Equipment Design ; Facial Injuries ; therapy ; First Aid ; instrumentation

OBJECTIVETo explore the effect of Bushen Gujin Recipe (BGR) on serum and synovial expression of interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α) in knee osteoarthritis (KOA) model rabbits.

METHODSTotally 36 8-month-old healthy male New Zealand white rabbits were randomly divided into 4 groups, i.e., the normal control group, the model group, the Western medicine group (Meloxicam, at the daily dose of 6 mg/kg), and the TCM group (BGR, at the daily dose of 53 g/kg), 9 in each group. Modeling was performed in all rabbits except those in the normal control group by using Hulth A method. All medication was performed for 8 consecutive weeks. Contents of IL-1 and TNF-α were detected using ELISA from serum, partial synovial tissue of the front knee joint, cartilage and subchondral bone of the medial femoral condyle.

RESULTSThe joint space became narrowed in the Western medicine group, ranging between the model group and the TCM group. The articular surface was rough with obvious osteophytes. The joint space was slightly narrower in the TCM group; the articular surface was slightly rough with mild osteophytes. Compared with the normal control group, contents of IL-1 and TNF-α in serum and synovial increased in the model group (P < 0.01). Compared with the model group, contents of IL-1 and TNF-α in serum and the synovial fluid decreased in the two treatment groups (P < 0.01). There was no statistical difference in contents of IL-1 and TNF-α between the Western medicine group and the TCM group.

CONCLUSIONBGR promoted the synthesis of cartilage matrix and carti- lage repair through inhibiting the secretion of IL-1 and TNF-α, and prolonging cartilage degeneration.

Animals ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Interleukin-1 ; metabolism ; Knee Joint ; Male ; Osteoarthritis, Knee ; drug therapy ; metabolism ; Rabbits ; Synovial Fluid ; Synovial Membrane ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

Objective To investigate the methods and therapeutic effects of image-guided percutaneous needle iniection of methylprednisolone and injectable calcium sulfate for simple bone cysts.Methods Thirty-seven patients with simple bone cysts from 0ctober 2006 to August 2010 were analysed retrospectively in our hospital,including 26 males and 11 females with the average age of 13.2 years(range,8-22 years).Five cases of proximal femus lesions,with proximal thigh pain,limp and other symptoms.Thirty-two cases of proximal humeral lesions,16 patients had proximal pain and other symptoms of upper arm,the other 16 cases were asymptomatic.Preoperative AP and lateral X-ray.CT and MRl were taken.Under the C-arm X-ray monitor.two needles were inserted into the proximal and distal of cysts respectively,Omnipaque contrast was iniected to confirm the two needles is interlinked,then repeated rinsing with normal saline,then 120 mg methylprednisolone and iniectable calcium sulfate were injected,till the cysts were full up.Patients after treatment were assessed according to modified Neer X-ray criteria.Resuits The average hospitalization was 2.3 days (range.1-3 days).X-ray was reviewed every month,additional injection was performed if bone cysts stopped decreasing for 2 consecutive months,iniection 2 times in 6 eases,and 31 cases were injected only once.After 3 months follow.up 37 cases,according to modified Neer X-ray criteria,6 eases regarded as grade Ⅱ,8 as grade Ⅲ,23 as grade Ⅳ;after 6 months,31 patients were followed up,including 2 cases as grade Ⅱ,4 cases as grade Ⅲ,25 as grade Ⅳ;after 24 months of follow-up 26 cases,3 as grade Ⅲ,23 as grade Ⅳ;after 36 months follow-up,19 cases were all grade Ⅳ.Conclusion Imaging-guided percutaneous iniection of methylprednisolone and inieetable calcium sulfate for simple bone cysts has demonstrated,with less trauma,lower complications incidence and quicker recovery.

OBJECTIVETo investigate the protective effect of histone acetylation against hypoxic-ischemic cortical injury in neonatal rats.

METHODSA total of 90 neonatal rats aged 3 days were divided into three groups: sham-operation, cortical injury model, and sodium butyrate (a histone deacetylase inhibitor) treatment. The rats in the model and the sodium butyrate treatment groups were intraperitoneally injected with lipopolysaccharide (0.05 mg/kg), and then right common carotid artery ligation was performed 2 hours later and the rats were put in a hypoxic chamber (oxygen concentration 6.5%) for 90 minutes. The rats in the sham-operation group were intraperitoneally injected with normal saline and the right common carotid artery was only separated and exposed without ligation or hypoxic treatment. The rats in the sodium butyrate treatment group were intraperitoneally injected with sodium butyrate (300 mg/kg) immediately after establishment of the cortical injury model once a day for 7 days. Those in the sham-operation and the model groups were injected with the same volume of normal saline. At 7 days after establishment of the model, Western blot was used to measure the protein expression of histone H3 (HH3), acetylated histone H3 (AH3), B-cell lymphoma/leukemia-2 (Bcl-2), Bcl-2-associated X protein (BAX), cleaved caspase-3 (CC3), and brain-derived neurotrophic factor (BDNF). Immunofluorescence assay was used to measure the expression of 5-bromo-2'-deoxyuridine (BrdU) as the cortex cell proliferation index.

RESULTSThe sodium butyrate treatment group had a significantly lower HH3/AH3 ratio than the model group (P<0.05), which suggested that the sodium butyrate treatment group had increased acetylation of HH3. Compared with the model group, the sodium butyrate treatment group had a significant increase in Bcl-2/Bax ratio, a significant reduction in CC3 expression, and a significant increase in BDNF expression (P<0.05). The sodium butyrate treatment group had a significant increase in the number of BrdU-positive cells in the cortex compared with the model group (P<0.05), and BrdU was mainly expressed in the neurons.

CONCLUSIONSIncreased histone acetylation may protect neonatal rats against cortical injury by reducing apoptosis and promoting regeneration of neurons. The mechanism may be associated with increased expression of BDNF.

Acetylation ; Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Brain-Derived Neurotrophic Factor ; analysis ; Butyric Acid ; therapeutic use ; Cerebral Cortex ; pathology ; Female ; Histones ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the target cells and molecules with sodium valproate induced differentiation of human glioma cells.

METHODSNude mice bearing human glioma xenogenic graft subcutaneously were treated with sodium valproate. The expressions of HDAC1 and Tob genes of xenografts were analyzed with semiquantitative RT-PCR. The CD133+ cells (BTSCs) were isolated from glioma specimens by immunomagnetic sorting, and cultured in the medium containing FCS or in the serum-free medium supplemented with growth factors, respectively, followed by treatment with sodium valproate in vitro for 21 days. The cell surface markers were detected with flow cytometry and confocal microscopy.

RESULTSSodium valproate inhibited the growth of subcutaneous xenografs bearing on nude mice (P<0.05), and up-regulated the HDAC1 expression (P<0.01), down-regulated the Tob expression (P<0.05). The cell surface markers of BTSCs were detected by flow cytometry after sodium valproate treatment for 21 days. In the FCS group, the GFAP or beta-tubulin III positive cells increased significantly (P<0.01), but in the growth factor group, no statistical differences were observed in the GFAP or beta-tubulin III expression (P>0.05). The results of confocal microscopy indicated that the GFAP+ or beta-tubulin III+ cells coexpressed with Nestin.

CONCLUSIONSHDAC1 and Tob genes were the potential target molecules in reversion of the differential inhibition of human glioma cells with sodium valproate. The BTSCs undergoing the processes of differentiation were the target cells for sodium valproate.

AC133 Antigen ; Actins ; analysis ; Animals ; Antigens, CD ; analysis ; Brain Neoplasms ; metabolism ; pathology ; prevention & control ; Cell Differentiation ; drug effects ; Flow Cytometry ; Gene Expression ; drug effects ; Glial Fibrillary Acidic Protein ; analysis ; Glioma ; metabolism ; pathology ; prevention & control ; Glycoproteins ; analysis ; Histone Deacetylases ; genetics ; Humans ; Intermediate Filament Proteins ; analysis ; Mice ; Mice, Nude ; Microscopy, Confocal ; Nerve Tissue Proteins ; analysis ; Nestin ; Peptides ; analysis ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Cells, Cultured ; Tumor Suppressor Proteins ; metabolism ; Valproic Acid ; pharmacology ; Xenograft Model Antitumor Assays ; methods

Objective To analyse the preliminary clinical results of intensity modulated radiation therapy (IMRT) for 122 untreated nasopharyngeal carcinoma (NPC)pafients.Methods 122 NPC pa- tients received IMRT alone from Feb.2001 to Jun.2004,with 31 females and 91 males,and a median age of 45 years(range 25-66).According to the Fuzhou Stage Classification,there were StageⅠ11 patients, StageⅡ34,StageⅢ62,and StageⅣa 15.IMRT was carried out using an inverse planning system (COR- VUS 5.0,Peacock plan) developed by the NOMOS Corp.The treatment was given with the Multi-leaf Inten- sity Modulating Collimator (MIMIC) using a slice-by-slice arc rotation approach.The prescription dose was 68 Gy/30f to the nasopharynx gross tumor volume (GTV_(nx)),60-66 Gy/30f to positive neck lymph nodes (GTV_(nd)),60 Gy/30f to the first clinical target volume (CTV_1) and 54 Gy/30f to the second clinical target volume (CTV_2).Kaplan-Meier method was used to calculate the overall survival rate (OS),distant metas- tasis-free survival rates (DMFS),and local-regional control rates from the last date of therapy.Log-rank test was used to detect the difference between groups.Results The median follow-up time was 20 months ( range 6 to46 months).The 1-,2-,and 3-year OS was 95.2%,91.4%,85.1%,DMFS was 91.9%, 88.6%,85.6%,and the local-regional control rates was 96.5%,93.2%,93.2%,respectively.Statistics of the local control rate was insignificant either for advanced T(T3+T4) stage or early T(T1+T2) stage diseases(P=0.148).The 2-year regional control rate was insignificant either for patients with N(+) or N (-),but the 2-year DMFS was significant both for patients with N(+) and N(-)lesions(P=0.004).For 17 patients who failed,there were two with residual disease and one with recurrence at the primary site (17.6%),three patients in the neck (17.6%),twelve patients (70.6%) in distant metastases.Conclu- sions Intensity modulated radiation therapy does provide excellent local-regional control for untreated NPC, especially in patients with advanced T stage or N(+) lesion.Distant metastasis is the main cause of failure. N (+) is significantly correlated with distant metastasis.

OBJECTIVETo evaluate the feasibility, toxicity and tumor control of intensity modulated radiation therapy (IMRT) for recurrent nasopharyngeal carcinoma.

METHODSFourty-nine patients (Karnofsky performance status (KPS) >or= 80) with local-regional recurrence in the nasopharynx were treated with full course IMRT. Three patients with cervical lymph node metastasis (N1 2 and N3 1) were further supplemented with 5 to 6 courses of chemotherapy (Cisplatin + 5-Fu) after IMRT.

RESULTSThe results of treatment plan showed that the mean dose of covering gross tumor volume (GTV) (D(95)) in the nasopharynx was 68.09 Gy and the mean volume of GTV (V(95)) receiving the 95% dose was 98.46%. The mean dose of GTV, clinical target volume CTV1 and CTV2 in the targets were 71.40 Gy, 63.63 Gy and 59.81 Gy. The median follow-up time was 9 months (range 3 to 16 months). The local-regional progression-free survival was 100% with local-regional residual disease in 3 (6.1%) cases but was complicated with nasopharyngeal mucosa necrosis in 14 (28.6%) cases after IMRT.

CONCLUSIONIntensity modulated radiation therapy, as a re-treatment option for recurrent nasopharyngeal carcinoma, is able to improve the tumor target coverage and spare the adjacent critical structures. As high dose IMRT can result in radio-necrosis of nasopharyngeal mucosa, the prescription dose of GTV should be suitably decreased to 60 - 65 Gy.

Adult ; Aged ; Carcinoma, Squamous Cell ; pathology ; radiotherapy ; Female ; Follow-Up Studies ; Humans ; Lymphatic Metastasis ; Male ; Middle Aged ; Nasopharyngeal Neoplasms ; pathology ; radiotherapy ; Neoplasm Recurrence, Local ; radiotherapy ; Neoplasm Staging ; Radiation Injuries ; pathology ; Radiotherapy Dosage ; Radiotherapy Planning, Computer-Assisted ; Radiotherapy, Conformal ; methods

OBJECTIVETo study the clinical manifestations of rheumatic disorders with macrophage activation syndrome (MAS) in children.

METHODSThe authors characterized MAS by carrying out a retrospective study on patients who were identified during the past 12 years in Tianjin Children's Hospital.

RESULTSSix cases (4 females, 2 males) were studied. Four had typical systemic onset juvenile idiopathic arthritis (SOJIA), two had systemic lupus erythematosus (SLE) with lupus nephritis. Clinical manifestations at diagnosis, which occurred in the lower activity state of these primary diseases, included high spiking fever (in 5 cases) or high fever (in 1), hepatosplenomegaly (in 6), lymphadenopathy (in 6), profound decrease of all 3 blood cell lines (in 6), significant injury of liver (in 6), diseminated intravascular coagulation (DIC)-like picture (in 2), and central nervous system dysfunction (in 3). Hypofibrinogenemia, elevated liver enzymes and hypertriglyceridemia were found consistently. The phagocytic histiocytes with plasmacytosis were found in 3 bone marrow smears (not done in others). MAS was presumed to have been precipitated by viral infections in 3 patients, two had evidences for herpes simplex virus infection and one for hepatitis A virus infection. The treatment regimen was tailored to each patient, as the clinical course was variable.

CONCLUSIONSMAS may not only be most frequently seen in children with SOJIA, but also in those with other rheumatic diseases, and may be a syndrome that is more common than previously thought. Infection may be main trigger factor for MAS. The immunoapheresis combined with immunochemotherapy may be optimal for severe injury of the liver in patients with MAS.

Adolescent ; Arthritis, Juvenile ; complications ; pathology ; Child ; Child, Preschool ; Female ; Humans ; Lupus Erythematosus, Systemic ; complications ; pathology ; Macrophage Activation Syndrome ; etiology ; pathology ; Male ; Retrospective Studies

Objective The expressions of inflammatory factors and brain edema after traumatic brain injury (TBI) are the main factors for deterioration of the condition.TBI after drunkenness is even more difficult to be managed than simple TBI.This study was to discuss the effects of drunkenness on the inflammatory factors TNF-o and IL-6 and the aquaporin-4 (AQP-4) protein in rats after TBI.Methods Forty-eight male adult SD rats were randomly divided into a TBI and an ethanol (ETH) pretreatment group.TBI was induced using the Feeney's method after intraperitoneal injection of 3％ chloral hydrate at 30 mg/kg (the TBI group) or following gavage of ETH (the ETH group).At 1,3 and 5 days after modeling,modified neurological function scores (mNSS) were obtained,the expressions of TNF-α,IL-6 and AQP-4 protein determined by Western blot,and the levels of TNF-α.IL-6 and AOP-4 mRNA measured by RT-PCR at 6,24 and 72 hours.Results Compared with the TBI group,the ETH group showed significantly decreased mNSS at 1 day (9.00±0.63 vs 7.17±1.72,P＜0.05),3 days (7.00±1.10 vs 4.83±1.47,P＜0.05) and 5 days after modeling (5.50±1.05 vs 3.83± 0.75,P＜ 0.05),but remarkably up-regulated expressions of TNF-α (0.068± 0.008 vs 0.257 ± 0.008,P＜ 0.01),IL-6 (0.102 ±0.013 vs 0.320±0.016,P＜0.01) and APQ4 (0.054±0.007 vs 0.212±0.015,P＜0.01) at 6 hours,as well as at 24 and 72 hours (P＜0.01).Conclusion Drunkenness may increase the expressions of inflammatory factors and brain edema after traumatic brain injury and consequently aggravate secondary brain injury.

BACKGROUNDEpidermal growth factor receptor (EGFR) mutations in lung carcinomas can make the disease more responsive to the treatment with tyrosine kinase inhibitors. We aimed to evaluate the prevalence of EGFR mutations in a large series of lung carcinomas.

METHODSWe examined 1195 consecutive lung cancer patients for EGFR mutations in exons 18, 19, and 21 using direct sequencing of polymerase chain reaction products. A detailed smoking history was obtained. Patients were categorized as never smokers (< 100 lifetime cigarettes), former smokers (quit > 1 year ago), or current smokers (quit < 1 year ago).

RESULTSThere were EGFR mutations in 9 (4.5%) of 201 squamous carcinomas, in 1 (2%) of 50 large cell carcinomas, and in 1 (2.3%) of 44 small cell carcinomas that were investigated. Three hundred and twenty-seven mutations were found in the series of 858 adenocarcinomas (38.1%). Among 858 lung adenocarcinomas, we detected EGFR mutations in 250 (48.6%) of 514 never smokers, 39 (33.9%) of 115 former smokers, and 38 (16.6%) of 229 current smokers. Significantly fewer EGFR mutations were found in people who smoked for more than 15 pack-years (P = 0.0002) or stopped smoking less than 15 years ago (P = 0.033) compared with individuals who never smoked.

CONCLUSIONSAdenocarcinoma is the most frequent EGFR mutation pathologic type in lung cancer. The likelihood of EGFR mutations in exons 18, 19 and 21 decreases as the number of pack-years increases. Mutations were less common in people who smoked for more than 15 pack-years or who stopped smoking cigarettes less than 15 years ago. These data can assist clinicians in assessing the likelihood of exons 18, 19, or 21 EGFR mutations in Chinese patients with lung cancer when mutational analysis is not feasible.

Adenocarcinoma ; genetics ; DNA Mutational Analysis ; Exons ; genetics ; Female ; Humans ; Lung Neoplasms ; genetics ; Male ; Mutation ; Polymerase Chain Reaction ; Receptor, Epidermal Growth Factor ; genetics ; Smoking ; adverse effects