Objective:To explore the effect of early intermittent enteral nutrition (EN) in critically ill patients after cardiac surgery.Methods:We developed an early EN feeding regimen for critically ill patients after cardiac surgery. A prospective analysis was conducted on 178 critically ill patients admitted to the Cardiothoracic Surgery Intensive Care Unit of a tertiary hospital in Shanghai from May 2022 to May 2023. They were divided into the control group ( n=88) and the observation group ( n=90) using a random number table method. The control group received routine EN feeding, while the observation group received early intermittent EN feeding. Comparison between groups was performed in terms of the tolerability and interruption of EN administration, nutrition related outcome indicators, and prognosis indicators. Results:The observation group had significantly lower rates of abdominal distension, diarrhea, nausea and vomiting (or reflux), and EN interruption, as well as shorter duration of EN interruption, compared to the control group ( P<0.05). After 7 days of early EN, 87.8% of patients in the observation group met the calorie goal, which was significantly higher than that of 22.5% in the observation group ( P<0.05). The nutritional related indicators (serum prealbumin, hemoglobin, actual intake of nutritional fluids) were also better in the observation group patients compared to the control group ( P<0.05). The duration of mechanical ventilation and length of ICU stay in the observation group were significantly shorter than those in the control group, with statistical significance ( P<0.05). There was no significant difference in the length of hospital stay between the two groups. Conclusion:Early EN program can improve the symptoms of feeding intolerance in patients, reduce the occurrence and duration of feeding interruption, increase the rate of calorie goal fulfillment, improve nutritional status,and promote patient recovery and outcome in critically ill patients after cardiac surgery.

【Objective】 To analyze the changes in antibody titer of voluntary blood donors after receiving the COVID-19 vaccine, so as to provide reference for blood donation strategy, follow-up vaccine development and COVID-19 prevention and treatment for healthy people. 【Methods】 1) The serum from voluntary blood donors 2, 4, 8, 12, 16 and 20 weeks after inoculation with two-shot vaccines (inactivated vaccine or recombinant protein vaccine) was collected, and SARS-CoV-2 total antibody (IgG+ IgM+ IgA) detection (colloidal gold method) and neutralizing antibody detection (UPT immunoluminescence method) were conducted. 2) The obtained data were grouped according to collection time, age and gender, and differences between groups were analyzed by t test and ANOVA using SPSS 2.0 statistical software to clarify the trend of total antibodies and neutralizing antibodies. 【Results】 Neutralizing antibodies and total antibodies (IgG+ IgM+ IgA) from voluntary blood donors vaccinated inactivated vaccine or recombinant vaccine had the same trend of change, both reached their peak at the 2nd and 4th week, respectively, after inoculation, and then decreased gradually. The antibody produced by the recombinant protein vaccine had a higher titer than that from inactivated vaccine, and had slower decline and more lasting protection. The neutralizing antibody and total antibody (IgG+ IgM+ IgA) from different genders and ages were not statistically different. 【Conclusion】 Neutralizing antibodies reached its peak in the second week after vaccination, and total antibody titer reached its peak in the fourth week; both were independent of age and gender. After receiving the vaccine, voluntary blood donors should follow the latest instructions on blood donation intervals issued by the government.

【Objective】 To explore the changes of blood routine, biochemical indexes and coagulation indexes of voluntary blood donors after COVID-19 vaccination, so as to provide a scientific basis for blood donation strategy and to ensure blood safety. 【Methods】 From March to August 2021, 55 blood donors who had received COVID-19 vaccination were sampled at the 2^nd, 4^th and 8^th weeks after vaccination for blood routine, biochemical and coagulation indexes testing. The changes were analyzed. 【Results】 At the second week after vaccination, abnormal blood routine indicators occurred 16(5.82%) occasions, abnormal biochemical indicators 159(36.14%) occasions; at the 4^th week after vaccination, abnormal blood routine indicators 14(5.10%) occasions and abnormal biochemical indexes 151(34.32%) occasions. There was no difference in blood routine and biochemical indexes before and after vaccination(P>0.05). Among the coagulation indexes, the incidence of abnormal increase of FⅧ activity at the 2^nd, 4^th and 8^th weeks after vaccination were 34.5%(19/55), 40%(22/55) and 50.9%(28/55), respectively. The the incidence of abnormal increase of TT were 3.6%(2/55), 7.2%(4/55) and 21.8%(12/55), respectively. Both TT and FⅧ activity had a tendency of increasing(P<0.05), APTT had an decreasing trend(P<0.05), and FIB content took on dynamical changes(P<0.05). 【Conclusion】 The blood indicators of blood donors after receiving COVID-19 vaccination are almost within the normal reference values. They can donate regularly according to the required interval, which may help to improve the potential transient changes of coagulation function.

Objective: To evaluate the protective effect of granulocyte-colony stimulating factor(G-CSF) on neonatal rats after hypoxic-ischemic brain damage(HIBD)and its effect on endoplasmic reticulum (ER) stress. Methods: According to the random number table, a total of 54 Sprague-Dawley (SD) rats aged 7 days were divided into 3 groups(18 rats in each group): Sham group, HIBD group and G-CSF group, and the improved Rice method was used to establish a neonatal rat model of HIBD.A dose of 50 μg/kg of G-CSF was administered intraperitoneally 1 hour after HIBD (G-CSF group), while the rats in HIBD group and Sham group received saline only.At 24 hours of HIBD, pups were euthanized to quantify brain infarct volume by using 2, 3, 5-Triphenyltetrazolium chloride.Hematoxylin-Eosin (HE) staining was used to observe the changes of brain structure.Neuronal cell death was determined by using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). Then the expressions of glucose-regulated protein 78 (GRP78), cysteinyl aspartate specific proteinase 12 (Caspase-12), CCAAT/enhancer binding-protein homologous protein (CHOP) were assessed by Western blot and immunofluorescence staining. Results: Twenty-four hours after operation, HE staining showed that no significant neuronal damage was observed in Sham group.The brain tissue structure of rats in the HIBD group was significantly damaged, while some improvement was observed in the G-CSF group.The infarction volume in HIBD group[(25.40±5.15)%] increased compared with that in the Sham group[(0.31±0.15)%] and the G-CSF group[(16.36±4.97)%], and the differences were statistically significant(all P<0.05). There was increased positive expression of GRP78 protein in HIBD group, compared with that in the Sham group and the G-CSF group[(49.38±10.06)% vs.(9.12±4.50)%, (30.61±6.35)%], and the differences were statistically significant (all P<0.05). The percentage of apoptosis in the hippocampal CA1 region and conex in HIBD group [(44.84±11.54)%, (48.23±14.07)%] were higher than those in the G-CSF group [(17.87±7.20)%, (26.18±9.96)%], and the differences were statistically significant (all P<0.05). The expression of GRP78, CHOP and Caspase-12 in the HIBD group (0.63±0.24, 0.72±0.21, 0.68±0.25) were higher than those in the Sham group (0.20±0.08, 0.28±0.08, 0.23±0.07), and the G-CSF group (0.39±0.13, 0.51±0.18, 0.48±0.16), and the differences were statistically significant (all P<0.05). Conclusions G-CSF exerts neuroprotective effect on the neonatal rats after HIBD.G-CSF may be an effective treatment of HIBD by reducing ER stress-induced neuronal apoptosis.

OBJECTIVE： To study the relationships of polymorphism of MTRR gene rs1801394 locus and SLCO1B1 gene rs11045879 locus with drug concentration of methotrexate （MTX） and high-dose MTX （HD-MTX）-induced ADR in acute lymphoblastic leukemia （ALL） children. METHODS： From Oct. 2015 to Sept. 2018， 70 ALL hospitalized children of Han nationality in Sichuan area who received HD-MTX treatment and were in consolidation chemotherapy were selected retrospectively from Sichuan People’s Hospital. The blood concentration of MTX at 48 and 72 hours after administration was measured by EMIT. The genetic typing of MTRR gene rs1801394 locus and SLCO1B1 gene rs11045879 locus were detected with real-time PCR. The relationships of the polymorphism of MTRR gene and SLCO1B1 gene with MTX blood concentration [dose-corrected concentration （c48 h/D，48 h）， the proportion of children with different concentration of MTX （≤0.1， ＞0.1 μmol/L）] and ADR （such as myelosuppression， liver function damage， gastrointestinal response， mucosal damage， rash， etc.） were analyzed. Binary Logistic regression analysis for the correlation of ADR with different influencing factors （gene polymor- phism， blood concentration of MTX， immunophenotyping， body mass index， etc.） was carried out by Wald method. RESULTS： Totally 31， 32， 7 children with MTRR gene AA， AG and GG genotype， while 23， 37， 10 children with SLCO1B1 gene TT， TC and CC genotype were detected. The distribution of each genotype in 70 children conformed to Hardy-Weinberg equilibrium （P＞0.05）. There was no significant difference in c48 h/D（48 h） of children and the proportion of children with different concentration of MTX （72 h） among difterent genotypes of MTRR and SLCO1B1 gene （P＞0.05）. There was statistical significance in the incidence of liver function injury in children with different genotypes of MTRR gene （P＜0.05）， and the AA genotype was significantly higher than the AG+GG genotype （P＜0.05）. There was no correlation of MTRR gene polymorphism with the incidence of other ADR， neither SLCO1B1 gene polymorphism with the incidence of ADR （P＞0.05）. The results of Binary Logistic regression analysis showed that liver function damage in ALL children was related to the gene polymorphism of MTRR； gastrointestinal reaction was related to whether the plasma concentration was more than 0.1 μmol/L at 72 h； mucosal damage was related to the immune type and BMI of children； the occurrence of skin allergy was correlated with body weight of children（P＜0.05）. CONCLUSIONS： Gene polymorphism of MTRR rs1801394 locus may associated with the occurrence of HD-HTX-induced liver function injury in ALL children， but its polymorphism and gene polymorphism of SLCO1B1 rs11045879 locus are not related to MTX blood concentration in ALL children.

Objective: To investigate the role of granulocyte-colony stimulating factor (G-CSF) on the regulation of inflammatory cytokines in neonatal hypoxic-ischemic brain damage(HIBD) rat model, and to explore the possible mechanism involved in G-CSF neuroprotective effect via the mammalian target of Rapamycin/p70 ribosomal S6 protein kinase (mTOR/p70S6K) signaling pathway. Methods: A group of postnatal day 7 (P7) Sprague-Dawley rat pups (90 cases) were randomly divided into sham-operated group, hypoxia-ischemia(HI) group, G-CSF group, Rapamycin (RAP) group and control group, and the improved Rice method was used to establish a neonatal rat model of HIBD.One hour before HI induction, Rapamycin was administered intraperitoneally with a dose of 250 μg/kg, and the control group was given equal volume of ethanol injected intraperitoneally.One hour after HI, a dose of 50 μg/kg of G-CSF was injected intraperitoneally into the G-CSF group, Rapamycin group and control group.The same volume of normal saline was injected intraperitoneally into HI group and sham-operated group.Forty-eight hours after HI, Western blot was used to detect the protein levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-10, and the mTOR/p70S6K signaling pathway in brain tissue.Neuron injury of the hippocampal CA1 region and the cortex was assessed by Nissl staining, and infarct volume detected by 2, 3, 5-triphenyltetrazolium chloride staining. Results: The G-CSF group and control group were associated with significantly reduced infarction volume compared to the HI group [(12.87±1.54)%, (11.90±1.31)% vs.(24.21±3.28)%], and the differences were statistically significant(P<0.05). There was an increased positive neuron cell number in the ipsilateral hemispheres of the hippocampal CA1 region in the G-CSF group and the control group [(61.00±4.90) cell/field and (61.67±6.40) cell/field] and cortex [(92.67±6.68) cell/field and (90.17±4.45) cell/field] compared with those in HI group [(42.62±4.46) cell/field and (70.83±6.97) cell/field], and the differences were all statistically significant (all P<0.05). The expression levels of TNF-α and IL-1β were significantly decreased in the G-CSF group and the control group, compared with those in HI group(TNF-α: 0.67±0.07, 0.55±0.05 vs.0.86±0.05; IL-1β: 0.65±0.06, 0.52±0.10 vs.0.86±0.06), and the differences were all statistically significant (all P<0.05). There was increased expression levels of IL-10, p-mTOR/mTOR and p-p70S6K/p70S6K in the G-CSF group and the control group, compared with those in HI group (IL-10: 0.68±0.04, 0.62±0.05 vs.0.34±0.02; p-mTOR/mTOR: 0.53±0.02, 0.51±0.01 vs.0.26±0.01; p-p70S6K/p70S6K: 0.89±0.03, 0.90±0.03 vs.0.55±0.02), and the differences were all statistically significant(all P<0.05). There was an increased infarct volume in Rapamycin group [(25.70±1.50)%], compared with the G-CSF group and the control group, and there were decreased number of positive neuron cell count in the hippocampal CA1 region [(40.67±3.50) cell/field] and cortex [(68.33±8.17) cell/field], increased expression levels of TNF-α and IL-1β (0.97±0.06 and 0.98±0.10, respectively), decreased expression levels of IL-10, p-mTOR/mTOR and p-p70S6K/p70S6K (0.21±0.02, 0.30±0.01 and 0.55±0.01, respectively) in the Rapamycin group, and the differences were all statistically significant (all P<0.05). Conclusions G-CSF may inhibit inflammatory responses after HIBD by up-regulating the mTOR/p70S6K signaling pathway in neonatal HI encephalopathy.

Objective To investigate the effects of granulocyte-colony stimulating factor (G-CSF) on neuronal apoptosis after hypoxia-ischemia brain damage (HIBD) and the possible role of the mTOR/p70S6K signaling pathway in neonatal rats.Methods Ninety seven-day-old Sprague-Dawley rats were assigned into 5 equal groups (n=18):sham group,HIBD group,G-CSF group,rapamycin group and ethanol group by random number table method.Pups were subjected to unilateral carotid artery ligation followed by 2hrs hypoxia or sham surgery.HIBD animals received normal saline,G-CSF (50 μg/kg),G-CSF combined with rapamycin (250 μg/kg) or ethanol (vehicle for rapamycin).Pups were euthanized 48hrs post-HIBD to quantify the percentage of brain infraction area.The pathomorphologic changes in the hippocampal CA 1 area and cortex were observed by Nissl staining.Neuronal cell death was determined using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL).mTOR,activated mTOR (p-mTOR),p70S6K,activated p70S6K (p-p70S6K),Cleaved Caspase-3 (CC3),Bax,and Bcl-2 were quantified using Western blot analysis.Results G-CSF treatment resulted in significantly reduced percentage of brain infraction area (P＜0.05) and neuronal apoptosis in the hippocampal CA1 area and cortex (P＜0.05) after HIBD in neonatal rats.However,rapamycin administration reversed the neuroprotective effect of G-CSF.G-CSF administration ameliorated the pathomorphologic damage in the ipsilateral hemisphere.Compared with the HIBD group,the Nissl stained neurons significantly increased in the G-CSF group (P＜0.05).Furthermore,G-CSF increased the expression ofp-mTOR,p-p70S6K and Bcl-2 but decreased the expression levels of CC3 and Bax in the ipsilateral hemisphere,which were all significantly reversed by rapamycin (P＜0.05).Conclusion G-CSF may attenuate caspase activation and reduce neuronal apoptosis by up-regulating the activity of mTOR/p70S6K signaling pathway after experimental HIBD in rat pups.

OBJECTIVE:To promote the working performace of automatic medicine packing machine in our hospital. METH-ODS:Combined with the problems we met in the use of the automatic medicine packing machine,the reconstructions of software functions,such as drug inventory management,drug identification,specific drug sub-package and document printing of non-pack-age drug,were introduced. Related indicators were compared before and after reconstruction. RESULTS:After the software recon-struction,compared with 2012,loss events of expire drug due to poor sales fell by 70% in 2013;drug dispensing errors related to medicine packing machine dropped by 1/2;the time of drug checking shortened by 1/5. CONCLUSIONS:The software program re-construction of automatic medicine packing machine can improve the work efficiency of pharmacy and the accuracy of drug dispens-ing,further guarantee the quality and safety of drugs,and meet the practical demand of our hospital.

OBJECTIVETo analyze the relationship between metabolites of polycyclic aromatic hydrocarbons (PAHs) and serum uric acid levels in coke oven workers and to provide new clues to the pathogenic mechanism of PAHs.

METHODSA total of 1302 coke oven workers were divided into four groups, namely control group and low-, intermediate-, and high-dose exposure groups. The concentrations of ambient PAHs at each workplace were determined by high-performance liquid chromatography. The detailed information on the occupational history and health of workers was collected by questionnaire survey and physical examination, and so were their blood and urine samples. Serum uric acid and creatinine levels were measured using a Hitachi 7020 automatic biochemical analyzer. Ten urinary PAH metabolites were detected by gas chromatography-mass spectrometry.

RESULTSSerum uric acid levels were the highest in the high-dose exposure group, followed by the intermediate- and low-dose exposure groups, and were the lowest in the control group. There were significant correlations between serum uric acid levels and the quartiles of 1-hydroxynaphthalene and 1-hydroxyphenanthrene (P < 0.05). After adjustment for PAH metabolite-related relationship, only urinary 1-hydroxyphenanthrene was significantly correlated with serum uric acid levels (P = 0.001). After adjustment for confounding factors and using the 1st quartile of 1-hydroxyphenanthrene as a reference, the odds ratio for hyperuricemia in subjects with the 2nd, 3rd, and 4th quartiles of 1-hydroxyphenanthrene were 1.55, 1.57, and 2.35, respectively.

CONCLUSIONUrinary 1-hydroxyphenanthrene is associated with a dose-response increase in serum uric acid levels in coke oven workers, and exposure to phenanthrene in PAHs may be a risk factor for hyperuricemia.

As an inhibitory amino acid similar to gama-aminobutyric acid,taurine can activate the corticostriatal pathway as an endogenous ligand for glycine receptors,establishing equilibrium between the excitatory and inhibitory processes in the brain.In mammalian brains,taurine concentrations increase during the developmental period of the brain until weaning,and subsequently decline reaching stable concentrations in adulthood.With abilities of anti-oxidative stress,anti-inflammatory and anti-apoptosis,taurine can improve the hypoxic-ischemic brain injury,promote the proliferation and differentiation of neurons and affect brain development,It needs more investigations to prove when and how taurine supplementation during gestation,baby,children or adult can assist the development of the brain and prevent the damage of the brain from hypoxic and ischemic damage.