Effects of Ligusticum Chuanxiong extract on MPP+-induced SH-SY5Y cells in Parkinson’s syndrome model via miR-23a-3p/SNCA axis / 西安交通大学学报(医学版)

【Objective】 To explore the effects of Ligusticum Chuanxiong extract on MPP+-induced SH-SY5Y cell damage and Parkinson’s syndrome. 【Methods】 1-methyl-4phenylpyridine ion (MPP+) interfered with SH-SY5Y to establish a cell model of elderly Parkinson’s syndrome (SH-SY5Y-MPP+). After intervention with Ligusticum Chuanxiong extract, cell proliferation and apoptosis as well as miR-23a-3p and SNCA expressions were detected. In addition, the changes of SH-SY5Y-MPP+ after regulating the expression of miR-23a-3p and SNCA were observed, and the relationship between miR-23a-3p and SNCA was verified by dual luciferase reporter. 【Results】 The cell proliferation capacity of SH-SY5y-MPP+ was significantly lower than that of SH-SY5Y, while the apoptosis rate was higher than that of SH-SY5Y (P<0.05). Under the intervention of Ligusticum Chuanxiong extract, the proliferation ability of SH-SY5Y-MPP+, and Bcl-2 and SNCA protein increased, the apoptosis rate, miR-23a-3p, and Bax proteins decreased (P<0.05). Both silencing miR-23a-3p and increasing SNCA could promote the proliferation of SH-SY5Y-MPP+ and inhibit apoptosis, while increasing miR-23a-3p and silencing SNCA were the opposite (P<0.05). The online target gene prediction website found that miR-23a-3p and SNCA had complementary sites that could bind, and the dual luciferase reporter enzyme showed that the firefly activity of SNCA-wt was significantly inhibited after the miR-23a-3p mimic sequence was transfected (P<0.05). After increasing miR-23a-3p, the expression of SNCA protein in SH-SY5Y-MPP+ decreased, while silencing miR-23a-3p was the opposite (P<0.05). Rescue experiments showed that the intervention effect of Ligusticum Chuanxiong extract on SH-SY5Y-MPP+ was completely reversed by increasing miR-23a-3p or silent SNCA (P>0.05); the effect of increasing miR-23a-3p on SH-SY5Y-MPP+ increased SNCA reversion (P>0.05). 【Conclusion】 Ligusticum Chuanxiong extract can affect the biological behavior changes of SH-SY5Y induced by MPP+ by regulating the miR-23a-3p/SNCA axis, which may be a new direction for the treatment of elderly Parkinson’s syndrome in the future.

Comparing computer-aided therapy with conventional physiotherapy in Parkinson’s disease: An equivalence study

@#Objective: The present study investigated, whether computer-aided therapy in patients with Parkinson’s disease is equivalent/non-inferior to conventional Lee Silvermann Voice Treatment (LSVT)-BIGtherapy in respect to motor outcome as measured by the Unified Parkinson’s Disease Rating Scale (MDS-UPDRS-III) and quality of life as measured by the Parkinson’s Disease Questionnaire (PDQ-39). Methods: In this controlled, rater-blinded study, 34 patients were included and 24 patients randomized to train seven standard exercises of the BIG-therapy either by a computer (BeBIG-group) or by a certified LSVT-BIG therapist (ThBIG-group) over four weeks. Equivalence was assessed by comparing the confidence interval of the BeBIG-group to the equivalence margin of the ThBIG-group. Results: There were no significant group differences in respect to age, disease duration, L-dopa equivalent daily dose or clinical stage of the disease. Both groups profited significantly from the therapy as demonstrated by an improvement in the MDS-UPDRS-III of 9.17 point in the BeBIG-group and of 8.92 points in the ThBIG-group. There was a non-significant decrease in the PDQ-39 of 9.23 points in the BeBIG-group and 4.23 points in the ThBIG-group. However, equivalence could not be demonstrated as the improvement of the BeBIG-group exceeded the confidence interval of the ThBIG-group. Conclusion: Physical training by a computer as well as by a therapist improves motor symptoms and quality of life in Parkinson’s disease. Both therapies are not equivalent, superiority of the computerized training can however not be concluded, as the study was only designed to test for non-inferiority. Therefore, computerized training can be considered as an add-on-therapy

CADASIL with clinical manifestations of lumbago, hunchback and Parkinson’s syndrome / 中华医学遗传学杂志

Objective@#To report a patient with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) manifesting as lumbago, hunchback and Parkinson’s syndrome.@*Methods@#A 49-years-old male CADASIL patient was reported. Results of clinical examination, neuroimaging and genetic testing were analyzed. His family members were also subjected to genetic testing. Related literature was reviewed.@*Results@#The patient had no typical symptoms of CADASIL such as headache, repeated stroke, dementia and emotional disorders, but progressive Parkinson’s syndrome, late onset lumbago, hunchback, dysphagia, and diplopia. Brain MRI showed left basal ganglia and external capsule lacunar infarction. Genetic testing revealed a point mutation c. 1630C>T (p.R544C) in exon 11 of the NOTCH3 gene. A heterozygous mutation was detected in the same gene in his mother, elder sister and younger brother, all of whom showed different clinical phenotypes.@*Conclusion@#The clinical features of CADASIL are heterogeneous. Lumbago, humpback, and Parkinson’s syndrome may be a rare clinical phenotype of CADASIL.

Report of 2 cases of atypical occupational chronic mercury poisoning / 中国职业医学

OBJECTIVE: To analyze the clinical characteristics of atypical occupational chronic mercury poisoning cases and explore ways to avoid misdiagnosis. METHODS: The clinical data of 2 atypical occupational chronic mercury poisoning cases were retrospectively analyzed. RESULTS: The two cases were in the same instrument factory. They were engaged in the inspection and filling of thermometers, with a long history of occupational mercury exposure. The main clinical manifestations were the nervous system damage. In the two cases,one case showed severe pain in limbs and joints accompanied with neurasthenia syndrome, oral-gingivitis and increased urine mercury; while the other one showed Parkinson's syndrome-like involuntary tremor whenever at rest or activity accompanied with neurasthenic syndrome and increased urine mercury,without oral-gingivitis. The physical examination showed notable finger tremor,tongue tremor,and eyelid tremor,and one case had coarse tremor of upper limb. Both cases were diagnosed as occupational chronic mercury poisoning. CONCLUSION: The nervous system is the most common site of involvement of patients with occupational chronic mercury poisoning,whose clinical manifestations are diverse. Clinicians should raise awareness of mercury poisoning,consult medical history in detail and reduce misdiagnosis.

Observation the treatment effect of edaravone on vascular Parkinson syndrome / 中国基层医药

Objective To analyze the clinical treatment effect of edaravone on vascular Parkinson syndrome. Methods 78 patients in our hospital who accepted treatment were selected as the study samples.They were divided into two groups which included treatment group (n =39)and control group (n =39)by random number table meth-od.The control group were given routine treatment,mainly including madopar,aspilin and cripar,however,the treat-ment group administered edaravone on the basis of conventional treatment.After total 2 periods of treatment,the score of UPDR,therapeutic efficacy and adverse reactions were recorded and compared.Results The therapeutic effective rate was 92.31% in the treatment group,which was significantly higer than that of the control group (66.66%),and the difference was statistical significance (χ2 =4.251,P 0.05).The patients in the observation group mental,e -motional and behavioral score were lower than those of the control group (t =4.568,4.113,4.345,all P <0.05),and there was no adverse reaction in the treatment group. Conclusion The treatment of edaravone in vascular Parkinson syndrome can obviously enhance the therapeutic effect,improve the treatment efficiency,has less adverse reaction and good tolerance,it is worth for clinical reference.

Reversible Parkinsonism Associated With Acute Arsenic Intoxication

No abstract available.

Espontánea reversibilidad de un síndrome de parkinson tardío y de alteraciones cognitivas frontales; después de una intoxicación aguda con órganofosforados / Reversible parkinson syndrome and cognitive impairments due organophosphate acute poisoning

Clásicamente, la intoxicación aguda por órganofosforados produce una crisis colinérgica, que con frecuencia es continuada con un cuadro de debilidad muscular, expresión de un síndrome intermedio. La génesis de estos cuadros está relacionada con la inactivación de la acetilcolinesterasa por el insecticida. Mecanismos diferentes darían origen a polineuropatías y síndromes extrapiramidales tardíos. Se describe un paciente intoxicado agudamente con órganofosforados, que desarrolló una florida crisis colinérgica, que requirió ventilación mecánica invasiva. Después de tres semanas, ya recuperado de una neumonía y del síndrome colinérgico, se pudo definir un daño cognitivo de apariencia frontal, y se apreció la progresiva aparición de hipomimia, rigidez generalizada, bradikinesia y temblor, que configuraron un síndrome de Parkinson. Esta condición clínica se mantuvo al menos por dos semanas, siendo seguida de manera espontánea por una progresiva y completa mejoría del cuadro extrapiramidal y cognitivo. La literatura ha reportado, sólo por excepción casos similares, en los que se destacó tanto la aparición tardía del cuadro parkinsoniano, como su completa y espontánea remisión. Aunque la patogenia del cuadro parkinsoniano no está completamente establecida, existen evidencias experimentales que demuestran que los órganofosforados producen modificaciones en el transporte y en la recaptación de la dopamina. En este paciente se confirmó la doble acción patogénica de los órganofosforados, que habiéndose iniciado con un síndrome colinérgico agudo, finalizó con un compromiso dopaminérgico tardío. La completa recuperación de ambos efectos, permite encasillar a estos insecticidas como generadores de alteraciones funcionales, más que de gestores de daños o cambios estructurales.

Acute organophosphate poisoning usually produces a cholinergic crisis followed by muscular weakness or intermediate syndrome. The basis for these clinical manifestations is inactivation of acetylcholinesterase at the nicotinic and muscarinic nerve terminals and junctions. Different mechanism might lead to polyneuropathy and late extrapyramidal syndromes. We report a case of a male patient who ingested organophosphate with suicidal intentions. He developed a typical cholinergic crisis and required invasive mechanical ventilation. Three weeks later, frontal cognitive impairment was noticed and masklike face, generalized rigidity, bradykinesia and tremor progressively developed until a Parkinson syndrome was established. After his clinical condition had remained stable for at least two weeks, overt spontaneous improvement in motor and cognitive functions was observed. Similar reports in literature are infrequent. Although the pathophysiology that underlies extrapyramidal manifestations due organophosphate poisoning remains unclear, experimental evidence demostróte that organophosphate compounds impair dopamine transport and uptake. This case report suggests that organophosphate might act through a double pathogenic action i.e an initial acute cholinergic syndrome and a delayed disfunction in dopaminergic pathways. Complete spontaneous resolution of both effects allow us to classify organophosphate substances as a cause of functional impairment in the basal ganglia.

Parkinson's Syndrome Caused by Organophosphate Intoxication: A case report

Organophosphate intoxication causing the extrapyramidal symptom is not frequent. A case of Parkinson's syndrome caused by organophosphate intoxication was observed, of which is reported with the quantitative measurement of tremor using Tri-axial accelerometry. A fifty nine year-old male was admitted to Wonju Christian Hospital after the intake of organophosphate for the purpose of suicide and three days after the accident, involuntary movements were detected. The encephalography and MRI showed no abnormality. With Tri-axial accelerometry, we detected less than 4 Hz resting tremor. The tremor did not response to L-dopa, and in the follow up examination performed 149 days after the accident, an increase in amplitude was detected. Gait disturbance and dysarticulation became more severe. In a case of the organophosphate intoxication patient, very rare Parkinson's syndrome findings were detected, and the tremor during the resting period was measured quantitatively by electromyography and Tri-axial accelerometry.

One Case of Parkinson's Syndrome in a Shipyard Painter Exposed to Mixed Organic Solvents / 대한산업의학회지

BACKGROUND: It is well-known that organic solvents can cause various neurologic toxicities, and in particular, it had been reported that Parkinson's syndrome can be caused by organic solvents. CASE REPORT: A 53-year-old man who had worked for 13 years as a shipyard spray and brush painter and manifested with moderate cognitive disorder and was diagnosed with chronic toxic encephalopathy. We can assume he had had considerable exposure to organic solvents considering the estimates of the amounts of organic solvents in his work place. He had no specific medical history. The Minnesota Multiphasic Personality Inventory (MMPI) showed mild cognitive deficit, depression, and anxiety. Single Photon Emission Computed Tomography (SPECT) indicated a slightly decreased flow at the edge of the left temporal brain area, while T2 brain Magnetic Resonance Imaging (MRI) showed no specific signs except for ischemic changes in small vessels in the periventricular and subcortical white matter. He was also diagnosed with both carpal tunnel syndrome and peripheral neuropathy through a neuroconductive study. Several years later, he developed progressive bradykinesia and rigidity and, later, resting tremors in the left hand. He was diagnosed with Parkinson's disease and treated with dopaminergic agents, but there was no effect. After that, he was given deep brain stimulation, both. As a result, his tremor is improved. but, the rigidity remained. Three years later, He has continuously received dopaminergic therapy. but, he complains about tremors in both hands and more greatly reduced cognitive function. CONCLUSION: In this case, we assumed by patient's work history and exposure estimates that he was exposed to excessive levels of organic solvents. The clinical symptoms of this patient were very similar to those from Parkinson's disease, but the psychological symptom appeared earlier than the other symptoms and there was no response to dopaminergic agents. We conclude that this case is likely Parkinson's syndrome caused by organic solvents.

One Case of Parkinson's Syndrome in a Shipyard Painter Exposed to Mixed Organic Solvents / 대한산업의학회지

BACKGROUND: It is well-known that organic solvents can cause various neurologic toxicities, and in particular, it had been reported that Parkinson's syndrome can be caused by organic solvents. CASE REPORT: A 53-year-old man who had worked for 13 years as a shipyard spray and brush painter and manifested with moderate cognitive disorder and was diagnosed with chronic toxic encephalopathy. We can assume he had had considerable exposure to organic solvents considering the estimates of the amounts of organic solvents in his work place. He had no specific medical history. The Minnesota Multiphasic Personality Inventory (MMPI) showed mild cognitive deficit, depression, and anxiety. Single Photon Emission Computed Tomography (SPECT) indicated a slightly decreased flow at the edge of the left temporal brain area, while T2 brain Magnetic Resonance Imaging (MRI) showed no specific signs except for ischemic changes in small vessels in the periventricular and subcortical white matter. He was also diagnosed with both carpal tunnel syndrome and peripheral neuropathy through a neuroconductive study. Several years later, he developed progressive bradykinesia and rigidity and, later, resting tremors in the left hand. He was diagnosed with Parkinson's disease and treated with dopaminergic agents, but there was no effect. After that, he was given deep brain stimulation, both. As a result, his tremor is improved. but, the rigidity remained. Three years later, He has continuously received dopaminergic therapy. but, he complains about tremors in both hands and more greatly reduced cognitive function. CONCLUSION: In this case, we assumed by patient's work history and exposure estimates that he was exposed to excessive levels of organic solvents. The clinical symptoms of this patient were very similar to those from Parkinson's disease, but the psychological symptom appeared earlier than the other symptoms and there was no response to dopaminergic agents. We conclude that this case is likely Parkinson's syndrome caused by organic solvents.

A COMPARATIVE STUDY ON THE TRANSPLANTATION OF FRESH AND FREEZINGSTORED ADRENAL MEDULLARY TISSUE TO THE RAT BRAIN / 解剖学报

A comparative study on the cellular survival of grafts and the behavior improvement in the rats was performed following tissue transplantation of either fresh or freezing-stored adrenal medulla. The fresh or freezing-stored adrenal medullary tissues were transplanted into the head of caudate nucleus in the animal models with unilateral 6-hydroxydopamine lesions of the substantia nigra. Experimental groups got some improvement after operation in rotation behavior induced by apomorphine, and the differences were significant between experimental and control groups. Among the transplanted rats, those received fresh tissue seemed to show more improvement than those received freezing-stored tissue, but the statistical difference was not significant. With regard to fluorescent intensity of the adrenal cells, it showed to be stronger in the experimental group received fresh graft than the group received freezing-stored graft, but the difference was no statistically significant either. No essential difference could be found between experimental groups as to the cellular apperance and staining features in the grafts.