Objective: To explore the relationship between processed food consumption and blood pressure level of students in a university in Yunnan Province, so as to provide the reference for preventing hypertension in university students. Methods: In October 2021, a cluster sampling method was used to select 4 781 freshmen from a university in Kunming, Yunnan Province. The frequency of processed food consumption of university students was assessed by using the dietary frequency questionnaire, and height, weight and blood pressure were measured. Mann-Whitney test and Kruskal-Wallis test were used to compare the differences in blood pressure level of university students with different demographic variables, and the association between processed food consumption and blood pressure level was analyzed with a generalized linear model. Results: Among the students of a university in Yunnan Province, the detection rates of systolic prehypertension and hypertension were 33.86% and 1.23%, and the detection rates of diastolic prehypertension were 32.13% and hypertension 7.22%. The results of generalized linear model analysis showed that after controlling for demographic variables and other variables that might affect the blood pressure level of university students, the consumption of processed food (bread and cake: β =0.15, 95% CI =0.01-0.29) and ultra processed food (coffee beverage: β =-0.29, 95% CI =-0.54--0.03) were associated with systolic blood pressure level( P <0.05). The consumption of processed food (salted duck egg: β =0.21, 95% CI =0.01-0.41) was correlated with the diastolic blood pressure of college students ( P <0.05). Conclusions Processed food consumption in university students may increase the risk of high blood pressure.The education of healthy eating among college students should be strengthened to reduce the consumption of processed foods.

BACKGROUND: LY01005 (Goserelin acetate sustained-release microsphere injection) is a modified gonadotropin-releasing hormone (GnRH) agonist injected monthly. This phase III trial study aimed to evaluated the efficacy and safety of LY01005 in Chinese patients with prostate cancer. METHODS: We conducted a randomized controlled, open-label, non-inferiority trial across 49 sites in China. This study included 290 patients with prostate cancer who received either LY01005 or goserelin implants every 28 days for three injections. The primary efficacy endpoints were the percentage of patients with testosterone suppression ≤50 ng/dL at day 29 and the cumulative probability of testosterone ≤50 ng/dL from day 29 to 85. Non-inferiority was prespecified at a margin of -10%. Secondary endpoints included significant castration (≤20 ng/dL), testosterone surge within 72 h following repeated dosing, and changes in luteinizing hormone, follicle-stimulating hormone, and prostate specific antigen levels. RESULTS: On day 29, in the LY01005 and goserelin implant groups, testosterone concentrations fell below medical-castration levels in 99.3% (142/143) and 100% (140/140) of patients, respectively, with a difference of -0.7% (95% confidence interval [CI], -3.9% to 2.0%) between the two groups. The cumulative probabilities of maintaining castration from days 29 to 85 were 99.3% and 97.8%, respectively, with a between-group difference of 1.5% (95% CI, -1.3% to 4.4%). Both results met the criterion for non-inferiority. Secondary endpoints were similar between groups. Both treatments were well-tolerated. LY01005 was associated with fewer injection-site reactions than the goserelin implant (0% vs . 1.4% [2/145]). CONCLUSION: LY01005 is as effective as goserelin implants in reducing testosterone to castration levels, with a similar safety profile. TRIAL REGISTRATION ClinicalTrials.gov, NCT04563936.
Humans ; Male ; Antineoplastic Agents, Hormonal/therapeutic use* ; East Asian People ; Gonadotropin-Releasing Hormone/agonists* ; Goserelin/therapeutic use* ; Prostate-Specific Antigen ; Prostatic Neoplasms/drug therapy* ; Testosterone

Alzheimer's disease (AD) is associated with the impairment of white matter (WM) tracts. The current study aimed to verify the utility of WM as the neuroimaging marker of AD with multisite diffusion tensor imaging datasets [321 patients with AD, 265 patients with mild cognitive impairment (MCI), 279 normal controls (NC)], a unified pipeline, and independent site cross-validation. Automated fiber quantification was used to extract diffusion profiles along tracts. Random-effects meta-analyses showed a reproducible degeneration pattern in which fractional anisotropy significantly decreased in the AD and MCI groups compared with NC. Machine learning models using tract-based features showed good generalizability among independent site cross-validation. The diffusion metrics of the altered regions and the AD probability predicted by the models were highly correlated with cognitive ability in the AD and MCI groups. We highlighted the reproducibility and generalizability of the degeneration pattern of WM tracts in AD.
Humans ; White Matter/diagnostic imaging* ; Diffusion Tensor Imaging/methods* ; Alzheimer Disease/complications* ; Reproducibility of Results ; Cognition ; Cognitive Dysfunction/complications* ; Brain/diagnostic imaging*

Facial paralysis causes both physical pain and psychological distress to patients. It is difficult for a patient with facial paralysis to engage with a normal social life and at work. Progresses have been made in recent years in the treatment of facial paralysis. More attentions have been caught by masseteric to facial nerve transposition, which has advantages of adjacency in location, abundancy in nerve supply and reliability in the outcome and now has deemed an important option of facial reanimation. It has not been long since the application of the technique of masseteric to facial nerve transposition in China, therefore it still lacks a universal guidance on practice. In order to achieve the aim of better quality control and popularisation of the technique, hereby a consensus with suggestions on facial reanimation with masseteric to facial nerve transposition is proposed as the reference for surgeons specialised in facial reanimation. This consensus is proposed, discussed and drafted by experts from plastic and reconstructive surgery, oral and maxillofacial surgery, head and neck surgery and neurosurgery.

Objective:To discuss the diagnostic methods, clinical features and treatment options of bronchogenic cysts.Methods:A total of 86 patients with bronchogenic cysts and 5 patients with esophageal cysts and esophageal cysts were selected from January 2011 to May 2020 in the Affiliated Tumor Hospital of Harbin Medical University. There were 37 males and 49 females with bronchogenic cysts, aged 23 to 70(49.27±10.70)years old. According to the location of the disease, the patients were divided into mediastinal type(65 cases, 75.6%); intrapulmonary type(21 cases, 24.4%); bronchogenic cyst originating from the esophagus(9 cases, 10.5%).Results:The preoperative diagnosis coincidence rate was 9.3% in 8 cases. The rate of thoracoscopic surgery(59.3% in 51 cases), compared with the indwelling time of thoracic drainage tube after thoracotomy[(3.80±1.25) days vs.(4.97±1.54)days, P<0.001] and hospital stay[(7.08±1.75) days vs.(9.60±2.58)days, P<0.001] significantly shortened. 65 cases(71.4%, 65/91) were successfully followed up, with a median follow-up time of 34(2-111) months, and no recurrence was found. Conclusion:Bronchial cysts have no characteristic clinical manifestations, and it is difficult to make a clear diagnosis before surgery. Chest MRI has a great advantage in the diagnosis of cysts. For most cases, thoracoscopic surgery can achieve better clinical treatment results and has minimally invasive advantages. It is difficult to distinguish between bronchogenic cysts that originated in the esophagus and esophageal cysts, and there is no significant difference in clinical characteristics.

Objective:To detect the expression level of RAB39B gene and the effect of RAB39B on autophagy and α-synuclein, and then investigate the role of RAB39B gene mutation c.536dupA in the pathogenesis of Parkinson′s disease.Methods:Based on the novel RAB39B gene c.536 dupamutation identified in the previous work, the recombinant expression plasmid (pcDNA3.1-HA-RAB39B-536) of RAB39B gene with this mutation and wild-type recombinant expression plasmid (pcDNA3.1-HA-RAB39B) of RAB39B gene were constructed, and the recombinant expression plasmid was transfected into N2a cells with liposome as experimental group. The control group was made up with N2a cells transfected with plasmid pcDNA3.1-HA-RAB39B. Real-time polymerase chain reaction, Western blotting, immunofluorescence and immunoprecipitation techniques were used to detect the expression level of mutant RAB39B gene and the effects of RAB39B on autophagy and α-synuclein.Results:In the N2a cell model, the transcription level of mutant RAB39B was about twice that of wild type RAB39B, while the protein level of mutant RAB39B (0.30±0.00) was significantly lower than that of wild type (1.50±0.25, t=8.313, P<0.05). After adding proteasome inhibitor MG132, the protein level of mutant RAB39B increased (0.70±0.10, t=6.925, P<0.05); the level of microtubule-associated protein 1 light chain 3 BⅡ/Ⅰ of mutant RAB39B (3.11±0.30) was significantly lower than that of wild type (7.03±0.20, t=18.831, P<0.05); overexpression of wild type and mutant RAB39B did not affect the level of endogenous α-synuclein; overexpression of wild-type RAB39B resulted in elevated level of exogenous wild-type (p.A53T; from 0.60±0.11 to 1.25±0.08, t=8.254, P<0.05) and mutant (from 0.55±0.08 to 1.15±0.08, t=9.293, P<0.05) α-synuclein. Conclusions:The stability of the RAB39B protein decreased with the appearance of c.536 dupA mutation, the mutant protein may be degraded through the ubiquitin-proteasome pathway, and this mutation may affect the autophagy level of cells. RAB39B protein may interact with α-synuclein in vivo and may be involved in the maintenance of the stable level of α-synuclein.

Objective:To report the clinical, electrophysiological and genetic features in a Chinese family with distal hereditary motor neuropathy type V (dHMN-V) and screen the pathogenic mutant gene.Methods:A family with the history of inherited peripheral neuropathy was recruited in the First Affiliated Hospital of Zhengzhou University in July 2017. The clinical features and electrophysiological data were investigated. Genetic testing on well-established genes associated with hereditary peripheral neuropathy was conducted by targeted high throughput sequencing and the candidate variant was screened in the family and normal controls.Results:There were four affected individuals in the family. The proband, a 25-year-old male, was characterized by weakness and atrophy in the distal extremities primarily affected the upper extremities without sensory impairment. Electrophysiological study showed chronic neurogenic pattern in the upper and lower limb muscles. The motor conduction showed reduced velocity and compound muscle action potential amplitude, while the sensory conduction studies results were normal. The grandfather, a maternal uncle and a cousin of the proband exhibited similar clinical manifestations and electrophysiological abnormality. Genetic testing revealed a heterozygous mutation, c.880G>A(p.G294R), in the GARS gene in the proband. Proband′s mother and two other affected individuals carried the mutation which was confirmed by Sanger sequencing. The mutation site was not found in the unaffected members from the family and 300 unrelated normal controls. The variant is a novel mutation which has not been reported in dbSNP, ExAC and 1000 Genomes Project databases. Conclusion:The results suggest that the novel c.880G>A(p.G294R) mutation of the GARS gene is responsible for the Chinese patients with dHMN-V, and the findings broaden the mutational spectrum of GARS gene.

Objective To analyze the clinical manifestations and genetic mutations in 3 pedigrees with hereditary spastic paraplegia (HSP).Methods Three pedigrees diagnosed as having HSP in our hospital from January 2014 to November 2015,were chosen;the clinical manifestations,electrophysiology and imaging features of the patients in these three families were analyzed.Genomic DNA was extracted from peripheral venous blood,and the targeted gene capturing was employed to identify the disease-causing genes of these patients.Results The patients from the first family was familiar HSP,and the main clinical features were progressive lower limbs weakness and abnormal gait without cognitive impairment;the patients from the second family were familiar HSP and those from the third family were HSP without family history,and the main clinical features of the two pedigrees were slowly progressive spastic paraplegia and cognitive impairment.In addition,thin corpus callosum was visible in MR imaging of family three.Genetic testing showed the first family presented with a known mutation c.715C＞T ofA TL1 exon 7 and the loci co-segregated in the family.The second family presented with novel compound heterozygous mutations in the SPG11 gene:c.3099_3103delGTTTG mutation of exon 17and c3817 3818insTGA mutation of exon 22;novel compound heterozygous mutations in the SPG11 gene in the third family were detected as follows:c.6194C ＞G mutation of exon 32 and c.5121+1C＞T splicing mutation ofintro 29.Conclusions Four novel mutations in SPG11 gene and one known mutation in A TL1 gene are found,which enriches the known HSP mutation types.Targeted gene capture is an efficient and rapid tool for identifying the causation of some complex and genetically heterogeneous neurodegenerative diseases.

Objective To look for more serum biomarkers supporting the diagnosis of multiple system atrophy ( MSA) and providing more evidence for early treatment.Methods All patients and healthy controls were enrolled from January 2011 to March 2015 in the First Affiliated Hospital of Zhengzhou University.Demographic features and biochemical examination results were collected.The t test was used to compare the lipid levels between MSA patients and controls.LSD-t test was used to compare the lipid levels among subtypes of MSA patients.Multivariate Logistic regression analysis was conducted to analyze the influencing factors.The relevance between lipid levels and onset age, disease duration and Hoehn & Yahr stage was calculated by Spearman correlation coefficients.Results Participants included 195 MSA patients and 195 age-and gender-matched controls with no neurological diseases.The levels of total cholesterol ((4.33 ±0.90) mmol/L), triglyceride ((1.27 ±0.71) mmol/L), low-density lipoprotein (LDL;(2.70 ±0.76) mmol/L) were significantly lower in patients than in controls ((4.52 ±0.85), (1.47 ± 0.86), (2.85 ±0.71) mmol/L ,t=2.056,2.528 and 2.149 respectively, all P<0.05).The levels of total cholesterol ((4.28 ±0.96) mmol/L) and triglyceride ((1.20 ±0.64) mmol/L) were significantly lower in MSA-P patients than in control group ((4.52 ±0.85), (1.47 ±0.86) mmol/L;LSD-t=1.983, 2.566, both P<0.05).After adjusting for age, gender and histories, the odds ratio ( OR) was 0.31 (95%CI 0.15-0.65, P =0.002 ) for MSA patients in the highest quartile of triglyceride and 0.38 (95%CI 0.17 -0.83,P=0.016) for those in the highest quartile of high-density lipoprotein (HDL), compared with the lowest quartiles.And HDL level was in a significantly positive correlation with onset age (r=0.15, P=0.039).Conclusion Our data suggest that triglyceride and HDL may be associated with the prevalence of MSA, and the lower levels of HDL, the earlier onset of MSA.

Objective To investigate the influence of one kind of defective gene NOTCH3 (R90C) of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) in proliferation of oligodendrocyte lineage cells HS683 and their related molecular mechanism.Methods (1) A pCMV-Sport6.0 was chosen as the expression vector and site-directed mutation was used to construct the mutant NOTCH3 (p.R90C) expression vector;eukaryotic cell transfection technique was used to respectively transfect the pCMV-Sport6.0 empty vector,wild NOTCH3 vector (p.NOTCH3) and mutant NOTCH3 (p.R90C) expression vector to HS683 cells (blank control vector group,wild NOTCH3 vector group,and mutant NOTCH3 vector group);the protein expressions of NOTCH3,p53,phosphorylated p53 and p21 were detected by Westem blotting.(2) Wild NOTCH3 vector group,mutant NOTCH3 vector group and mutant NOTCH3 vector+pifithrin-α group were divided,and after wild NOTCH3 vector (p.NOTCH3) and mutant NOTCH3 (p.R90C) vector transfection,the latter two groups were added 0 or 1 μmol/L pifithrin-α,respectively;CCK-8 assay was employed to test the proliferation oftransfected HS683 cells 24,48 and 72,and 96 h after transfection.Results (1) As compared with wild NOTCH3 vector group,mutant NOTCH3 vector group had significantly lower absorbance value 24,48 and 72 h after transfection (P＜0.05);72 h after transfection,wild NOTCH3 vector group and mutant NOTCH3 vector group had significantly higher NOTCH3 protein expression as compared with blank control vector group (P＜0.05),and mutant NOTCH3 vector group had significantly higher p53,phosphorylated-p53 and p21 protein expressions as compared with wild NOTCH3 vector group and blank control vector group (P＜0.05).(2) The absorbance value in the mutant NOTCH3 vector+pifithrin-α group was significantly increased as compared with that in the mutant NOTCH3 vector group 48,72 and 96 h after transfection (P＜0.05).Conclusion Mutation of NOTCH3 (R90C) may inhibit the proliferation of oligodendrocyte cell lineage via p53 dependent way,which might play a direct role in demyelination pathology of CADASIL caused by NOTCH3(R90C).