The clinical experiences and proven cases of distinguished doctor of TCM, professor WU Xu, on acupuncture for acute upper abdominal pain is introduced. Professor WU's manipulation characteristics of acupuncture for acute upper abdominal pain, including acute cholecystitis, kidney stone, acute stomach pain, are one-hand shape but both hands in nature, moving like Tai Chi, force on the tip of needle, movement of qi mainly. The main technique posture is one-hand holding needle with middle finger for pressing, the needle is hold by thumb and index finger, and is assisted by middle finger. The special acupuncture experience of emergency is treatment according to syndrome differentiation, combination of acupuncture and moxibustion, selecting acupoint based on experience, blood-letting acupuncture therapy and so on.
Abdominal Pain ; therapy ; Acupuncture Points ; Acupuncture Therapy ; Acute Pain ; therapy ; Adult ; Female ; Humans ; Male

OBJECTIVETo suggest a chemical surface treatment for titanium and to initiate the formation of hydroxycarbonated apatite (HCA) on titanium surface during in vitro bioactivity tests in simulated body fluid (SBF).

METHODSTo improve the bone-bonding ability of Ti implants, commercially pure titanium (cpTi) by a simple chemical pre-treatment in orthophosphoric acid (H(3)PO(4)) with different density was activated, and then the phosphorylation specimens were soaked in SBF to investigate the function of biomineralization.

RESULTSThe scanning electron microscope (SEM) photographs showed that the surfaces of the pre-treated samples were characterized by a complex construction, which consisted of a mesh-like morphology matrix (a micro-roughened surface) and an uniform surface with different morphous of titanium dihydrogen orthophosphate [Ti(H(2)PO(4))(3)] crystal. After 14 days in SBF a homogeneous biomimetic apatite layer precipitated.

CONCLUSIONSThese data suggest that the treatment of titanium by acid etching in orthophosphoric acid is a suitable method to provide the titanium implant with bone-bonding ability.

Acid Etching, Dental ; methods ; Biomimetics ; Body Fluids ; Coated Materials, Biocompatible ; Dental Bonding ; Dental Implants ; Microscopy, Electron, Scanning ; Phosphoric Acids ; chemistry ; Phosphorylation ; Surface Properties ; Titanium ; chemistry

OBJECTIVETo investigate the safety and tolerance of adjuvant dose-dense chemotherapy with paclitaxel and epirubicin for high-risk breast cancer.

METHODSFrom January 2004 to December 2006, 101 patients with high-risk breast cancer after surgical resection were enrolled into this study. The patients were divided into two groups: dose-dense and regular groups. Each patient received 6 cycles of chemotherapy with intravenous administration of paclitaxel (175 mg/m2, on D3) and epirubicin (60 mg/m2, on Dl and D2). The dose-dense group had repeated treatment every two weeks, while the regular group repeated it every three weeks. G-CSF was used in a dose of 3 microg/kg on D5-D9 during each cycle in the dose-dense group. While in the regular group, it was used only under the condition that grade II neutropenia occurred.

RESULTSThe toxicity could be evaluated in 101 patients. Major grade II-IV toxicities included: neutropenia, nausea, vomiting and alopecia. The incidence of grade III-IV neutropenia was 16.0% in the dose-dense group versus 54.9% in the regular group (P = 0.000); postponing of chemotherapy was 2.4% versus 6.0% (P = 0.027). Ninety-eight patients completed the chemotherapy as planed. After a median follow-up of 24 months, the median DFS and OS were not reached. The relapse-free rate and survival rate were 89.8% and 100% in the dose-dense group, which were 87.8% and 93.9% in the regular group. The relapse-free rate of the high-risk patients in the dose-dense group was 86.8% versus 81.3% in the regular group, and the corresponding survival rate was 100% versus 90.6%.

CONCLUSIONAdjuvant dose-dense chemotherapy with paclitaxel and epirubicin is safe, tolerable and promising for high-risk breast cancer.

Adult ; Antineoplastic Combined Chemotherapy Protocols ; administration & dosage ; adverse effects ; therapeutic use ; Breast Neoplasms ; drug therapy ; pathology ; surgery ; Chemotherapy, Adjuvant ; Epirubicin ; administration & dosage ; adverse effects ; Female ; Follow-Up Studies ; Granulocyte Colony-Stimulating Factor ; administration & dosage ; therapeutic use ; Humans ; Lymphatic Metastasis ; Mastectomy ; methods ; Middle Aged ; Nausea ; chemically induced ; Neoplasm Recurrence, Local ; Neoplastic Cells, Circulating ; Neutropenia ; chemically induced ; Paclitaxel ; administration & dosage ; adverse effects ; Survival Rate ; Vomiting ; chemically induced ; Young Adult

OBJECTIVETo demonstrate expression and single nucleotide polymorphisms (SNP) of human kallikrein 10 (KLK 10) in colorectal cancer (CRC) and to correlate the KLK 10 expression level with clinicopathological factors of CRC.

METHODSKLK 10 expression in 63 cases of tumoral and nontumoral colorectal tissues at the mRNA and protein levels were evaluated by quantitative real-time RT-PCR (qRT) and Western blot methods. KLK 10 protein was localized by immunohistochemistry. The KLK 10 genomic DNA from 16 cases of paired normal and cancerous colorectal tissues was PCR-amplified and examined for SNP by direct sequencing.

RESULTSThe KLK 10 mRNA expression was detected by qRT in 61 of 63 (97%) CRC specimens. The KLK 10 expression was much higher in tumor tissue than in the corresponding normal mucosal tissue at the mRNA and protein levels. The KLK 10 mRNA expression level significantly correlated with the lymphatic invasion (P < 0.05) and clinical stage of CRC (P < 0.05). No mutations or polymorphisms were detected in exon 1, 2 and 5 of KLK 10 gene in CRC. A SNP in codon 50 of exon 3, GCC (alanine) to TCC (serine) was identified. The genetic changes of exon 4 were located at codon 106 [GGC (glycine) to GGA (glycine)], codon 112 [ACG (threonine) to ACC (threonine)], codon 141 [CTA (leucine) to CTG (leucine)], and codon 149 [CCG (proline) to CTG (leucine)]. All these SNP were identical in tumor as well as the corresponding normal tissue DNA from the same individuals.

CONCLUSIONSThe KLK 10 expression is up-regulated in CRC and higher expression of KLK 10 closely correlate with advanced disease stage, which predicts a poorer prognosis, however, further follow-up study is needed.

Adult ; Aged ; Aged, 80 and over ; Blotting, Western ; Colorectal Neoplasms ; genetics ; metabolism ; pathology ; Female ; Humans ; Kallikreins ; biosynthesis ; genetics ; Lymphatic Metastasis ; Male ; Middle Aged ; Neoplasm Staging ; Polymerase Chain Reaction ; Polymorphism, Single Nucleotide ; RNA, Messenger ; genetics

BACKGROUNDMedian sternotomy is considered the most usually performed procedure in cardiac operations. This study aimed to assess clinical effectiveness of bilateral pectoralis major muscle flaps (BPMMF) for management of sternal osteomyelitis and mediastinal infection following median sternotomy.

METHODSClinical data were collected and retrospectively analyzed from twelve patients who underwent the BPMMF transposition for management of sternal osteomyelitis and mediastinal infection following median sternotomy from January 2006 to June 2009. Procedure consisted of rigorous debridement of necrotic tissues, dead space obliteration using the BPMMF, and placement of drainage tubes connected to a negative pressures generator for adequate drainage.

RESULTSNo patients died of drainage, and all 12 patients had viable BPMMF when discharged from hospital. At 1 week post discharge, 2 patients presented with sternal infection but recovered following local debridement and medication. No patients showed infection recurrence during the follow-up period over 10 months.

CONCLUSIONSSternal osteomyelitis and mediastinal infection following median sternotomy may be effectively managed through rigorous debridement of infected soft tissues, resection of the damaged sternal segment, transposition of the BPMMF to fill the damaged sternum resulting from debridement, and adequate postoperative drainage.

Adolescent ; Adult ; Aged ; Debridement ; Follow-Up Studies ; Humans ; Male ; Mediastinitis ; surgery ; Middle Aged ; Osteomyelitis ; surgery ; Retrospective Studies ; Sternotomy ; adverse effects ; Sternum ; surgery ; Surgical Flaps ; Surgical Wound Infection ; surgery

OBJECTIVETo explore the relationship between gamma-synuclein gene expression and CpG island demethylation in colorectal cancer(CRC), and the relationship between the demethylation and clinicopathological factors of CRC.

METHODSThe expression of gamma-synuclein mRNA was examined in 30 pairs of tumor tissues and tumor-matched non-neoplastic adjacent tissues(NNAT) by RT-PCR. CRC cell lines including COLO205, LoVo, and SW480 were used and treated with a demethylating agent, 5-aza-2'-deoxycytidine(5-aza-C). Before and after the treatment, the expression of gamma-synuclein mRNA in the cells was determined by RT-PCR, and bisulfite sequencing PCR was also used to analyze methylation status of CpG island. The methylation status of gamma-synuclein was then examined in 67 CRC samples and 30 NNAT samples by nested methylation-specific PCR (NMSP) and real time methylation-specific PCR(real-time MSP). The relationship between the demethylation of gamma-synuclein in CRC and clinicopathological factors was analyzed.

RESULTSThe mean gamma-synuclein mRNA expression was 0.66+/-0.34 in CRC samples, which was much higher than 0.45+/-0.26 in NNAT samples(P=0.011). 5-aza-C could induce expression and demethylation of gamma-synuclein in COLO205, LoVo and SW480 cells. gamma-Synuclein gene was demethylated in 80.0%(24/30) of the CRC samples and 50.0%(15/30) of the NNAT samples. The demethylated status of gamma-synuclein was much higher in CRC samples than that in NNAT samples(P=0.030), and was significantly correlated with clinical stage, lymph node involvement, and distant metastasis of CRC(P<0.05).

CONCLUSIONThe upregulation of gamma-synuclein expression in CRC is primarily attributed to the demethylation of CpG island, which may be used as a marker for prognosis.

Cell Line, Tumor ; Colorectal Neoplasms ; genetics ; metabolism ; pathology ; CpG Islands ; DNA Methylation ; Gene Expression Regulation, Neoplastic ; Humans ; Prognosis ; RNA, Messenger ; genetics ; gamma-Synuclein ; genetics ; metabolism

Objective To compare the antibody response between preterm and full-term infants after primary immunization of hepatitis B vaccine (HepB).Methods Infants who were aged 7-12 months and had completed primary immunization with 5 μg HepB made by recombinant dexyribonucleic acid techniques in saccharomyces cerevisiae (HepB-SC) or 10 μg HepB made by recombinant dexyribonucleic acid techniques in Hansenula polymorpha (HepB-HP) on 0-1-6 schedule were investigated in four provinces (municipality) including Beijing,Shandong,Jiangsu and Guangxi of China.Among them,all preterm infants were selected to form the preterm group and the 1:1 matching full-term infants with the same month-age,gender and residence were randomly selected to form the full-term group.Their HepB history was determined by immunization certificate and all of their parents were interviewed with standard questionnaire to get their birth information.Blood samples were obtained from all anticipants and were tested for Anti-HBs by chemiluminescence microparticle immuno-assay (CMIA).Results Total anticipants were 648 pairs of infants.The rates of non-response,low-response,normal-response and high-response after the primary immunization were 1.39％,8.64％,45.83％ and 44.14％ in the preterm group,respectively.The corresponding rates were 1.08％,9.26％,44.91％ and 44.75％ in the full-term group.The above four rates did not show significant differences between the two groups (P＞0.05).The geometric mean concentrations (GMC) of anti-HBs in the pre-term and full-term group were 755.14 and 799.47 mIU/ml respectively.There was no significantly difference in the GMCs between the two groups (P＞0.05).Results from multivariable conditional logistic analysis showed that preterm was not an influencing factor to the antibody response after HepB primary immunization among newborns even after debugging the other influencing factors.Conclusion The autibody response after HepB primary immunization were similar among the preterm and full-term infants.The preterm newborns could be immunized under the same HepB immunization strategy.

Objective To compare the antibody response induced by primary immunization with 5 μ g and 10 μ g hepatitis B vaccine made by recombinant DNA techniques among the newborns.Methods Healthy infants who had completed primary immunization with 5 μg hepatitis B vaccine made by recombinant dexyribonucleic acid techniques in Saccharomyces (Hep-SC) or 10 μg hepatitis B vaccine made by recombinant dexyribonucleic acid techniques in Hansenula polymorpha (HepB-HP) were included in the study.Kids under study were 7-12 months of age and had been on 0-1-6 schedule.Standardized questionnaire was used and blood samples were collected.The titer of antibody to hepatitis B surface antigen (anti-HBs) was detected by Chemiluminescence Microparticle Imunoassay (CMIA).If anti-HBs happened to be under 10 mIU/ml,HBV DNA was further detected by nested-PCR to distinguish occult hepatitis B virus infection.Sero-conversion rate and titer of anti-HBs were compared between the two kinds of hepatitis B vaccines.Multivariate analysis was used to find the relationship between the kind of hepatitis B vaccine as well as the antibody response after debugging the other influencing factors including month-age,gender,birth-weight,premature birth and mother' s HBsAg status.Results 8947 infants vaccinated with 5 μg HepB-SC and 4576 infants vaccinated with 10 μg HepB-HP were investigated.In the 5 μg group,the rates of non-,low-,normal- and high-response were 1.88％,15.18％,61.42％ and 21.52％ respectively.In the 10 μg group,the corresponding rates were 0.15％,2.16％,29.42％ and 68.26％ respectively.The non-,low-,normal-response rates were all higher in 5 μg group than in 10 μg group (P＜0.01),while the high-response rate was much higher in 10 μg group than in 5 μ g group (P＜0.01).The geometric mean concentration (GMC) of anti-HBs were 354.81 mIU/ml (95％ CI:338.84-363.08 mIU/ml) and 1778.28 mIU/ml (95％CI:1698.24-1819.70 mIU/ml) in the 5 μg group and 10 μg group respectively.The GMC was statistically higher in the 10 μg group than in the 5 μg group (P＜0.001).The seroconversion rate and GMC were significantly different between the two groups even after debugging the other influencing factors.Conclusion Better anti-HBs response could be achieved by primary immunization with 10 μg HepB-HP than with 5 μg HepB-SC among newborns.

Objective: To explore the effects and molecular mechanism of the selective JAK1inhibitor SHR0302 and Ruxolitinib on myeloproliterative neoplasms (MPN) cell line SET2 and primary cells in vitro. Methods: Cell proliferation was detected by CCK8 kit. Colony forming experiment was conducted to evaluate erythroid burst colony formation unit (BFU-E) of primary cells from MPN patients. Multi-factor kits were used to detect six inflammatory cytokines. Phosphorylated proteins of Jak-Stat signaling pathway were tested by Western blot. Results: At different time points after treated with SHR0302 and Ruxolitinib, the inhibition of cell proliferation was dose dependent by both drugs (P<0.01) . The inhibitory rates of 2.5 μmol/L SHR0302 and 0.1 μmol/L Ruxolitinib on SET2 cells for 72 h were comparable, i.e. (59.94±0.60) % and (64.00±0.66) %, respectively, suggesting that the inhibitory effect of SHR0302 was weaker than that of Ruxolitinib. Similarly, both SHR0302 and Ruxolitinib inhibited BFU-E in primary marrow cells from MPN patients in a dose-dependent manner. SHR0302 1.0 μmol/L produced similar degree of inhibition compared to Ruxolitinib 0.2 μmol/L. Except IL-12, the expression of other 5 cytokines (IL-6, TNF-α, IL-1β, IL-2, IL-8) was significantly inhibited by 1.6 μmol/L SHR0302 in SET2 cells at 24 h (P<0.01) , while Ruxolitinib 1.0 μmol/L had the same effect. Several phosphorylated molecules of Jak-Stat signaling pathway were significantly inhibited by SHR0302 in SET2 cells only for 3 h. P-stat1 (Tyr701) , p-stat3 (Tyr705) were down-regulated when treated with SHR0302 1.0 μmol/L (P<0.05) , p-jak1 (tyr1022/1023) and p-stat5 (Tyr694) were inhibited at 5.0 μmol/L (P<0.05) . Ruxolitinib significantly inhibited the downstream STAT protein at 0.1 μmol/L. Again, the inhibitory effect of SHR0302 on protein expression was weaker than that of Ruxolitinib. Conclusion: SHR0302 can effectively inhibit the proliferation of MPN cell line and patients' primary cells, as well as the expression of inflammatory factors. The molecular mechanism is possibly related to the down-regulation of phosphorylated proteins of Jak-Stat signaling pathway. Overall, the anti-proliferative and anti-inflammatory effects of SHR0302 are weaker than those of Ruxolitinib.
Anti-Inflammatory Agents ; Cell Line ; Cell Proliferation/drug effects* ; Histone-Lysine N-Methyltransferase ; Humans ; Janus Kinase 1 ; Nitriles ; Pyrazoles ; Pyrimidines ; Sulfuric Acids

BACKGROUNDAngiotensin II (Ang II) is a major contributor to the development of heart failure. However, the molecular and cellular mechanisms that underlie this process remain elusive. Inadequate angiogenesis in the myocardium leads to a transition from cardiac hypertrophy to dysfunction, and our previous study showed that Ang II significantly impaired the angiogenesis response. The current study was designed to examine the role of Jagged1-Notch signaling in the effect of Ang II during impaired angiogenesis and cardiac hypertrophy.

METHODSAng II was subcutaneously infused into 8-week-old male C57BL/6 mice at a dose of 200 ng·kg-1·min-1 for 2 weeks using Alzet micro-osmotic pumps. N-[N-(3, 5-difluorophenacetyl)-L-alanyl]-S-phenylglycine tert-butyl ester (DAPT), a γ-secretase inhibitor, was injected subcutaneously during Ang II infusion at a dose of 10.0 mg·kg-1·d-1. Forty mice were divided into four groups (n = 10 per group): control group; Ang II group, treated with Ang II; DAPT group, treated with DAPT; and Ang II + DAPT group, treated with both Ang II and DAPT. At the end of experiments, myocardial (left ventricle [LV]) tissue from each experimental group was evaluated using immunohistochemistry, Western blotting, and real-time polymerase chain reaction. Data were analyzed using one-way analysis of variance test followed by the least significant difference method or independent samples t-test.

RESULTSAng II treatment significantly induced cardiac hypertrophy and impaired the angiogenesis response compared to controls, as shown by hematoxylin and eosin (HE) staining and immunohistochemistry for CD31, a vascular marker (P < 0.05 for both). Meanwhile, Jagged1 protein was significantly increased, but gene expression for both Jag1 and Hey1 was decreased in the LV following Ang II treatment, compared to that in controls (relative ratio for Jag1 gene: 0.45 ± 0.13 vs. 0.84 ± 0.15; relative ratio for Hey1 gene: 0.51 ± 0.08 vs. 0.91 ± 0.09; P < 0.05). All these cellular and molecular effects induced by Ang II in the hearts of mice were reduced by DAPT treatment. Interestingly, Ang II stimulated Hey1, a known Notch target, but did not affect the expression of Hey2, another Notch target gene.

CONCLUSIONSA Jagged1-Hey1 signal might mediate the impairment of angiogenesis induced by Ang II during cardiac hypertrophy.

Animals ; Cardiomegaly ; chemically induced ; metabolism ; Cell Cycle Proteins ; metabolism ; Immunohistochemistry ; Jagged-1 Protein ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Myocardium ; metabolism ; Neovascularization, Physiologic ; drug effects ; Signal Transduction ; drug effects