Objective To summarize the clinical manifestation ,the main pathogenic bacteria distribution and drug resistance of neonatal community acquired sepsis late onset in our hospital .Methods Retrospectively analyse the clinical material of 122 cases (41 premature cases and 81 cases of full term) with neonatal community acquired sepsis late onset ,which were clinically diagnosed , from January 2009 to December 2012 in our hospital .Results The main clinical manifestation of neonatal community acquired sep-sis late onset was poor response(64 .7% ) ,repellent milk(57 .4% ) ,temperature changes(61 .5% ) ,and the respiratory tract and um-bilical region were the main infection ways .42 cases were checked out with pathogen in the 122 cases ,blood culture positive rate was 34 .4% ,and there was no statistically differences between the premature and the full term infant group ,In the 42 cases ,there were 29 cases with staphylococcus ,including 10 cases of staphylococcus aureus ,14 cases of coagulase negative staphylococcus and 5 cases of enterococcus ;and there were 10 cases are checked out with e .coli .All of the coccus detected were resistant to penicillin and erythromycin ,but sensitive to vancomycin ,teicoplanin ,linezolid .The e .coli was sensitive to amikacin ,imipenem ,meropenem ,and al-so had a higher sensitivity to cefazolin ,ceftriaxone ,cefepime ,cefoperazone and nitrofurantoin .Conclusion Blood culture positive rate is not high in neonatal community acquired sepsis late onset ,and its′clinical manifestations are nonspecific .The main pathogenic bacteria is coagulase negative staphylococcus ,staphylococcus aureus ,followed by escherichia coli .

Serine protease inhibitor (serpin) is a kind of serine protease activity regulator,which including nine subfamilies (SERPIN A ～ I).SERPINE (Serpin Peptidase Inhibitor,Clade E) can regulate many important life processes.In this paper,the physical and chemical properties,mechanisms and regulatory factors of SERPINE1 and SERPINE2 in the two important members of SERPINE family are introduced,and the research progress of SERPINE family in the fibrosis related diseases is described.

OBJECTIVE: The current study was designed to examine the expression of Skp2 gene in laryngeal squamous cell carcinoma (LSCC) and to investigate the role of Skp2 gene in tumorigenesis and progression of LSCC. METHOD: FQ-PCR method was used to examined the expression of Skp2 gene in 40 LSCC and 10 normal laryngeal mucosa tissues, and relationship between its expression and clinical biological factors of patients with LSCC was analyzed. RESULT: The median copy number of Skp2 mRNA expression in LSCC was 6622.54 copy/microg RNA, the median copy number of Skp2 mRNA expression in normal laryngeal mucosa tissues was 0 copy/microg RNA, there was a very significant difference between them (P < 0.01); The positive rate of Skp2 mRNA expression in LSCC and adjacent normal laryngeal tissue were 50%, 0, respectively (P < 0.01). The median copy number of Skp2 RNA expression in LSCC with cervical lymph node metastasis was 617138.4 copy/microg RNA, the median copy number of Skp2 mRNA expression in LSCC without cervical lymph node metastasis was 0 copy/microg RNA, there was a very significant difference between them (P < 0.05); The positive rate of Skp2 mRNA expression in LSCC with and without cervical lymph node metastasis were 100.00%, 35.48%, respectively (P < 0.01). CONCLUSION Skp2 gene might have relation with the cervical lymph node metastasis of LSCC. FQ-PCR is an accurate assay to detecting expression of Skp2 mRNA in patient with LSCC. The level of Skp2 mRNA expression might be a new and more accurate marker, and it can be used to predict cervical lymph node metastasis of LSCC.
Adult ; Aged ; Aged, 80 and over ; Carcinoma, Squamous Cell ; genetics ; Female ; Gene Expression ; Humans ; Laryngeal Neoplasms ; genetics ; Lymphatic Metastasis ; Male ; Middle Aged ; Polymerase Chain Reaction ; methods ; RNA, Messenger ; genetics ; S-Phase Kinase-Associated Proteins ; genetics ; metabolism

This article presented the maternal and infant outcomes of glycogen storage disease type Ⅲa (GSDⅢa) in a woman with full-term pregnancy. The woman exhibited symptoms of hypoglycemia when she was three months old, which were alleviated with intravenous glucose infusion. At the age of 19, during surgical treatment for scoliosis, she was found with liver cirrhosis, splenomegaly, and thrombocytopenia. Glycogen debranching enzyme deficiency was detected through liver biopsies, leading to the clinical diagnosis of GSDⅢ (unspecified genotype). The patient was admitted after conceiption due to "irregular lower abdominal pain for 1 day" at 34 weeks and 3 days. Through multidisciplinary management in the late pregnancy, which included medication adjustments, dietary instruction, and platelet transfusions both at half an hour before and during the operation, the patient underwent a cesarean section at 37 +1 weeks of gestation and delivered a healthy boy with normal Apgar scores at 1, 5, and 10 min. The mother followed a high-protein diet postpartum and the newborn experienced hypoglycemia after birth. Intravenous glucose was supplied to the infant, restabilizing his blood glucose. Maternal and neonatal blood glucose both remained stable. Postpartum whole-exome sequencing identified compound heterozygous variants in the mother, which were in the AGL gene at chr1:100379102-100379103 with gene variant information of NM_000642.2:c.3971_3972delAT(p.Tyr1324*) and at chr1:100345603 with gene variant information of NM_000642.2:c.1735+1G>T, confirming the diagnosis of GSDⅢa. The newborn carried a heterozygous variant in the AGL gene at chr1:100379102-100379103 with gene variant information of NM_000642.2:c.3971_3972delAT(p.Tyr1324*). Postpartum follow-ups showed stable blood glucose levels for the mother and normal growth and development for the newborn.

OBJECTIVE To explore the role and underlying mechanism of tournefolic acid B （TAB） on the improvement of glucose metabolism and renal function in diabetic nephropathy （DN） model mice. METHODS DN model mice were established by high-fat diet combined with streptozotocin， and then randomly divided into model group， positive control group （vitamin E， 20 mg/kg）， TAB low-dose， medium-dose and high-dose groups （1， 2， 4 mg/kg）， with 12 mice in each group； normal control group was given regular diet. Each group was given relevant medicine or normal saline intragastrically， once a day， for 4 consecutive weeks. The glucose metabolic function was estimated by fasting blood glucose， glucose tolerance test， insulin tolerance test and serum insulin concentration. The renal coefficients and biochemical indicators related to renal function [serum uric acid， blood urea nitrogen， creatinine levels， and ratio of urine microalbumin to creatinine] were detected in mice； the contents of biochemical indicators related to oxidative stress [superoxide dismutase （SOD）， glutathione peroxidase （GSH-Px）， malondialdehyde （MDA）， 8-hydroxydeoxyguanosine （8-OHdG）] were determined in renal tissue of mice； the pathological morphology of renal tissue was observed； the expressions of extracellular matrix （ECM） deposition related factors [transforming growth factor β1 （TGF- β1）， fibronectin （Fn）， type Ⅳ collagen （Col Ⅳ）] and protein kinase B （Akt）/nuclear factor erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） pathway related proteins were determined in renal tissue of mice. RESULTS Compared with normal control group， fasting blood glucose， area under glucose tolerance curve， area under insulin tolerance curve， serum insulin content， the levels of uric acid， urea nitrogen and creatinine @qq.com and ratio of urinary microalbumin to creatinine in serum， the contents of MDA and 8-OHdG and the protein expressions of TGF-β1， Fn and Col Ⅳ were increased significantly in model group （P＜0.05）， while the contents of SOD， GSH-Px and the protein expressions of p-Akt， Nrf2， HO-1 in renal tissue were decreased significantly （P＜0.05）； the significant thickening of the basement membrane， accumulation of mesangial matrix， glomerulosclerosis and interstitial fibrosis of the renal tubules were all found. Compared with model group， above indexes of mice were all reversed significantly in TAB groups （P＜0.05）， and pathological changes were alleviated in a dose-dependent manner. CONCLUSIONS TAB can improve blood glucose metabolism and kidney function and alleviate renal tubulointerstitial fibrosis in DN model mice， the mechanism of which may be associated with activating the Akt/Nrf2/HO-1 signaling pathway and suppressing ECM deposition.