Analysis of blood component transfusion and some adverse reactions in myelodysplastic syndroms patients / 中国输血杂志

【Objective】 To analyze the blood transfusion and adverse reactions in myelodysplastic syndroms (MDS) patients, so as to improve transfusion management in MDS patients. 【Methods】 The diagnosis and treatment information of MDS patients with blood transfusion in our hospital from January 2003 to December 2022 were collected, and the component transfusion and adverse reactions were investigated. 【Results】 The average infusion volume of red blood cells(RBCs) and platelets were respectively (27.46±43.11 ) and (16.41±24.81 ) in 799 MDS patients, which had no correlation with gender and blood type. The incidence of adverse reactions was 18.27% (146/799), with the most common adverse reactions as delayed serologic transfusion reaction (DSTR) (9.01%, 72/799), followed by non hemolytic fever reaction (4.76%, 38/799) and allergic reaction (4.38%, 35/799). Compared with all patients with transfusion, DSTR was more common in females (P<0.05), with elder age and had more RBCs consumption (all P<0.01). 86.11%(62/72) were Rh system, and 40.28% (29/72) had 2 or more antibodies. The occurrence time of DSTR in some patients was not related to the volume of RBCs trans infusion. 【Conclusion】 MDS patients, with more average transfusion volume and higher incidence of adverse reactions especially DSTR, were recommended a strictly limited transfusion schedule and Rh phenotype matching RBC products. The investigation of immune status of MDS patients at different periods is helpful to provide new aspects and therapeutic measures for the pathogenesis of DSTR, and the antibody screening time may adjusted appropriately.

Efficacy of bedside gastric ultrasound in guiding enteral nutrition therapy in patients with spontaneous cerebral hemorrhage / 中华麻醉学杂志

Objective:To evaluate the efficacy of bedside gastric ultrasound in guiding enteral nutrition therapy in the patients with spontaneous cerebral hemorrhage.Methods:Sixty-one patients with spontaneous intracerebral hemorrhage in the intensive care unit (ICU) of our hospital, aged 18-60 yr, with the European malnutrition risk screening score in 2002 was ≥ 3, who could not eat orally, were selected.All patients received decompression or aneurysm clipping under general anesthesia.Patients were divided into 2 groups using a random number table method: control group ( n=30) and ultrasound group ( n=31). Nutrient infusion pump was used to infuse standard whole protein formula enteral nutrition continuously through a nasogastric tube.In control group, gastric residual volume, residual traits and bowel sounds were evaluated according to gastric drainage to start or adjust enteral nutrition treatment.In ultrasound group, the antral motility index and gastric residual volume were monitored by the modified antral single section method under ultrasound to start or adjust enteral nutrition treatment.The starting time of enteral nutrition, time to reach the target feeding amount, rate of reaching the target feeding standard within 96 h, interruption of enteral nutrition, duration of hospitalization in ICU, and occurrence of intraperitoneal hypertension, aspiration, diarrhea, gastrointestinal bleeding and new pulmonary infection during enteral nutrition therapy were recorded. Results:Compared with control group, the initiation time of enteral nutrition and time to reach the target feeding amount were significantly shortened, the interruption rate of enteral nutrition was decreased, the rate of reaching the target feeding standard within 96 h was increased, the incidence of aspiration and new pulmonary infection was decreased ( P<0.05), and no significant change was found in the duration of hospitalization in ICU and incidence of intraperitoneal hypertension, diarrhea and upper gastrointestinal bleeding in ultrasound group ( P>0.05). Conclusions:Bedside gastric ultrasound-guided enteral nutrition therapy can improve the therapeutic effect with higher safety in the patients with spontaneous intracerebral hemorrhage.

Effect of self-made Qingyuan Shenghua decoction on coagulation dysfunction in patients with sepsis / 中华危重病急救医学

Objective:To observe the effects of self-made Qingyuan Shenghua decoction on coagulation dysfunction in patients with sepsis, and to explore its possible mechanism.Methods:Eighty patients with sepsis and coagulation dysfunction admitted to the department of critical care medicine of Chengdu First People's Hospital from March 2018 to April 2020 were enrolled. The patients were divided into control group and observation group according to random number table method, with 40 cases in each group. Patients in both groups received basic treatment for sepsis. On this basis, the observation group was administrated with self-made Qingyuan Shenghua decoction, one dose a day, 100 mL in the morning and 100 mL in the evening; the control group was given the same amount of normal saline. Both groups were treated for 7 days. Prothrombin time (PT), activated partial thromboplastin time (APTT), international normalized ratio (INR), fibrinogen (Fib), D-dimer, platelet count (PLT), white blood cell count (WBC), C-reactive protein (CRP), and procalcitonin (PCT) were measured before and after treatment, and acute physiology and chronic health evaluation Ⅱ (APACHEⅡ) and sequential organ failure assessment (SOFA) were calculated. The length of intensive care unit (ICU) stay, the incidence of multiple organ dysfunction syndrome (MODS) and 28-day mortality was recorded.Results:The indexes of coagulation function and inflammation in the two groups were significantly improved after treatment, the improvement of various indexes in the observation group were better than those in the control group [PT (s): 16.01±1.08 vs. 19.21±1.38, APTT (s): 55.33±15.29 vs. 79.41±12.69, INR: 1.30±0.21 vs. 1.65±0.22, Fib (g/L): 2.87±0.89 vs. 5.44±1.13, D-dimer (mg/L): 2.56±1.67 vs. 6.41±2.42, PLT (×10 9/L): 125.79±18.51 vs. 95.46±18.50, WBC (×10 9/L): 7.50±0.78 vs. 12.75±4.09, CRP (mg/L): 21.27±9.32 vs. 65.44±13.40, PCT (μg/L): 1.15±0.58 vs. 6.31±1.29], and the differences were statistically significant (all P < 0.05). After treatment, APACHEⅡ and SOFA scores in the two groups decreased significantly compared with those before treatment, and the decrease in the observation group were more obvious than those in the control group (APACHEⅡ score: 10.29±1.86 vs. 15.35±2.06, SOFA score: 5.51±1.08 vs. 7.65±1.58, both P < 0.05). The length of ICU stay was shortened in the observation group than that in the control group (days: 12.22±9.48 vs. 20.22±15.35, P < 0.05). The incidence of MODS [35.0% (14/40) vs. 47.5% (19/40)] and the 28-day mortality [45.0% (18/40) vs. 47.5% (19/40)] was lower than that of the control group, but there was no statistical difference (both P > 0.05). Conclusion:Self-made Qingyuan Shenghua decoction can effectively improve the prognosis of patients with coagulation dysfunction and sepsis, and its mechanism may be related to inhibition of inflammatory reaction and improvement of coagulation function.

HNF1A-AS1 inhibits proliferation, migration and invasion of IL-6-induced hemangioma endothelial cells by targeting miR-363-3p / 中华医学遗传学杂志

OBJECTIVE@#To explore the effect of HNF1A-AS1 on the proliferation, migration and invasion of IL-6-induced hemangioendothelial cells (HemEC) and possible mechanism.@*METHODS@#RT-qPCR was used to detect the expression level of HNF1A-AS1 and miR-363-3p in the tumor tissue and adjacent normal skin tissue from 35 patients with hemangioma. Pearson correlation was used to analyze the correlation between the expression of HNF1A-AS1 and miR-363-3p in tumor tissues. HemEC were isolated and cultured in vitro.Dual luciferase reporter gene experiment was used to study the regulatory effect between HNF1A-AS1 and miR-363-3p. IL-6 was added to HemEC transfected with si-NC, si-HNF1A-AS1, si-HNF1A-AS1 and anti-miR-NC, or si-HNF1A-AS1 and anti-miR-363-3p, respectively. CCK-8 method and clone formation experiment were used to detect cell proliferation in each group. Transwell method was used to detect cell migration and invasion in each group. Western blotting was used to detect the expression of Ki67, MMP-2 and MMP-9 proteins in each group.@*RESULTS@#Compared with normal skin tissues, the expression of IL-6 mRNA in hemangioma tissues was increased (P<0.05), and the expression of IL-6 mRNA in the proliferative phase was lower than that in the degenerative phase (P<0.05). Expression of HNF1A-AS1 in hemangioma tissue was increased (P<0.05), while that of miR-363-3p was decreased (P<0.05), and the two were negatively correlated (r=-0.758, P<0.05). HNF1A-AS1 down-regulated the expression of miR-363-3p in HemEC.IL-6 promoted the expression of HNF1A-AS1, OD value, number of colonies, number of migration and invasion of HemEC cells, and the expression of Ki67, MMP-2 and MMP-9proteins (P<0.05), while reduced the expression of miR-363-3p (P<0.05). Down-regulating si-HNF1A-AS1 reduced the IL-6-induced HemEC cell OD value, colony numbers, migration and invasion and the expression of Ki67, MMP-2 and MMP-9 proteins (P<0.05). Down-regulating miR-363-3p attenuated the inhibitory effect of down-regulating si-HNF1A-AS1 on the proliferation, migration and invasion of HemEC cells induced by IL-6 (P<0.05).@*CONCLUSION@#Expression of HNF1A-AS1 is increased in hemangioma tissues. Down-regulating HNF1A-AS1 may inhibit proliferation, migration and invasion of IL-6-induced hemangioma endothelial cells by targeted up-regulation of miR-363-3p.

Effects of sleep fragmentation on vascular cognitive impairment and relationship with central inflammation and oxidative stress in rats / 中华麻醉学杂志

Objective:To evaluate the effects of sleep fragmentation on vascular cognitive impairment (VCI) and the relationship with central inflammation and oxidative stress in rats.Methods:Forty-eight male Sprague-Dawley rats, aged 8-10 weeks, weighing 210-240 g, were divided into 4 groups ( n=12 each) by a random number table method: sham operation group (group Sham), sham operation + sleep fragmentation group (group Sham+ SF), group VCI and VCI+ sleep fragmentation group (group VCI+ SF). VCI was induced by ligating bilateral common carotid arteries of anesthetized rats.In VCI+ SF and Sham+ SF groups, the sleep fragmentation model was established starting from day 26 after inducing VCI, and the contextual fear conditioning test and open field test were performed on day 29.After the end of the contextual fear conditioning test, the contents of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-6) were determined by enzyme-linked immunosorbent assay, the hippocampal superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), malondialdehyde (MDA) and iron contents were measured using microplate method, and the expression of nuclear factor-kappa B (NF-κB), caspase-3 and glutathione peroxidase 4 (GPX4) was determined using Western blot. Results:Compared with group Sham, the number of crossing lattices and standing on back legs and percentage of time spent freezing were significantly decreased, the contents of SOD and GSH-Px were decreased, the contents of MDA, IL-6, TNF-α and iron were increased, the expression of NF-κB and caspase-3 was up-regulated, and the expression of GPX4 was down-regulated in group VCI ( P<0.05). Compared with Sham+ SF and VCI groups, the number of crossing lattices and standing on back legs and percentage of time spent freezing were significantly decreased, the contents of SOD and GSH-Px were decreased, the contents of MDA, IL-6, TNF-α and iron were increased, the expression of NF-κB and caspase-3 was up-regulated, and the expression of GPX4 was down-regulated in group VCI+ SF ( P<0.05). Conclusion:Sleep fragmentation can aggravate VCI, and the mechanism may be related to the induction of central inflammation and oxidative stress, which leads to increased apoptosis and ferroptosis in hippocampal neurons of rats.

Hippocampal neuronal ferroptosis involved in cognitive dysfunction in rats with sepsis-related encephalopathy through the Nrf 2/GPX4 signaling pathway / 中华危重病急救医学

Objective@#To evaluate the effects of ferroptosis in hippocampal neurons on cognitive dysfunction in rats with sepsis-associated encephalopathy (SAE) and its potential molecular mechanisms.@*Methods@#① Screening experiment of SAE modeling conditions: 42 healthy male Sprague-Dawley (SD) rats were divided into normal saline (NS) control group (n = 6) and lipopolysaccharide (LPS) 5, 15, 30 mg/kg groups (each n = 12) according to the random number table method. The SAE modeling conditions were determined by survival and the changes in mean arterial pressure (MAP) and heart rate (HR) within 72 hours, the percentage of stiffness status, the levels of serum inflammatory factors including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), neuron specific enolase (NSE, a marker of neuronal injury), serum iron and lactic acid (Lac) contents, and the morphological changes in CA1 of hippocampus after 72 hours. ② Deferoxamine (Def) intervention experiment: according to the results of screening experiments, 28 healthy male SD rats were divided into NS control group (n = 8), SAE group (n = 10) and Def+SAE group (n = 10) according to the random number table method. In the Def+SAE group, 100 mg/kg Def was injected intraperitoneally 12 hours before the modeling, once every 12 hours, with a total of 7 times; the rats in the NS control group and SAE group were injected with the same amount of NS. Then the cognitive function of rats was evaluated by fear conditioning test for the percentage of stiffness status; serum IL-6, TNF-α and NSE levels were determined by enzyme-linked immunosorbent assay (ELISA); the levels of serum Lac, serum iron and hippocampal malondialdehyde (MDA) and iron contents were determined by chemical colorimetric; the protein expressions of nuclear factor E2 related factor 2 (Nrf 2), glutathione peroxidase 4 (GPX4) and NAPDH oxidase 1 (NOX1) in hippocampus were determined by Western Blot; morphological changes in hippocampal CA1 were observed after hematoxylin and eosin (HE) staining.@*Results@#① Compared with the NS control group, intraperitoneal injection of 15 mg/kg LPS could significantly reduce the MAP and HR as time prolonged, and the reduction was most significant at 72 hours. The 72-hour survival rate was significantly reduced and cognitive function was impaired. The levels of serum IL-6, TNF-α, Lac and NSE were increased while the serum iron content was decreased significantly. The morphology of vertebral cells in hippocampal CA1 was irregular and some of the cells were obviously vacuolated. In the LPS 5 mg/kg group, there were no significant changes in vital signs, inflammation, organ function or cognitive dysfunction, while the symptoms of septic shock were apparent in the LPS 30 mg/kg group. Therefore, SAE model was reproduced by intraperitoneal injection of 15 mg/kg LPS for 72 hours. ② Compared with the NS control group, the percentage of stiffness in the SAE group was significantly reduced. The levels of serum IL-6, NSE and hippocampal MDA, iron were significantly increased. The serum iron contents and hippocampal Nrf 2 and GPX4 protein expressions were significantly reduced, while the hippocampal NOX1 protein expression was significantly increased. The morphology of vertebral cells in hippocampal CA1 was irregular and the cytoplasm was deeply stained. The results indicated that the level of oxidative stress in the hippocampus of SAE rats was increased, the neuron degenerations were obvious, and the cognitive function of rats were impaired. Compared with the SAE group, the percentage of stiffness in the Def+SAE group was significantly increased [(63.4±6.4)% vs. (47.6±6.0)%, P < 0.05]. The levels of serum IL-6, NSE, iron and hippocampal MDA, iron were significantly reduced [serum IL-6 (ng/L): 73.14±8.31 vs. 99.86±12.37, serum NSE (μg/L): 3.67±0.51 vs. 5.92±0.79, serum iron (mg/L): 68.43±8.12 vs. 134.60±15.63, hippocampal MDA (mol/g): 4.62±0.90 vs. 6.62±0.84, hippocampal iron (μg/g): 155.32±17.86 vs. 221.54±27.54, all P < 0.05]. The hippocampal protein expressions of Nrf 2 and GPX4 were significantly increased [Nrf 2/β-actin: 0.41±0.07 vs. 0.18±0.03, GPX4/β-actin: 0.74±0.09 vs. 0.40±0.06, all P < 0.05] while the hippocampal NOX1 protein expression was significantly reduced (NOX1/β-actin: 0.62±0.08 vs. 1.11±0.16, P < 0.05). The vertebral cells was significantly improved as compared with the SAE group. These findings showed that the oxidative stress level in hippocampus of the Def+SAE group was reduced, neuron degeneration was significantly alleviated, and the cognitive function of the rats was significantly improved.@*Conclusions@#The cognitive function of rats with SAE was significantly impaired, the hippocampal neurons were obviously damaged and ferroptosis was increased. Def pretreatment could significantly reduce iron deposition and ferroptosis in hippocampal neurons of SAE rats and improve cognitive dysfunction, which may be related to activation of Nrf 2/GPX4 signaling pathway.

Hippocampal neuronal ferroptosis involved in cognitive dysfunction in rats with sepsis-related encephalopathy through the Nrf 2/GPX4 signaling pathway / 中华危重病急救医学

To evaluate the effects of ferroptosis in hippocampal neurons on cognitive dysfunction in rats with sepsis-associated encephalopathy (SAE) and its potential molecular mechanisms. Methods ① Screening experiment of SAE modeling conditions: 42 healthy male Sprague-Dawley (SD) rats were divided into normal saline (NS) control group (n = 6) and lipopolysaccharide (LPS) 5, 15, 30 mg/kg groups (each n = 12) according to the random number table method. The SAE modeling conditions were determined by survival and the changes in mean arterial pressure (MAP) and heart rate (HR) within 72 hours, the percentage of stiffness status, the levels of serum inflammatory factors including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), neuron specific enolase (NSE, a marker of neuronal injury), serum iron and lactic acid (Lac) contents, and the morphological changes in CA1 of hippocampus after 72 hours. ② Deferoxamine (Def) intervention experiment: according to the results of screening experiments, 28 healthy male SD rats were divided into NS control group (n = 8), SAE group (n = 10) and Def+SAE group (n = 10) according to the random number table method. In the Def+SAE group, 100 mg/kg Def was injected intraperitoneally 12 hours before the modeling, once every 12 hours, with a total of 7 times; the rats in the NS control group and SAE group were injected with the same amount of NS. Then the cognitive function of rats was evaluated by fear conditioning test for the percentage of stiffness status; serum IL-6, TNF-α and NSE levels were determined by enzyme-linked immunosorbent assay (ELISA); the levels of serum Lac, serum iron and hippocampal malondialdehyde (MDA) and iron contents were determined by chemical colorimetric; the protein expressions of nuclear factor E2 related factor 2 (Nrf 2), glutathione peroxidase 4 (GPX4) and NAPDH oxidase 1 (NOX1) in hippocampus were determined by Western Blot; morphological changes in hippocampal CA1 were observed after hematoxylin and eosin (HE) staining. Results ① Compared with the NS control group, intraperitoneal injection of 15 mg/kg LPS could significantly reduce the MAP and HR as time prolonged, and the reduction was most significant at 72 hours. The 72-hour survival rate was significantly reduced and cognitive function was impaired. The levels of serum IL-6, TNF-α, Lac and NSE were increased while the serum iron content was decreased significantly. The morphology of vertebral cells in hippocampal CA1 was irregular and some of the cells were obviously vacuolated. In the LPS 5 mg/kg group, there were no significant changes in vital signs, inflammation, organ function or cognitive dysfunction, while the symptoms of septic shock were apparent in the LPS 30 mg/kg group. Therefore, SAE model was reproduced by intraperitoneal injection of 15 mg/kg LPS for 72 hours. ② Compared with the NS control group, the percentage of stiffness in the SAE group was significantly reduced. The levels of serum IL-6, NSE and hippocampal MDA, iron were significantly increased. The serum iron contents and hippocampal Nrf 2 and GPX4 protein expressions were significantly reduced, while the hippocampal NOX1 protein expression was significantly increased. The morphology of vertebral cells in hippocampal CA1 was irregular and the cytoplasm was deeply stained. The results indicated that the level of oxidative stress in the hippocampus of SAE rats was increased, the neuron degenerations were obvious, and the cognitive function of rats were impaired. Compared with the SAE group, the percentage of stiffness in the Def+SAE group was significantly increased [(63.4±6.4)% vs. (47.6±6.0)%, P < 0.05]. The levels of serum IL-6, NSE, iron and hippocampal MDA, iron were significantly reduced [serum IL-6 (ng/L): 73.14±8.31 vs. 99.86±12.37, serum NSE (μg/L): 3.67±0.51 vs. 5.92±0.79, serum iron (mg/L): 68.43±8.12 vs. 134.60±15.63, hippocampal MDA (mol/g): 4.62±0.90 vs. 6.62±0.84, hippocampal iron (μg/g): 155.32±17.86 vs. 221.54±27.54, all P < 0.05]. The hippocampal protein expressions of Nrf 2 and GPX4 were significantly increased [Nrf 2/β-actin: 0.41±0.07 vs. 0.18±0.03, GPX4/β-actin: 0.74±0.09 vs. 0.40±0.06, all P < 0.05] while the hippocampal NOX1 protein expression was significantly reduced (NOX1/β-actin: 0.62±0.08 vs. 1.11±0.16, P < 0.05). The vertebral cells was significantly improved as compared with the SAE group. These findings showed that the oxidative stress level in hippocampus of the Def+SAE group was reduced, neuron degeneration was significantly alleviated, and the cognitive function of the rats was significantly improved. Conclusions The cognitive function of rats with SAE was significantly impaired, the hippocampal neurons were obviously damaged and ferroptosis was increased. Def pretreatment could significantly reduce iron deposition and ferroptosis in hippocampal neurons of SAE rats and improve cognitive dysfunction, which may be related to activation of Nrf 2/GPX4 signaling pathway.

Analyzing Antenatal Test and Outcomes of Rh-negative Pregnant Women / 实用妇产科杂志

Objective:To study antenatal immunity test and outcomes of Rh-negative pregnant women.Methods:287cases(1.25％ in 22880 cases)of Rh-negative pregnant women delivered in Shanghai Sixth People hospital from January 1 st,2010 to December 31,2016 were retrospectively analyzed.Rh(D) blood group was identified by a micro column gel method,and the same as serum anti-D antibody.The Rh phenotype detection was done Serology method and the hemolytic disease of the newborn was used indirect antiglobulin test,serum free antibody test,absorption and elution test.Some Rh negative pregnant women were implemented autologous blood at 37 weeks of gestation.Results:Among 287 cases of Rh-negative,12 cases had anti-D antibody and the positive rate was 4.18％.Among the 12 cases of anti-D positive,their Rh phenotype were all ccdee and they all had history of childbearing.In 90 cases which had one history of birth,there were ten cases had anti-D antibody (11.11％),in 15 cases which had two history of birth,there were two cases had anti-D antibody(13.33％).287 Rh negative pregnant women had 290 child births,among which 8 newborn had neonatal hemolytic disease,the incidence rate was 2.75％ (8/290).In the 12 cases of anti-D positive,there were 1 case died because of fetal neonatal hemolytic disease and 7 cases were cured and 4 cases were normal with free of jaundice symptoms.There were 146 pregnant women implementation of autologous donation safely.According to the delivery way of childbirth,287 cases were divided by cesarean section and vaginal delivery,comparing postpartum haemorrhage amount with autologous donantion and unautologous donation,respectively,the result showed that they had no significant difference(P ＞0.05).Conclusions:It should be pay attention to the pregnant women who had childbearing history and whose Rh phenotype is ccee,which tend to produce anti-D immune antibody.However,this does not necessarily lead to hemolytic disease.Based on maternal and fetus conditions,autologous donation is safe and valuable in Rh-negative pregnant.

A report of four cases of hemolytic disease caused by red blood cell immune in neonates antibodies / 临床儿科杂志

Objective To investigate the laboratory ifndings, clinical manifestations and treatment in hemolytic disease caused by red cell immune antibodies in neonates. Methods The laboratory and clinical data from 4 cases of hemolytic disease of neonates caused by red cell immune antibodies were retrospectively analyzed. Results IgG antibody were detected in all mothers of 4 cases during pregnancy and they were anti-E, anti-D, anti-Jkb and the autoantibody with the titer being 16, 2048, 1 and 16 respectively. The four neonates were all full-term. The jaundice appeared 6 h to 3 d after birth with varying degrees of skin stained yellow, with or without anemia. Serology and elution test found the existence of antibody same as the one on their maternal red cells and the titer was 4, 512, 0, and 2, respectively. All neonates were treated by phototherapy. Two servere cases were also treated by whole blood exchange and red blood cells transfusion. The prognosis were good in all neonates. Conclusions Prenatal immune hematological tests facilitated early detection of irregular erythrocyte antibodies and thus assessment of the risk of hemolytic dis-ease of the fetus and neonates.