ObjectiveTo evaluate the therapeutic effect of Huazhuo SanJie Chubi presciption （HSCD） on chronic gouty arthritis （CGA） rats with low-grade inflammation and to explore the underlying mechanism with a focus on macrophage polarization. MethodsThe 41 male 6-week-old SD rats were randomly allocated， using the random number table， to a normal group （n=8） and a model group （n =33）. CGA with low-grade inflammation was induced in the model group by daily gavage of potassium oxonate （250 mg·kg^-1·d^-1） and hypoxanthine （300 mg·kg^-1·d^-1）， combined with intra-articular injection of a monosodium urate （MSU） crystal suspension （50 μL， 25 g·L^-¹） into the left ankle twice weekly. After 4 weeks of modeling， 3 rats were randomly selected from each group for model validation. The remaining successfully modeled rats were randomly divided into a model group， an HSCD group （10.35 g·kg^-1·d^-1， gavage once daily）， an M1 polarization agonist group （L-methionine sulfoximine， 300 mg·kg^-1， subcutaneous injection every other day）， an M1 polarization agonist + HSCD group， an M2 polarization inhibitor group （PD0325901， 10 mg·kg^-1·d^-1， gavage once daily）， and M2 polarization inhibitor + HSCD group. The corresponding drug or drug combination was administered according to group assignment， whereas rats in the normal and model groups received 0.5% carboxymethyl cellulose sodium （CMC-Na） vehicle （10.35 g·kg^-1·d^-1， gavage once daily）. All interventions were continued for four weeks. During the intervention period， except for the normal group， potassium oxonate （250 mg·kg⁻¹） and hypoxanthine （300 mg·kg^-1） were co-administered by gavage every other day to maintain the model. At the end of treatment， serum uric acid （SUA）， ankle joint diameter and joint swelling index were measured. The levels of high-sensitivity C-reactive protein （hs-CRP）， interleukin-1β （IL-1β）， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， chemokine C-C motif ligand 2 （CCL2）， S100 calcium-binding protein A8/A9 （S100A8/A9）， interleukin-10 （IL-10） and arginase-1 （Arg-1） in serum and joint fluid were determined by enzyme-linked immunosorbent assay （ELISA）. High-frequency ultrasound was used to assess MSU deposition in the ankle joint. Hematoxylin-eosin （HE） staining was performed to evaluate synovial histopathological changes. Quantitative Real-time PCR and immunofluorescence were used to detect the mRNA and protein expression of the M1 macrophage polarization markers inducible nitric oxide synthase （iNOS） and the M2 macrophage polarization marker scavenger receptor cysteine-rich type 1 protein M130 （CD163） in synovial tissue. ResultsCompared with the normal group， the model group showed significantly elevated SUA level and joint swelling index， and increased levels of pro-inflammatory cytokines， CCL2， and S100A8/A9 in both serum and joint fluid （P<0.05）， accompanied by MSU deposition and synovial inflammation in the ankle joint. The mRNA and protein expression levels of macrophage polarization M1/M2 markers iNOS and CD163 in synovial tissues were also significantly up-regulated （P<0.05）. Compared with model group， rats in HSCD group had significantly lower SUA levels， attenuated joint swelling， reduced serum levels of pro-inflammatory cytokines， and decreased levels of CCL2 and S100A8/A9 in both serum and joint fluid， accompanied with alleviated MSU deposition and synovial inflammation （P<0.05）. HSCD markedly downregulated the mRNA and protein expression of M1 marker iNOS （P<0.05）， whereas it had no significant effect on the expression of M2 marker CD163. Compared with the M1 polarization agonist group， the M1 polarization agonist + HSCD group showed significantly reduced joint swelling， lower serum levels of pro-inflammatory cytokines， and decreased levels of CCL2 and S100A8/A9 in joint fluid （P<0.05）. In addition， synovial inflammatory cell infiltration and angiogenesis were attenuated， and iNOS mRNA and protein expression levels were significantly reduced （P<0.05）. Compared with the M2 polarization inhibitor group， the M2 polarization inhibitor + HSCD group exhibited reduced joint swelling， decreased levels of CCL2 and S100A8/A9 in joint fluid and ameliorated synovial inflammation （P<0.05）， whereas the levels of anti-inflammatory mediators （IL-10， Arg-1） and CD163 mRNA and protein expression were not significantly increased. ConclusionHSCD alleviates low-grade inflammation in CGA rats， at least in part， by inhibiting macrophage polarization toward the M1 phenotype.

ObjectiveThis paper aims to observe the effect of Huazhuo Sanjie Chubi prescription （HSCD） on the gouty bone erosion model rats and investigate its action mechanism. MethodsThirty-six two-month-old male SD rats were randomly divided into the blank group with nine rats and the modeling group with 27 rats. The rats in the modeling group were administered hypoxanthine solution at 300 mg·kg^-1·d^-1 and potassium oxonate solution at 250 mg·kg^-1·d^-1， combined with intra-articular injection of 200 μL monosodium urate （MSU） crystal suspension at 25 g·L^-1 into the right ankle joint （joint injection once every three days）， so as to induce the gouty bone erosion model. After four weeks of modeling， three rats were selected from these two groups to validate the model. The modeled 24 rats were randomly divided into the model group， HSCD group （10.35 g·kg^-1·d^-1）， allopurinol group （20 mg·kg^-1·d^-1）， and inhibitor group （LY294002， 10 mg·kg^-1·d^-1）， with six rats per group. Except for the blank group， rats in all other groups continued to receive hypoxanthine solution at 300 mg·kg^-1 and potassium oxonate solution at 250 mg·kg^-1 via gavage concurrently with administration to maintain modeling intervention. The rats in the HSCD group and allopurinol group received administration by gavage at the above doses. The rats in the inhibitor group received an intraperitoneal injection at the above dose. The rats in the blank group and model group received saline （10.35 g·kg^-1·d^-1） by gavage for four consecutive weeks. After administration， ankle joint swelling of the rats in all groups was observed， and the diameters were measured. Bone volume fraction （BV/TV） and bone surface area to bone volume （BS/BV） were observed and quantitatively analyzed by Micro-CT. Histopathological changes in the ankle joint were observed by hematoxylin-eosin （HE） staining and safranin O-fast green staining. The uric acid in the rats' serum was determined by enzyme colorimetry. The levels of inflammatory factors， including tumor necrosis factor-α （TNF-α）， interleukin （IL）-1β， and IL-6 were measured by enzyme-linked immunosorbent assay （ELISA）. The protein expressions of receptor activator of nuclear factor-κB ligand （RANKL） and phosphorylated （p）-phosphatidylinositol-3-kinase （PI3K） in ankle joint tissues of rats were detected by immunofluorescence staining. The mRNA levels of the proteins related to the bone erosion， including RANKL， tartrate-resistant acid phosphatase （TRAP）， cathepsin K （CTSK）， and matrix metalloproteinase-9 （MMP-9） in the ankle joint tissues of rats were determined by real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. The expressions of the proteins related to the bone erosion， including RANKL， CTSK， TRAP， MMP-9， and the proteins related to the PI3K/protein kinase B （Akt） signaling pathway， including PI3K， Akt， mammalian target of rapamycin （mTOR）， p-PI3K， phosphorylated protein kinase B （p-Akt）， and phosphorylated mammalian target of rapamycin （p-mTOR）， were detected by Western blot. ResultsCompared with the blank group， the modeling group showed marked ankle swelling and increased diameter. Micro-CT revealed an uneven articular surface and honeycomb-like bone erosion in the ankle joint. Quantitative analysis showed decreased BV/TV and increased BS/BV （P<0.05）. HE staining revealed a narrowed joint space， rough and discontinuous cartilage surfaces， reduced and unevenly distributed chondrocytes， partial hypertrophy， and blurred tidemarks， confirming successful model establishment. After four weeks of intervention， compared with those in the blank group， the rats in the model group exhibited severe ankle swelling and increased diameters （P<0.05）. Micro‑CT showed that the ankle joint surface was irregular， and bone erosion exhibited a honeycomb‑like morphology. The microstructural parameters of the bone revealed a decreased BV/TV and an increased BS/BV （P<0.05）. Histopathological examination revealed a narrowed joint space and severe articular cartilage destruction. The levels of uric acid in the serum and inflammatory factors （IL-1β， IL-6， and TNF-α） were increased （P<0.05）. The mRNA and protein levels of the proteins related to bone erosion in joint tissue， including RANKL， CTSK， TRAP， and MMP-9， were upregulated （P<0.05）. The ratios of p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR in the proteins related to the PI3K/Akt signaling pathway were increased （P<0.05）. RANKL and p-PI3K protein fluorescence intensities were elevated （P<0.05）. Compared with those in the model group， the above indicators in all other administration groups showed varying degrees of improvement. The HSCD group and inhibitor groups exhibited more significant effects in reducing ankle swelling， improving bone erosion， bone microstructure （significant decrease in BV/TV and increase in BS/BV）， and the pathology of cartilage erosion， lowering inflammatory factor levels， downregulating the proteins related to the bone erosion， and suppressing activation of the PI3K/Akt/mTOR pathway （P<0.05）. The uric acid levels in rats' serum were reduced in both HSCD and allopurinol groups （P<0.05）. Compared with those in the HSCD group， the rats in the allopurinol group had larger ankle diameters （P<0.05）， more severe bone erosion and bone microstructure damage （P<0.05）， worse improvement of the pathology of cartilage erosion， higher levels of IL-6 and TNF-α （P<0.05）， elevated expressions of the proteins related to the bone erosion， higher expression ratio of proteins related to the PI3K/Akt signaling pathway （P<0.05）， and higher fluorescence intensities of RANKL and p-PI3K proteins （P<0.05）. The inhibitor group achieved comparable results to the HSCD group in improvements of bone microstructure and the reduction of IL-1β and IL-6， stronger suppression of TNF-α and PI3K/Akt/mTOR signaling pathway activation （P<0.05）， but weaker effects on cartilage repair and serum uric acid reduction （P<0.05）. ConclusionHSCD effectively reduces uric acid levels in serum， suppresses inflammatory factor secretion， and downregulates the expressions of proteins related to bone erosion， including RANKL， CTSK， TRAP， and MMP-9 in the joint tissues. Its action mechanism of improving gouty bone erosion may be associated with inhibition of the PI3K/Akt signaling pathway.

ObjectiveTo explore the possible mechanisms of Tongfengning （痛风宁， TFN） in treating hyperuricemia （HUA） of spleen deficiency with exuberance of dampness syndrome. MethodsTen of 60 mice were randomly selected， and were fed with regular diet as the control group， while the remaining 50 mice were fed with high-fat and high-sugar diet combined with excessive exercise and potassium oxonate-allopurinol suspension to establish an HUA animal model of syndrome of spleen deficiency with exuberance of dampness. After the successful modeling， in order to better observe the effects of TFN on the intestinal microbiota of the model mice， a mixed antibiotic suspension was administered by gavage to induce further dysbiosis of the intestinal microbiota in the model mice. Fifty sucessfully modeled mice were randomly divided into model group， TFN group， allopurinol group， probiotics group， and an allopurinol + probiotics group， 10 in each group. The TFN group was administered TFN liquid at a dosage of 19.11 g/（kg·d） by gavage. The allopurinol group was administered allopurinol suspension at a dosage of 78 mg/（kg·d） by gavage. The probiotics group was administered live combined Bifidobacterium and Lactobacillus tablets suspension at a dosage of 3 g/（kg·d） by gavage. The allopurinol + probiotics group was administered allopurinol at a dosage of 78 mg/（kg·d） and live combined Bifidobacterium and Lactobacillus tablets suspension at a dosage of 3 g/（kg·d） by gavage. The control group and model group were administered normal saline at a dosage of 19.11 ml/（kg·d） by gavage. The interventions were continued for 21 days. In order to maintain a stable high blood uric acid state， all groups but the control group continued modeling while receiving drug intervention. The changes in spleen deficiency syndrome scores， blood uric acid levels， microbial community structure， acetic acid and butyric acid content in intestinal lavage fluid， adenosine deaminase （ADA） and xanthine oxidase （XOD） content in small intestine tissue， as well as ATP-binding cassette transporter G2 （ABCG2）， glucose transporter 9 （GLUT9） protein and mRNA expression in the small intestine tissue were compared among the groups of mice. ResultsCompared with the control group， the model group showed increased spleen deficiency syndrome scores， blood uric acid levels， relative abundance of phylum Firmicutes， Firmicutes/Bacteroidetes ratio， abundance of Bacteroides genus， Klebsiella genus， and Enterococcus genus， acetic acid content in intestinal lavage fluid， ADA and XOD content in small intestine tissue， as well as GLUT9 protein and mRNA expression （P<0.05）. The number of operational taxonomic units （OTUs） of intestinal microbiota， relative abundance of Bacteroidetes phylum， abundance of Lactobacillus genus and uncultured Bacteroides genus， butyric acid content in intestinal lavage fluid， and ABCG2 protein and mRNA expression in small intestine tissue were significantly decreased （P＜0.05）. Compared with the model group， in the group treated with TFN， probiotics， and allopurinol + probiotics， the spleen deficiency syndrome score， blood uric acid level， relative abundance of Firmicutes， acetic acid content in intestinal lavage fluid， ADA and XOD content in small intestine tissue， GLUT9 protein and mRNA expression significantly decreased. The number of gut microbiota OTUs， relative abundance of proteobacteria， butyric acid content in intestinal lavage fluid， ABCG2 protein and mRNA expression in small intestine tissue significantly increased （P＜0.05）. In the probiotics group， the ratio of Firmicutes to Bacteroidetes decreased. In the TFN group， the abundance of Lactobacillus and uncultured Bacteroidetes significantly increased， while the abundance of Parabacteroides， Klebsiella， and Enterococcus significantly decreased （P＜0.05）. Compared with the TFN group， allopurinol group and the probiotics group showed elevated blood uric acid levels， abundance of Bacteroidetes， ADA and XOD levels in intestinal tissue， and GLUT9 mRNA expression. The relative abundance of Firmicutes， abundance of lactobacilli， and ABCG2 mRNA expression significantly decreased. The probiotics group showed elevated GLUT9 protein expression in intestinal tissue. The probiotics group and the allopurinol plus probiotics group showed significantly higher scores for spleen deficiency syndrome in mice， and lower levels of butyric acid in mouse intestinal lavage fluid. The allopurinol group showed decreased numbers of OTUs in mouse intestinal flora， decreased abundance of proteobacteria， and butyric acid levels in intestinal lavage fluid. The allopurinol group also showed decreased ABCG2 protein expression in intestinal tissue， increased acetic acid levels in intestinal lavage fluid， increased abundance of Klebsiella， and significantly elevated GLUT9 protein expression （P＜0.05）. ConclusionsThe treatment of HUA with TFN may be associated with the regulation of intestinal probiotics （such as lactobacilli） and pathogenic bacteria （such as Klebsiella）， as well as the production of bacterial metabolites such as acetic acid and butyric acid. It may also involve reducing the expression of ADA and XOD in the intestines， decreasing intestinal uric acid production， upregulating the expression of intestinal epithelial urate transporter ABCG2， downregulating GLUT9 expression， and promoting intestinal uric acid excretion. These factors are related to the syndrome of spleen deficiency with exuberance of dampness.

Objective To evaluate the effect of ganglioside ( GM-1) preconditioning on endoplas-mic reticulum stress ( ERS)-dependent apoptosis during spinal cord injury induced by bupivacaine in rats. Methods One hundred and eight clean-grade healthy male Sprague-Dawley rats, aged 8 weeks, weighing 250-300 g, were divided into 3 groups ( n=36 each) using a random number table method: control group (group C), bupivacaine group (group B) and GM-1 pretreatment group (group G). In group B, 5％bupivacaine 0. 12 μl/g was intrathecally injected at 1. 5 h intervals, 3 times intotal. In group G, GM-120μl ( 30 mg/kg) was intrathecally injected, and 24 h later bupivacaine was intrathecally injected according to the method previously described in group B. Immediately after intrathecal injection and at 1, 3, 5, 7 and 14 days after intrathecal injection, the maximum percentage of anti-nociceptive effects (％MPE) was detected, the hindlimb motor function score ( BBB score) was evaluated, and spinal cord tissues were har-vested for determination of cell apoptosis ( using TUNEL) and expression of caspase-12 and CCAAT/enhan-cer-binding protein homologous protein ( CHOP ) protein and mRNA ( by Western blot or quantitative real-time polymerase chain reaction) . The apoptosis rate was calculated. Results Compared with group C, the％MPE and apoptosis rate were significantly increased, the BBB score was decreased, and the expression of CHOP and caspase-12 protein and mRNA was up-regulated in group B ( P＜0. 05) . Compared with group B, the ％MPE and apoptosis rate were significantly decreased, the BBB score was increased, and the ex-pression of CHOP and caspase-12 protein and mRNA was down-regulated in group G ( P＜0. 05) . Conclu-sion GM-1 preconditioning reduces bupivacaine-induced spinal cord injury possibly through inhibiting ERS-dependent apoptosis in rats.

OBJECTIVETo explore the correlation between cytogenetic findings and clinical manifestations of Turner syndrome.

METHODS607 cases of cytogenetically diagnosed Turner syndrome, including those with a major manifestation of Turner syndrome, were analyzed with conventional G-banding. Correlation between the karyotypes and clinical features were analyzed.

RESULTSAmong the 607 cases, there were 154 cases with monosomy X (25.37%). Mosaicism monosomy X was found in 240 patients (39.54%), which included 194 (80.83%) with a low proportion of 45,X (3 ≤ the number of 45, X ≤5, while the normal cells ≥ 30). Structural X chromosome abnormalities were found in 173 patients (28.50%). A supernumerary marker chromosome was found in 40 cases (6.59%). Most patients with typical manifestations of Turner syndrome were under 11 years of age and whose karyotypes were mainly 45,X. The karyotype of patients between 11 and 18 years old was mainly 45,X, 46,X,i(X)(q10) and mos45,X/46,X,i(X)(q10), which all had primary amenorrhea in addition to the typical clinical manifestations. The karyotype of patients over 18 years of age were mainly mosaicism with a low proportion of 45,X, whom all had primary infertility. 53 patients had a history of pregnancy, which included 48 with non-structural abnormalities of X chromosome and 5 with abnormal structure of X chromosome.

CONCLUSIONGenerally, the higher proportion of cells with an abnormal karyotype, the more severe were the clinical symptoms and the earlier clinical recognition. Karyotyping analysis can provide guidance for the early diagnosis of Turner syndrome, especially those with a low proportion of 45,X.

Abortion, Spontaneous ; genetics ; Adolescent ; Adult ; Amenorrhea ; genetics ; Child ; Child, Preschool ; Chromosomes, Human, X ; genetics ; Cytogenetic Analysis ; methods ; Female ; Humans ; Infant ; Infant, Newborn ; Karyotyping ; Middle Aged ; Mosaicism ; Pregnancy ; Sex Chromosome Aberrations ; Turner Syndrome ; genetics ; pathology ; Young Adult

Objective The incidence rate of pressure ulcer is high in critical patients and off-loading mattresses and reposi-tioning are known as effective interventions for the prevention of pressure ulcers .However, evidence is lacking for selection of the right type of mattresses and suitable interval of repositioning .This study was to compare the effects of two types of off-loading mattresses with two different repositioning intervals in preventing pressure ulcers in critical patients . Methods According to the design of this ran-domized controlled trial , we made a training plan concerning the participants , methods of intervention and comparison , criteria and methods of observation , and methods of recording , and trained 26 nurses from 7 hospitals .Using non-inferiority design and the method of stratified blocked randomization , we divided 1194 patients with the risk of pressure ulcer into a trial group ( n=596) and a control group ( n=598) , a viscoelastic sponge mattress with every-four-hours repositioning used for the former and an automatic aeration mat-tress with every-two-hours repositioning for the latter , both for 7 successive days .We examined the patients every day , recorded the in-cidence and stages of pressure ulcer , and compared the data obtained between the two groups of patients . Results The total inci-dence rate of pressure ulcer was 1.09%(13/1194), significantly lower in the trial than in the control group (0.34%[2/596] vs 1.84%[11/598], P=0.012). Conclusion A viscoelastic sponge mattress with every-four-hours repositioning is superior to an automatic aeration mattress with every-two-hours repositioning and therefore is preferred to the latter in preventing the incidence of pressure ulcer in critical patients in the ICU .

OBJECTIVE:To establish a method for the simultaneous determination of syringinand and pedunculoside in Zhuang medicine Yuyang powder. METHODS:HPLC was performed on the column of Agilent ODS with mobile phase of acetonitrile-water (gradient elution)at a flow rate of 1 ml/min,the detection wavelength was 210 nm,the column temperature was 30℃,and the in-jection volume was 5μl. RESULTS:The linear range was 0.71-3.55μg for syringin(r=0.999 7)and 1.62-8.10μg for pedunculoside (r=0.999 8), respectively;RSDs of precision, stability and reproducibility tests were lower than 3%;recoveries were 100.8%-104.9%(RSD=1.7%,n=6) and 96.0%-100.8%(RSD=2.2%,n=6). CONCLUSIONS:The method is simple,stable and reproducible,and can be used for the simultaneous determination of syringinand and pedunculoside in Zhuang medicine Yuyang powder.

BACKGROUND:Stem cel transplantation has achieved good results in the treatment of cerebral ischemia, and how to reduce apoptosis of transplanted cel s has become the focus of the therapy.
OBJECTIVE:To investigate the injured effect of tumor necrosis factor alpha (TNF-α) on bone marrow mesenchymal stem cel s and its mechanism.
METHODS:Primary cultured bone marrow mesenchymal stem cel s from Sprague-Dawley rats were treated with 200μg/L TNF-αfor 6 hours. Cel vitality was assayed by MTT, and cel apoptosis was observed by Hoechst33342 staining. Apoptotic rate was detected by Annexin-V/PI double staining. Level of oxidative stress was evaluated by determination of malondialdehyde and superoxide dismutase levels. The protein expressions of phosphorylated-Akt, Akt, phosphorylated-FoxO1, FoxO1 were detected by western blot analysis.
RESULTS AND CONCLUSION:After treatment with TNF-α, the cel vitality of bone marrow mesenchymal stem cel s decreased, the apoptotic rate increased, and the cel s were arrested in the S phase. Moreover, the oxidative stress level was elevated, and the protein expression of phosphorylated-Akt and phosphorylated-FoxO1 was significantly reduced compared with the control group (P<0.05). These results suggest that TNF-αat high level contributes to the S-stage arrest, responsible for the apoptosis processes of bone marrow mesenchymal stem cel s via the Akt-FoxO1 pathway.

Objective To discuss the impact of the neurotoxity of bupivacaine and bupivacaine-induced cellular neurotoxicity caused by pretreatment of ganglion (GM-1 )monoglyceride on the ex-pression of caspase-3.Methods The mouse neuroblastoma cells-N2a cells was used as a research object to carry out the following experiments:(1)To observe the damage effects of different concen-trations of bupivacaine on N2a cells and find out the most suitable damage concentration to establish cell damage model.The N2a cells were interacted with bupivacaine with different concentrations [0μmol/L (group C),600 μmol/L (group B1),900 μmol/L (group B2),1 200 μmol/L (group B3), 1 500 μmol/L (group B4),2 000 μmol/L (group B5)]for 6,12,24,36 h and then evaluated by CCK-8 cell survival.Each experiment was repeated three times.The protective function of GM-1 to bupiva-caine-induced N2a cells damage.The N2a cells were treated with different concentrations (0.1μmol/L (group BG1),1.0 μmol/L (group BG2),10 μmol/L (group BG3))of GM-1 pretreatment 24 h,CCK-8 was evaluated in cell viability,Western Blot method was used to detect damaged cells caspase-3 expression levels.Each experiment was repeated three times.Results (1)Bupivacaine could significantly damage N2a cells,the greater the bupivacaine concentration,the longer the action time,the stronger neurotoxicity.(2)GM-1 bupivacaine nerve injury had a significant protective effect in a dose-related manner.The maximum of protective dose of this experiment was 10 μmol/L.Conclusion Bupivacaine can significantly damage N2a cells,correlating with both dose and time double positively,while GM-1 pretreatment significantly reduced the expression of caspase-3 induced by bupivacaine.

Objective To explore the characteristics of surface electromyogram (sEMG) of the forearm muscles of Parkinson's disease patients with or without load. Methods 26 Parkinson's disease patients and 28 healthy individuals participated in this study. All the subjects performed isometric contraction for elbow flexion without load or with a load of 1.5 kg. The sEMG signals were collected by surface elec-trodes and processed by linear time and frequency domain method. Results The values of median frequency (MF) and mean power frequen-cy (MPF) were higher in the patients than in the healthy controls without load (P<0.05). The value of average EMG (AEMG) was lower in the patients than in the healthy controls with a load of 1.5 kg (P<0.001). For the patients, the values of MF and MPF were higher without load than with a load of 1.5 kg (P<0.001), and the value of AEMG was lower without load than with a load of 1.5 kg (P<0.001). For the healthy controls, only the value of AEMG was lower without load than with a load of 1.5 kg (P<0.001). Conclusion The values of MF and MPF are higher in Parkinson's disease patients than in the healthy controls without load while the value of AEMG is lower in Parkinson's dis-ease patients than in the healthy controls with load.