1.Clinical study of ivermectin/metronidazole in the treatment of patients with intestinal acariasis
Yangqing SUN ; Xuewen LIU ; Weichao LIANG ; Dayun LIN ; Weimin YAO
Chinese Journal of Primary Medicine and Pharmacy 2006;0(05):-
Objective To compare the efficacy and safety of ivermectin with metronidazole in patients with intestinal acariasis.Methods 24 patients with typical intestinal acariasis were selected and divided into two groups,each group had 12 members.Double-blind,randomized clinical trial of ivermectin versus metronidazole was assigned.Results 24 patients completed 3 courses.The total cure rate of ivermectin and metronidazole were 100%(12/12) and 25%(3/12),respectively.There was statistical difference between the two groups(P
2.Study of the relationship between the onset of peptic ulcers and meteorological factors.
Dayun LIU ; Anning GAO ; Guodu TANG ; Wangyue YANG
Chinese Medical Journal 2003;116(12):1940-1942
OBJECTIVETo discuss the relationship between the onset of peptic ulcers (PU) and meteorological factors (MF).
METHODSIn reviewing records from 17 hospitals in the city of Nanning from 1992 to 1997, we found 24, 252 cases of PU in 104, 121 samples of gastroscopic examinations. We then calculated the detectable rate of PU (DRPU) during each season every five days (FD) and made a correlated analysis with the seasonal MF during the same period in Nanning. Finally, we made a multiple regressive correlated analysis of DRPU and the 5MF for the same period of the year. A forecast model based on the MF of the previous FD was established. The real value and the forecast value was being tested and verified.
RESULTSFrom 1992 to 1997, the DRPU is: winter and spring > summer and autumn (P < 0.005). There is a close relationship between the DRPU and the average temperature (AT), the average highest temperature (AHT), the average lowest temperature (ALT), average air pressure (AAP) and the average dew point temperature (ADT) of the five days of the same period of the year (the correlated coefficients are -0.5348, -05167, -0.5384, 0.4579 and -0.4936, respectively), with P < 0.01. The AT, AHT, ALT, AAP and ADT of the previous FD are of great value in forecasting the onset of PU, with its real value and forecast value corresponding to 66.6%.
CONCLUSIONSThere exists a close relationship between DRPU and the AT, AHT, ALT, AAP and ADT of the FD for the same period. A mid-term medical meteorological forecast of the onset of PU can be made more accurately and reliably according to the close relation between the DRPU and some MF of the previous FD.
Forecasting ; Humans ; Meteorological Concepts ; Peptic Ulcer ; epidemiology ; Pressure ; Seasons ; Temperature
3. Acrolein Induces Systemic Coagulopathy via Autophagy-dependent Secretion of von Willebrand Factor in Mice after Traumatic Brain Injury
Wenxing CUI ; Xun WU ; Dayun FENG ; Jianing LUO ; Yingwu SHI ; Wei GUO ; Haixiao LIU ; Qiang WANG ; Liang WANG ; Shunnan GE ; Yan QU
Neuroscience Bulletin 2021;37(8):1160-1175
Traumatic brain injury (TBI)-induced coagulopathy has increasingly been recognized as a significant risk factor for poor outcomes, but the pathogenesis remains poorly understood. In this study, we aimed to investigate the causal role of acrolein, a typical lipid peroxidation product, in TBI-induced coagulopathy, and further explore the underlying molecular mechanisms. We found that the level of plasma acrolein in TBI patients suffering from coagulopathy was higher than that in those without coagulopathy. Using a controlled cortical impact mouse model, we demonstrated that the acrolein scavenger phenelzine prevented TBI-induced coagulopathy and recombinant ADAMTS-13 prevented acrolein-induced coagulopathy by cleaving von Willebrand factor (VWF). Our results showed that acrolein may contribute to an early hypercoagulable state after TBI by regulating VWF secretion. mRNA sequencing (mRNA-seq) and transcriptome analysis indicated that acrolein over-activated autophagy, and subsequent experiments revealed that acrolein activated autophagy partly by regulating the Akt/mTOR pathway. In addition, we demonstrated that acrolein was produced in the perilesional cortex, affected endothelial cell integrity, and disrupted the blood-brain barrier. In conclusion, in this study we uncovered a novel pro-coagulant effect of acrolein that may contribute to TBI-induced coagulopathy and vascular leakage, providing an alternative therapeutic target.
4.Acrolein Aggravates Secondary Brain Injury After Intracerebral Hemorrhage Through Drp1-Mediated Mitochondrial Oxidative Damage in Mice.
Xun WU ; Wenxing CUI ; Wei GUO ; Haixiao LIU ; Jianing LUO ; Lei ZHAO ; Hao GUO ; Longlong ZHENG ; Hao BAI ; Dayun FENG ; Yan QU
Neuroscience Bulletin 2020;36(10):1158-1170
Clinical advances in the treatment of intracranial hemorrhage (ICH) are restricted by the incomplete understanding of the molecular mechanisms contributing to secondary brain injury. Acrolein is a highly active unsaturated aldehyde which has been implicated in many nervous system diseases. Our results indicated a significant increase in the level of acrolein after ICH in mouse brain. In primary neurons, acrolein induced an increase in mitochondrial fragmentation, loss of mitochondrial membrane potential, generation of reactive oxidative species, and release of mitochondrial cytochrome c. Mechanistically, acrolein facilitated the translocation of dynamin-related protein1 (Drp1) from the cytoplasm onto the mitochondrial membrane and led to excessive mitochondrial fission. Further studies found that treatment with hydralazine (an acrolein scavenger) significantly reversed Drp1 translocation and the morphological damage of mitochondria after ICH. In parallel, the neural apoptosis, brain edema, and neurological functional deficits induced by ICH were also remarkably alleviated. In conclusion, our results identify acrolein as an important contributor to the secondary brain injury following ICH. Meanwhile, we uncovered a novel mechanism by which Drp1-mediated mitochondrial oxidative damage is involved in acrolein-induced brain injury.
5. Antagonism of Protease-Activated Receptor 4 Protects Against Traumatic Brain Injury by Suppressing Neuroinflammation via Inhibition of Tab2/NF-κB Signaling
Jianing LUO ; Xun WU ; Haixiao LIU ; Wenxing CUI ; Wei GUO ; Kang GUO ; Hao GUO ; Kai TAO ; Fei LI ; Yingwu SHI ; Dayun FENG ; Guodong GAO ; Yan QU ; Hao YAN
Neuroscience Bulletin 2021;37(2):242-254
Traumatic brain injury (TBI) triggers the activation of the endogenous coagulation mechanism, and a large amount of thrombin is released to curb uncontrollable bleeding through thrombin receptors, also known as protease-activated receptors (PARs). However, thrombin is one of the most critical factors in secondary brain injury. Thus, the PARs may be effective targets against hemorrhagic brain injury. Since the PAR1 antagonist has an increased bleeding risk in clinical practice, PAR4 blockade has been suggested as a more promising treatment. Here, we explored the expression pattern of PAR4 in the brain of mice after TBI, and explored the effect and possible mechanism of BMS-986120 (BMS), a novel selective and reversible PAR4 antagonist on secondary brain injury. Treatment with BMS protected against TBI in mice. mRNA-seq analysis, Western blot, and qRT-PCR verification in vitro showed that BMS significantly inhibited thrombin-induced inflammation in astrocytes, and suggested that the Tab2/ERK/NF-κB signaling pathway plays a key role in this process. Our findings provide reliable evidence that blocking PAR4 is a safe and effective intervention for TBI, and suggest that BMS has a potential clinical application in the management of TBI.