1.Clinical value of procalcitonin detection in neonatal necrotizing enterocolitis
Xiaoyan HU ; Yuxin ZHOU ; Songzhou XU ; Yueyu LIN ; Fang ZHAO
Clinical Medicine of China 2016;32(4):325-327
Objective To investigate the clinical value of of procalcitonin detection in neonatal necrotizing enterocolitis (NEC).Methods Sixty cases eligible NEC infants were randomly divided into observation group and control group(n=30 each group).All the infants were divided into Ⅰ grade group(19cases),Ⅱ-Ⅲ grade group(41 cases) according to NEC classification.All infants received PCT detection after NEC diagnosis.The observation group received antibiotic treatment base on the serum PCT levels.The control group received antibiotic treatment according to treatment routine and physician's clinical experience.Results PCT increased in 28 (46.7%) of the 60 NEC infants.In the Ⅰ grade group and Ⅱ-m grade group,the proportion of PCT increased cases were 26.3%,61.3% respectively,and the PCTmax in PCT positive cases were (0.81±0.25) μg/L,(1.76±0.89) μg/L respectively,the differences were signifiacnt(x2 =4.627,t=-2.608,P<0.05).The time of antibiotic usage in observation group was significantly less than that in control group ((4.9±3.0) d vs.(8.6±2.5) d,t=-3.645,P<0.01).The fasting time and the cure time of the two groups had no significant difference (P> 0.05).Conclusion PCT detection can help to understand the cause and severity of NEC.Using antibiotics according to PCT levels can reduce the time of antibiotic usage without affecting the effect of the NEC treatment.
2.Distribution of pathogen species and antibiotic resistance of pathogens from intravenous catheter-related bloodstream infections in pediatric intensive care unit
Yuxiong GUO ; Yueyu SUN ; Minquan ZHONG ; Shaoru HE ; Tieying HOU ; Yanjun CHANG ; Xiaoyuan LIN
Chinese Journal of Applied Clinical Pediatrics 2015;30(12):929-933
Objective To investigate the clinical characteristics,distribution and drug sensitivity of pathogens causing intravenous catheter-related bloodstream infections (CRBSIs) in pediatric intensive care unit (PICU) so as to use antibiotics reasonably.Methods All patients with CRBSIs in PICU of Guangdong General Hospital from September 2009 to September 2014 were investigated and the drug resistance profiles of pathogens causing CRBSIs were also analyzed retrospectively.Results Between 2009 and 2014,there were totally 10 834 catheter days and 23 episodes of CRBSIs with an incidence of 2.1 infections per 1 000 catheter days.Catheter indwell time < 7 days in 9 cases (39.1%),8 to 14 days in 10 cases (43.5%),14 to 21 days in 4 cases (17.4%).There were 13 strains (56.6%) of gram-positive bacteria,5 strains (21.7%) of gram-negative bacteria and 5 strains (21.7%) of fungi.The main pathogens causing CRBSIs were coagulase negative Staphylococci (7 strains,30.4%),Staphylococcus aureus (3 strains,13.0%),Candida albicans(3 strains,13.0%),Candida parapsilosis(2 strains,8.7%),and Enterobacter cloacae (2 strains,8.7 %).The susceptibility to Vancomycin,Linezolid and Teicoplanin of coagulase negative Staphylococ cus such as S.epidermidis and to Imipenem,Piperacillin/Tazobactam,Cefoperazone/ Sulbactam and Amikacin of gram-positive bacteria arrived at 100.0%,respectively.The candida were 100% susceptible to Amphotericin B,5-Flucytosine,Fluconazole and Voriconazole.Twenty-one cases (91.3%) received antibiotic treatment versus no antibiotic in 2 cases (8.7%).The average number of antibiotic kinds administered on the patients with fungal infection was 4.4,bacteria were 1.4.Ten cases (43.5%) treatment with 1 kind of antibiotic,4 cases (17.4%) with 2,4 cases (17.4%) with 3,5 cases (21.7%) with more than 3.Twenty-two cases (95.7%) cured and 1 case died (4.3%).Conclusions The major species of pathogen causing CRBSIs was coagulase negative staphylococci in PICU.It is critical for clinicians to guard against fungal infection because of prolonged catheter indwelling time and more antibiotics administered before indwelling catheter.It is effective way to prevent the CRBSIs by reasonably using antibiotics and shortening the time of catheter indwelling.Monitoring CRBSIs pathogenic bacteria distribution and drug susceptibility helps reasonable administration of antibiotics in the earlier time.
3.Neonatal Schaaf-Yang syndrome: a case report and literature review
Huaqing ZHANG ; Jingjing CHEN ; Yueyu LIN ; Jinfeng LI ; Songzhou XU
Chinese Journal of Neonatology 2024;39(1):30-33
Objective:To study the clinical and genetic features of neonatal Schaaf-Yang Syndrome (SYS).Methods:The clinical data of a newborn with SYS admitted to our hospital in October 2022 were retrospectively analyzed. Using "Schaaf-Yang syndrome", "newborn", "preterm", "neonate" as keywords, we searched the CNKI, Wanfang Database, VIP database, Chinese Medical Journal Full Text Database, PubMed, Embase, Web of Science and the Cochrane Library for literature published during the date of establishment to March 24th, 2023. The clinical and genetic features of neonatal SYS from published literature were summarized.Results:The patient in this case was a female preterm infant with a gestational age of 33 +3 weeks, characterized by epiglottic collapse, hypotonia, poor response, weak sucking and swallowing, respiratory failure, and abnormalities such as bilateral low ear position and short limbs. The patient received symptomatic treatment, often failed to withdraw the ventilator, and had difficulty intubating. Meanwhile, whole exome sequencing identified a de novo truncated variant c.2892del (p.Trp965Glyfs*3) in the MAGEL2 gene of the patient. At 30 d after birth, the patient died after giving up treatment by her family. A total of 11 retrieved literatures had neonatal records, including 17 cases. The clinical features involved joint contracture (15/17), hypotonia (14/17), respiratory failure (12/17), and feeding difficulties (12/17). Most of the gene variation was truncated mutation, and only 1 heterozygote deletion mutation was found. These gene variation included c.1996dupC(p.Gln-666Profs*47) variation in 7 cases, c.1912C>T(p.Q638X) variation in 3 cases, c.1996C>T(p.Q666*) in 1 case, c.2847-2883del37 in 1 case, c.2118delT(p.Leu708Trpfs*7) in 1 case, c.1850G>A(p.RP617*) in 1 case, c.2167delG (p.Ala723Profs*4) in 1 case, c.2005C>T(p.Gln669) in 1 case, c.2892del(p.Trp965Glyfs*3) in 1 case, respectively. Conclusions:The main manifestations of neonatal SYS included hypotonia, feeding difficulties, respiratory failure and joint contracture. Most of the mutations were truncated mutations of c.1996dupC (p.Gln-666Profs*47).
4.The antitumor effect of tanshinone IIA on anti-proliferation and decreasing VEGF/VEGFR2 expression on the human non-small cell lung cancer A549 cell line.
Jun XIE ; Jiahui LIU ; Heng LIU ; Shihui LIANG ; Meigui LIN ; Yueyu GU ; Taoli LIU ; Dongmei WANG ; Hui GE ; Sui-Lin MO
Acta Pharmaceutica Sinica B 2015;5(6):554-563
The effects of tanshinone IIA on the proliferation of the human non-small cell lung cancer cell line A549 and its possible mechanism on the VEGF/VEGFR signal pathway were investigated. The exploration of the interaction between tanshinone IIA and its target proteins provides a feasible platform for studying the anticancer mechanism of active components of herbs. The CCK-8 assay was used to evaluate the proliferative activity of A549 cells treated with tanshinone IIA (2.5-80 μmol/L) for 24, 48 and 72 h, respectively. Flow cytometry was used for the detection of cell apoptosis and cell cycle perturbation. VEGF and VEGFR2 expression were studied by Western blotting. The binding mode of tanshinone IIA within the crystal structure of the VEGFR2 protein was evaluated with molecular docking analysis by use of the CDOCKER algorithm in Discovery Studio 2.1. The CCK-8 results showed that tanshinone IIA can significantly inhibit A549 cell proliferation in a dose- and time-dependent manner. Flow cytometry results showed that the apoptosis rate of tested group was higher than the vehicle control, and tanshinone IIA-treated cells accumulated at the S phase, which was higher than the vehicle control. Furthermore, the expression of VEGF and VEGFR2 was decreased in Western blot. Finally, molecular docking analysis revealed that tanshinone IIA could be stably docked into the kinase domain of VEGFR2 protein with its unique modes to form H-bonds with Cys917 and π-π stacking interactions with Val848. In conclusion, tanshinone IIA may suppress A549 proliferation, induce apoptosis and cell cycle arrest at the S phase. This drug may suppress angiogenesis by targeting the protein kinase domains of VEGF/VEGFR2.