24 cases of renal failure induced by chemotherapy were treated with Wuling powder plus additives.Theresult of clinical amelioration was 87.5%.with a to-tal effective yielded marked actions of promoting ap-petite in animals,lowering serum urea nitrogen,cre-atinine,2 microglobulin.It also decreased the inhibi-tion of PDD on the enzyme activity of renal Na~+—K~+ATP.Microscopic exam revealed the pathological le-sion of kidney to be milder in the tested group.

Objective: To investigate the effects of plateau environment exposure on the reproductive system of male rats, so as to provide the reference for mechanisms of reproductive damage in plateau environment. Methods: Sixty SPF-grade 12-week-old male Wistar rats were randomly divided into the plain-exposed group, the 1 day-, 3 day-, 7 day-, 14 day- and 28 day- plateau-exposed groups. The rats in the plain-exposed group were raised under normal conditions for 28 days, while the rats in the plateau-exposed groups were raised in a simulated high-altitude plateau chamber. After the completion of the designated feeding periods, the rats were sacrificed under anesthesia, and testicular tissue and abdominal aortic blood were collected to detect the testicular index and evaluate sperm quality. Histological and cellular morphologies of the testicular tissue were analyzed. Additionally, the levels of malondialdehyde (MDA), superoxide dismutase (SOD) and reactive oxygen (ROS) in the testicular tissue were determined, along with serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone (T). Conclusions Plateau environment may cause a decrease in testicular index and sperm quality, impair mitochondrial function, induce oxidative stress, and thus affect reproductive system of male rats. However, there are signs of self-repair in the reproductive system with the increase of exposure duration.

Clinical observation revealed that combined use of Decoction of Radix Astragali seu Hedysari and Poria withlarge dose of Cisplatin.none of the cases showed ab-normality in BUN,Cr.with improvement of biochemi-cal indices,there was also diuretic actions observed.Ahgdraton contrel group revealed worse result.The ex-periment proves that the Decoction is capable of pre-venting and ameliorating the harmful effect on kidneyinduced by Cisplatin in rats.

Postoperative delirium, one of the common complications in patients with hip fracture, has a high incidence and poor prognosis. As there have been no effective treatments for this complication, early prediction and intervention is the most effective method available to reduce its occurrence. This study reviews the types and characteristics of the patients who suffer from postoperative delirium after hip fracture, as well as the risk factors that have been currently found. The risk prediction models for postoperative delirium are also analyzed and compared in hip fracture patients from the perspectives of cohorts included, research design, model construction and validation methods, model performance, and clinical application. The limitations of existing models are analyzed to foresee the development trend of future delirium prediction models for hip fracture patients. This study aims to help clinical healthcare professionals to identify as soon as possible those who will face a high risk for postoperative delirium after hip fracture surgery and to work out algorithms for targeted prevention and management.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective To analyze the relative indicators associated with warm ischemia time (WIT).Methods We established the porcine donor after cardiac death (DCD) model and monitored biochemical parameters (glucose,lactate,pyruvate,glycerol,and glutamate) changes of porcine livers at different WIT by microdialysis technique.The pathological changes were also observed during different WIT by HE staining.Results As the extension of WIT,the morphology injury of the graft aggravated:glucose and pyruvate levels slightly declined in the early stage,and then increased with WIT entension;glycerol levels increased with WIT entension;lactate levels and lactate/pyruvate ratio increased significantly after 20 min of WIT.The expression of lactate and lactate/pyruvate ratio were increased with the prolonged WIT.Pearson correlation analysis of all factors with liver ischemia time and liver pathological injury degree (P＜0.05) showed the obvious correlation between lactate,lactate/pyruvic acid ratio with liver ischemia time and liver pathological injury degree,and of positive correlation (P＜0.001,and correlation coefficients were 0.682 and 0.453 respectively).The ROC curve analysis revealed that the area under the curve was 0.950 for lactate,and 0.885 for pyruvate,respectively.When the critical value of lactic acid was 2.3736,the sensitivity was 90％ and specificity was 95％.When the critical value of lactate/pyruvate ratio was 0.0257,the sensitivity was 80％ and specificity was 83％.Conclusion The level of lactic acid and lactate/pyruvate ratio are significantly related to the WIT.These factors may be used as a predictor of donor liver warm ischemia injury.Reference range of these indicators needs further discussion based on larger sample research.