1.Clinjcal Study Chemotherapeutic Renal Failure Treated with Wuling Powder with Additives
Jianghua CHENG ; Hao LONG ; Dehui ZHAO ; Xiao WANG ; Jiali ZHU ; Liping ZHU ; Zhaoming HUANG
Journal of Traditional Chinese Medicine 1993;0(01):-
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.
2.Reproductive damage of male rats exposed to plateau environment
BU Zihan ; ZHOU Hao ; LI Jiahao ; ZHANG Bin ; ZHANG Chunlei ; CHANG Dehui
Journal of Preventive Medicine 2024;36(8):727-730,736
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.
3.Toxicity of Large Dose of Cisplatin on Kidney-Pre-vented by Decoction of Radix Astragali seu Hedysariand Poria
Jianhua CHEN ; Suole ZHANG ; Zhaoming HUANG ; Hao LONG ; Jiali ZHU ; Dehui ZHAO ; Xiao WANG ; Liping ZHU ; Weixin LIU ; Zhiping LI
Journal of Traditional Chinese Medicine 1993;0(06):-
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.
4.Research progress concerning risk factors and prediction models of postoperative delirium in patients with hip fracture
Weili ZHANG ; Chen QIU ; Dan KONG ; Dehui HAO ; Yuan GAO
Chinese Journal of Orthopaedic Trauma 2023;25(12):1095-1099
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.
5.Extracellular Ubiquitin Enhances Autophagy and Inhibits Mitochondrial Apoptosis Pathway to Protect Neurons Against Spinal Cord Ischemic Injury via CXCR4
Hao FENG ; Dehui CHEN ; Huina CHEN ; Dingwei WU ; Dandan WANG ; Zhengxi YU ; Linquan ZHOU ; Zhenyu WANG ; Wenge LIU
Neurospine 2025;22(1):157-172
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.
6.Extracellular Ubiquitin Enhances Autophagy and Inhibits Mitochondrial Apoptosis Pathway to Protect Neurons Against Spinal Cord Ischemic Injury via CXCR4
Hao FENG ; Dehui CHEN ; Huina CHEN ; Dingwei WU ; Dandan WANG ; Zhengxi YU ; Linquan ZHOU ; Zhenyu WANG ; Wenge LIU
Neurospine 2025;22(1):157-172
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.
7.Extracellular Ubiquitin Enhances Autophagy and Inhibits Mitochondrial Apoptosis Pathway to Protect Neurons Against Spinal Cord Ischemic Injury via CXCR4
Hao FENG ; Dehui CHEN ; Huina CHEN ; Dingwei WU ; Dandan WANG ; Zhengxi YU ; Linquan ZHOU ; Zhenyu WANG ; Wenge LIU
Neurospine 2025;22(1):157-172
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.
8.Extracellular Ubiquitin Enhances Autophagy and Inhibits Mitochondrial Apoptosis Pathway to Protect Neurons Against Spinal Cord Ischemic Injury via CXCR4
Hao FENG ; Dehui CHEN ; Huina CHEN ; Dingwei WU ; Dandan WANG ; Zhengxi YU ; Linquan ZHOU ; Zhenyu WANG ; Wenge LIU
Neurospine 2025;22(1):157-172
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.
9.Extracellular Ubiquitin Enhances Autophagy and Inhibits Mitochondrial Apoptosis Pathway to Protect Neurons Against Spinal Cord Ischemic Injury via CXCR4
Hao FENG ; Dehui CHEN ; Huina CHEN ; Dingwei WU ; Dandan WANG ; Zhengxi YU ; Linquan ZHOU ; Zhenyu WANG ; Wenge LIU
Neurospine 2025;22(1):157-172
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.
10. The prognostic significance of minimal residual disease detection after first induction treatment in adult acute lymphoblastic leukemia patients treated with autologous stem cell transplantation
Zoufang HUANG ; Jie XU ; Mingwei FU ; Tingyu WANG ; Mu HAO ; Wei LIU ; Lugui QIU ; Dehui ZOU
Chinese Journal of Hematology 2019;40(2):105-110
Objective:
To investigate the prognostic significance of detection of minimal residual disease after first induction treatment (MRD1) in adult acute lymphoblastic leukemia (ALL) patients treated with autologous stem cell transplantation (auto-HSCT).
Methods:
The clinical data of 87 ALL patients who underwent auto-HSCT during February 2006 to April 2017 with MRD1 detection data by flow cytometry were analyzed retrospectively. The relationship between MRD1 and relapse and survival of ALL patients after auto-HSCT was studied.
Results:
Of 87 patients, 26 (29.9%) were MRD1 positive. The proportion of high-risk immunophenotype (pro-B, pro-T, pre-T, mature T) was significantly higher in MRD1-positive patients than that in MRD1 negative patients (34.6%