OBJECTIVETo evaluate clinical outcomes of anterior cruciate ligament (ACL) and posterior cruciate ligament (PCL) reconstruction under arthroscopy combined with limited open repair of medial collateral ligament (MCL) for the treatment of multiple ligament injuries of knee joints.

METHODSFrom March 2006 and June 2012,the data of 14 patients (14 knees) with multiple injuries of ACL, PCL, and MCL were collected. There were 8 males and 6 females with an average age of (31.8 +/- 8.1) years old (ranged, 20 to 49 years old). All the patients were performed with X-ray and MRI examination, and the results showed that 10 patients had combined with injuries of anterior cruciate ligament (ACL), posterior cruciate ligament (PCL) and medial collateral ligament (MCL); 4 patients had ALC,PCL and posterolateral corner (PLC) injuries. Four patients had medial meniscus injuries and 2 patients had lateral meniscus injuries. The MCL,PLC and meniscus injuries were treated with operation on the first stage, and functional exercises were performed 3 weeks after fixation. The reconstruction operation of ACL and (or) PCL was performed at the second stage under arthroscopy 3 to 6 months later when the movement range of knee joint recovered to the normal level with obvious relaxation.

RESULTSAll incisions healed by primary intention. All the patients were followed up with a mean duration of 48.9 months (ranged, 24 to 80 months). The Lysholm score was improved from preoperative 19.6 +/- 0.9 to the latest follow-up 87.1 +/- 2.8 (t=12.3, P<0.01). The International Knee Documentation Committee (IKDC) rating: 9 cases nearly recovered to normal, 5 cases were abnormal.

CONCLUSIONFor multiple ligament injuries in the knee, staged repair and reconstruction can effectively restore knee joint stability and function.

Adult ; Anterior Cruciate Ligament ; surgery ; Anterior Cruciate Ligament Injuries ; Female ; Follow-Up Studies ; Humans ; Knee Injuries ; physiopathology ; surgery ; Knee Joint ; physiopathology ; surgery ; Male ; Middle Aged ; Posterior Cruciate Ligament ; injuries ; surgery ; Reconstructive Surgical Procedures ; Treatment Outcome ; Young Adult

OBJECTIVETo investigate the clinical efficacy of modified Sanmiao Powder (SMP) in treating chronic uric acid nephropathy (CUAN).

METHODSNinety-four patients with CUAN were equally randomized to the treated group and the control group. Conventional treatment was given to all patients and the treated group was administered with SMP additionally for 12 weeks. Changes of symptoms were observed, and laboratory indexes, as urinary protein quantity (UPro), urinary RBC count (URBC), urinary beta2 microglobulin (beta2-M), urinary beta-N-acetylglucosaminidase (NAG), blood urea nitrogen (BUN), serum creatine (SCr) and serum uric acid (SUA), were detected before and after treatment.

RESULTSThe total effective rate in the treated group was 87.2% (41/47), and in the control group was 61.7% (21/47), showing significant difference between groups (P < 0.01); significant improvement of UPro, URBC, beta2-M, NAG, BUN, SCr and SUA were shown in the treated group (P < 0.05, P < 0.01); but in the control group, only URBC count was significantly decreased (P < 0.05), no statistically significant change of other indexes was found (P > 0.05). SUA decreased in both groups (P < 0.01), which was markedly lower in the treated group than in the control group (P < 0.05); SCr and BUN were also decreased in the treated group (P < 0.01).

CONCLUSIONSCombined therapy of SMP and conventional Western medicine shows a favorable effect in treating CUAN. It could not only reduce SUA, but also alleviate the albuminuria and hematuria, lower the urinary levels of beta2-M and NAG to improve renal function.

Adult ; Aged ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Kidney Diseases ; drug therapy ; etiology ; Male ; Medicine, Chinese Traditional ; methods ; Middle Aged ; Phytotherapy ; Uric Acid

OBJECTIVETo investigate the tumor suppression efficacy of histone deacetylase inhibitor, phenylbutyrate (PB), in combination with DNA methylation inhibitor 5-Aza-2-deoxycytidine (5-Aza-CdR) in the treatment of Kasumi-1 xenograft tumor in nude mice and its mechanism.

METHODSThe nude mice model of Kasumi-1 xenograft tumor was established by subcutaneous inoculation. Latency of tumor formation, the ability of Kasumi-1 cells pre treated with PB to form the xenograft tumor, and the tumor suppression activity of PB and 5-Aza-CdR by intraperitoneal injection in xenografted mice model were detected. Cell differentiation and cell cycle parameters of the tumor cells were analyzed by flow cytometry analysis, apoptosis by TUNEL in situ hybridization, and tumor microvessel density (MVD) by immunohistochemistry study.

RESULTSThe latency of tumor formation in mice with or without previous lienectomy was 17 approximately 23 and 40 approximately 50 days, respectively. Tumor cells xenografted could not be found in other tissues than in inoculation area, and still harbored the specific t(8;21) and AML1-ETO fusion gene. When the xenografted mice models treated with PB, 5-Aza-CdR, or both, the tumor growth inhibition rates were 49.07%, 25.69% and 87.46% (P < 0.05), the apoptosis indexes (AI) of tumor cells were (2.25 +/- 0.85)%, (1.32 +/- 0.68)%, and (5.41 +/- 1.56)% (P < 0.05), and the microvessel densities (MVD) were 21.69 +/- 6.25, 28.34 +/- 4.24 and 9.48 +/- 3.21 (P < 0.01), respectively. All the data above were significantly different from that in control (P < 0.05). The expression of CD11b and CD13 antigen of the tumor cells was increased in xenografted mice model treated with PB when compared with the control \[(12.08 +/- 1.02)% and (54.91 +/- 2.72)%\], respectively (P < 0.01), and tumor cells showed a cell cycle arrest with increased G(0)/G(1)-phase cells and decreased S-phase cells.

CONCLUSIONPB inhibited the growth of Kasumi-1 xenograft tumor by inducing tumor cell apoptosis and differentiation, and suppressing its angiogenesis in vivo. 5-Aza-CdR could significantly enhance the antitumor activity of PB.

Animals ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Deoxycytidine ; administration & dosage ; Disease Models, Animal ; Flow Cytometry ; Humans ; In Situ Nick-End Labeling ; Leukemia, Myeloid, Acute ; drug therapy ; pathology ; Mice ; Mice, Nude ; Phenylbutyrates ; administration & dosage ; Tumor Burden ; drug effects ; Xenograft Model Antitumor Assays

OBJECTIVETo explore the blockade effect of phenylbutyrate (PB), a histone deacetylase inhibitor, on the in vitro biological function of AML1/ETO to reverse its transcription repression and induce Kasumi-1 cells to differentiate and apoptosis.

METHODSKasumi-1 cells were treated with PB at different concentrations in suspension culture. Cell proliferation was analysed by MTT assay, morphological changes by light and electron microscopy, expression of myeloid-specific differentiation antigen and cell cycle by flow cytometry, cell apoptosis by annexin V staining, agarose gel electrophoresis and flow cytometry.

RESULTSPB treatment caused a dose-dependent inhibition of the cell proliferation. The IC(50) was about 2.3 mmol/L. PB treatment led to a progressive decline in the fraction of S-phase cells and increase in G(0)/G(1) cells. PB induced a time- and dose-dependent increase in expression of myeloid cell surface protein CD(11b) and CD(13). A dose-dependent increase in early apoptosis for 2 days treatment, late apoptosis for 3 days treatment. The DNA ladder of apoptosis was observed on agarose gel electrophoresis for 5 days treatment. Morphological features of monocytoid differentiation and apoptosis were seen on Wright-Giemsa staining smears.

CONCLUSIONPB treatment could inhibit proliferation of Kasumi-1 cells, induce partial differentiation, apoptosis and accumulation of cells in G(0)/G(1) phase.

Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Division ; drug effects ; Cell Line, Tumor ; Dose-Response Relationship, Drug ; Histone Deacetylase Inhibitors ; Humans ; Leukemia, Myeloid, Acute ; pathology ; Phenylbutyrates ; pharmacology

OBJECTIVETo further verify the transcriptional repression domains in ETO and their relationship with histone deacetylase (HDAC).

METHODSEither of the ETO two zinc fingers was mutated respectively by site-directing mutagenesis. The truncation fragments of ETO were amplified by polymerase chain reaction (PCR) and cloned into eukaryotic expression plasmid pFA-CMV. By the means of DNA transfection and analysis of the transcription derived from the promoter of reporter gene, the transcriptional regulation domains of ETO was determined.

RESULTSThe expression plasmids carrying truncated ETO and ETO with point mutation at either zinc finger were successfully constructed. Two repression domains were found within ETO, which were located at two zinc finger motifs and 275 - 487 amino acid residues, respectively.

CONCLUSIONThe transcription repression by ETO was mediated by two separated domains and closely associated with HDAC, which may be used as therapeutic target for acute myeloid leukemia M(2b).

Core Binding Factor Alpha 2 Subunit ; chemistry ; genetics ; Gene Expression Regulation, Leukemic ; genetics ; Genetic Vectors ; Histone Deacetylases ; physiology ; Humans ; In Vitro Techniques ; Leukemia, Myeloid, Acute ; enzymology ; genetics ; Oncogene Proteins, Fusion ; chemistry ; genetics ; RUNX1 Translocation Partner 1 Protein ; Transcription, Genetic ; Transfection ; Zinc Fingers ; genetics

Objective To evaluate and analyze the efficacy and safety of endoscopic papillectomy for tumors of major duodenal papilla. Methods The clinical data of three patients with tumors of major duodenal papilla who were treated by endoscopic papillectomy were retrospectively reviewed, and the clinical outcome was summarized. Results The success rate of endoscopic papillectomy was 100.0% (3/3), and the complete resection was 100.0% (3/3). No short-term complication occurred in 3 cases. The recurrence rate was 0.0% (0/3). Conclusion Endoscopic papillectomy is an effective method for treating tumors of major duodenal papilla.

OBJECTIVETo investigate the normal range of (CAG)n in spinocerebellar ataxia type 1 (SCA1) gene and spinocerebellar ataxia type 3 (SCA3/MJD) gene in 110 normal subjects of Han population in Northeastern China, to assess the genotypes for clinically diagnosed spinocerebellar ataxia(SCA) individuals including 25 patients from 8 families and 6 sporadic patients, and to make presymptomatic and prenatal diagnosis.

METHODSDNA fragments from the normal subjects and the patients were detected by fluorescence-PCR. Homozygosities were selected for DNA sequencing.

RESULTSThe normal ranges of (CAG)n of SCA1 and SCA3/MJD were 20-39 and 14-38 repeats respectively, SCA1 was found mostly to be 26 and 27 repeats, allele frequency 34.09% and 20.91%; heterozygosity was 84.55%, SCA3/MJD was found mostly to be 14 repeats, allele frequency 39.55%, heterozygosity was 78.18%.(CAG)(68) of SCA3/MJD gene of one affected individual had been found in a family but no CAG mutative expansion in related members was observed.

CONCLUSIONThe normal ranges of CAG repeats vary with areas and races. SCAs genotyping is the first choice in presymptomatic and prenatal diagnosis.

Ataxin-1 ; Ataxin-3 ; Ataxins ; China ; DNA ; chemistry ; genetics ; Family Health ; Female ; Gene Frequency ; Genotype ; Humans ; Machado-Joseph Disease ; diagnosis ; genetics ; Male ; Nerve Tissue Proteins ; genetics ; Nuclear Proteins ; genetics ; Pedigree ; Repressor Proteins ; Sequence Analysis, DNA ; Spinocerebellar Ataxias ; diagnosis ; genetics ; Trinucleotide Repeat Expansion ; genetics ; Trinucleotide Repeats ; genetics

OBJECTIVETo investigate the expression of high mobility group box-1 (HMGB1) in the lung tissue and bronchoalveolar lavage fluid (BALF) of asthmatic mouse models and the influence of dexamethasone (DM).

METHODSEighteen female Balb/C mice were randomly divided PBS control group, OVA group and OVA/DM group, and asthmatic mouse models were established in the latter two groups. The airway responsiveness of the mice was assessed by whole-body plethysmography, and the cells in the BALF were counted and classified, with the supernatants of the BALF collected for detection of the level of HMGB1 by ELISA. The left lung of the mice was collected for HE staining, and the expression of HMGB1 in the right lung tissue was detected by Western blotting.

RESULTSAsthmatic mouse models were successfully established. The level of HMGB1 in the BALF was significantly higher in OVA group than in the control group (6.31 ± 4.05 ng/ml vs 2.59 ± 0.73 ng/ml, P = 0.017), but no significant difference was found between OVA/DM group (3.39 ± 0.50 ng/ml) and OVA group (PP = 0.052). The expression of HMGB1 relative to tubulin was significantly higher in OVA group than in the control group (2.08 ± 0.87 vs 0.85 ± 0.30, P = 0.032), but similar between OVA/DM group (1.15 ± 0.48) and OVA group (PP = 0.133).

CONCLUSIONThe expression of HMGB1 is obviously increased in the lung and BALF of asthmatic mice and DM produces no significant effect on HMGB1 expression, suggesting that HMGB1 may serve as a new therapeutic target for asthma treatment.

Animals ; Asthma ; drug therapy ; metabolism ; Bronchoalveolar Lavage Fluid ; chemistry ; Dexamethasone ; therapeutic use ; Female ; HMGB1 Protein ; genetics ; metabolism ; Lung ; metabolism ; Mice ; Mice, Inbred BALB C

OBJECTIVETo investigate whether phenylbutyrate (PB) combined with 5-aza-2'-deoxycytidine (5-Aza-CdR)could inhibit transcription repression and induce t(8;21) acute myelogenous leukemia (AML) Kasumi-1 cells to differentiate and undergo apoptosis.

METHODSKasumi-1 cells were treated with PB and 5-Aza-CdR at different concentrations in suspension culture. Cellular proliferation was determined by the MTT assay, expression of myeloid-specific differentiation antigen and cell cycles were analyzed by flow cytometry. Cell apoptosis were assessed using AnnexinV/PI staining and flow cytometry.

RESULTSTreatment of Kasumi-1 cells with PB caused a dose-dependent inhibition of proliferation, with an IC(50) of 2.3 mmol/L. When combined with 5-Aza-CdR, PB resulted in a greater growth inhibition with an IC(50) of 1.95 mmol/L. Treatment of Kasumi-1 cells with PB resulted in cell cycle arrest at G(0)/G(1), while combined treatment with PB and 5-Aza-CdR led to cell cycle arrest at G(2)/M. Expression of myeloid cell differentiation antigens CD11b and CD13 induced by PB was enhanced when Kasumi-1 cells were pretreated with low dose of 5-Aza-CdR. High, but not low, concentrations of 5-Aza-CdR could enhance early apoptosis of Kasumi-1 cells induced by PB.

CONCLUSIONPhenylbuty rate, when combined with 5-Aza-CdR, inhibits AML cell in vitro proliferation and increases apoptosis in a synergistic fashion.

Acute Disease ; Apoptosis ; drug effects ; Azacitidine ; administration & dosage ; analogs & derivatives ; pharmacology ; CD11b Antigen ; metabolism ; CD13 Antigens ; metabolism ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; Drug Synergism ; Humans ; Leukemia, Myeloid ; immunology ; pathology ; Phenylbutyrates ; pharmacology

OBJECTIVE: To compare the behavioral improvement to find the best transplantation approach for treating brain injury through transplanting amniotic-derived mesenchymal stem cells into brain injured rats in different ways. METHODS: Eighty brain injured Wista rats were randomly divided into a control group with brain injury alone (n=20) and a treatment group(n=60) which were further evenly divided into Group A (transplanted through the vena caudalis), Group B (transplanted through the ventriculus cerebri lateralis), and Group C (transplanted through the injured brain area). Each group was transplanted with amniotic-derived esenchymal stem cells, and their therapeutic efficacy would be evaluated through the neurological severity score (NSS). RESULTS: Compared with other groups, the behaviors of Group C had markedly improved. There was statistically significant difference in the 2 groups (P<0.05). Compared with the control group, the behaviors of Group A and Group B had marked improvement. There was statistically significant difference in the 3 groups (P<0.05). However, there was no significant difference between Group A and the control group (P>0.05). CONCLUSION Transplanting the amniotic-derived mesenchymal stem cells into the injured brain area may be effective for brain injury in rats.
Amnion ; cytology ; Animals ; Brain Injuries ; therapy ; Female ; Male ; Mesenchymal Stem Cell Transplantation ; methods ; Mesenchymal Stem Cells ; cytology ; physiology ; Nerve Regeneration ; physiology ; Random Allocation ; Rats ; Rats, Wistar