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Objective To explore the clinical effect of microsurgical clearance combined with vacuum sealing drainage(VSD) for chronic osteomyelitis,and to analyze its complications.Methods 80 patients with chronic osteomyelitis in the People's Hospital of Xuecheng District from January 2014 to January 2015 were selected and randomly divided into two groups according to the digital table ,with 40 cases in each group .The observation group was treated with microsurgical clearance combined with VSD , the control group was given microsurgical clearance treatment.The changes of inflammatory factors were compared at 1 week after treatment,and the number of wound dressing,the percentage of wound healing and the time of clinical healing were analyzed .Results After treatment for 1 week,the levels of tumor necrosis factor -α(TNF-α),interleukin-1(IL-1) and high-sensitivity C-reactive protein(hs-CRP) in the observation group were (12.0 ±0.1)μg/L,(0.6 ±0.1)μg/L,(10.7 ±1.0) mg/L, respectively,which were significantly lower than those in the control group [(18.5 ±0.6) μg/L,(0.9 ±0.2)μg/L, (31.2 ±2.0) mg/L](t=67.584,9.899,57.983,all P<0.05).The number of dressing in the observation group was less than that in the control group [(7.4 ±1.2) times vs.(7.3 ±1.2) times,t=16.499,P<0.05)].The recovery rate of the wound in the observation group was higher than that in the control group [(47.4 ±2.9)％ vs. (16.4 ±1.2)％,t=62.470,P<0.05].The clinical healing time in the observation group was shorter than that in the control group[(25.3 ±1.8)d vs.(33.2 ±2.7)d,t=15.397,P<0.05)].The incidence rate of complications such as infection ,hematoma and wound unhealing in the observation group was 7.5％,which was lower than 35.0％in the control group (χ2 =7.470,P <0.05).Conclusion Microsurgical treatment combined with VSD in the treatment of patients with chronic osteomyelitis can effectively reduce the inflammatory reaction, so it can promote wound healing and reduce related complications .
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Objective The content of urea and amino acids in sweat fingerprints is examined by ultraviolet spectrophotometry at ambient temperature of 25 and relative humidity of 65%. Methods In the fingerprint of sweat, urea and amino acids are chemically reacted to produce blue and blue purple matter.Their concentrations are calculated by ultraviolet spectrophotometerand the two ratios are calculated to infer the remaining time. Results Left time of sweat fingerprints shows a linear correlation with urea and amino acid ratio, the linear regression equation is Y=-3.227X+6.706, the female is Y=-3.672X+6.546, the regression equation is Y=-3.276X+6.638.Conclusion The remaining time of human sweat fingerprints is linearly related to the ratio of urea to amino acidsand the regression relation can be used to infer the time of fingerprint retention.
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<p><b>OBJECTIVE</b>To explore the clinical characteristics and genetic mutations in two children with Omenn syndromes.</p><p><b>METHODS</b>Peripheral venous blood samples were collected from 2 children suspected with severe combined immunodeficiency (SCID) and their family members. The samples were subjected to RAG1 and RAG2 gene sequencing and TCR Vβ subclone analysis.</p><p><b>RESULTS</b>Both patients had recurrent infections, erythroderma rashes and alopecia baldness. One patient has fit with immunophenotype T-B-NK+, while another was consistent with typical Omenn syndrome combined with T+B-NK+ immunophenotype, IgE and eosinophil increase. Both children have carried compound heterozygous mutations of the RAG1 gene. The first patient carried c.1328 G>A (p.R443K) and c.2486-2490delGGAAA (p.R829fsX869) mutations, both were of de novel type. The second patient has carried c.1209C>T (p.R403W) and c.2892delT (p.ASN964LYSfs*14), with c.2892delT (p.ASN964LYSfs*14) being a de novel mutation. The parents of both patients were heterozygous carriers. The same mutations were not found in 100 healthy children. Both patients' 24 TCR Vβ subfamilies have presented monoclonal or oligoclonal peaks, with TCR Vβ polymorphism being severely disrupted.</p><p><b>CONCLUSION</b>Three novel mutations have been identified in two children with Omenn syndrome, which featured early onset and rapid progression. Early recognition of the disease and prompt treatment may reduce the mortality.</p>
Subject(s)
Adult , Female , Humans , Infant , Male , Base Sequence , DNA-Binding Proteins , Genetics , Heterozygote , Homeodomain Proteins , Genetics , Molecular Sequence Data , Mutation , Nuclear Proteins , Genetics , Pedigree , Severe Combined Immunodeficiency , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To explore use of interleukin-10 receptor (IL-10R) gene mutation in diagnosis and pathogenesis of neonatal inflammatory bowel disease (IBD) in 2 suspected cases.</p><p><b>METHOD</b>Two cases of sibling brothers who had suspected IBD from Guangzhou Women and Children's Medical Center Affiliated to Guangzhou Medical University during the year 2010-2014 were enrolled in the study. The proband, male, 26 days old, weight 3.73 kg, presented with recurrent fever, increased stool frequency since 9 days of age, and was hospitalized at the age of 6 months in 2014. The proband's brother, male, 6 months old, weight 8 kg, had repeated bloody and mucous diarrhea for more than five months, recurrent fever five days, and was hospitalized in 2010. The blood samples were collected from the children and their families for IL-10 receptor genes including IL-10 receptor α subunit (IL-10RA) and β subunit (IL-10RB) PCR amplification. Reverse transcription polymerase chain reaction (RT-PCR) was used to amplify the proband IL-10RA transcripts. Sequencing was performed on the PCR products forward and reversely. Western blot analysis was used for protein expression of the proband and normal control's IL-10RA and P-STAT3 (Tyr705) expression after IL-10 stimulation, TNF-α level was detected using Human TNF-α ELISA Kit after PBMC was cultured and stimulated.</p><p><b>RESULT</b>The proband and his brother were IBD patients. Genome sequencing showed mutation in c.537G>A, namely the exon 4 and intron 4 connections changed CA/GT for CG/GT. Sequencing of the RT-PCR products and T-A clone showed that the mutation was (c.519-537del GGTGCCGGGAAACTTCAC, p.LYS173ASNfs*7), as the splice mutation. Two gene mutations were novel mutation. The parents were the mutations carrier. Both of the children were compound heterozygous mutations in IL-10RA. The Western blot analysis showed that the patient and normal children can express IL-10RA protein, however, the function of IL-10RA had obvious defects in the patient, IL-10RA downstream signaling pathways P-STAT3 had no expression. The average level of TNF-α secreted by PBMC after LPS + IL-10 co-stimulation in patient was significantly increased as compared with control group ((2 100±356) vs. (200±50) ng/L, t=9.154, P=0.001), suggesting that interleukin-10-dependent negative feedback regulation is disrupted in the patient.</p><p><b>CONCLUSION</b>IL-10 receptor mutations can cause neonatal-IBD, for which common treatment effect is poor. Early diagnosis and allogeneic stem-cell transplantation performed may save the children's life.</p>
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Purpose The aim is to study the transduction of m urine stem cell factor(SCF) into umbilical blood cells by LipofectinRMmediated and expression in them.Methods Murine SCF cDNA encoding extra cellu lar domain was isolated using PCR from plasmid pRC/CMV(containing SCF gene), and then recombined into the expression vector pcDNA3,and transferred into enrichme nt cultural umbilical blood cells. Semi-quantitative RT-PCR was used to examin e the expression on mRNA level.And the effects of supernatant of transfected umb ilical blood cells were investigated alone or in coordinate with GM-CSF by colo ny formation test of human bone marrow cells in semisolid culture.Results SCF mRNA was expressed in transfected umbilical blood cells.The su pernat ant of transfected umbilical blood cells could increase the number of CFU-GM, s ynergizing with GM-CSF.Conclusion The supernatant of umbil ical b lood cells transfected with vector containing mSCF gene can stimulate the colony formation of human bone marrow cells in combination with GM-CSF.