major surgery plus: total joint replacement; lung operations; colonic resection; radical neck dissection; neurosurgery; cardiac surgery)</p><p>² Arthroscopic, laparoscopic, etc</p><p>³ Time from incision to closure</p><p>⁴ Time from induction to discontinuation of anesthetic agents</p><p>Patient Demographics and Anesthesia/Surgery Data, Beijing, China (N = 830).</p

Incidence of intraoperative hypothermia, patient warming and clinical outcome (N = 830).

<p>¹ passive warming includes comforter, blanket etc</p><p>² active warming includes electric heated blanket, space heater etc</p><p>Incidence of intraoperative hypothermia, patient warming and clinical outcome (N = 830).</p

Memory of stochastic single-cell apoptotic signaling promotes chemoresistance in neuroblastoma

Gene expression noise is known to promote stochastic drug resistance through the elevated expression of individual genes in rare cancer cells. However, we now demonstrate that chemoresistant neuroblastoma cells emerge at a much higher frequency when the influence of noise is integrated across multiple components of an apoptotic signaling network. Using a JNK activity biosensor with longitudinal high-content and in vivo intravital imaging, we identify a population of stochastic, JNK-impaired, chemoresistant cells that exist because of noise within this signaling network. Furthermore, we reveal that the memory of this initially random state is retained following chemotherapy treatment across a series of in vitro, in vivo, and patient models. Using matched PDX models established at diagnosis and relapse from individual patients, we show that HDAC inhibitor priming cannot erase the memory of this resistant state within relapsed neuroblastomas but improves response in the first-line setting by restoring drug-induced JNK activity within the chemoresistant population of treatment-naive tumors