Xanthan gum is a microbial, natural high molecular weight polysaccharide produced by a the bacterium Xanthomonas campestris. Due to its exceptional rheological properties, its numerous areas of application cover a broad range. This review focuses on various aspects of xanthan production, properties, degradation, and application.

0.05).The different tilt angles impacted patients' fear psychology(?2=8.038,P=0.018).The order of the extent of children's fear psychology represented from low to high at the angle of 60?,70? and 80?,respectively.The extent of the children's fear psychology had positive correlation with the tilt angle(r=0.669,P=0.002).Conclusions The tilt test angle does not affect the positive rate of HUTT and the hemodynamics in children undergoing HUTT with angles from 60? to 80?.The children at the tilt angle 60? had less fear than at the angle of 70? or 80?.The 60? tilt angle of HUTT in children is recommended in the clinical practice.

AIM: To detect whether N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) inhibits epithelial-mes-enchymal transition in A549 cells induced by TGF-β1 through suppressing the expression of heat shock protein 27 (HSP27) and zinc finger proteins Snail (including SNAI1and SNAI2) which ultimately inhibited the deposition of type I and type III collagens.METHODS:The colocalizations of HSP27 and SNAI1/SNAI2 respectively on A549 alveolar epi-thelial cells induced by TGF-β1 were measured by confocal microscopy .The expression of HSP27, SNAI1 and SNAI2 at mRNA level was detected by real-time PCR.Western blotting analysis was used to detect the expression of HSP 27, SNAI1 and SNAI2 on epithelial-mesenchymal transition in A549 cells induced by TGF-β1 and also the deposition of type I and type III collagens in A549 cells transfected with HSP27shRNA prior to TGF-β1 stimulation.RESULTS: Compared with control group, TGF-β1 increased the expression of HSP27, SNAI1, SNAI2, type I and type III collagen, which decreased significantly followed by Ac-SDKP intervention.The expression of SNAI1, type I and type III collagen decreased signifi-cantly after transfected with HSP27shRNA in A549 cells, which had the similar effect on Ac-SDKP intervention.CON-CLUSION:Ac-SDKP inhibits the transition of cultured A 549 cells to myofibroblasts and attenuates collagen synthesis by suppressing the expression of HSP 27 and zinc finger proteins SNAI 1 and SNAI2.

BACKGROUND:Establishment of in vitro culture system of human placental microvascular endothelial cel s with high purity is very important. In recent studies, some scholars have successful y obtained a large number of placental microvascular endothelial cel s by three-stepenzyme digestion and magnetic separation method, but the procedures were extremely complex and it had great damage to the cel s. Therefore, how to separate human placental microvascular endothelial cel s easily and obtain high-purified cel s has become a research hotspot.
OBJECTIVE:To investigate an efficient method to isolate and purify human placental microvascular endothelial cel s from early vil us microvessels, observe the cel growth and identify the cel s.
METHODS:The vil i from normal early pregnancies (6-8 weeks) after artificial abortion were col ected aseptical y. Using two-step digestion procedure and discontinuous Percol density gradient centrifugation method, human placental microvascular endothelial cel s were obtained. Then the cel s were identified by trypsin digestion method and repeated adherence method.
RESULTS AND CONCLUSION:Human placental microvascular endothelial cel s were isolated successful y from early vil i. The primary cel s adhered to the wal s after inoculated for 24 hours and entered logarithmic phase at 10 days. 80%of the cel s achieved a confluence at 12-13 days after inoculating. The subculture cel s grew swiftly with the typical cobblestone appearance. Immunofluorescence staining showed that, cultured human placental microvascular endothelial cel s demonstrated a strong positive reaction to von Wil ebrand factor antigen and CD31, accounting for 100%. MTT assay results showed that, human placental microvascular endothelial cel s at passage 5 exhibited an S-shaped growth curve. High-purity human placental microvascular endothelial cel s can be obtained by proteolytic enzymes digestion and discontinuous Percol density gradient centrifugation method, and the purity is detected by trypsin digestion method and repeated adherence method.

OBJECTIVETo evaluate the clinical efficacy of autologous semitendinosus and gracilis tendon grafting with anchor repair for the treatment of chronic achilles tendon rupture and severe scarring.

METHODSFrom April 2010 to October 2012,26 patients with chronic achilles tendon rupture(with Myerson type III ) and severe scarring were treated with autologous semitendinosus and gracilis tendon grafting with anchor repair. There were 19 males and 7 females,with an average age of 32 years old (ranged, 22 to 47 years). The time from injury to surgery was from 3 to 12 months (7 months on average). The plantar flexion strength of all injuried feet attenuated and single heel rise test were positive in 26 cases before operation. Plaster immobilization and routine rehabilitation therapy were performed after operation. Clinical effects were evaluated by Arner-lindholm criterion and complications were observed after operation.

RESULTSAll the patients were followed up from 12 to 24 months with a mean of 16 months. No complications such as achilles tendon re-rupture, wound infection, etc were found during follow-up period. According to the Arner-Lindholm standard, 15 cases got excellent results and 11 good.

CONCLUSIONUsing autologous semitendinosus and gracilis tendon grafts with anchor repair to treat chronic achilles tendon rupture and severe scarring is a perfect surgical procedure.

Achilles Tendon ; injuries ; surgery ; Adult ; Chronic Disease ; Cicatrix ; surgery ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Rupture ; Young Adult

Objective To investigate the changes of iodide uptake and the expression of thyroidspecific genes in poorly differentiated follicular thyroid carcinoma (FTC) cells after transfection of human TSH receptor (hTSHR) gene in vitro. Methods The recombinant eukaryotic expression plasmid PcDNA3. 1/hTSHR-cDNA was transformed into DH5a bacterial for amplification and then the recombinant plasmid was extracted. The recombinant was identified with PCR amplifying, restriction enzyme digestion analysis and DNA sequencing. The recombinant plasmid pcDNA3.1/hTSHR was transfected into FTC-133 cell line by lipofectin methodin vitro. Immunofluorescence, iodide uptake studies and real time-PCR were applied to detect target protein expression. Statistical analysis was performed with t-test using SPSS 13. 0 software. Results Kpn Ⅰ and Xba Ⅰ restriction enzyme digestion, PCR amplifying and DNA sequencing confirmed that pcDNA3. 1/hTSHR was successfully constructed. After transfection of the recombinant plasmid pcDNA3. 1/hTSHR-cDNA and the stimulation of hTSH, the tumor cells displayed the expression of hTSHR protein at cell surface and cytoplasm. The iodine uptake in pcDNA3. 1/hTSHR transfected cells was 2. 9 times higher than that of control(pcDNA3.1(+) transfected cells) group(t = 28.63, P ＜0. 01). The expression of TSHR,NIS, TPO and Tg (mRNA levels) in pcDNA3. 1/hTSHR transfected cells were also significantly elevated by 1.74 (t =5.959, P＜0.01), 7.2 (t =3.807,P＜0.05), 2.88 (t=4.769,P＜0. 01) and 2.67 times (t=6.388,P ＜0.01) respectively compared to those of the control group. Conclusion The study demonstrates that iodide uptake may be reactivated by hTSHR receptor gene transfection in poorly differentiated FTC cell.

[Abstract ] Objective Silicosis is one of the most serious occupational diseases in China .In this study,we explored the reg -ulatory effect of N-acetyl-seryl-aspartyl-lysyl-proline ( Ac-SDKP ) on angiotensin ( Ang ) Ⅱ-induced extracellular signal-regulated ki-nase ( ERK1/2) and Jun N-terminal kinase ( JNK) signals and its inhibitory effect on the differentiation of human embryonic lung MRC-5 fibroblasts to myofibroblasts via Ang Ⅱ-induced ERK1/2 and JNK signals . Methods Human embryonic lung MRC-5 fibro-blasts were induced by Ang Ⅱand pre-treated with the JNK signal inhibitor ( SP600125 ) , the ERK1/2 signal inhibitor ( PD98059 ) or Ac-SDKP.The proliferation of the cells was measured by MTT assay .The expressions of αS-MA, SRF, p-ERK1/2 and p-JNK were determined by immunocytochemical staining , and the expression levels of these proteins and collagen Ⅰwere detected by Western blot .Results The A value of Ang Ⅱ group (0.56 ±0.08) measured by MMT assay was 2.07 fold as control group ( 0.27 ±0.05 ). Pretreatment with SP600125 , PD98059 and Ac-SDKP, the A value were (0.39 ±0.02), (0.40 ±0.03) and (0.36 ±0 0.5) that had a statistical significance with Ang Ⅱgroup.The up-regulation of colla-gen type Ⅰ,α-SMA, SRF were induced by Ang Ⅱ by 4.50, 3.50 and 3.00 fold compared with control group.Moreover, the expression of p-ERK1/2 and p-JNK were increased as 6.71 and 7.90 fold as control. Pre-treatment with Ac-SDKP could inhibit p-JNK and p-ERK1/2 to 29.79% and 46.84% compared with AngⅡ group. Conclusion Ac -SDKP can inhibit the differentiation of human embryonic lung MRC-5 fibroblasts to myofibroblasts by regulating AngⅡ-induced JNK and ERK1/2 signals.

Objective:To investigate the factors and mechanisms in forming uric acid stones in patients with type 2 diabetes (T2DM).Methods:106 patients with diabetes were divided into observation group and control group according to the combination of urinary calculi,53 cases in each group,The differences of clinical data and biochemical indexes between the two groups were compared,The relationship between type 2 diabetes mellitus and urinary stones was analyzed by multi factor regression analysis.Results:There were no significant difference in observation group and control group in age,sex,SBP,DBP,TC,FBG,2hPBG and HbA1C (P＞0.05),and there were of statistical difference significance in BMI,urinary pH,HOMA-IR,SUA,TUA in the two gruops (P ＜0.05) and the Logistic regression analysis showed blood uric acid,the urinary pH,HOMA-IR,SUA were independent risk factors in urolithiasis in T2DM (P ＜ 0.05).Conclusion:High uric acid hematic disease,high uric acid excretion,insulin resistance,overweight or obesity,high blood triglycerides in patients with type 2 diabetes is risk factors for urinary stone formation,in which blood uric acid,urinary pH,HOMA-IR is the independent risk factor for type 2 diabetic patients with urinary calculi.

OBJECTIVETo study the role of N-methyl-D-aspartate-receptor (NMDAR) expression in the development of hearing damage in neonatal rats with hyperbilirubinemia.

METHODSSixty seven-day-old Sprague-Dawley rats were randomly injected with bilirubin of 100 microg/g (low-dose treatment group) or 200 microg/g (high-dose treatment group) or normal saline (control group). Auditory brainstem response (ABR) was examined. The concentrations of bilirubin in blood and brain were measured. NMDAR expression in the cochlear nucleus slices was examined by immunohistochemistry assay.

RESULTSABR reflecting threshold obviously increased, and I, II and III wave latency as well as I-II, II-III and I-III interval were more prolonged in the two bilirubin treatment groups when compared with the control group. The NMDAR expression in the cochlear nucleuse in the two bilirubin treatment groups was obviously lower than that in the control group. The NMDAR expression in the cochlear nucleuse was negatively correlated with the brain bilirubin content and the ABR reflecting threshold in the two bilirubin treatment groups.

CONCLUSIONSAn increased NMDAR activity may play an important role in hearing damage following hyperbilirubinemia.

Animals ; Animals, Newborn ; Bilirubin ; analysis ; Cochlear Nucleus ; chemistry ; Evoked Potentials, Auditory, Brain Stem ; Female ; Hearing Disorders ; etiology ; Hyperbilirubinemia ; complications ; metabolism ; Immunohistochemistry ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate ; analysis

BACKGROUNDMutations in fumarylacetoacetate hydrolase (FAH) gene can lead to tyrosinemia type 1 (HT1), a relatively rare autosomal recessive disorder. To date, no molecular genetic defects of HT1 in China have been described. We investigated a Chinese family with a HT1 child to identify mutations in FAH.

METHODSDNA sequencing was used for mutations screening in FAH gene. Real-time polymerase chain reaction (PCR) was performed to determine the FAH gene expression level. To confirm the presence of degradation by the nonsense-mediated mRNA decay pathway (NMD), the fragments containing R237X mutations were analyzed by primer introduced restriction analysis-polymerase chain reaction (PIRA-PCR) and cDNA sequencing. Finally, the effects of the mutations reported in this study were predicted by online softwares.

RESULTSA boy aged 3 years and 8 months was diagnosed clinically with HT1 based on his manifestations and biochemical abnormalities. Screening of FAH gene revealed two heterozygous mutations R237X and L375P transmitted from his mother and father respectively. In this pedigree, the amount of FAH mRNA relative to a healthy control was 0.44 for the patient, 0.77 for his mother and 1.07 for his father. Moreover, both PIRA-PCR and cDNA sequencing showed significant reduction of the FAH mRNA with R237X nonsense mutation. The missense mutation of L375P was not reported previously and prediction software showed that this mutation decreased the stability of protein structure and affected protein function.

CONCLUSIONSThis is the first case of HT1 analyzed by molecular genetics in China. The R237X mutation in FAH down- regulates the FAH gene expression, and the L375P mutation perhaps interrupts the secondary structure of FAH protein.

Child, Preschool ; China ; Humans ; Hydrolases ; genetics ; Male ; Molecular Sequence Data ; Mutation ; Mutation, Missense ; genetics ; Nonsense Mediated mRNA Decay ; genetics ; Real-Time Polymerase Chain Reaction ; Tyrosinemias ; genetics