Objective To observe the effect of pre-hospital and intra-hospital collaborative ther-apeutic model in the treatment of patients with acute cerebral infarction.Methods A total of 67 pa-tients with acute cerebral infarction were selected as the research objects,and they were divided into observation group(n=37)and control group(n=30)according to the therapeutic model.The con-trol group was conducted with the traditional therapeutic model,while the observation group was con-ducted with the pre-hospital and intra-hospital collaborative therapeutic model.The time efficiency of intravenous thrombolysis,early recovery of nerve function and oxidative stress indexes were compared between the two groups.Results There was no significant difference in the time from onset to visit between the two groups(P＞0.05);the time from seeing a doctor to thrombolysis and the time from seeing a doctor to signing the informed consent for intravenous thrombolysis in the observation group were significantly shorter than those in the control group(P＜0.05).On the hospital admission,there was no significant difference in the National Institutes of Health Stroke Scale(NIHSS)score be-tween the two groups(P＞0.05);at the time points of 7 days after admission and 90 days after thrombolysis,the NIHSS scores of patients in the observation group were significantly lower than that in the control group(P＜0.05).There were no significant differences in the levels of serum glutathione peroxidase(GSH-Px)and malonaldehyde(MDA)between the two groups(P＞0.05);the level of serum superoxide dismutase(SOD)in the observation group was significantly higher than that in the control group(P＜0.05).One patient died in the control group,with a mortality rate of 3.33％;no patient died in the observation group.Conclusion Pre-hospital and intra-hospital collaborative therapeutic model can effectively improve the time efficiency of intravenous thrombolysis for patients with acute cerebral infarction,alleviate the neurological damage,and reduce degree of oxidative stress reaction and death risk.

Objective To observe the effect of pre-hospital and intra-hospital collaborative ther-apeutic model in the treatment of patients with acute cerebral infarction.Methods A total of 67 pa-tients with acute cerebral infarction were selected as the research objects,and they were divided into observation group(n=37)and control group(n=30)according to the therapeutic model.The con-trol group was conducted with the traditional therapeutic model,while the observation group was con-ducted with the pre-hospital and intra-hospital collaborative therapeutic model.The time efficiency of intravenous thrombolysis,early recovery of nerve function and oxidative stress indexes were compared between the two groups.Results There was no significant difference in the time from onset to visit between the two groups(P＞0.05);the time from seeing a doctor to thrombolysis and the time from seeing a doctor to signing the informed consent for intravenous thrombolysis in the observation group were significantly shorter than those in the control group(P＜0.05).On the hospital admission,there was no significant difference in the National Institutes of Health Stroke Scale(NIHSS)score be-tween the two groups(P＞0.05);at the time points of 7 days after admission and 90 days after thrombolysis,the NIHSS scores of patients in the observation group were significantly lower than that in the control group(P＜0.05).There were no significant differences in the levels of serum glutathione peroxidase(GSH-Px)and malonaldehyde(MDA)between the two groups(P＞0.05);the level of serum superoxide dismutase(SOD)in the observation group was significantly higher than that in the control group(P＜0.05).One patient died in the control group,with a mortality rate of 3.33％;no patient died in the observation group.Conclusion Pre-hospital and intra-hospital collaborative therapeutic model can effectively improve the time efficiency of intravenous thrombolysis for patients with acute cerebral infarction,alleviate the neurological damage,and reduce degree of oxidative stress reaction and death risk.

Cucurbitaceae is an important family of flowering plants containing multiple species of important food plants, such as melons, cucumbers, squashes, and pumpkins. However, a highly efficient genetic transformation system has not been established for most of these species (Nanasato and Tabei, 2020). Watermelon (Citrullus lanatus), an economically important and globally cultivated fruit crop, is a model species for fruit quality research due to its rich diversity of fruit size, shape, flavor, aroma, texture, peel and flesh color, and nutritional composition (Guo et al., 2019). Through pan-genome sequencing, many candidate loci associated with fruit quality traits have been identified (Guo et al., 2019). However, few of these loci have been validated. The major barrier is the low transformation efficiency of the species, with only few successful cases of genetic transformation reported so far (Tian et al., 2017; Feng et al., 2021; Wang JF et al., 2021; Wang YP et al., 2021). For example, Tian et al. (2017) obtained only 16 transgenic lines from about 960 cotyledon fragments, yielding a transformation efficiency of 1.67%. Therefore, efficient genetic transformation could not only facilitate the functional genomic studies in watermelon as well as other horticultural species, but also speed up the transgenic and genome-editing breeding.
CRISPR-Cas Systems ; Citrullus/genetics* ; Cucurbitaceae/genetics* ; Gene Editing ; Plant Breeding ; Transformation, Genetic

OBJECTIVEA remote wireless electrocardiogram (ECG) monitoring system is designed by using the CC2530 micro-controller as the device core.

METHODSAcquisition, conversion and data processing for ECG signals are realized on CC2530 micro-controllers. And the ECG data is transmitted to the coordinator by using ZigBee. It realizes the real-time monitoring of ECG signals and heart rate variability (HRV) data.

RESULTSThe test results show that the maximum error of the designed ECG monitoring analyzer is 3 beats per minute and the average error is 1.6 beats per minute, which can meet the requirement of pharmaceutical industry standards of the People's Republic of China.

CONCLUSIONSThe ECG monitoring analyzer has good portability, high measurement precision and good practical application values.

Objective: To investigate the history, risk factors for prognosis of malignant biliary stricture (MBS) patients receiving conservative therapy after endoscopic retrograde cholangiopancreatography(ERCP) and to set up a predictive model for overall survival (OS). Methods: MBS patients who underwent ERCP and conservative therapy in Xijing Hospital and PLA No.451 Hospital from January 2009 to December 2013 were enrolled to the present study. Predictive factors associated with OS were identified in the training cohort by stepwise multivariate Cox regression analysis. A predictive model was then developed and externally validated in the validation cohort. Results: Between January 2009 and December 2013, 152 and 149 patients were eligible to the training and validation cohort respectively. In the training cohort, tumors were mainly originated from bile duct (33.6%), pancreas (23.5%) or ampulla (20.4%). 76.3% (116/152) patients died during the observation period. The median OS for the training population was 5.0 months (3.9-6.2 months). CA19-9≥1 000 U/mL, non-ampulla tumor, metastasis, pre-ERCP total bilirubin≥7 mg/dL and hilar stricture were identified as independent predictive factors of poor OS (all P<0.05). Based on these factors, the COMTH predictive model was developed. The median OS of patients with COMTH>8 in the training and validation cohorts were both 3.0 months, which were significantly shorter than those with COMTH≤8 (10.0 and 6.9 months in the training and validation cohorts respectively, both P<0.001). Conclusion The prognosis of MBS patients undergoing ERCP is poor. The survival chance of patients with COMTH>8 is even more dismal.

Objective To investigate the protective effect of heat shock protein (HSP) 70 on the acute lung injury (ALI) of rats with heat stroke.Methods Sixty four rats were randomly (by employing a random number table) assigned into a sham-heated group (Sham group),heat stress group (HS group),and HS plus gluttamine treatment group (HS+GLN group) and HS plus quercet in treatment group (HS+QU group),16 each.All rats were housed in a artificial climate chamber,with the rats in the sham groups exposed to a temperature of 23 ℃ and humidity of 55％ ± 5％,while the rats of HS,HS+GLN and HS+QU groups to an ambient temperature of 39 ℃ and humidity of 65％.During heat stress or sham heating,rectal temperature (Tr),systolic blood pressure (SBP) and pulse rate (PR) were monitored to observe the difference in heat stress response among the groups.The time point at which the SBP started to drop from the peak level was taken as the point of HS onset.At the onset of HS,heat exposure was terminated,then the rats were immediately removed from the chamber,and returned to room temperature.The rats were scarified 0h and 6h after HS onset respectively.After bronchoalveolar lavage fluid (BALF) was collected,the lungs of all animals were harvested for pathological examination of lung injury.The concentrations of IL-1β,TNF-α and IL-6 in BALF and HSP70 in lung homogenate were measured by using an enzyme linked immunosorbent assay kit.Results Compared with HS and HS+QU groups,the rats in HS+GLN group required significantly greater heat load to induce HS (P＜0.001),and had longer survival time span after HS onset.Compared with Sham group,the concentration of HSP70 in lung homogenate in HS group increased in a time-dependent manner (P＜0.001).In comparison with HS group,the concentration of HSP70 in lung homogenate from HS+GLN group was significantly elevated at each time point (P＜0.001),while the treatment with QU significantly inhibited the expression of HSP70 (P＜0.001).The concentration of IL-1β,TNF-α and IL-6 in BALF significantly decreased in HS+GLN group compared with those in HS group and HS+QU group (P＜0.001).The pathological results showed that the lung injury was milder in HS+GLN group,while the opposite in HS+QU group.Conclusion HSP70 could protect HS rats against ALI by enhancing their thermo-tolerance and inhibiting inflammatory response.

Objective To investigate the role of oxidative stress in acute liver injury in a heat stroke model of conscious rats,and to explore its underlying mechanism.Methods Thirty-two rats were randomly (by using a random number table) assigned into a sham-heated control group (Sham group,n=8),a sham-heated group treated with NAC (Sham-NAC group,n=8),a heat stroke group (HS group,n=8) and a heat stoke group treated with NAC (HS-NAC,n=8).Rats were prepared with pre-warm chamber to initiate heat stoke.The change of rectum temperature (Tr),heart rate (HR) and systolic blood pressure (SBP) were monitored,and the time point of HS onset was recorded.Rats were sacrificed 12h after HS onset.ALT,serum TBIL,IL-6,IL-1β,TNF-α,MDA,T-SOD and GSH in the liver homogenates were measured.Liver tissues were harvested for determining the concentration of reactive oxygen species (ROS),neutrophil infiltration and the histological changes.Results During HS onset,no significant differences were observed in Tr,HR,SBP and heat exposure time between HS group and HS-NAC group (P＞0.05).However,the survival time was significantly longer in HS-NAC group than in HS group (P=0.039).12 hours after HS onset,the concentrations of ROS and MDA in the liver homogenates were significantly higher in HS group than in the other groups (P=0.000),while the concentrations of T-SOD and GSH were much lower than in the other groups (P=0.000).The serum concentrations of ALT and TBIL were significantly higher in HS group than in the other groups (P=0.000).Compare with HS group,the pathological injury was alleviated in HS-NAC group (P=0.000).The neutrophil infiltration level and the concentrations of IL-6,IL-1 β and TNF-α in liver tissue were significantly higher in HS group than in HS-NAC group (P=0.000).Conclusion Oxidative stress may play an important role in the pathogenesis of HS liver injury through its cytotoxic effect and by inducing inflammatory responses.

Objective To investigate the clinical significance of β2-microglobulin(β2-MG),glycated hemoglobin(HbA1c) and cystain C(CysC) in the diagnosis of early diabetic kidney injury.Methods Seventy cases of diabetic nephropathy(group DN) and 110 cases of simple diabetes(group DM) admitted and treated in our hospital from June to November 2015 were selected as the research subjects and performed the contrastive study with the 50 volunteers undergoing physical examination (control group)in the same period.The levels of β2-MG,HbA1c,CysC,SCr and Urea were compared among three groups.Results Compared with the control group,the SCr and Urea levels in the DM group had no statistically significant difference (P>0.05),while the β2-MG,HbA1c and CysC levels in the DM group were significantly higher than those in the control group(P<0.05);the levels of β2-MG,HbA1c,CysC,SCr and Urea in the DN group were significantly higher than those in the control group and DM group,the differences were statistically significant (P<0.05).The positive rates of single index detection and combined detection of β2-MG,HbA1c and CysC I the DN group were significantly higher than those in the DM group,and the differences were statistically significant (P<0.05).Conclusion For the patients with diabetes,β2-MG,HbA1c and CysC can better reflect the early damage of renal function,their joint detection is conducive to the diabetic treatment and disease condition monitoring.

Objective To investigate the effect of gradient heat stress on phagocytosis of hepatic Kupffer cells (KCs) in vitro in rats. Methods Rat Kupffer cells were isolated in vitro and the temperature for gradient heat stress was set at 37, 39, 41 and 43℃. After thermal stimulation, cell injury was detected by PI and Hochest33342 staining. CCK-8 assay was used to investigate difference in cellular proliferation rate over 24h between the groups. Flow cytometry was used to investigate the influence of heat stress on the phagocytosis of KCs. Results Compared to the normal control group, cells in each heat stress group exhibited varying degrees of damage, especially cells in 43℃ group. The ratio of damage cells increased with the increase of heat stress severity (P<0.05). Proliferation assay indicated that the proliferation rate of cells in each heat stress group was significantly decreased in comparison with normal control group 6h after heat stress (P<0.05). After 12h recovery, decrease in proliferation rate was observed only in 43℃ group (P<0.001), and no difference in the rate of proliferation could be observed between the heat stress groups and normal control group after 24h recovery. Flow cytometry showed, that the phagocytosis of KCs decreased in heat stress groups compared with control group, especially in 43℃ group (P<0.05). This phenomenon disappeared after 24h recovery. Conclusion Heat stress can inhibit the phagocytosis of rat liver KCs through its cytotoxic effect on KCs, and subsequently inhibits its proliferative ability. Further investigation of the effect of heat stress on KCs may help understand the pathogenesis of heat stress.

Objective To explore the protective effect of propofol on endothelial cells during heat stress and its protective effect to mitochondra. Methods Heat stress model of human umbilical vein endothelial cell was established when cells were incubated at 43℃ for 2h, then further incubted at 37℃, 5%CO2 for 6h. The experimental group was subdivided into six groups, including 37℃ group, 37℃ plus intralipid group (negative control group), 37℃ plus propofol group, 43℃ plus propofol group, 43℃ plus intralipid group, H2O2 plus propofol group (positive control group); Pretreated with 50μmol/L propofol, 0.2ml intralipid or 25μmol/L H2O2 before heat stress at 43℃, while the cells in the control group were incubated at 37℃. Cell viability was tested by CCK-8. ROS, mitochondrial membrane potential and the changes in mitochondrial permeability transition pore were determined by flow cytometry. The level of ATP was detected by fluorescein-luciferase. The changes of caspase-9 and caspase-3 were analyzed by Caspase Activity Assay Kit. Results HUVESs cell viability and damage of mitochondra were significantly decreased after heat stress. Compared with 43℃ heat stress group, pretreatment with propofol induced the recovery of cell viability and the ROS levels were significantly decreased in HUVEC cells (P<0.05). Meanwhile, the number of cells representing the decrease of mitochondrial membrane potential (the proportion of JC-1 monomer) was significantly decreased (P<0.05) by propofol. The average fluorescence intensity of calcein which representing the MPTP changes and intracellular ATP content was significantly increased (P<0.05). In addition, the activation of mitochondrial apoptotic pathway mediated by caspase-9/3 was also inhibited. Conclusions Propofol have anti-oxidative, anti-apoptosis and mitochondria protective effect against endothelial cell injury during heat stress.