Objective To investigate the method for the normal three‐dimensional ultrasound imaging and the characteristics of the fetal hard palate .Methods 210 single fetus free of deformity were examined using three‐dimensional ultrasound(3DUS) .Offline analysis was made after reconstruction ,the hard palate was observed and the width was measured .Results With reconstruction ,the fetal palate was clearly displayed 1.97 cases in 210 cases were successfully displayed (93 8.% ) .The front palate and both frontalis processus of maxillary bone composed similar triangular structure in the coronal plane .The retral part showed sustained linear hyperechoic and the radian increased along with the gestational age .Early palate showed flaky hyperechoic in the cross section and it became horse‐shoe shaped in the second or third trimester pregnancy surrounded by alveolar bone .Linear regression yielded the following formula for the hard palate width (PW) according to gestational age (GA):PW= -0 5.47+0 0.13 × GA( r =0 9.82 ,P <0 0.01) .Conclusions 3DUS acquired palate images fast and easily .The hard palate in the coronal ,sagittal and cross plane showed obvious characteristic images in different gestational stages .With increasing gestational age ,the curvature ,width ,trend and the contrast with the surrounding tissue had the corresponding changes . The successful three‐dimensional image reconstruction of the postnasal triangle and the retral part of fetal hard palate would have an important significance in terms of assessing its continuity and integrity .

Objective To explore whether chlamydia pneumoniae(CP) infection causes the coronary artery morphology change in children and their reciprocity.Methods Serum immunoglobin M(IgM) and immunoglobin G(IgG) antibody to CP were detected by enzymelinked immunosorbent assay(ELISA) in 52 hospitalized children aged 1 month to 10 years and 5 months old in respiratory ward in our hospital,serum interleukin-6(IL-6),triglyceride(TG) and peripheral blood C-reactive protein(CRP) were also determined,morphology change of coronary artery of the patients were harvested by colored doppler echocardiogram.Results In the 52 cases,21 cases were positive of IgM,28 cases were positive of IgG,3 cases were positive both IgM and IgG.Twelve cases were high of CRP,5 cases were high of IL-6,9 cases were high of TG.In the 52 patients,the different levels of IgM,IgG,IL-6,CRP and TG had not coronary artery morphology change.Conclusion CP infection in the children does not cause the coronary artery to occur morphology change.

Objective To explore the function of fluorescent probe JC-1 in detecting the changes of mitochondrial membrane potential(△?m)in early apoptotic cells.Methods After 2-ME was used to induce MUTZ-1 cell apoptosis,cells were dyed with fluorescent probe JC-1,and then the changes of △?m in the early stage of apoptotic cells were analyzed by flow cytometry or detected under fluorescent microscope. Results The control cells with high △?m are those forming JC-1 aggregates in the inner membrane of mitochondria,thus showing orange-red fluorescence.2-ME caused decrease of △?m in MUTZ-1 cells,in which JC-1 maintains monomeric form,thus showing only green fluorescence.The decreases of △?m were in a time-dependent manner,which were significantly higher than those in control group(P

Definite therapeutic effect has obtained by TCM in treating acute cerebral hemorrhage (ACH) according the TCM theory of "blood circulating outside the vessels is the stasis" using breaking stagnant and eliminating blood stasis (Poxue Zhuyu) method, but no material involving the natural development of stoke in superacue stage (0 - 4 hrs after onset of the disease) being presented so far. It has been proved by randomized, double-blinded multi-centeric clinical trials that recombinant activated factor VII (rF VII a) could decreased the morbidity and disability of patients suffered from ACH, suggesting that use hemostasis treatment in ACH during superacu stage should be stressed, and the drugs for Poxue Zhuyu should be used cautiously in the period of 0 - 4 hrs after onset. The hemorrhagic disorder could be eliminated by using drugs for Poxue Zhuyu and other medicines in rational combination.
Cerebral Hemorrhage ; drug therapy ; Drugs, Chinese Herbal ; therapeutic use ; Factor VIIa ; biosynthesis ; genetics ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; Phytotherapy ; Recombinant Proteins ; biosynthesis ; genetics ; therapeutic use

OBJECTIVETo explore clinical effects of internal fixation in treating displaced clavicle fracture combined with coracoid process.

METHODSFrom January 2005 to July 2012, 9 patients with displaced clavicle fracture combined with coracoid process were treated by internal fixation. Among them, there were 6 males and 3 females with an average age of 40.1 (ranged from 20 to 57) years old. According to Eyres classification: 3 cases were type II B, 1 case was type II A, 3 cases were type III B, and 2 cases were type V A. All patients had history of injury, and diagnosed as coracoid fracture X-ray and CT before operation. Herscovici criteria was used to evaluate function of shoulders joint after operation.

RESULTSSeven of 9 patients were followed up from 6 to 18 (averaged 11) months. The incisions were healed at stage I, coracoid process obtained bony healing, and reduction of acromioclavicular joint well. According to Herscovici criteria, 6 patients got excellent results and 1 in good.

CONCLUSIONInternal fixation for the treatment of displaced clavicle fracture combined with coracoid process could restore physiological anatomical position of coracoid process, and benefit for recovery of limb function.

Adult ; Clavicle ; injuries ; Female ; Fracture Fixation, Internal ; methods ; Fractures, Bone ; surgery ; Humans ; Male ; Middle Aged ; Recovery of Function ; Scapula ; injuries ; Shoulder Joint ; injuries

The study was aimed to investigate the mechanism of proliferation inhibition and apoptosis of MDS-RAEB MUTZ-1 cells induced by 2-methoxyestradiol (2-ME), the cell proliferation was determined by MTT assay, apoptosis rate was determined with annexinV-FITC/PI double staining and cell cycle was analyzed by flow cytometry (FCM) after MUTZ-1 cells were treated with different concentrations of 2-ME; the changes of morphologic features of MUTZ-1 cells were observed with Wright-Giemsa's staining; lactate dehydrogenase was determined by Beckman Counter; and agarose gel electrophoresis was used to verify whether 2-ME can induce apoptosis of MUTZ-1 cells. The results showed that 2-ME inhibited the proliferation of MUTZ-1 cells in a dose-and time-dependent manner and caused a sustained arrest at G(2)/M phase in MUTZ-1 cells; the typical apoptotic morphological features appeared in MUTZ-1 cells; the production of lactate dehydrogenase was up-regulated and the marked DNA ladder pattern of internucleosomal fragmentation was observed. It is concluded that the mechanism of proliferation inhibition and apoptosis of MUTZ-1 cells induced by 2-ME is probably related with the G(2)/M cell cycle arrest; 2-ME may be a potentially adjunctive anticancer drug useful to treat myelodysplastic syndrome.
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; Estradiol ; analogs & derivatives ; pharmacology ; Humans ; L-Lactate Dehydrogenase ; metabolism ; Myelodysplastic Syndromes ; pathology

AIMTo determine whether the cardioprotection of ischemic postconditioning and heptanol in ischemic heart against ischemia/reperfusion (I/R) is mediated by gap junction.

METHODSThe effect of ischemic postconditioning, heptanol at different doses (0.03, 0.06, 0.30, and 0.60 mg/kg) and AAP10 (10 mg/kg) on the intact rat heart during 30 min ischemia and 2 h of reperfusion was observed. Ischemic postconditioning was achieved by 3 cycles of 10 s reperfusion/10 s regional ischemia starting at the beginning of the reperfusion. The infarct size and the arrhythmia scores were measured. The effect of ischemic postconditioning, heptanol at different doses (0.05, 0.10, 0.50 and 1.00 mmol/L) and AAP10 (1 x 10(-7)mol/L) on the isolated heart during 30 min ischemia and 2 h of reperfusion was observed. Ischemic postconditioning was achieved by 6 cycles of 10 s reperfusion/10 s global ischemia starting at the beginning of the reperfusion. The arrhythmia scores and conduction velocity of ventricle muscle were measured.

RESULTSIn the intact rat heart model, ischemic postconditioning and heptanol reduced infarct size and arrhythmia scores. In the Langendorff perfused rat heart model, ischemic postconditioning and heptanol reduced arrhythmia scores and conduction velocity of ventricle muscle. Administration of AAP10, an opener of gap junction attenuated the cardioprotection of ischemic postconditioning and heptanol.

CONCLUSIONThe cardioprotection of ischemic postconditioning and heptanol may be related to the attenuation of gap junction communication on myocardiac ischemia/reperfusion injury.

Animals ; Gap Junctions ; physiology ; Heptanol ; pharmacology ; Ischemic Postconditioning ; methods ; Male ; Myocardial Ischemia ; physiopathology ; Myocardial Reperfusion Injury ; physiopathology ; prevention & control ; Rats ; Rats, Sprague-Dawley

The tetrapeptide N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP), a physiological regulator of cell proliferation, has been principally reported as a potent inhibitor of the proliferation of haematopoietic stem cells and progenitors. The purpose of this study was to investigate whether the AcSDKP may directly affect the proliferative potential of human bone marrow mesenchymal stem cells (MSCs) in vitro. We added AcSDKP to the cultures of human bone marrow mononuclear cells and measured the number and average area of MSC colonies. MTT colorimetric assay and mitotic index determination were further used to examine the proliferative state of the third passage MSCs in subcultures with or without the addition of AcSDKP. In addition, we evaluated whether AcSDKP may kill MSCs by the trypan blue dye exclusion test. The results showed that the colony forming capacity, the number of viable cells and the mitotic index were reduced in human bone marrow MSCs cultured in 1x10(-12) mol/L to 1x10(-9) mol/L AcSDKP. Maximum inhibitory activity appeared in 1x10(-11) mol/L of AcSDKP. No difference in percent of living cells was observed between the MSC subcultures with and without the addition of AcSDKP. As a result, AcSDKP within a certain range of concentrations has negatively regulatory effects on the proliferation of human bone marrow MSCs in vitro.
Bone Marrow Cells ; cytology ; Cell Proliferation ; drug effects ; Cells, Cultured ; Down-Regulation ; physiology ; Growth Inhibitors ; physiology ; Humans ; Mesenchymal Stromal Cells ; cytology ; Oligopeptides ; physiology

OBJECTIVETo determine the detection rate of Helicobacter pylori (Hp) in children with Meckel's diverticulum (MD) and its clinical significance among children with MD.

METHODSEighty-one children with MD were divided into two groups according to the presence (n=45) or absence (n=36) of digestive hemorrhage. The detection rates of Hp in MD tissues and stomach tissues were determined by immunohistochemistry. The detection rates of Hp were compared between the two groups and between the MD tissues with different clinical features in the hemorrhage group.

RESULTSThe detection rate of Hp in MD tissues for the hemorrhage group was 76% (34/45), which was significantly higher than that for the non-hemorrhage group (47%, 17/36) (P<0.05). The detection rate of Hp in stomach tissues for the hemorrhage group (87%, 39/45) was insignificantly higher than that for the non-hemorrhage group (67%, 24/36) (P>0.05). Among patients in the bleeding group, the detection rate of Hp in MD tissues showed no relationship with age, sex, preoperative hemorrhage frequency, amount of hemorrhage, length of MD, basal diameter of MD, and pathological type (P>0.05), but was related to location of MD, presence or absence of ulcer, and depth of ulcer (P<0.05). For the hemorrhage group, a significant positive correlation was found between the detection rates of Hp in MD tissues and stomach tissues (P<0.05), as shown by the Spearman correlation analysis.

CONCLUSIONSThe detection rate of Hp in MD tissues is increased in children with MD complicated by digestive hemorrhage. Hp infection may play some role in the hemorrhage process among children with MD.

Adolescent ; Child ; Child, Preschool ; Female ; Gastric Mucosa ; microbiology ; Gastrointestinal Hemorrhage ; etiology ; microbiology ; Helicobacter pylori ; isolation & purification ; Humans ; Immunohistochemistry ; Infant ; Male ; Meckel Diverticulum ; complications ; microbiology

OBJECTIVETo modify the current PCR-based method for rapid and efficient preparation of small interfering RNA (siRNA) expression cassette to improve the efficiency of RNA interference.

METHODSThe U6 promoter sequence was amplified by PCR using the genomic DNA of K562 cells as the template, and cloned into pMD18-T vector which served as the template for further PCR amplification with the primers on the plasmid. The amplified product was directly used as the template for preparing siRNA expression cassette. The siRNA expression cassette targeting p53 gene was amplified, verified by sequencing, and transfected into SH-SY5Y cells. After a 48-hour transfection, the cells were harvested and the total RNA was for RT-PCR for evaluating the effect of RNA interference.

RESULTSThe sequencing result confirmed the correct U6 promoter sequence cloned from K562 cells. After transfection of SH-SY5Y cells for 48 h with siRNA expression cassette, the p53 gene expression was inhibited at the mRNA level in comparison with the control cells as demonstrated by RT-PCR detection.

CONCLUSIONThe siRNA expression cassette prepared using the established method described hereby can be well applicable in RNA interference research.

Gene Silencing ; Gene Targeting ; methods ; Genetic Vectors ; genetics ; Humans ; K562 Cells ; Polymerase Chain Reaction ; RNA, Small Interfering ; biosynthesis ; genetics ; RNA, Small Nuclear ; Tumor Suppressor Protein p53 ; biosynthesis ; genetics