Objective:To explore whether the optic nerve sheath diameter (ONSD) within 24 hours of intensive care unit (ICU) admission is the predictor of 28-day delirium or coma and death in etiologically diverse critically ill patients.Methods:A prospective, observational study was conducted. The critically ill patients admitted to the emergency ICU of Cangzhou Central Hospital from January 2021 to October 2022 were enrolled. Bedside ultrasound monitoring ONSD was performed within 24 hours of ICU admission. The consciousness status was assessed daily during ICU hospitalization. Coma was defined as Glasgow coma scale (GCS) score < 8 or Richmond agitation-sedation scale (RASS) score -4 or -5. Delirium was defined as responsiveness to verbal stimulation and with a positive confusion assessment method-intensive care unit (CAM-ICU). A positive result of CAM-ICU was defined as acute change or fluctuating course of mental status+inattention+altered level of consciousness or disorganized thinking. X-tile software analysis was used to visualize the best cut-off value for creating divisions in predicting 28-day coma or delirium and death, and then Kaplan-Meier curves were plotted. ONSD≥the optimal cut-off value from X-tile analysis was defined as ONSD broadening. ONSD broadening and related indicators were enrolled, and multivariate Cox regression analysis was used to analyze the risk factors of 28-day coma or delirium and 28-day death in etiologically diverse critically ill patients.Results:A total of 321 critically ill patients were enrolled. Of them, 49 had primary brain injury, 54 had hypoxic ischemic brain injury (HIBI) after cardiac arrest, 70 had acute heart failure, 73 had sepsis, and 75 had other causes. Coma affected 184 patients (57.3%), and delirium affected 173 patients (53.9%). At 28 days of follow-up, 100 patients died, 16 patients remained comatose and 20 patients remained delirious. In all patients, as the GCS score decreased upon admission to the ICU, there was a gradually increasing trend in ONSD [GCS score 15 group: 5.20 (4.93, 5.43) mm, GCS score 10-14 group: 5.30 (4.90, 5.65) mm, GCS score 6-9 group: 5.40 (5.10, 5.80) mm, GCS score < 6 group: 5.70 (5.20, 5.96) mm, P < 0.05]. X-tile software analysis showed that in all patients and five etiological subgroups, ONSD broadening was a predictor for 28-day coma or delirium, and the optimal cut-off value was obtained (5.60 mm for all patients, 4.90 mm for primary brain injury, 5.75 mm for HIBI after cardiac arrest, 5.40 mm for acute heart failure, 5.90 mm for sepsis, and 5.75 mm for other causes). The Kaplan-Meier curves were plotted according to the optimal cut-off values, and the results showed that the higher the ONSD, the higher the incidence and duration of coma or delirium within 28 days in above patient population. X-tile software analysis showed that in all patients, and HIBI after cardiac arrest, sepsis and other causes patients, ONSD was a predictor for 28-day death, and the optimal cut-off value was obtained (6.20 mm for all patients, 5.85 mm for HIBI after cardiac arrest, 5.35 mm for sepsis, and 6.10 mm for other causes). The Kaplan-Meier curves were plotted according to the optimal cut-off values, and the results showed that the higher the ONSD, the higher the 28-day survival rate and the shorter survival duration in above patient population. Multivariate Cox regression analysis showed that ONSD broadening was an independent risk factor for 28-day coma or delirium in all patients [hazard ratio ( HR) = 1.513, 95% confidence interval (95% CI) was 1.093-2.095, P = 0.013] and patients with primary brain injury ( HR = 5.739, 95% CI was 2.112-15.590, P = 0.001). However, ONSD broadening was not independently associated with 28-day death in all patients or in the five etiological subgroups. Conclusions:ONSD within 24 hours of ICU admission is an independent risk factor for 28-day coma or delirium in etiologically diverse critically ill patients. It serves as a predictor for 28-day coma or delirium in 5 subgroups of etiology including primary brain injury, HIBI after cardiac arrest, acute heart failure, sepsis, and other causes, but not for 28-day death.

Objective To investigate the effect of atractylenolide Ⅲ(A Ⅲ)on stroke in spon-taneously hypertensive rats by regulating microRNA-296-5p(miR-296-5p)expression.Methods The spontaneously hypertensive rats(SHR)were given 0.9％sodium chloride solution freely for 2 months,and then fed with 1％sodium chloride solution to establish the stroke model of SHR.The rat models were randomly grouped into Model group,A Ⅲ low-dose group(A Ⅲ-L group),A Ⅲ high-dose group(A Ⅲ-H group),positive drug nimodipine group(Nim group),miR-296-5p agonist group(miR-296-5p agomir group),agomir NC group,A Ⅲ-H+miR-296-5p agomir group,and A Ⅲ-H+agomir NC group,with 12 in each group.The changes in neurological symptom scores,av-erage arterial pressure,survival time,and platelet adhesion rate were detected and recorded;hema-toxylin and eosin(HE)staining was applied to detect pathological changes in the CA1 region of the rat hippocampus;quantitative reverse transcription polymerase chain reaction(qRT-PCR)was ap-plied to detect the expression of miR-296-5p in the hippocampal CA1 region.Results Compared with the NC group,the Model group showed increases in neurological symptom score,mean arterial pressure,platelet adhesion rate,miR-296-5p expression,shortened survival time,and severe pathological damage to the hippocampal CA1 area(P＜0.05);compared with the Model group,the neurological symptom scores,mean arterial pressure,platelet adhesion rate,and miR-296-5p expression in the A Ⅲ-L,A Ⅲ-H,and Nim groups decreased,the survival time was prolonged,and the pathological damage in the CA1 area of the hippocampus was alleviated(P＜0.05);compared with Model group and agomir NC group,neurological symptom score,mean arterial pressure,platelet adhesion rate and miR-296-5p expression of rats in the miR-296-5p agomir group were increased,survival time was shortened,and pathological damage in hippocampal CA1 region was aggravated(P＜0.05).compared with the A Ⅲ-H group and the AⅢ-H+agomir NC group,the neurological symptom score,average arterial pressure,platelet adhesion rate and miR-296-5p expression of rats were in-creased,the survival time was shortened,and the pathological damage in hippocampal CA1 region was serious in the AⅢ-H+miR-296-5p agomir group(P＜0.05).Conclusion A Ⅲ may treat SHR stroke by inhibiting the expression of miR-296-5p.

Objective To investigate the effect of atractylenolide Ⅲ(A Ⅲ)on stroke in spon-taneously hypertensive rats by regulating microRNA-296-5p(miR-296-5p)expression.Methods The spontaneously hypertensive rats(SHR)were given 0.9％sodium chloride solution freely for 2 months,and then fed with 1％sodium chloride solution to establish the stroke model of SHR.The rat models were randomly grouped into Model group,A Ⅲ low-dose group(A Ⅲ-L group),A Ⅲ high-dose group(A Ⅲ-H group),positive drug nimodipine group(Nim group),miR-296-5p agonist group(miR-296-5p agomir group),agomir NC group,A Ⅲ-H+miR-296-5p agomir group,and A Ⅲ-H+agomir NC group,with 12 in each group.The changes in neurological symptom scores,av-erage arterial pressure,survival time,and platelet adhesion rate were detected and recorded;hema-toxylin and eosin(HE)staining was applied to detect pathological changes in the CA1 region of the rat hippocampus;quantitative reverse transcription polymerase chain reaction(qRT-PCR)was ap-plied to detect the expression of miR-296-5p in the hippocampal CA1 region.Results Compared with the NC group,the Model group showed increases in neurological symptom score,mean arterial pressure,platelet adhesion rate,miR-296-5p expression,shortened survival time,and severe pathological damage to the hippocampal CA1 area(P＜0.05);compared with the Model group,the neurological symptom scores,mean arterial pressure,platelet adhesion rate,and miR-296-5p expression in the A Ⅲ-L,A Ⅲ-H,and Nim groups decreased,the survival time was prolonged,and the pathological damage in the CA1 area of the hippocampus was alleviated(P＜0.05);compared with Model group and agomir NC group,neurological symptom score,mean arterial pressure,platelet adhesion rate and miR-296-5p expression of rats in the miR-296-5p agomir group were increased,survival time was shortened,and pathological damage in hippocampal CA1 region was aggravated(P＜0.05).compared with the A Ⅲ-H group and the AⅢ-H+agomir NC group,the neurological symptom score,average arterial pressure,platelet adhesion rate and miR-296-5p expression of rats were in-creased,the survival time was shortened,and the pathological damage in hippocampal CA1 region was serious in the AⅢ-H+miR-296-5p agomir group(P＜0.05).Conclusion A Ⅲ may treat SHR stroke by inhibiting the expression of miR-296-5p.

【Objective】 To establish a routine screening method for unexpected antibodies of blood donors, analyze the results of centralized screening for unexpected antibody of blood donors in the blood center, and compare the cost of centralized and decentralized screening modes. 【Methods】 A total of 35 591 blood donors were screened for unexpected antibodies from March 31, 2021 to July 31, 2021, using microcolumn gel method. Unexpected antibody screening reactive samples were further confirmed by the Transfusion Research Institute of Shenzhen Blood Center, and the demographic characteristics were further determined through the analysis of unexpected antibody positive population. The direct cost and indirect cost of centralized and decentralized unexpected antibody screening mode were compared. 【Results】 Forty unexpected antibody positive samples were confirmed in Shenzhen, with the positive rate at 0.11%(40/35 591), among which MNS, Rh and Lewis system accounted for 35% (14/40), 32.5% (13/40) and 17.5% (7/40), respectively. Males and females accounted for 45% (18/40) and 55% (22/40), respectively (P<0.01). No significant difference was noticed by age and repeated-donor or not (P>0.05). Unexpected antibody screening in a centralized way saved about 1.16 million yuan per year. 【Conclusion】 It is necessary to carry out unexpected antibody screening for all blood donors, and centralized screening is more economical than decentralized screening.

AIM: To evaluation the effects of esketamine and butorphanol on postoperative pruritus induced by epidural morphine injection in cesarean delivery parturients. METHODS: A total of 162 parturients who underwent elective cesarean section under continuous epidural anesthesia in Taizhou Central Hospital (Taizhou University Hospital), were selected and randomly divided into esketamine group (group K), butorphanol group (group B) and blank control group (group C). 5min after umbilicus amputation, parturients in group K was injected with 3 mg morphine diluent through epidural catheter, and esketamine 0.2 mg/kg intravenously. Parturients in groups B and C were given the same dose of morphine,and butorphanol 10 μg/kg or the same volume of normal saline, respectively. The incidence of postoperative pruritus at different times, the degree of pruritus and incidence of other adverse reactions were compared among three groups. RESULTS: The highest incidence of pruritus occurred within 4 hours after operation. The incidence of postoperative pruritus at 4 hours in group K and B was significantly lower than that in group C (3.7% vs. 3.7% vs. 29.6%, P < 0.05), the total incidence of postoperative pruritus within 48 hours was also significantly lower than that in group C (13.0% vs. 11.1% vs. 40.7%, P < 0.05), and the incidence of moderate to severe pruritus was also significantly lower than that of group C (5.6% vs. 3.7% vs. 31.5%, P < 0.05). There was no significant difference between group K and group B (all P > 0.05). There were no significant differences in the incidence of postoperative nausea, vomiting, dizziness and postoperative pain scores among three groups (P > 0.05). CONCLUSION: Both esketamine and butorphanol can reduce the incidence and degree of pruritus caused by epidural morphine injection in parturients, without affecting the analgesic effect of morphine and without increasing the incidence of adverse reactions. Esketamine is as effective and safe as butorphanol in preventing pruritus after cesarean section.

Objective: To retrospectively analyze the efficacy and prognostic factors of postoperative intensity modulated radiotherapy for grade Ⅱ gliomas. Methods: Retrospective analysis was conducted on patients with postoperative grade Ⅱ glioma in our hospital from Jan. 2010 to Dec. 2018. The primary endpoint was progression-free survival, and the secondary endpoint was overall survival. Correlative analyses of prognosis by age, gender, initial resection status, the maximum diameter of the lesions, bi-hemisphere, astrocytoma, chemoradiation, adjuvant chemotherapy were conducted. Results: A total of 109 cases with grade Ⅱ glioma were enrolled. The follow-up rate was 91.75%, including 10 cases dead and 27 relapsed. There were 24 cases (88.9%) of in-field failure, and 3 cases (11.1%) of out-field failure. 14 cases of recurrence occurred in 81 cases of total resection group, accounting for 17.3%, and 13 in 28 cases of subtotal resection group, accounting for 46.4%. The recurrence rate in the subtotal resection group was significantly higher than that in the total resection group (χ ²=9.484, P<0.05). The 1-, 2-, 3-, 4- and 5-year progression-free survival rates were 92.5%, 86.0%, 80.6%, 77.5% and 66.8%, respectively. The 2-, 3-, 4- and 5-year overall survival rates were 97.2%, 90.8%, 87.7% and 84.5%, respectively. Multivariate analysis showed that patients with subtotal resection(HR=3.608, P<0.05) and bi-hemisphere(HR=3.183, P<0.05)were significantly correlated with the progression free survival. Conclusions Postoperative intensity modulated radiotherapy for grade Ⅱ gliomas can achieve a better PFS. Recurrence in the radiation field is the main failure mode. Initial resection status and bi-hemisphere of tumor are important influential factors for PFS of grade Ⅱ gliomas patients.

Based on the noninvasive detection indeices and fuzzy mathematics method, this paper studied the noninvasive, convenient and economical cardiovascular health assessment system. The health evaluation index of cardiovascular function was built based on the internationally recognized risk factors of cardiovascular disease and the noninvasive detection index. The weight of 12 indexes was completed by the analytic hierarchy process, and the consistency test was passed. The membership function, evaluation matrix and evaluation model were built by fuzzy mathematics. The introducted methods enhanced the scientificity of the evaluation system. Through the Kappa consistency test, McNemer statistical results ( = 0.995 > 0.05) and Kappa values (Kappa = 0.616, < 0.001) suggest that the comprehensive evaluation results of model in this paper are relatively consistent with the clinical, which is of certain scientific significance for the early detection of cardiovascular diseases.
Cardiovascular Diseases ; diagnosis ; Cardiovascular System ; Fuzzy Logic ; Humans ; Models, Cardiovascular ; Research

Objective To investigate the effects of inhibiting NgR on retinal ganglion cells density and synaptophysin expression of diabetic rat.Methods Thirty-two SD male rats were randomly divided into normal control group,diabetic group,siNgR group and scNgR group,8 rats in each group.Normal control group was given no any treatment.Diabetes model was induced by intraperitoneal injection of 50 mg · kg-1 streptozotocin in diabetic group,siNgR group and scNgR group,and the blood giucose more than 16.7 mmol · L-1 at 72 hours was set as the successfully model.The rats of siNgR group were intravitreally administrated with anti-NgR nucleotide and the rats of scNgR group intravitreally administrated with negative nucleotide.Eight weeks later,HE staining was conducted to detect density of retinal ganglion cell (RGC),immunofluorescence was used to evaluate the expression and distribution of synaptophysin (a marker of synaptic number).Relative expression of NgR and synaptophysin in retina were analyzed by Western blot.Results RGC density in normal control group,diabetes group,siNgR group and scNgR group were (624.33 ± 3.51) mm-2,(420.00 ± 2.65) mm-2,(621.67 ± 1.53) mm-2,(416.67 ± 2.52) mm-2,respectively.There was significant difference among four groups (F =5985.37,P ＜ 0.01).Compared with normal control group,RGC density in diabetes group and scNgR group were obviously decreased (all P ＜0.01),but siNgR group had no obviously change (P ＞ 0.05).The synaptophysin mainly expressed in the inner and outer network layer.Compared with normal control group,the positive expression of synaptophysin in diabetes group and scNgR group were decreased,but siNgR group had no obviously change.The relative expression of NgR in normal control group,diabetes group,siNgR group and scNgR group were (11.26 ±0.02) ％,(19.38 ± 0.10) ％,(11.17 ± 0.02) ％,(19.47 ± 0.31) ％,respectively.There was significant difference among four groups (F =2466.09,P ＜ 0.01).Compared with normal control group,the relative expression of NgR in diabetes group and scNgR group were obviously decreased (all P ＜ 0.01),but siNgR group had no obviously change (P ＞0.05).The relative expression of synaptophysin in normal control group,diabetes group,siNgR group and scNgR group were (35.76 ± 0.15) ％,(25.47 ± 0.36) ％,(35.28 ± 0.12) ％,(25.03 ± 0.75) ％,respectively.There was significant difference among four groups (F =583.70,P ＜ 0.01).Compared with the normal control group,the expression of synaptophysin in diabetic group and scNgR group were decreased increased (all P ＜ 0.01),while there was no significant difference in siNgR group (P ＞ 0.05).Conclusion Inhibiting the expression of NgR in the retina of diabetic rats can help to restore the number of synapses and protect the damaged RGC.

Objective To investigate the effects of nerve growth factor (NGF) on retinal synaptic plasticity of diabetic mellitus rat and its underlying mechanisms.Methods A total of 24 clean SD male rats were randomly divided into three groups (n =8),and they were control group,diabetic group and treatment group.In the latter two groups,a model of diabetic rats was induced by streptozotocin,and then the rats of treatment group were injected intraperitoneally 800 U · kg-1 NGF once a day after the model was induced successfully.Both control group and diabetic group were given the same amount of normal saline.Twelve weeks later,MDA content and SOD activity were detected;meanwhile,the expression of retinal synaptophysin was detected by immunofluorescence,and the expressions of retina synaptophysin and Caspase-3 were detected by Western blot.Results The difference of MDA content in the three groups was statistically significant (F =85.46,P ＜ 0.01);and the content of MDA in the diabetic group was significantly higher than that in the control group (P ＜0.01),while its content in the treatment group was significantly lower than that in the diabetic group (P ＜0.01).The difference of SOD activity in the three groups was statistically significant (F =17.76,P ＜0.01);and the SOD activity in the diabetic group was significantly lower than that in the control group (P ＜0.01),while its activity in the treatment group was significantly higher than that in the diabetic group (P ＜0.01).The difference of immunofluorescence intensity of synaptophysin in the three groups was statistically significant (F =395.42,P ＜ 0.01);immunofluorescence intensity of synaptophysin in the diabetic group was attenuated compared with the control group (P ＜0.01),while the intensity in the treatment group was enhanced compared with the diabetic group(P ＜0.01).The difference of the relative expression of synaptophysin in the three groups was statistically significant (F =17.27,P ＜ 0.01);and the expression of synaptophysin in the diabetic group was significantly downregulated compared with the control group (P ＜ 0.01),while its expression in the treatment group was upregulated compared with the diabetic group (P ＜ 0.01).The difference of relative expression of Caspase 3 protein in the three groups was statistically significant (F=217.13,P ＜0.01);and the expression level of Caspase 3 in the diabetic group was significantly higher than that in the control group (P ＜0.01),while its level in the treatment group was significantly lower than that in the diabetic group (P ＜ 0.01).Conclusion NGF can help to inhibit the apoptosis of retinal cell,restore the number of retina synapse by reducing the oxidative stress in diabetic retina,which suggests that NGF may be involved in the changes of synaptic plasticity in diabetic retina via oxidative stress pathway.

Objective To investigate the associations of baseline serum uric acid, bilirubin levels with short-term outcome in patients with acute ischemic stroke. Methods The clinical data in successive patients with acute ischemic stroke were colected, including the serum levels of uric acid and bilirubin on admission, the National Institutes of Health Stroke Scale (NIHSS) score, and the modified Rankin scale (mRS) score at discharge or at day14 (mRS 0-2 was defined as good outcome, > 2 was defined as poor outcome). Results A total of 162 patients with ischemic stroke were enroled, including 114 in the good outcome group and 48 in the poor outcome group. There were significant differences in proportions of the patients with diabetes melitus (51. 75% vs. 75. 00% ; χ2 = 7. 526, P = 0. 006), previous history of stroke or transient ischemic attack (TIA) (18. 42% vs. 50. 00% ; χ2 = 17. 790, P = 0. 001), as wel as the baseline diastolic blood pressure (87. 061 ± 12. 245 mmHg vs. 82. 375 ± 10. 949 mmHg; t = 2. 293, P = 0. 023; 1 mmHg =0. 133 kPa), high-density lipoprotein cholesterol (1. 604 ± 0. 299 mmol/L vs. 1. 265 ± 0. 206 mmol/L; t =3. 227, P = 0. 002), fasting glucose (2. 875 ± 0. 438 mmol/L vs. 8. 160 ± 0. 592 mmol/L; t = - 4. 761, P <0. 001), uric acid (289. 365 ± 77. 168 μmol/L vs. 248. 206 ± 66. 206 μmol/L; t = 3. 111, P = 0. 002), total bilirubin (14. 673 ± 2. 213 μmol/L vs. 10. 395 ± 2. 714 μmol/L; t = 3. 779, P = 0. 001 ), direct bilirubin (6. 036 ± 1. 392 μmol/L vs. 4. 956 ± 1. 379 μmol/L; t = 2. 088, P = 0. 038), and indirect bilirubin (8. 634 ± 2. 307 μmol/L vs. 5. 439 ± 1. 223 μmol/L; t = 4. 219, P < 0. 001) levels between the 2 groups. Multivariate logistic regression analysis showed that the previous history of stroke or TIA (odds ratio [ OR ] 3. 751, 95% confidence interval [CI ] 1. 395-10. 091; P = 0. 009) and baseline NIHSS score (OR 2. 723, 95% CI 1. 093-6. 783; P = 0. 031) were the independent risk factors for poor outcome of ischemic stroke; while uric acid (OR 0. 357, 95% CI 0. 141-0. 900; P = 0. 029), high-density lipoprotein (OR 0. 262, 95% CI 0. 079-0. 870; P = 0. 029), and indirect bilirubin (OR 0. 117, 95% CI 0. 025-0. 539; P = 0. 006) were independently correlated with good outcome. Conclusions The increased baseline uric acid and indirect bilirubin levels are the favorable factors for good outcome in patients with acute ischemic stroke.