Acupuncture Therapy ; Aged ; Combined Modality Therapy ; Female ; Humans ; Male ; Middle Aged ; Parkinson Disease ; drug therapy ; therapy

AIM: To observe the effect of microRNA-16 (miR-16) on the megakaryocytic differentiation of K562 cells, and to explore the potential mechanism.METHODS:miR-16 was over-expressed or silenced by transfection with miR-16 mimics or inhibitor in K562 cells.The level of miR-16 was detected by real-time PCR.The expression of CD41, CD42b and CD61, as megakaryocytic differentiation markers, was detected by flow cytometry.The effect of miR-16 on the expression of myeloblastosis oncogene ( MYB) was measured by Western blotting, and flow cytometry was performed to confirm whether the effect of miR-16 on expression of CD41, CD42b and CD61 was mediated by MYB.RESULTS:Transfection with miR-16 mimics dramatically elevated the level of miR-16 and the expression of CD41, CD42b and CD61 in the K562 cells.Transfection with miR-16 inhibitor decreased the level of miR-16 and the expression of CD41, CD42b and CD61 in the K562 cells (P<0.05).The expression of MYB was regulated by miR-16, and MYB silencing reversed the regulation of CD41, CD42b and CD61 induced by miR-16.CONCLUSION:miR-16 regulates the megakaryocytic dif-ferentiation of K562 cells by targeting MYB.

Objective To investigate the clinical and pathologic features in patients of microscopic polyangiitis (MPA) with peripheral nerve abnormality.Methods We collected clinical data of 6 patients with MPA that was confirmed by immunological,pathological and clinical findings.Electroneurophysiologic examinations and sural nerve biopsies were performed in these patients.Two normal controls were included in these studies.Results All of 6 patients developed asymmetric polyneuropathies.Electrodiagnostic studies showed reduced amplitudes of the sensory nerve action potential and compound motor action potential with mild impaired conductive velocities.The patients presented vasculitis changes with cell infiltration by monocytes and lymphocytes.Sural nerve biopsies found loss of myelinated fibers in all of the patients indicating axonal degeneration.Some of them associated with regeneration clusters of myelinated fibers.Conclusions Asymmetric neuropathy with sensory nerve injuries is the mainfeature in the MPA associated polyneuropathy.Electrodiagnostic examination indicated axonal lesions in mononeuritis multiplex.Sural nerve biopsies confirmed the active axonal lesions and vasculitis.

Objective To investigate expression and significance of matrix metalloproteinase-2(MMP-2),MMP-9 and tissue inhibitor of metalloproteinase-1(TIMP-1) in rats with glomerular sclerosis made by doxorubicin.Methods Forty Wistar male rats(8-week-old) were randomly assigned into 2 groups:sham operated and model groups.Rats in model group were nephrectomized after anesthesia and injected with adriamycin(5 mg/kg) after 1 week.Rats in sham operated group was subjected to sham operation and injected with normal saline after 1 week through the tail vein.All rats were killed in the 12th week.Immuno-histochemistry was performed on renal tissue to detect Collagen Ⅳ(Col-Ⅳ),fibronectin(FN),MMP-2,-9 and TIMP-1.Results Immunohistochemistry staining indicated that expressions of MMP-2,-9 in model group decreased significantly compared to sham operated group(Pa

Objective To study the expression of ?-smooth muscle actin(?-SMA)in glomerulosclerosis rats and its relationship with renal function.Methods Forty healthy Wistar rats were equally divided into 2 groups including sham operated group and model control group.Rats in model groups were uninephrectomized and injected with daunorubicin(5 mg/kg)after 1 week through the tail vein.Twenty-four hours of urinary protein excretion,serum creatinine(Scr),blood urea nitrogen(BUN)were measured at the 12th week.Renal pathology was evaluated.Immunohistochemistry(SupervisionTM)was performed on renal glomeruli tissue to detect the expression of ?-SMA.Reverse transcription polymerase chain reaction(RT-PCR)was used to examine the expression levels of ?-SMA mRNA in glomeruli.SPSS 13.0 software was used to analyze the two variables.Results In model control group,the urinary protein,Scr,BUN significantly increased(Pa

Objective To investigate the incidence rate, high risk factors and hemodynamic changes of patent ductus arteriosus (PDA) in premature infants, and to give suggestions abo ut clinical monitoring and management of PDA in premature infants. Methods Echocardiography was performed on 86 non-ventilated or weaned from ventilator-pr emature infants at 2 to 5 days of age,whose gestational age was 28 to 36 weeks. All premature infants diagnosed as PDA were followed up clinically and by Echoc ardiography until discharged. Results Twenty-two infants diagnosed as PDA at mean 3 days of age, mean gestational age was (33.l?2.0) weeks. Ductus in 16 infants (out of 20 infants) closed spontaneo usly when repeated echocardiography at mean 8.5 days of age. For 4 remaining PDA infants, ductus closed in 2 cases (l treated with indomethacin). One ductus reo pened because of sepsis, and 3 infants discharged with opened ductus at their 2l , 40 and 47 days of age respectively. Single and multiple Logistic analysis indi cated that the lower the birth-weight ,the higher the incidence of PDA (?2=2. 8907 P=0.0891); neonatal asphyxia and suffered from severe diseases (neonat al respiratory distress syndrome, sepsis) were high risk factors of PDA (?2= 4.3729 P=0.0365;?2=11.6590 P=0.0006). Premature infants with PDA h ad good heart function,although their LA/AO ratio increased slightly (1.0810?0. 18 vs 1.00?0.07,P= 0.048).Conclusions PDA incidence at 3 days of life in 33 weeks premature infants is 25.6%, 85% PDA disappeares spontaneously during follow-up. Low birth-weight asphyxia, severe diseases and symptomatic PDA are high risk factors of PDA. Ductus can reopen in premature infants. J Appl Clin Pediatr,2005,20(2):129-131

In this study, the effect of heparin-derived oligosaccharide (HDO) on platelet-derived growth factor (PDGF) induced vascular smooth muscle cells (VSMCs) proliferation and the related signal transduction mechanisms were investigated. MTT assays were used to measure VSMCs proliferation. Cell cycle distribution was analyzed by flow cytometry. The level of key regulatory proteins in PKC, MAPK and Akt/PI3K pathways were determined by RT-PCR, Western blot and immunocytochemical methods. Meanwhile, mRNA expressions of some proto-oncogenes were assayed by RT-PCR method. Our data showed that HDO (0.01, 0.1 and 1 μmol · L(-1)) inhibited 30 ng · mL(-1) PDGF-induced VSMCs proliferation in a dose-dependent manner, blocked the G1/S transition and inhibited the level of key regulatory proteins and some proto-oncogenes (P < 0.05). The results showed that HDO may decrease the key regulatory proteins expression, hence suppress the transcription of proto-oncogene and G1/S transition, finally inhibiting VSMCs proliferation.
Cell Cycle ; Cell Proliferation ; drug effects ; Cells, Cultured ; Flow Cytometry ; Heparin ; pharmacology ; Humans ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; cytology ; drug effects ; Oligosaccharides ; pharmacology ; Platelet-Derived Growth Factor ; pharmacology ; Signal Transduction

Objective: The BCR-ABL fusion gene induced by reciprocal translocation of t (9; 22) (q34; q11) plays an important role in the pathogenesis of chronic myeloid leukemia (CML). Using recombinant ade-noviruses carrying the N-terminal oligomerizaton domain (OD) of the BCR/ABL and chimeric ubiquitin ligase β-TrCP, this study was to investigate the effect of the targeted degradation of oncoprotein BCR-ABL by Ubiqui- tin-Proteasome System on the proliferation of leukemia call line K562. Methods: The recombinant adenovirus-es carrying wild-type β-TrCP gene (Ad5β-TrCP-OD-HA), mutational β-TrCP gene (Ad5 A F-TrCP-OD-HA)and green fluorescent protein gene (Ad5GFP)were amplified in 293 calls and co-infected into K562 cells respec- tively. The rates of infection were analyzed by flow cytometry (FCM). Recombinant protein and BCR-ABL ex-pression was detected by Western blot. Cell proliferation was determined by cell counting and methylcellu- cose clonal cell culture. Cell cycle was observed through FCM. Untreated K562 cells were used as blank con-trols. Result: The leukemia K562 cell lines with exogenous recombinant β-TrCP-OD-HA and F-TrCP-OD-HA gene were established. The infection rates in the three groups were over 66.4% and recombinant protein sus-tained to be expressed. Ad5β-TrCP-OD-HA down-regulated the expression of BCR-ABL and inhibited prolifer-ation of K562 cells. FCM showed that the percentage of cells at S phase was decreased to 10.88%±2.42%, while that of cells at G_0/G_1 was increased to 85.6%±5.61%, with a significant difference (P<0.05). No changes were found in the cell cycle in groups of Ad5 △ F-TrCP-OD-HA and Ad5GFP. Conclusion: There is sustained ex-pression of recombinant β-TrCP-OD-HA protein in K562 cells infected by recombinant adenovirus.β-TrCP-OD-HA could inhibit the proliferation and clonogenicity of K562 cells through targeted degradation of oncoprotein BCR-ABL and arresting the progression of call cycle.