Effect of Zero-valent Iron Nanoparticles and Melatonin on Yield and Quality of Fritillaria przewalskii in Domesticated Cultivation Conditions / 中国实验方剂学杂志

Objective:To investigate the effect of iron nanoparticles and melatonin on yield and quality of <italic>Fritillaria przewalskii</italic> and provide technical support for its domesticated cultivation. Method:Hundred grain weight was measured by conventional method；alkaloid content was detected according to protocols of the edition of 2020 <italic>Chinese Pharmacopoeia</italic>，chlorophyll，hydrogen peroxide，malondialdehyde，superoxide dismutase （SOD），peroxidase （POD） and catalase （CAT） were detected by spectrophotometric analysis，auxins，cytokinins，gibberellins，salicylic acid，jasmonic acid and abscisic acid were detected by ultra performance liquid chromatography tandem mass spectrometry analysis. Result:Zero-valent iron nanoparticles and melatonin significantly increased the hundred grain weight without affecting the quality. The effect of the two treatments on physiological and biochemical indexes in different stages were quite different，but the effects on content of endogenous hormones were basically the same. Correlation analysis showed that hundred grain weight was negatively correlated with malondialdehyde content，SOD activity and jasmonic acid content，but positively correlated with POD activity，salicylic acid content，gibberellins content，auxin content and abscisic acid content. The two treatments were separated effectively by principal component analysis，indicating that there were some differences in the mechanisms of growth promoting. The treatment of zero-valent iron nanoparticles mainly affected auxins，salicylic acid and abscisic acid. The treatment of melatonin mainly affected SOD，malondialdehyde and gibberellins. Conclusion:Zero-valent iron nanoparticles and melatonin can be used as a simple and practical technology to improve the stress resistance and yields of <italic>F. przewalskii</italic> in domesticated cultivation conditions.

Comparison of the curative effect between delayed PCI and medical therapy on ST-segment elevation acute myocardial infarction / 天津医药

Objective To investigate and compare the curative effect between delayed percutaneous coronary intervention (PCI) for patients with acute myocardial infarction presenting 12-24 hours from symptom onset and medical therapy on acute myocardial infarction patients presenting with ST-segment elevation (STEMI). Methods Using a prospective,open,parallel,controlled research approach,186 patients with STEMI were divided into delayed PCI group(n=89),which received PCI within 12-24 hours after STEMI and medical therapy group(n=97),which received medical therapy after STEMI. All patients were followed up 1-6 months with average follow-up (5.6 ± 1.4) months. Data of hospitalization period, the cardiac structures detected by echocardiography such as left atrial diameter (LAD), left ventricular diastolic diameter(LVDd),left ventricular ejection fraction LVEF,left ventricular fractional shortening(LVFS),composite end point events and major adverse cardiac events(MACE)were compared between the two groups.Results Compared with medical therapy group, the hospitalization cycle was significantly shorter in delayed PCI group. Data of the LAD and LVDd were significantly decreased,but LVEF and LVFS were increased in delayed PCI group compared with those of medical therapy group at 30 d and 6-month follow-up. The incidence of MACE and composite end point events were significantly less in delayed PCI group than those of medical therapy group (P<0.05). Conclusion Delayed PCI treatment can decrease the time of hospital stay and decrease the incidence rates of MACE and composite end point events,and improve left ventricular function and prognosis of patients.

Progress in researches on latent class analysis based subtyping of depression / 上海交通大学学报（医学版）

Depression is a highly heterogeneous syndrome. Homogeneous subtypes according to symptomatology of illness may contribute to development of individualized treatment, assessment on outcomes and prognosis. Latent class analysis is a flexible statistical approach to determine classes with similar symptom profiles in a heterogeneous group, which has been widely used in data-driven subtyping of depression to increase accuracy of subtyping. This article reviewed existing symptom-based subtypes of depression and findings of researches on latent class analysis based illness subtyping.

Fine mapping of a pure paroxysmal kinesigenic dyskinesia family / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To fine map the gene responsible for pure paroxysmal kinesigenic dyskinesia in a Chinese family.</p><p><b>METHODS</b>Six additional markers flanking the tightly linked markers were chosen in the candidate region resulting from a whole genome-wide scanning and tested by parameter and nonparameter analysis using Linkage and Genehunter softwares to fine map the candidate region.</p><p><b>RESULTS</b>Evidence for linkage of the pure paroxysmal kinesigenic dyskinesia to chromosome 3 was further confirmed. A maximum two-lod score of 2.82 at theta=0 was obtained with D3S3669. Critical recombinants place the PKD gene between D3S1314 and D3S1265.</p><p><b>CONCLUSION</b>A new locus of pure paroxysmal kinesigenic dyskinesia (PKD) is localized within a 10.2 cM interval on 3q28-29, between markers D3S1314 and D3S1265.</p>

A follow-up study on features of sensory gating P50 in treatment-resistant depression patients / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Depressive disorder is a well-known chronic, recurrent and disabling mental disease with high direct and indirect costs to society in both western and eastern cultures. Approximately 40% of depressed patients show only partial or no response to initial or even multiple antidepressant medications and are usually called treatment-resistant depression (TRD) patients. The present work was to measure the features of sensory gating (SG) P50 in TRD patients with the intent of understanding the characteristics of this disease.</p><p><b>METHODS</b>In 50 TRD patients, 39 non-treatment-resistant depression (NTRD) patients and 51 healthy controls (HC), auditory evoked potential P50 was measured using the conditioning/testing paradigm presented with auditory double clicks stimuli, and 36 TRD patients had repeated measurements after an 8-week venlafaxine treatment course.</p><p><b>RESULTS</b>All the depressive disorder patients, including the TRD and NTRD groups, showed an increased testing stimulus wave (S2-P50) amplitude compared to controls (P < 0.01 and P < 0.05), but there was no significant difference between the TRD and NTRD groups (P > 0.05). There were significant differences in the ratio of testing stimulus (S2) and conditioning stimulus (S1) (S2/S1) and in the value of 100 x (1 - S2/S1) among the three groups. Compared to the baseline, TRD patients had no significant changes of features and different expression of P50 after acute treatment (P > 0.05). Meanwhile, a statistically significant positive correlation of S2/S1 with the scores of the 17-item Hamilton Rating Scale for Depression (HAMD-17) (P < 0.01), and a significantly negative correlation of S1 - S2, 100 x (1 - S2/S1) with the scores of HAMD-17 (P < 0.01) were observed in the TRD patients' baseline measurement, but there was no correlation after venlafaxine treatment (P > 0.05).</p><p><b>CONCLUSIONS</b>Both the TRD and NTRD patients had obvious SG deficits, with a more severe deficit in TRD patients. Although, with a correlated relationship to the severity of depressive symptoms, SG P50 deficit might be suggested as a trait marker for TRD, and a combination of S2/S1 ratio, S1 - S2 and 100 x (1 - S2/S1), was recommended for electrophysiological measurement in TRD patients.</p>

A preparative method of chronic experiment autoimmune encephalomyelitis / 中南大学学报(医学版)

OBJECTIVE@#To explore the model of chronic experimental autoimmune encephalomyelitis (EAE)for the further study of multiple sclerosis.@*METHODS@#A total of 72 female SPF C57BL/6J mice (inbred strain, aged 8 approximately 10 weeks), were randomly divided into an EAE group, a blank group and an adjuvant group, and each group was divided into 3 subgroups: an onset group, a peak group and a chronic phase group. The EAE group was immunized with mMOG35-55.@*RESULTS@#At the end of the study, and 83.3% of the mice in EAE group suffered the onset, and 8.3% of the mice died. The highest clinical score reached grade 5, namely paralysis of the whole body and then death. In the EAE group, after being immunized first, the mice were all anosis during the first 13 days. They got ill on the third week, and in about 20 approximately 24 days the clinical symptom reached the peak, and in 28 approximately 32 days the chronic phase arrived,when parts of the clinical symptoms got relieved. On the contrary, both the adjuvant group and the blank group were healthy all the time. Characteristic appearance was detected in the EAE group.@*CONCLUSION@#Antigen emulsion, mixture of artificially synthesized mMOG35-55 and complete Freundos adjuvant can successfully induce chronic EAE in the mice. The model of EAE duplicated in our study has the characteristics of high incidence, low death rate and stability, which can be used to carry out further research on multiple sclerosis.

Quantitative analysis of SMN gene copies in spinal muscular atrophy / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To study the genetic basis in the patients with clinical diagnosis of spinal muscular atrophy(SMA) but without survival motor neuron telomeric copy (SMN-T) deletion; the relationship between the SMN-C (centromeric) copies and the phenotype; and the distribution of SMN-C and SMN-T copies in the SMA patients, the carriers and the controls.</p><p><b>METHODS</b>Quantitative PCR analysis of SMN-T and SMN-C copies were carried out in 45 patients, 25 consanguineous and 33 control individuals. The patients were identified by clinical manifestation and muscular pathology. Two internal standards of SMN-T and cystic fibrosis transmembrane conductance regulator (CFTR) were constructed. Nonradioactive and nonfluorescence-labelling competitive PCR were used. The numbers of SMN-T and SMN-C copies were determined by calculating the ratios of SMN-T/CFTR and SMN-C/CFTR.</p><p><b>RESULTS</b>Quantitation of SMN-T gene copies in SMA patients revealed that nine cases of type I-III were homozygously deleted. Two cases of type III had only one copy and four cases of type III had two copies. SMA IV and other type cases had two copies. Nine cases of consanguineous individuals had one copy, but other 16 had two copies. All of the normal individuals had two copies. Analysis of SMN-C copies showed that SMA I had < or = 2 copies, II-III had < or = 3 copies, SMA IV and others had 0-3 copies, the consanguineous individuals and normal individuals had 0-3 copies.</p><p><b>CONCLUSION</b>The number of copies determined by PCR quantitative assay of SMN-T is in accordance with the result of PCR qualitative assay of homozygous deletion. Quantitative assay of the number of copies can find out the cases and the carriers of heterozygous deletion. The SMA phenotype is related to the number of copies of SMN-C; the smaller the number of copies the patient has, the severer the patient's phenotype will be. The pathogenesis of SMA IV and other types of SMA may not relate to SMN gene.</p>

Preliminary linkage analysis of a Chinese family with benign familial infantile convulsion / 中华儿科杂志

<p><b>OBJECTIVE</b>Benign familial infantile convulsions (BFIC) is a recently recognized autosomal dominant inherited disorder. This epileptic syndrome typically begins between 3 and 12 months of age with clusters of partial seizures in most cases and carries a good prognosis. So far, three loci have been linked to chromosome 19q12.1-13.1, chromosome 2q24 and chromosome 16p12-q12. The authors performed linkage analysis on this pedigree.</p><p><b>METHODS</b>A four-generation Chinese family was investigated. The total number of members was 32 in this family and two neurologists in Xiangya Hospital gave systemic physical examinations and interictal neurological examinations to nineteen members of this family. Venous blood samples were taken for genetic analysis. DNA was extracted from peripheral blood leukocytes using phenol-chloroform method. Seventeen microsatellite markers spanning the critical regions on chromosomes 19q12-13.1, 2q24, and 16p12-q12 were genotyped. These markers included D19S49, D19S250, D19S414, D19S416 and D19S245 for the 19q region, D2S2380, D2S399, D2S111, D2S2195, D2S2330 and D2S2345 for the 2q region, D16S401, D16S3131, D16S3093, D16S517, D16S3120 and D16S415 for the 16p-q region. The DNA from each sample was amplified for the 17 markers. After polymerase chain reactions (PCR), PCR products of chromosome 19 with markers D19S49, D19S250, D19S414, D19S416 and D19S245 were subjected to electrophoresis on 8% denatured polyacrylamide gel for at least 2 hours and 20 minutes. Then the length of the PCR products was judged in the Strategene Eagle Eye II automated gel image analyzer. For the markers from chromosome 2 and 16, PCR products were scanned at ABI 377 autosequencer. The data of PCR products were analyzed using the software Genescan v3.1, Genetyper v2.1 (Applied Biosystem, CA. USA) and GenoDB v1.0. After Mendelian checking, the eligible genotyping data were used for linkage analysis. LOD scores were calculated by using MLINK program of LINKAGE v5.1, under an assumption of autosomal dominant inheritance and the estimated penetrance was 0.9. The allele frequencies of each marker were assumed to be equal and the disease-allele frequencies were designated to be 1/10,000. The LOD scores were calculated at combination rate (theta) 0.0, 0.1, 0.2, 0.3, and 0.4.</p><p><b>RESULTS</b>Among the 17 selected microsatellite markers, which cover the previously reported regions, seven markers' data (D16S3131, D16S517, D16S3120, D16S3093, D2S2380, D19S250 and D19S414) were omitted due to failed genotyping, low genetic heterogeneity, or failure to pass Mendelian checking. Omission of these markers was to ensure the reliability of our raw data. The two-point LOD scores were below zero for all the markers and the maximum LOD scores at theta = 0.0 were less than -2 for markers D19S49, D19S416, D19S245, D16S401, D16S415, D2S399, D2S111, D2S2195, D2S2330 and D2S2345. Thus, the linkage result showed no evidence that the disease locus is linked to any of these selected markers, which excludes the previously reported candidate regions found in other ethnic families.</p><p><b>CONCLUSION</b>There is no evidence that this Chinese family was linked to one of the following loci: 19q12.1-13.1, 16p12-q12 and 2q24. The results indicated that BFIC showed genetic heterogeneity and the Chinese BFIC families might be mapped on another new locus.</p>

The gene expression patterns of genetic P77PMC epilepsy-prone rats' hippocampus / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To find out the differentially expressed genes in the hippocampus of the rats with genetic epilepsy so as to lay a foundation for exploring the pathogenesis of epilepsy by means of cDNA array technology.</p><p><b>METHODS</b>Gene expression patterns in the hippocampus of the genetic epilepsy-prone P77PMC rats and normal Wistar rats were established using the alpha-32P-labeled cDNA probes hybridized with the Atlas Rat cDNA Expression Array, and then were analyzed by an image analysis instrument to get the differentially expressed genes.</p><p><b>RESULTS</b>Fifteen genes were found having differential expression patterns in hippocampus between the P77PMC rats and the Wistar rats, while there may be many other differentially expressed genes left undiscovered due to having no appropriate image analysis software. And among the fifteen genes, the expression levels of twelve genes in the P77PMC rats were higher than those in the Wistar rats, while the expression levels of the other three genes were lower. The results of reverse transcription-polymerase chain reaction(RT-PCR) have demonstrated the reliability of cDNA arrays method.</p><p><b>CONCLUSION</b>cDNA array is a powerful tool for identifying differential expression genes of epilepsy on large scales. There are several differentially expressed genes in hippocampus of the P77PMC rats and the Wistar rats. All these identified genes could play potentially important roles in the pathogenesis of epilepsy.</p>

Advance in researches on survival of motor neurons protein and its interaction proteins / 中华医学遗传学杂志

Survival of motor neurons(SMN) protein is the product of spinal muscular atrophy(SMA) gene. Now the function researching of SMN protein has become hotspot field to discuss the pathogenic mechanism of SMA. The construction, distribution and function of SMN protein are reviewed in this paper.