A Preliminary Study on the Microwave Ablation of Multifocal Papillary Thyroid Microcarcinoma.

RATIONALE AND OBJECTIVES: To evaluate the feasibility, efficiency, and safety of microwave ablation (MWA) for multifocal papillary thyroid microcarcinoma (PTMC). METHODS: This was a retrospective study, and the data of patients who underwent MWA for multifocal PTMC from October 2016 to December 2021 were reviewed. After ablation, the changes in tumor size and volume, as well as the rates of technical success, tumor disappearance, disease progression, and complications, were assessed. According to the tumor location, the cases were further divided into a unilateral multifocal disease (UMD) subgroup and a bilateral multifocal disease (BMD) subgroup. Further analyses were carried out. RESULTS: There was a total of 94 cases enrolled in the present study, which included 24 males and 70 females. The median age was 40 years (22-66 years); the median follow-up time was 14 months (6-48 months). Complete ablation was achieved in all enrolled cases. Therefore, the technical success rate was 100%. Due to expanding ablation, the MD and volume of the ablation zone increased at the 1st and 3rd months after ablation and decreased from the 12th month after ablation (p < 0.05 for all). The total complete tumor disappearance rates were 45/94 (47.87%) overall, 40.625% (13/32) in the UMD subgroup and 51.61% (32/62) in the BMD subgroup (p = 0.312). The total disease progression rates were 4.26% (4/94) overall, 6.25% (2/32) in the UMD subgroup and 3.23% (2/62) in the BMD subgroup (p = 0.881). The overall complication rate was 4.26% (4/94). CONCLUSION: This preliminary study indicates that MWA is a safe and effective treatment for multifocal PTMC.

Preliminary Study of Microwave Ablation for Multifocal Papillary Thyroid Microcarcinoma in Nonoperative Candidates.

PURPOSE: To study the feasibility, safety, and effectiveness of microwave ablation (MWA) in patients with multifocal papillary thyroid microcarcinoma (PTMC). MATERIALS AND METHODS: This retrospective study included patients who underwent MWA for multifocal PTMC (number of nodules ≤3). A total of 44 patients were included, and the mean age was 43 years (SD ± 11). After ablation, progression-free survival (PFS) at 6, 12, 24, 36, and 48 months; disease progression; change in tumor size and volume; tumor disappearance rate; and adverse events (AEs) were assessed, and the feasibility, safety, and effectiveness of MWA for PTMC were evaluated on the basis of statistical analysis. RESULTS: The median follow-up period was 18 months (interquartile range, 12-33 months). The PFS rates at 6, 12, 24, 36, and 48 months were 100.0%, 96.4%, 96.4%, 70.3%, and 52.7%, respectively. The disease progression rate was 11.4% (5 of 44 patients). The maximum diameter (MD) and volume of the ablation zone were larger at the 3-month follow-up than before ablation (median MD, 13.0 vs 7.0 mm; P < .001; median volume, 503.8 vs 113.0 mm3; P < .001). Subsequently, the tumors exhibited a reduction in both size and volume after 18 months (median MD, 4.0 vs 7.0 mm; P = .04; median volume, 12.6 vs 113.0 mm3; P = .055). At the end of the follow-up period, the complete response rate was 59% (26 of 44 patients). The overall AE rate was 6.8%. CONCLUSIONS: MWA is a feasible treatment for PTMC (number of nodules ≤3), and this study preliminarily demonstrated the safety and effectiveness of this technique.

A clinical study on microwave ablation of multifocal (≤ 3) T1N0M0 papillary thyroid carcinoma.

OBJECTIVE: To evaluate the feasibility, efficiency, and safety of microwave ablation (MWA) for T1N0M0 multifocal (≤ 3) papillary thyroid carcinoma (PTC). METHODS: This was a retrospective study, and patients who underwent MWA for multifocal (≤ 3) PTC were reviewed between October 2016 and December 2020. After ablation, the changes in tumor size and volume, as well as the rate of technical success, tumor disappearance, disease progression, and complications were assessed. RESULTS: There were a total of 57 cases enrolled in the present study, which included 18 males and 39 females. The mean age was 44 ± 11 years (22-66 years); the mean follow-up time was 18 ± 11 months (6-48 months). Complete ablation was achieved in all enrolled cases. Therefore, the technical success rate was 100%. Due to expanding ablation, the MD and volume of the ablation zone, as well as the VRR, increased at the 1st and 3rd months after ablation and decreased at 12 and 18 months after ablation (p < 0.05 for all). The total complete tumor disappearance rate was 43.9% (25/57), including 54% (24/44) in the T1a subgroup vs. 7.7% (1/13) in the T1b subgroup (p = 0.003). The total disease progression rate was 7% (4/57), including 9.1% (4/44) in the T1a subgroup vs. 0% (0/13) in the T1b subgroup (p = 0.142). The overall complication rate was 5.3% (3/57), including 6.8% (4/44) in the T1a subgroup vs. 0% (0/13) in the T1b subgroup (p = 0.206). CONCLUSION: This preliminary study indicates that MWA is a safe and effective treatment for T1N0M0 multifocal (≤ 3) PTC. KEY POINTS: • MWA is a promising alternative method for T1N0M0 multifocal (≤ 3) PTC.

Hyperhomocysteinemia Induces Rat Memory Impairment Via Injuring Hippocampal CA3 Neurons and Downregulating cAMP Response Element-Binding Protein (CREB) Phosphorylation.

Accumulated evidence demonstrated that an elevated plasma homocysteine level, hyperhomocysteinemia, induced cognitive impairment in animals, elderly and the patients with neurodegenerative diseases. To date, the underlying cellular and molecular mechanisms by which hyperhomocysteinemia induces cognitive impairment has not been clearly defined. The purpose of this study was to investigate the possible cellular and molecular mechanisms behind hyperhomocysteinemia signaling in rat memory impairment. The results from this study demonstrated that hyperhomocysteinemia induced neuronal damage and loss in hippocampal CA3 region and downregulated the cAMP response element-binding protein (CREB) phosphorylation. The findings of this study provide evidence that hyperhomocysteinemia induces rat memory impairment via injuring hippocampal CA3 neurons and downregulating CREB phosphorylation.

Comparison of the Efficacy of Danhong Injections at Different Time-points During the Perioperative Period of Acute Myocardial Infarction: A Systematic Review and Meta-analysis of Randomized Controlled Trials.

Objectives: Danhong injections (DHI) are widely used in the treatment of acute myocardial infarction (AMI). As there are no guidelines for the timing of DHI in the peri-percutaneous coronary intervention (PCI) period for AMI, we investigated the effects of DHI timing. Methods: We reviewed reports published before September 30, 2020 in PubMed, embase, the Cochrane Central Register of Controlled Trials, the Chinese BioMedical database, Chinese VIP database, Wanfang database, and Chinese National Knowledge Infrastructure database. Only randomized controlled trials of DHI with percutaneous coronary intervention for AMI were included. Methodological quality was assessed using the Cochrane evaluation manual 5.3.3 criteria. A meta-analysis was performed, and forest plots were drawn. Results: We included 23 studies which all revealed that patients in DHI groups had better efficacy than control groups. Subgroup analysis revealed that DHI administered intraoperatively and continued postoperatively was more effective in increasing left ventricular ejection fraction when compared to other time-points (p < 0.001). The pre- and intraoperative use of DHI could improve reflow more effectively than conventional treatment, while the effect was not significant in the postoperative intervention study (p = 0.654). The 16 postoperative interventions revealed that the effect of DHI at 14 days was better than that at 7 and 10 days for hs-CRP (p = 0.013), the 10-days treatment produced better results for CK-MB than for the other treatments (p < 0.001) and a dosage of 30 ml proved most effective for IL-6 (p < 0.001). Conclusion: DHI proved to be superior to conventional Western medicine in reducing the incidence of adverse cardiac events, promoting reperfusion, improving cardiac function, reducing inflammatory factors, and protecting the myocardium. DHI should be administered early in the perioperative period and continued postoperatively because of its ability to improve cardiac function. Furthermore, in the PCI postoperative, 30 ml is recommended to inhibit IL-6 levels, for patients with high hs-CRP, a course of 14 days is most effective, for patients with obvious abnormalities of CK-MB, a 10-days course of treatment is recommended. However, due to the limited number and quality of the original randomized controlled trials, our conclusions need large, multi-centre RCTs to validation.

In-vitro neuroprotective effect and mechanism of 2ß-hydroxy-δ-cadinol against amyloid ß-induced neuronal apoptosis.

Amyloid beta (Aß) neurotoxicity plays a causative role in the pathogenesis of Alzheimer's disease. Accumulating evidence demonstrates that Aß neurotoxicity is mediated by glutamate excitotoxicity. In our previous study, a sesquiterpenoid compound 2ß-hydroxy-δ-cadinol (HOC) which exhibited antiglutamate excitotoxicity effect was isolated from the fruits of Alpinia oxyphylla Miquel. Based on the antiglutamate excitotoxicity effect of HOC, in this study, we investigated the potential benefit of HOC in preventing Aß(1-42)-induced neuronal apoptosis in cultured rat hippocampal neurons. The neuroprotective effect of HOC against Aß(1-42)-induced neuronal apoptosis was assessed by Hoechst 33258 staining, reactive oxygen species (ROS) production, caspase-3 activation and caspase-3 activity. Results demonstrated that HOC treatment significantly prevented Aß(1-42)-induced neuronal apoptosis. The underlying molecular mechanisms of HOC in preventing Aß(1-42)-induced neuronal apoptosis may be via inhibiting Aß(1-42)-induced ROS production, attenuating Aß(1-42)-induced caspase-3 activation and inhibiting caspase-3 activity. This study suggests that HOC may be a potential agent for the prevention of Aß neurotoxicity.

Color-Tuning and Near-Sunlight White Emission in Highly Stable Rod-Spacer MOFs with Defective Dicubane Based Lead(II)-Carboxyl Chains.

The active lone pair electron effect and highly flexible coordination geometry of Pb2+ prevented the rational construction of metal-organic frameworks (MOFs) but promoted excellent fluorescence tuning. The regulation on organic and alkali templates facilitated the assemblies of three new Pb-MOFs: [Pb2(pia)2(DMA)]·DMA (1), [Pb2(pia)2(DMF)]·1.5DMF (2), and [Pb2(pia)2(DMF)]·NEt3 (3). They were rigid rod-spacer and double-walls frameworks, which possess defective dicubane [Pb4O6] based metal-carboxyl chains constructed from both semidirected and holodirected Pb2+ ions. These MOFs exhibited thermal stability up to 370 °C and unprecedented chemical stability in H2O and acidic (pH 2) and alkaline (pH 12) aqueous solutions, found for the first time in Pb-MOFs. A single-phase and rare-earth-free white-emitting phosphor, 1, was screen out, which showed a near-sunlight and human-vision-friendly broadband spectrum covering the full visible region, possessing the close-to-pure-white chromaticity coordinates of (0.332, 0.347), a near-daylight color temperature of 5696 K, and a high color rendering index of 95. The replacement of DMF as apical ligand and guest in 2 resulted in an intrinsic single and narrow emission at 562 nm with yellow color. The convenient yellow-and-blue color-tuning until white for 2 was realized by either solution or solid blending with blue-emissive H2pia, benefited from their highly matched excitation spectra. Using large NEt3 as template guest induced great framework distortion for 3 and led to white emission with chromaticity coordinates of (0.302, 0.294), stemming from nonequivalent dual emission at 450 and 545 nm. In-depth structure analysis revealed intra-/interchain Pb···Pb interactions in the lead(II)-carboxyl chains greatly affected the photochemical output.

Near sunlight continuous broadband white-light emission by single-phase Zn(ii)-1,3,5-benzenetricarboxylate MOFs.

A new white light MOF was constructed from low-cost 1,3,5-benzenetricarboxylate and nontoxic Zinc(ii) ions. The compound possessed the most sophisticated crystallographic asymmetric unit containing sixteen metal ions and twelve ligands. Near sunlight and human eye friendly white-light emission under a wide ultraviolet radiation range of 300 to 390 nm was observed for this photoemitter, without the use of expensive rare earth and complicated organic ligands.

Efficacy and safety of Hou Gu Mi Xi in patients with spleen qi deficiency syndrome who underwent radical gastrectomy for gastric cancer: protocol for a multicenter, randomized, double-blind, placebo-controlled trial.

BACKGROUND: Spleen qi deficiency (SQD), a syndrome based on traditional Chinese medicine (TCM) theory, is common in patients after radical gastrectomy. SQD manifests with chronic gastrointestinal disorders and systemic symptoms and is challenging to manage. Hou Gu Mi Xi (HGMX) is a dietary TCM formula for SQD. This study aims to evaluate the efficacy and safety of HGMX in patients with SQD who have undergone radical gastrectomy for gastric cancer. METHODS AND DESIGN: This study is a multicenter, randomized, double-blind, placebo-controlled trial. One hundred thirty patients with SQD who have undergone radical gastrectomy for gastric cancer will be assigned to receive either HGMX or placebo for 2 years. The main outcome will be changes in SQD symptoms assessed by the Spleen Qi Deficiency Symptoms Grading and Quantifying Scale. The secondary outcomes will be changes in quality of life assessed by the Short Form 36 scale, performance status as assessed by the Eastern Cooperative Oncology Group Performance Status scale, body weight, and body mass index. Progression-free survival will also be assessed as a secondary outcome. Adverse events (AEs), severe AEs, and study withdrawal due to AEs will be recorded to evaluate the safety of HGMX. DISCUSSION: The results of this trial will provide initial evidence for the use of HGMX as an alternative and complementary intervention to manage chronic postoperative complications in patients who have undergone radical gastrectomy for gastric cancer. TRIAL REGISTRATION: ClinicalTrials.gov, NCT03025152 . Registered on 17 January 2017.

Protein Phosphatase 2A B'α and B'ß Protect Centromeric Cohesion during Meiosis I.

During meiosis, the stepwise release of sister chromatid cohesion is crucial for the equal distribution of genetic material to daughter cells, enabling generation of fertile gametophytes. However, the molecular mechanism that protects centromeric cohesion from release at meiosis I is unclear in Arabidopsis (Arabidopsis thaliana). Here, we report that the protein phosphatase 2A regulatory subunits B'α and B'ß participate in the control of sister chromatid separation. The double mutant b'αß exhibited severe male and female sterility, caused by the lack of a nucleus or presence of an abnormal nucleus in mature microspores and embryo sacs. 4',6-Diamidino-2-phenylindole staining revealed unequal amounts of DNA in the mononuclear microspores. Transverse sections of the anthers revealed unevenly sized tetrads with or without a nucleus, suggesting a defect in meiocyte meiosis. An analysis of chromosome spreads showed that the sister chromatids separated prematurely at anaphase I in b'αß Immunoblotting showed that AtRECOMBINATION DEFECTIVE8 (AtREC8), a key member of the cohesin complex, was hyperphosphorylated in b'αß anthers and pistils during meiosis but hypophosphorylated in the wild type. Furthermore, yeast two-hybrid and bimolecular fluorescence complementation assays showed that B'α and B'ß interact specifically with AtREC8, AtSHUGOSHIN1 (AtSGO1), AtSGO2, and PATRONUS1. Given that B'α was reported to localize to the centromere in meiotic cells, we propose that protein phosphatase 2A B'α and B'ß are recruited by AtSGO1/2 and PATRONUS1 to dephosphorylate AtREC8 at the site of centromere cohesion to shield it from cleavage until anaphase II, contributing to the balanced separation of sister chromatids at meiosis.

CiteSpace-based Document Information Visualization of Literature Published by Journal of Forensic Medicine from 1985 to 2018 / 法医学杂志

Objective To analyze a knowledge web of the literature published by Journal of Forensic Medicine from its founding in 1985 to 2018, describe the evolving process of forensic science research and explore the research hotspots and frontiers at present. Methods The literature that was published by Journal of Forensic Medicine from 1985 to 2018 was collected and analyzed in terms of elements, such as emerging research hotspots, high frequency keywords, authors, dispatching units, location of institution and funding, by CiteSpace5.3 information visualization analysis software. Results All disciplines of forensic medicine were continually developing and maturing, and the publication volume of the literature on forensic pathology had the highest weight; in research hotspots, the two categories, research and identification each had their own emphasis; as the main source of contributions to the journal, research institutes accounted for 38.99% of the total number of publications; Shanghai ranked first among all regions with 1 046 articles published. The number of funded articles was generally on the rise, with the number of funded articles published largest in 2015. Conclusion As an authoritative academic journal in the field of forensic science in China, Journal of Forensic Medicine carries the development of forensic science and witnesses the institutional reform of universities and colleges, and offers a wide range of communication and cooperation in terms of technicality and application. Many scholars and scientific research institutions have gained progress continually in various research directions in the form of teamwork; and emerging research hotspots will continue to play a huge role in future practical applications.

Neuroprotective effect and mechanism of daucosterol palmitate in ameliorating learning and memory impairment in a rat model of Alzheimer's disease.

Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by progressive memory decline and cognitive impairment. Amyloid beta (Aß) has been proposed as the causative role for the pathogenesis of AD. Accumulating evidence demonstrates that Aß neurotoxicity is mediated by glutamate excitotoxicity. Daucosterol palmitate (DSP), a plant steroid with anti-glutamate excitotoxicity effect, was isolated from the anti-aging traditional Chinese medicinal herb Alpinia oxyphylla Miq. in our previous study. Based on the anti-glutamate excitotoxicity effect of DSP, in this study we investigated potential benefit and mechanism of DSP in ameliorating learning and memory impairment in AD model rats. Results from this study showed that DSP administration effectively ameliorated Aß-induced learning and memory impairment in rats, markedly inhibited Aß-induced hippocampal ROS production, effectively prevented Aß-induced hippocampal neuronal damage and significantly restored hippocampal synaptophysin expression level. This study suggests that DSP may be a potential candidate for development as a therapeutic agent for AD cognitive decline.

Neuroprotective Mechanisms of 9-Hydroxy Epinootkatol Against Glutamate-Induced Neuronal Apoptosis in Primary Neuron Culture.

Glutamate-induced neuronal apoptosis has been implicated in the pathogenesis of neurological disorders. 9-Hydroxy epinootkatol (9OHEN), a sesquiterpene compound with neuroprotective activity against glutamate-induced neuronal apoptosis, was isolated from Alpinia oxyphylla Miquel in our previous study. In this study, we investigated the neuroprotective mechanisms of 9OHEN against glutamate-induced neuronal apoptosis in primary cultured neurons. The results from this study demonstrated that 9OHEN protected cortical neurons from glutamate-induced neuronal apoptosis via inhibiting glutamate-induced activation of caspase-3, inhibiting glutamate-induced reactive oxygen species (ROS) production, inhibiting glutamate-induced nitric oxide (NO) production, and downregulating glutamate-induced neuronal nitric oxide synthase (nNOS) expression. This study suggest that 9OHEN might have therapeutic potential in treating glutamate-mediated neurological diseases.

Neuroprotective effect of biatractylenolide against memory impairment in D-galactose-induced aging mice.

Biatractylenolide, a sesquiterpene lactone, which exerted the neuroprotective effect against glutamate-induced excitotoxicity, was isolated from Atractylodis macrocephala in our previous study. In this study, we evaluated the neuroprotective effect of biatractylenolide against D-galactose-induced memory impairment and explored the potential mechanism of its action. The results showed that administration of biatractylenolide could significantly improve behavioral performance of D-galactose-treated mice in passive avoidance test and spatial learning-memory test. Administration of biatractylenolide could significantly decrease the formation of reactive oxygen species (ROS), decrease the activity of acetylcholinesterase (AChE), and increase the expression of synapsin I and protein kinase C (PKC) in D-galactose-treated mice. Our findings provide first evidence for the neuroprotective effect of biatractylenolide against D-galactose-induced memory impairment. The potential mechanisms underlying the neuroprotective effect of biatractylenolide in D-galactose-treated mice might be (i) attenuating oxidative damage via decreasing ROS formation, (ii) restoring cholinergic neurotransmission via decreasing AChE activity, and (iii) increasing the expression of memory-related proteins (synapsin I and PKC). Biatractylenolide may have therapeutic potential in aging-related memory impairment.

Neuroprotection of atractylenolide III from Atractylodis macrocephalae against glutamate-induced neuronal apoptosis via inhibiting caspase signaling pathway.

Glutamate-induced excitotoxicity appears to play a crucial role in neurological disorders. Neuroprotection against glutamate-induced excitotoxicity has been proposed as a therapeutic strategy for preventing and/or treating these excitotoxicity-mediated diseases. In the present study, atractylenolide III, which exhibited significantly neuroprotective effect against glutamate-induced neuronal apoptosis, was isolated from Atractylodes macrocephala by means of bioactivity-guided fractionation. The inhibitory effect of atractylenolide III on glutamate-induced neuronal apoptosis was in a concentration-dependent manner. The anti-apoptotic property of atractylenolide III might be mediated, in part, via inhibiting caspase signaling pathway. Atractylenolide III may have therapeutic potential in excitotoxicity-mediated neurological diseases.

Neuroprotective effect of Rhizoma Atractylodis macrocephalae against excitotoxicity-induced apoptosis in cultured cerebral cortical neurons.

Excitotoxicity has been implicated in neurological disorders. This study investigated the neuroprotective effect of the extract from Rhizoma Atractylodis macrocephalae on excitotoxicity-induced neuronal apoptosis in primary cultured cerebral cortical neurons. Excitotoxicity was induced by exposure of cortical neurons to glutamate. Neuronal apoptosis and the protective effect of Rhizoma Atractylodis macrocephalae extract were examined by multi-indices including cell viability assay, morphological features, DNA fragmentation and flow cytometric analysis. After exposure of cultured neurons to glutamate for 24 h, the neurons exhibited marked apoptotic-like death. Co-treatment of the neurons with glutamate and Rhizoma Atractylodis macrocephalae extract significantly elevated the cell viability, and reduced the number of apoptotic cells. These results demonstrate that Rhizoma Atractylodis macrocephalae is an effective neuroprotective agent against glutamate-induced excitotoxicity and may have therapeutic potential in excitotoxicity-mediated diseases.