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

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.

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 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

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 report the clinical and myopathological features in a patient with common variable immunodeficiency (CVID) with myositis.Methods A 33 years old man suffered from recurrent respiratory infection with fever over 10 years.The symptoms improved after anti-infection therapy.At the same time he presented with fatigue.Two years ago he developed general muscle weakness,hypertrophy and myotonia,especially in the hands,neck and thighs.Genetic test for myotonic dystrophy protein kinase (DMPK) and zinc finger protein 9 (ZNF9) was performed.Laboratory tests,electromyography,muscle ultrasound and muscle biopsy were performed.In addition to standard histological and enzyme histochemical stainings,immunohistochemical method was used with primary antibodies of mouse anti human monoclonal antibodies including CD8 for T-lymphocytes,CD20 for B-lymphocytes,CD68 for macrophages and MHC-Ⅰ for muscle membrane.Results Electromyography revealed myogenic changes and abound with myotonic potentials.There was muscle hypertrophy in muscle ultrasound.Lung biopsy showed chronic inflammatory changes.Serum hypoimmunoglobulin and anemia were found.Muscle biopsy showed muscle fiber necrosis and regeneration with lymphocyte and macrophage infiltration.There were no gene mutations in DMPK and ZNF9 gene.Conclusion Muscle hypertrophy and myotonia appeared in CVID with myositis.

Objective:To study the influence of protein transduction domain (PTD)-oligomerization domain (OD)-HA fusion proteins on apoptosis of bcr/abl-positive cell lines. Methods:bcr/abl-positive cells were treated with PTD-OD-HA protein. The apoptoses of the cells were detected by flow cytometry (FCM), DNA ladder and transmission electron microscopy (TEM), and the levels of apoptosis-related genes bax and bcl-2 were detected by RT-PCR and Western blotting. Results:FCM examination demonstrated that PTD-OD-HA protein induced the apoptosis of bcr/abl-positive cells; DNA ladder showed that the classic DNA ladders appeared in BaF3-P210 and K562 cells after 48 h treatment with PTD-OD-HA proteins; the apoptoses of BaF3-P210 cells were observed by TEM; the levels of bax in mRNA and protein increased in BaF3-P210 and K562 cells, and bcl-2 decreased. Conclusion:PTD-OD-HA proteins specifically induced the apoptosis of bcr/abl positive cells.