The Physiological Response of Apricot Flowers to Low-Temperature Stress.

The growth and development of apricot flower organs are severely impacted by spring frosts. To better understand this process, apricot flowers were exposed to temperatures ranging from 0 °C to -8 °C, including a control at 18 °C, in artificial incubators to mimic diverse low-temperature environments. We aimed to examine their physiological reactions to cold stress, with an emphasis on changes in phenotype, membrane stability, osmotic substance levels, and antioxidant enzyme performance. Results reveal that cold stress induces significant browning and cellular damage, with a sharp increase in browning rate and membrane permeability below -5 °C. Soluble sugars and proteins initially rise as osmoprotectants, but their content decreases at lower temperatures. Proline content consistently increases, suggesting a protective role. Antioxidant enzyme activities, including catalase (CAT), peroxidase (POD), superoxide dismutase (SOD), and ascorbate peroxidase (APX), exhibit a complex pattern, with initial increases followed by declines at more severe cold conditions. Correlation and principal component analyses highlight the interplay between these responses, indicating a multifaceted adaptation strategy. The findings contribute to the understanding of apricot cold tolerance and inform breeding efforts for improved crop resilience.

Prevalence, risk factors, and prognosis of central nervous system manifestations in antiphospholipid syndrome.

The central nervous system (CNS) is considered as one of the most frequently affected organs in antiphospholipid syndrome (APS). This study investigated the prevalence of CNS manifestations in APS and associated risk factors and evaluated stroke recurrence. We carried out this retrospective study from 2009 to 2021 at Peking University People's Hospital, which enrolled 342 APS patients, and 174 neurologic events were suffered by 119 patients (34.8%). Patients with and without CNS involvement were compared regarding demographics and laboratory parameters. The analysis showed that older age, livedo reticularis, and dyslipidaemia were significant related factors for CNS manifestations (P = 0.047, 0.038, and 0.030 respectively). The use of anticoagulants (P = 0.004), and/or hydroxychloroquine (P = 0.016) appeared to associated with a lower incidence of CNS manifestations. During a median follow-up of 4.1 years, 10 individuals developed new episodes of stroke in APS patients with previous ischemic strokes. Livedo reticularis, smoking and male gender may predict the risk of recurrent stroke (P = 0.020, 0.006, and 0.026 respectively). Collectively, our results indicated the protective and risk factors for CNS manifestations, as well as demonstrated that APS patients appeared at high risk of stroke recurrence despite current therapy.

A novel aGAPSS-based nomogram for the prediction of ischemic stroke in patients with antiphospholipid syndrome.

Background: Ischemic stroke (IS) is the most common and life-threatening arterial manifestation of antiphospholipid syndrome (APS). It is related to high mortality and severe permanent disability in survivors. Thus, it is essential to identify patients with APS at high risk of IS and adopt individual-level preventive measures. This study was conducted to identify risk factors for IS in patients with APS and to develop a nomogram specifically for IS prediction in these patients by combining the adjusted Global Anti-Phospholipid Syndrome Score (aGAPSS) with additional clinical and laboratory data. Methods: A total of 478 consecutive patients with APS were enrolled retrospectively. All patients were randomly assigned to the training and validation cohorts. Univariate and multivariate binary logistic analyses were conducted to identify predictors of IS in the training cohort. Then, a nomogram was developed based on these predictors. The predictive performance of the nomogram for the training and validation cohorts was evaluated by determining areas under the receiver operating characteristic curve (AUROC) and creating calibration plots. A decision curve analysis (DCA) was conducted to compare the potential net benefits of the nomogram with those of the aGAPSS. Results: During a mean follow-up period of 2.7 years, 26.9% (129/478) of the patients were diagnosed with IS. Binary logistic regression analysis revealed that five risk factors were independent clinical predictors of IS: age (P < 0.001), diabetes (P = 0.030), hyperuricemia (P < 0.001), the platelet count (P = 0.001), and the aGAPSS (P = 0.001). These predictors were incorporated into the nomogram, named the aGAPSS-IS. The nomogram showed satisfactory performance in the training [AUROC = 0.853 (95% CI, 0.802-0.896] and validation [AUROC = 0.793 (95% CI, 0.737-0.843)] cohorts. Calibration curves showed good concordance between observed and nomogram-predicted probability in the training and validation cohorts. The DCA confirmed that the aGAPSS-IS provided more net benefits than the aGAPSS in both cohorts. Conclusion: Age, diabetes, hyperuricemia, the platelet count, and the aGAPSS were risk factors for IS in patients with APS. The aGAPSS-IS may be a good tool for IS risk stratification for patients with APS based on routinely available data.

Network pharmacology-based analysis of the effects of puerarin on sarcopenia.

Background: With the acceleration of population aging, sarcopenia will place a heavy burden on families and society. Thus, effective treatments urgently need to be developed to slow down the development of sarcopenia. This study adopted a network pharmacological approach to explore the possible mechanisms of puerarin in treating sarcopenia. Methods: The potential therapeutic targets of puerarin were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) database, while the targets of sarcopenia were obtained from the GeneCards, DisGeNET, Online Mendelian Inheritance in Man (OMIM), and Therapeutic Target Database (TTD) databases. The protein-protein interaction (PPI) network was generated by BisoGenet, and core targets were identified by a topological analysis. To determine the potential targeting pathways, the core targets were further imported into the Metascape platform for the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. The results were visualized using an online bioinformatics tool. Results: We identified 53 targets for puerarin and 129 targets for sarcopenia. A total of 206 core targets, which were considered potential therapeutic targets, were identified from the merged PPI network. Further, the GO and KEGG analyses revealed that the functions of the core targets and related pathways were mainly associated with the cell cycle, apoptosis, protein synthesis, and proteolysis. Conclusions: Puerarin has the potential to treat sarcopenia through the regulation of the cell cycle, apoptosis, and protein homeostasis. Our study has laid a foundation for further studies on drug development and pharmacological experiments in the treatment of sarcopenia.

DNAJB2 c.184C>T mutation associated with distal hereditary motor neuropathy with rimmed vacuolar myopathy.

Distal hereditary motor neuropathy (dHMN), also known as distal spinal muscular atrophy (dSMA), comprises a group of inherited peripheral neuropathies with great clinical and genetic heterogeneity, mainly characterized by progressive atrophy and weakness of distal muscle without clinical or electrophysiological sensory abnormalities. Next-generation sequencing is widely applied as an effective diagnostic technique to discover pathogenic genes in patients with dHMN. To date, at least 23 causal genes have been identified to be associated with dHMN, several of which encode chaperones. Here, we report a dHMN patient due to a homozygous c.184C>T variant in the DNAJB2 gene with rare neuropathic and myopathic characteristics on pathological examination. These findings might broaden the mutational spectrum of DNAJB2 and expand the tissue involvement of DNAJB2-related presentations.

Variants in MME are associated with autosomal-recessive distal hereditary motor neuropathy.

OBJECTIVE: To identify a new genetic cause in patients segregating distal hereditary motor neuropathy (dHMN) with an autosomal recessive pattern. METHODS: Whole-exome sequencing was conducted in two siblings and was combined with segregation analysis. Additionally, 83 unrelated dHMN patients with unknown genetic cause were screened. RNA analysis was performed using blood lymphocytes and HEK293 cells transfected with mutant plasmids. Immunohistochemistry and Western blot analysis was applied to the nerve tissue. The enzymatic activities of mutant proteins were measured in the cultured cells to verify the pathogenicity of variants. RESULTS: The clinical features of the patients showed late-onset phenotype of distal motor neuropathy without sensory involvement. We identified that compound heterozygous variants of c.1342C>T and c.2071_2072delGCinsTT in the membrane metalloendopeptidase (MME) gene co-segregated with the phenotype in a dHMN family. In an additional group of 83 patients with dHMN, compound heterozygous variants of c.1416+2T>C and c.2027C>T in MME were identified in one patient. The splice site variant c.1416+2T>C results in skipping of exon 13. The stop variant c.1342C>T induces mRNA degradation via nonsense-mediated mRNA decay. Transcript levels of MME in the lymphocytes showed no significant differences between the patients and controls. We also identified that MME variants were associated with mild decrease in protein expression in the sural nerve and significant impairments of enzymatic activity. INTERPRETATION: Variants in the MME gene were associated with not only a Charcot-Marie-Tooth neuropathy phenotype but also with an autosomal-recessive dHMN phenotype. Loss of function may play a role in the pathogenesis of dHMN.

Current status and potential application of navigated transcranial magnetic stimulation in neurosurgery: a literature review.

Transcranial magnetic stimulation (TMS) is a noninvasive neurophysiologic technique that can stimulate the human brain. Positioning of the coil was often performed based merely on external landmarks on the head, meaning that the anatomical target in the cortex remains inaccurate. Navigated transcranial magnetic stimulation (nTMS) combines a frameless stereotactic navigational system and TMS coil and can provide a highly accurate delivery of TMS pulses with the guidance of imaging. Therefore, many novel utilities for TMS could be explored due to the ability of precise localization. Many studies have been published, which indicate nTMS enables presurgical functional mapping. This review aimed to provide a comprehensive literature review on nTMS, especially the principles and clinical applications of nTMS. All articles in PubMed with keywords of "motor mapping," "presurgical mapping," "navigated transcranial magnetic stimulation," and "language mapping" published from 2000 to 2018 were included in the study. Frequently cited publications before 2000 were also included. The most valuable published original and review articles related to our objective were selected. Motor mapping of nTMS is validated to be a trustful tool to recognize functional areas belonging to both normal and lesioned primary motor cortex. It can offer reliable mapping of speech and motor regions at cortex prior to operation and has comparable accuracy as direct electrical cortical stimulation. nTMS is a powerful tool for mapping of motor and linguistic function prior to operation, has high application value in neurosurgery and the treatment of neurological and psychiatric diseases, and has gained increasing acceptance in neurosurgical centers across the world.