Treatment of acromion base fractures with double plates internal fixation / 中国骨伤

<p><b>OBJECTIVE</b>To study clinical effects of double plates fixation for the treatment of acromion base fracutres.</p><p><b>METHODS</b>From January 2010 to May 2012, 7 patients with acromion base fractures were treated with double plates ORIF surgical treatment. There were 5 males and 2 females, with an average age of 36.3 years old (ranged, 24 to 62 years old). All fractures were acuted and closed injuries. The duration from injury to surgery was 4.6 days (ranged, 2 to 10 days). Hardegger functional criterion, Visual Analogue Scale (VAS) and complications of the patients were documented analysis.</p><p><b>RESULTS</b>All the patients were followed up,and the duration ranged from 4 to 13 months (averaged 8.9 months). The healing duration of fractures ranged from 8 to 14 weeks without any infection, shoulder instability, subacromial impingement syndrome, nonunion and failure of internal fixation. At the latest follow-up, the VAS ranged from 0 to 5. According to Hardegger criterion, 2 patients got an excellent result, 4 good and 1 poor.</p><p><b>CONCLUSION</b>Double plates ORIF plays a positive role in the treatment of acromion base fractures, which reduces complications and maximally restore the function of shoulder.</p>

Surgical treatment of acetabular type C1 acetabular fracture by posteroproximal-posteroanterior sequential reduction and internal fixation / 中国骨伤

<p><b>OBJECTIVE</b>To investigate the operative reduction techniques and clinical results of surgical treatment of type C1 (AO/ASIF) acetabular fracture by posteroproximal-posteroanterior sequential reduction and internal fixation.</p><p><b>METHODS</b>From August 2004 to January 2012, 13 patients with type C1 (AO/ASIF) acetabular fracture were treated by posteroproximal-posteroanterior sequential reduction and internal fixation. Of them, 8 cases were male and 5 cases were female with an average age of 42 years years old (ranged, 18 to 64). Pelvis 3-dimentional CT reconstruction were used to confirmed the classification of fracture, and the operation were performed during from 5 to 20 days with an average of 9.5 days. Operation time, blood loss, complications and reduction were recorded and evaluated. The function of hip joint were accessed at the final follow-up.</p><p><b>RESULTS</b>The operation time ranged from 190 to 290 min with an average of 240 min. The mean blood loss was 1 800 ml (ranged, 1 300 to 3 000 ml). One case had superficial infection and healed after 3 weeks. According to Matta reduction criteria, 8 cases obtained anatomical reduction, 4 cases got satisfied results and 1 cases got unsatisfied results. Eleven cases were followed up with an average of (24.0 +/- 8.0) months, and 2 cases were lost to follow-up. According to revised Mede d'Aubingne and Postel evaluation system, 7 cases got excellent results, 2 good, 1 moderate and 1 poor.</p><p><b>CONCLUSION</b>Posteroproximal-posteroanterior sequential reduction and internal fixation for the treatment of type C1 (AO/ASIF) acetabular fracture can achieve satisfied surgical proces and operation quality.</p>

Effect of erythropoietin on β-amyloid peptide-induced tau phosphorylation in SH-SYSY cells / 中华神经医学杂志

Objective To investigate the effect of erythropoietin (Epo) on tau hyperphosphorylation induced by β-amyloid peptide 25-35 (Aβ25-35) in SH-SY5Y cells. Methods MTT assay was employed to identify the changes in the viability of SH-SY5Y cells following Epo treatment at 0, 5, 10, 20, and 50 U. Western blot was used to detect the levels oftau phosphorylation at Ser396, Ser199 and Taul at different time points after treatment with 20 μmol/L Aβ25-35. The effect of a 3-hour EPO pretreatment at 5, 10, and 20 U on the actions of Aβ25-35 was evaluated. The inhibitory effect of Epo on Aβ25-35-induced neurotoxicity after pretreatment with the PI3K/Akt inhibitor LY294002 was assessed to explore the possible mechanism of Epo. Results The viability of SH-SY5Y cells showed no obvious changes in response to Epo exposure at different doses. Western blot showed that Aβ25-35 induced increased phosphorylation at Ser396 and Ser199 3 hatter the treatment. The phosphorylation reached the peak level at 6 h after Aβ25-35 treatment and gradually decreased after 12 h, but stilled maintained a significantly higher level at 24 h,compared with 0 min, 30 min (P<0.05). The total tau underwent no significant changes in response to Aβ25-35 treatment (P>0.05). Epo pretreatment at 5, 10, and 20 U efficiently inhibited Aβ25-35-induced tau phosphorylation in comparison with that in the control cells(P<0.05), and application of LY294002 resulted in obvious inhibition of the effect of Epo. Conclusion Epo can inhibit Aβ25-35-induced tau phosphorylation via PI3K/Akt signaling pathway, and this finding provides an important theoretical basis for studying the pathogenesis and management of AD.

Curative effect of the fibrinogen gel for sacral canal arachnoid cyst / 中国骨伤

<p><b>OBJECTIVE</b>To evaluate curative effect of the fibrinogen gel for treating sacral canal arachnoid cyst.</p><p><b>METHODS</b>Nineteen patients with sacral canal arachnoid cysts included 7 males and 12 females; The average age was 48.4 years ranging from 19 to 68 years. The course was from 2 weeks to 7 months. Of all the patients, 9 were in level of S1, 4 were in level of S1 to S2, 5 were in level of S2, 1 was in level of S1 to S3. Cystis wall greater partial excision adopted in 11 cases, partial resection in 8, then all patients were treated by spray painting fibrinogen gel.</p><p><b>RESULTS</b>Nineteen patients were followed-up for 13 to 30 months (mean 21.3 months). The clinical symptom disappeared completely in 18 patients, and only one patient urinated incapably, but after 2 weeks returned to normal. No one found recurrence by MRI after 12 months.</p><p><b>CONCLUSION</b>This method of fibrinogen gel for treating sacral canal arachnoid cyst has advantages of easy performing, safety, achieve good results, less neck symptoms and early commencing of mobilization.</p>

The prevalence of LRRK2 Gly2385Arg variant in Chinese Han population with Parkinson's disease.

We conducted a case-control study to determine the prevalence of the LRRK2 Gly2385Arg variant in patients with Parkinson's disease in Han population in mainland China. Heterozygous LRRK2 Gly2385Arg variant was identified in 14 of 235 patients with Parkinson's disease (5.69%), but not in 214 unrelated healthy controls. Multivariate analysis indicated the frequency of Gly2385Arg variant in the female patients with early age at onset is higher than their male counterparts. The founder haplotype analysis showed the variant carriers shared the same founder. Clinically, the LRRK2 Gly2385Arg carriers presented with classical Parkinson's disease symptoms. Our study indicates that the LRRK2 Gly2385Arg variant is a potential ethnic-specific genetic risk factor of Parkinson's disease within Chinese Han ethnicity.

Calbindin-28 in rats of Parkinson's disease after deep brain stimulation to subthaiamus nucleus / 中华神经科杂志

Objective To explore the mechanism of deep brain stimulation(DBS)therapy to Parkinson's disease(PD).Methods We produced hemi-parkinsonian rat model with stereotaxically injecting 6-OHDA to right medial forebrain bundle(MFB)and stimulated ipsilateral subthalamu nucleus (STN)with platinum electrodes chronically to investigate the influence of DBS to the expression of Calbindin-28,synaptophysin and tyrosine dioxydase(TH)in Striatum by Western blot.In addition,slices of bilateral PD rats after DBS were stained to observe the expression of Calbindin-28 and synaptophysin in substantia nigra by Immunohistochemistry.Results High frequency stimulation impaired the rotational frequency 31% of unilateral PD rats triggered by apomophine;Long-term DBS increased the expression of TH in innocent striatum of unilateral PD rats 78.6%?9.5%,since the ipsilateral striatum(lesion side) was TH depleted by 6-OHDA insults;Calbindin-28 expression in ipsilateral striatum of hemi-PD rats raised up 75.4%?15.0% and long-term DBS reduced the effect by 43.0%?7.1%,meanwhile Calbindin-28 positive neurons in substantia nigra compacta in sham,PD and DBS rats were 74.5?10.2,75.7?15.6, 33.1?7.8.However,Synaptophysin expression in substantia nigra and striatum kept stable even after long- term DBS.Conclusions Consistent to the treatment to PD patients,DBS to STN alleviated the motor disorder of PD rats,the treatment might be based on regulating the expression of Calbindin-28 and TH.

Prader-Willi syndrome and genomic imprinting / 中华儿科杂志

<p><b>OBJECTIVE</b>Prader-Willi syndrome (PWS) is an example of a human genetic disorder that involves imprinting genes on the proximal long arm of chromosome 15 and SNRPN gene as a candidate gene for this syndrome. The purpose of this study was to show the molecular genetic defects and genomic imprinting basis in Chinese PWS patients and to evaluate the clinical applications of a differential diagnostic test for PWS.</p><p><b>METHODS</b>Fluorescence in situ hybridization (FISH) and methylation-specific PCR (MSPCR) techniques were applied for 4 clinically suspected PWS patients. Using three probes, including SNRPN probe for identification of the critical locus in PWS region, D15Z1 and PML control probes for identification of the 15p arm and 15q arm, the authors detected the deletions 15q in PWS. MSPCR was based on sodium bisulfite treatment of DNA and PCR primers specific for the maternal and paternal allele.</p><p><b>RESULTS</b>When hybridized with mixed probes, it was found in 2 patients that the central specific signal was absent, but both the flanking control signals were retained, indicating SNRPN gene deletion of chromosome 15q11-13. Bisulfite-modified DNA from all PWS children amplified with methylated allele-specific primer pair showed only maternal 131bp PCR product, indicating the maternal uniparental disomy (UPD15).</p><p><b>CONCLUSION</b>Genomic imprinting plays an important role in the molecular pathogenesis of PWS that caused by paternal microdeletions of 15q11-q13 or maternal UPD of chromosome 15. The basic defect seemed to be an absence of function of PWS genes that are normally expressed only from the paternal chromosome 15. MSPCR is a rapid and simple PCR-based assay compared with other cyto-molecular tests and its results were consistent with the clinical diagnosis of PWS, so it seems to be a reliable diagnostic method for PWS patients who show abnormal methylation at SNRPN. The genetic differential tests for PWS are important in determining familial recurrence risk.</p>

The relationship between the dyskinesia in Parkinson disease and the degree of substantia nigra lesion / 中华老年医学杂志

Objective To explore the relationship between the genesis of dyskinesia and the degree of substantia nigra lesion in Parkinson disease(PD).Methods The hemi-parkinsonian rat model was established by injecting 6-OHDA stereotaxically to right medial forebrain bundle(MFB). Then the hemi-parkinsonian rat was injected intraperitoneally with levodopa methylester(25 mg?kg~(-1)?d~(-1),twice a day)for 21 days,the abnormal involuntary movements were estimated.After being sacrificed,the midbrain was removed,and the injured degree of dopaminergic neurons at substantia nigra was observed by tyrosine hydroxylase immunohistochemistry staining.The relationship between the abnormal involuntary movement scores and dopaminergic neurons loss at substantia nigra was evaluated by sigmoid equation analysis by using Excel software.Results The apomorphine-induced rotation rate above 7 r/min was found in 10 of 25 rats,those rats were regarded as successful hemi-parkinsonian model rats.After the treatment with levodopa methylester,8 of 10 rats displayed abnormal involuntary movements,including stereotype and contralateral rotation,the types of movements varied.Abnormal involuntary movements were appeared in the rats with dopaminergic neurons loss above 90%.The positive relationship was observed between the degree of lesion in substantia nigra and the severity of abnormal involuntary movements.Conclusions The severe loss of dopaminergic neurons at substantia nigra probably plays a role in the development of levodopa-induced dyskinesia in patient with Parkinson disease.

5-HT1A receptor agonist 8-OH-DPAT improves motor complications in Parkinson' s disease / 中华神经科杂志

Objective To investigate cellular and behavioural effects of 5-HT1A receptor agonist 8- OH-DPAT in a rat model of levodopa-induced motor complications.Methods The hemi-parkinsonian rat model was produced by stereotaxically injecting 6-OHDA to right medial forebrain bundle(MFB).Two sets of experiments were performed.First,rats were intrapefitoneally treated with levodopa 50 mg/kg plus benserazide 12.5 mg/kg twice a day for 22 days.On day 23,rats intraperitoneally received either 8-OH- DPAT(1 mg/kg)or 8-OH-DPAT plus WAY-100635(0.1 mg/kg)or dissolvent with each levodopa dose as controls.In the second set,rats were intraperitoneally treated either with levodopa(50 mg/kg)plus 8-OH- DPAT(1 mg/kg)or levodopa 50 mg/kg plus dissolvent,administered twice daily for 22 consecutive days. Rotational duration and frequency of off period were estimated.After sacrificed,subcellualr distribution of GluR1 and GluR1Ser845 phosphorylation was observed by Western blot.Results 8-OH-DPAT,reversing the shortened rotational duration induced by levodopa,prolonged the rotational duration by 27.8%?6.1% and reduced the frequency of failures to levodopa by 7.2%?1.7%.Co-administration of WAY-100635,a 5-HT1A receptor antagonist,with 8-OH-DPAT eliminated the effect of 8-OH-DPAT on motor complications, indicating that the observed 8-OH-DPAT responses were probably mediated via the 5-HT1A autoreceptor. Moreover,8-OH-DPAT could regulate subcellular distribution of GluR1 and reduce hyperphosphorylation of GluR1 Ser845 by 22.1%?3.5%,which was closely associated with levodopa-induced motor complications. Conclusions These results suggest that pharmaceuticals stimulating 5-HT1A receptors could be useful in the treatment and prevention of the motor complications in parkinsonian patients.

Experimental study on prevention of Parkinson disease by neutral amino acid / 中华老年医学杂志

Objective To investigate the effect of neutral amino acid on preventing Parkinson disease.Methods Mice were injected with L-Valine,L-Pheylalanine,D-Valine or L-Lysine before or after paraquat administration,by which prakinsonian mouse model was constructed.The paraquat immunoreactivity was observed within nigral cell bodies.Then neurodegeneration and ?-synuclein aggregation were observed by immunohistochemistry and Western blot.Results Paraquat immunoreactivity was abolished by the administration of L-Valine,L-Pheylalanine before paraquat exposure.Pre-treatment with these two amino acids also protected the paraquat-induced loss of nigrostriatal dopaminergic cells and formation of thioflavine S-positive aggregates.In contrast, paraquat-induced toxicity was unaffected if animals were injected with these two amino acids after paraquat exposure or pre-treated with D-Valine or L-Lysine.Conclusions L-type neutral amino acids such as L Valine and L-Pheylalanine can prevent paraquat-induced neurodegeneration and a synuclein pathology through a competitive inhibition mechanism with stereospecificity in the central nervous system (CNS).Neutral amino acid could protect the dopaminergic neuron in substantia nigra and may prevent Parkinson disease.