Three-Dimensional Printing of Large Objects with High Resolution by Dynamic Projection Scanning Lithography.

Due to the development of printing materials, light-cured 3D printing is playing an increasingly important role in industrial and consumer markets for prototype manufacturing and conceptual design due to its advantages in high-precision and high-surface finish. Despite its widespread use, it is still difficult to achieve the 3D printing requirements of large volume, high resolution, and high speed. Currently, traditional light-cured 3D printing technologies based on stereolithography, such as regular DLP and SLA, can no longer meet the requirements of the processing size and processing rate. This paper introduces a dynamic projection of 3D printing technology utilizing a digital micro-mirror device (DMD). By projecting the ultraviolet light pattern in the form of "animation", the printing resin is continuously cured in the exposure process to form the required three-dimensional structure. To print large-size objects, the three-dimensional model is sliced into high-resolution sectional images, and each layer of the sectional image is further divided into sub-regional images. These images are dynamically exposed to the light-curing material and are synchronized with the scanning motion of the projection lens to form a static exposure pattern in the construction area. Combined with the digital super-resolution, this system can achieve the layering and fine printing of large-size objects up to 400 × 400 × 200 mm, with a minimum feature size of 45 µm. This technology can achieve large-size, high-precision structural printing in industrial fields such as automobiles and aviation, promoting structural design, performance verification, product pre-production, and final part processing. Its printing speed and material bending characteristics are superior to existing DLP light-curing 3D printing methods.

Cardiac Involvement in COVID-19: A Global Bibliometric and Visualized Analysis.

Objective: Coronavirus disease 2019 (COVID-19), which was caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), had already resulted in widespread epidemics worldwide and millions of people's deaths since its outbreak in 2019. COVID-19 had also been demonstrated to affect people's cardiac function. However, the specific mechanism and influence of this damage were not clear yet. The purpose of the present study was to provide a bibliometric analysis of the current studies related to cardiac involvement after SARS-CoV-2 infection. Methods: A bibliometric literature search was performed on the web of science. The number and type of publications, countries, institutional sources, journals, and citation patterns were analyzed. In addition, qualitative and quantitative evaluations were carried out to visualize the scientific achievements in this field by using the VOSviewer software. Results: Web of science had recorded 2,24,097 documents on COVID-19 at the time of data collection (May 12, 2022). A total of 2,025 documents related to cardiac involvement were recorded at last. The countries with the most published articles were the United States of America (USA) (n =747, 36.9%), Italy (n =324, 16%), and England (n =213, 10.5%). Although the countries and institutions that published the most articles were mainly from the USA, the top three authors were from Germany, England, and Poland. Frontiers in Cardiovascular Medicine was the journal with the most studies (65 3.2%), followed by ESC Heart Failure (59 2.9%) and Journal of Clinical Medicine (56 2.8%). We identified 13,739 authors, among which Karin Klingel and Amer Harky had the most articles, and Shaobo Shi was co-cited most often. There existed some cooperation between different authors, but the scope was limited. Myocarditis and heart failure (HF) were the main research hotspots of COVID-19 on cardiac dysfunction and may be crucial to the prognosis of patients. Conclusions: It was the first bibliometric analysis of publications related to COVID-19-associated cardiac disorder. This study provided academics and researchers with useful information on the most influential articles of COVID-19 and cardiac dysfunction. Cooperation between countries and institutions must be strengthened on myocarditis and HF during COVID-19 pandemic.

Establishing a Risk Prediction Model for Atherosclerosis in Systemic Lupus Erythematosus.

Background and aims: Patients with systemic lupus erythematosus (SLE) have a significantly higher incidence of atherosclerosis than the general population. Studies on atherosclerosis prediction models specific for SLE patients are very limited. This study aimed to build a risk prediction model for atherosclerosis in SLE. Methods: RNA sequencing was performed on 67 SLE patients. Subsequently, differential expression analysis was carried out on 19 pairs of age-matched SLE patients with (AT group) or without (Non-AT group) atherosclerosis using peripheral venous blood. We used logistic least absolute shrinkage and selection operator regression to select variables among differentially expressed (DE) genes and clinical features and utilized backward stepwise logistic regression to build an atherosclerosis risk prediction model with all 67 patients. The performance of the prediction model was evaluated by area under the curve (AUC), calibration curve, and decision curve analyses. Results: The 67 patients had a median age of 42.7 (Q1-Q3: 36.6-51.2) years, and 20 (29.9%) had atherosclerosis. A total of 106 DE genes were identified between the age-matched AT and Non-AT groups. Pathway analyses revealed that the AT group had upregulated atherosclerosis signaling, oxidative phosphorylation, and interleukin (IL)-17-related pathways but downregulated T cell and B cell receptor signaling. Keratin 10, age, and hyperlipidemia were selected as variables for the risk prediction model. The AUC and Hosmer-Lemeshow test p-value of the model were 0.922 and 0.666, respectively, suggesting a relatively high discrimination and calibration performance. The prediction model had a higher net benefit in the decision curve analysis than that when predicting with age or hyperlipidemia only. Conclusions: We built an atherosclerotic risk prediction model with one gene and two clinical factors. This model may greatly assist clinicians to identify SLE patients with atherosclerosis, especially asymptomatic atherosclerosis.

Gut microbiota dysbiosis in stable coronary artery disease combined with type 2 diabetes mellitus influences cardiovascular prognosis.

BACKGROUND AND AIMS: Host-microbiota interactions involving metabolic pathways have been linked to the pathogenesis of atherosclerotic disease and type 2 diabetes. As stable coronary artery disease (SCAD) patients combined with type 2 diabetes have significantly increased risk for cardiac event, we focused on elucidating the role of microbiota affecting cardiometabolic disease development. METHODS AND RESULTS: We used multi-omics analyses (metagenomics and metabolomics) of fecal and serum samples from a prospective cohort including stable coronary artery disease combined with diabetes mellitus (SCAD + T2DM, n = 38), SCAD (n = 71), and healthy control (HC, n = 55). We linked microbiome features to disease severity in a three-pronged association analysis and identified prognostic bacterial biomarkers. We identified that bacterial and metabolic signatures varied significantly between SCAD and SCAD + T2DM groups. SCAD + T2DM individuals were characterized by increased levels of aromatic amino acids and carbohydrates, which correlate with a gut microbiome with enriched biosynthetic potential. Our study also addressed how metformin may confound gut dysbiosis and increase the potential for nitrogen metabolism. In addition, we found that specific bacterial taxa Ruminococcus torques [HR: 2.363 (08-4.56), P = 0.03] was predictive of cardiac survival outcomes. CONCLUSION: Overall, our study identified relationships between features of the gut microbiota (GM) and circulating metabolites, providing a new direction for future studies aiming to understand the host-GM interplay in atherosclerotic cardiovascular pathogenesis.

Establishment of an induced pluripotent stem cell line PUMCHi004-A from a hereditary transthyretin amyloid cardiomyopathy patient with transthyretin (TTR) p.Asp38Asn mutation.

Hereditary transthyretin amyloid cardiomyopathy is cardiac involvement in systemic transthyretin amyloidosis. For the first time, we generated induced pluripotent stem cell (iPSC) line of hATTR-CM carrying the TTR mutation p.Asp38Asn. We isolated peripheral blood mononuclear cells from the patient's peripheral blood. The reprogramming of PBMCs achieved a pluripotent state by the transfection of non-integrated episomal vectors. We demonstrated pluripotency with the presence of cell surface markers, the expression of pluripotency-related genes and the ability to form teratoma composed of three germ layers in vivo. This iPSC line is a useful model for studying the pathogenic mechanism of TTR p.Asp38Asn mutation.

Novel Method for Preparing a High-Performance Auxetic Foam Directly from Polymer Resin by a One-Pot CO2 Foaming Process.

So far, negative Poisson's ratio foam (auxetic foam) is usually prepared by the transformation of conventional polymer foam, and it is a challenge to prepare auxetic foam directly from polymer resin. In this work, a novel method based on the synergism between the phase transition of water and the permeability rate difference of the CO2 blowing agent from air in the foaming process is put forward to prepare auxetic foam directly from the polymer resin. Using this method, herein, nylon elastomer (NE) foam with auxetic behavior is successfully prepared from NE resin by a one-pot CO2 foaming method inside an autoclave aided by water; the obtained auxetic foam has a Poisson's ratio value of -1.29 and has excellent tensile cycle stability and energy absorption performance. This method breaks through the bottleneck for preparing auxetic foams from the polymer resin directly, which is also green and environment-friendly. It is believed that the abovementioned method also applies to other thermoplastic polymers, which paves a way for designing and preparing multifunctional auxetic foam materials in the future via a one-pot CO2 foaming process. Furthermore, this work first demonstrates that the transformation between auxetic foam and positive Poisson's ratio foam is reversible due to the closed cell structure, which provides an opportunity to reversibly adjust the performance and the shape of polymer foam materials.

Novel Method for Preparing Auxetic Foam from Closed-Cell Polymer Foam Based on the Steam Penetration and Condensation Process.

Auxetic materials are a class of materials possessing a negative Poisson's ratio. Here, we established a novel method for preparing auxetic foam from closed-cell polymer foam based on the steam penetration and condensation (SPC) process. Using polyethylene (PE) closed-cell foam as an example, the foams treated by the SPC process presented a negative Poisson's ratio during stretching and compression testing. The effect of steam-treated temperature and time on the conversion efficiency of negative-Poisson's ratio foam was investigated, and the mechanism of the SPC method for forming a reentrant structure was discussed. The results indicated that the presence of enough steam within the cells was a critical factor for the negative Poisson's ratio conversion in the SPC process. The pressure difference caused by steam condensation was the driving force for the conversion from conventional closed-cell foam to the negative-Poisson's ratio foam. Furthermore, the applicability of the SPC process for fabricating auxetic foam was studied by replacing PE foam by polyvinyl chloride foam with a closed-cell structure or replacing water steam by ethanol steam. The results verified the universality of the SPC process for fabricating auxetic foams from conventional foams with a closed-cell structure. In addition, we explored the potential application of the obtained auxetic foams by the SPC process in the fabrication of shape-memory polymer materials.

Sirtuins in mitochondrial stress: Indispensable helpers behind the scenes.

Mitochondria play an essential part in guaranteeing normal cellular physiological functions through providing ATP and participating in diverse processes and signaling pathways. Recently, more and more studies have revealed the vital roles of mitochondria in coping with stressors in the aging process, metabolic disturbances and neurological disorders. Mitochondrial stress responses, including the mitochondrial unfolded protein response (UPRmt), antioxidant defense, mitochondrial fission, mitochondrial fusion and mitophagy, are induced to maintain cellular integrity in response to stress. The sirtuin family, a group of NAD+-dependent deacetylases, has been the focus of much attention in recent years for their multiple regulatory functions, especially in aging and metabolism. Recent reports validated the significant link between mitochondrial stress responses and the sirtuin family, which may help to elucidate the pathogenesis and therapies for diseases such as Alzheimer's disease or Parkinson's disease. This review will summarize recent related studies and illuminate the interplay between sirtuins and mitochondrial stress.

Particle-size dependent melt viscosity behavior and the properties of three-arm star polystyrene-Fe3O4 composites.

The melt viscosity of three-arm star polystyrene (S3PS)-Fe(3)O(4) nanoparticle composites was studied by means of rheological measurements. The arm molecular weight (M(a)) of S3PS (or radius gyration) and the particle size of Fe(3)O(4) (radius (R(p)): 3 nm and 44 nm) showed a strong influence on the melt viscosity behavior (at low shear frequencies) of S3PS-Fe(3)O(4) composites. The reinforcement (viscosity increase) was observed in the composites where the M(a) was higher than the M(c) of PS (M(c): the critical molecular weight for chain entanglement). For M(a) < M(c), when the size of Fe(3)O(4) nanoparticles was changed, the melt viscosity of the composites exhibited either plasticization (melt viscosity reduction) or reinforcement. When the content of Fe(3)O(4) was low (1 wt%), the transformation from plasticization to reinforcement behavior could be observed, which strongly depended on the size ratio of the radius of gyration (R(g)) of S3PS to the size of nanoparticles (R(p)). In addition, the magnetic properties and thermal stability of S3PS-Fe(3)O(4) composites were studied.

Protective effect of a novel cystine C(60) derivative on hydrogen peroxide-induced apoptosis in rat pheochromocytoma PC12 cells.

Oxidative stress has been considered as a major cause of cellular injuries in a variety of clinical abnormalities, especially neural diseases. One of the effective ways to prevent the reactive oxygen species (ROS) mediated cellular injury is dietary or pharmaceutical augmentation of free radical scavengers. In the present study, we describe the synthesis and characterization of a novel cystine C(60) derivative (CFD). The compound was analyzed by FT-IR, (1)H NMR, (13)C NMR, LC-MS and elemental analysis. It contains five cystine moieties per C(60) molecule. This water-soluble amino-fullerene derivative was able to scavenge both superoxide and hydroxyl radical with biocompatibility. We investigated its potential protective effects on hydrogen peroxide-induced oxidative stress and apoptotic death in cultured rat pheochromocytoma (PC12) cells. Cells treated with hydrogen peroxide underwent cytotoxicity and apoptotic death determined by MTT assay, flow cytometry analysis, PI/Hoechst 33342 staining and glutathione peroxidase assay. The CFD was able to reduce the accumulation of reactive oxygen species and cellular damage caused by hydrogen peroxide in PC12 cells. RF assay demonstrated that CFD could penetrate through the cell membrane and it has played its distinguished role in protecting PC12 cells against hydrogen peroxide-induced cytotoxicity. The results suggest that CFD has the potential to prevent oxidative stress-induced cell death without evident toxicity. Hence, we can hypothesize that the protective effect of CFD on hydrogen peroxide-induced apoptosis is related to its scavenger activity.

Synthesis of beta-alanine C60 derivative and its protective effect on hydrogen peroxide-induced apoptosis in rat pheochromocytoma cells.

Oxidative stress has been considered as a major cause of cellular injuries in a variety of clinical abnormalities, especially prominent in neural diseases. One of the effective ways to prevent the reactive oxygen species (ROS) mediated cellular injury is dietary or pharmaceutical augmentation of some free radical scavenger. Water-soluble amino-fullerene derivative is a novel compound that behaves as a free radical scavenger with excellent biocompatibility. In the present study, we synthesized a novel beta-alanine C(60) derivative. The product was characterized by FT-IR, (1)H NMR, (13)C NMR, LC-MS and elemental analysis. We investigated the protective effect on hydrogen peroxide-induced oxidative stress and apoptotic death in cultured rat pheochromocytoma (PC12) cells. PC12 cells treated with hydrogen peroxide underwent apoptotic death determined by MTT, flow cytometry analysis and PI/Hoechst 33342 staining. Moreover, the scavenging ability of beta-alanine C(60) derivative to reactive oxygen species both in vivo and in vitro of PC12 cells was measured. The results suggest that beta-alanine C(60) derivative has the potential to prevent oxidative stress-induced cell death without evident toxicity. Hence, on the basis of the above-mentioned studies, we can hypothesize that the protective effect of beta-alanine C(60) derivative on H(2)O(2) induced apoptosis is related to their known scavenger activity toward ROS.

[Detection rate of human papillomavirus-16 in esophageal squamous cell carcinoma from different Chinese populations].

BACKGROUND & OBJECTIVE: Anyang in Henan Province of China is a hyperendemic area of esophageal cancer. The infection of human papillomavirus (HPV) is thought as an important pathogenesis of esophageal cancer in Anyang. This study was to detect infection rate and level of HPV-16 in esophageal squamous cell carcinoma (ESCC) patients from 3 different Chinese areas, and investigate its relationship with the pathogenesis of ESCC. METHODS: Infection status of HPV-16 in 119 ESCC specimens (43 collected from Anyang, 43 from Beijing, and the rest 33 from Mongolia nationality of Inner Mongolia) was detected by in situ hybridization (ISH) technique with digoxin-labeled HPV-16 E6 probe. RESULTS: HPV16 infection rates were 81.4%, 69.8%, and 63.6% in the specimens from Anyang, Beijing, and Inner Mongolia, respectively. Infection level of HPV-16 was significantly higher in Anyang group than in Beijing group (H=3.91, P<0.05) and Inner Mongolia group(H=4.22,P<0.05). There was no significant difference between the latter 2 groups. Furthermore, the proportion of strong expression of HPV16 (++ and +++) was significantly higher in Anyang group than in the other 2 groups(H=3.95, P<0.05). CONCLUSIONS: HPV-16 infection rate is high in the esophageal specimens from the 3 different areas. Infection status of HPV16 is serious in Anyang.

LMP7/TAP2 gene polymorphisms and HPV infection in esophageal carcinoma patients from a high incidence area in China.

Esophageal carcinoma is characterized by a widely ranged incidence variation among the different geographic regions. Anyang is a county in Henan Province of North China with the highest prevalence of esophageal carcinoma. Human papillomavirus (HPV) infection has been linked to the etiology of esophageal cancer in this area. In this study, we investigated correlations of the polymorphisms at low molecular weight polypeptide (LMP) and transporters with antigen processing (TAP) genes, with the risk of esophageal carcinoma. DNA extracted from either tumor specimens or esophageal epithelial cells was used to test HPV infection. Peripheral blood lymphocyte DNA was used for LMP/TAP genotyping. Polymerase chain reaction was performed to analyze HPV infection and LMP/TAP gene polymorphisms. The combined effect of LMP/TAP gene polymorphisms and HPV infection on esophageal carcinoma was analyzed by using unconditional logistic regression models. The TAP2 codons 379 isoleucine carriers and LMP7 codons 145 lysine carriers were found to be more susceptible to esophageal carcinoma (OR = 2.74, 95% CI = 1.15-6.49, P = 0.023 for TAP2; OR = 2.19, 95% CI = 1.09-4.37, P = 0.027 for LMP7). Patients carrying homozygous LMP7/TAP2 haplotype C, which contained the glutamine at LMP7 codons 145 and the isoleucine at TAP2 codons 379, were more prone to develop esophageal carcinoma (OR = 2.96, 95% CI = 1.13-7.81, P = 0.027). An additive effect on the risk of esophageal carcinoma development was found among individuals carrying LMP7/TAP2 haplotype C and infected by HPV (OR = 4.33, 95% CI = 2.53-7.42, P < 0.0001). LMP7/TAP2 haplotype C may act as the risk factor in esophageal carcinoma development and it may influence the tumorigenesis in HPV infected individuals.

[Relationship between polymorphism of IRF-3 gene codon 427 and esophageal cancer in Anyang population of China].

OBJECTIVE: To investigate the association between the single nucleotide polymorphisms (SNPs) of interferon regulatory factor 3 (IRF-3) gene and the susceptibility of esophageal cancer in Anyang area, Henan Province. METHODS: The genomic DNAs of 152 esophageal cancer patients and 191 health controls were extracted from the peripheral blood leukocytes. Three fragments covering codons 96, 194, 377, and 427 of the IRF-3 gene were amplified by polymerase chain reaction (PCR). The SNPs were revealed by DNA sequencing and the genotype of every sample was determined accordingly. The frequency distribution of the SNPs was analyzed by chi(2) test. RESULTS: There were no IRF-3 gene SNPs at codons 96, 194, or 377 in Anyang participants. There was significant difference in the SNPs at codon 427 between the healthy controls and esophageal cancer patients in Anyang area OR=2.38 (95%CI=1.15-4.95,P<0.05). CONCLUSION: The SNPs at codon 427 of the IRF-3 gene may relate to the susceptibility of esophageal cancer. The risk of esophageal cancer in participants with C allele is 2.38-fold compared to those with G allele.

p53 codon 72 polymorphism (C/G) and the risk of human papillomavirus-associated carcinomas in China.

BACKGROUND: Human papillomavirus (HPV) plays an important role in the development of carcinomas at various body sites. It was found previously that the p53 codon 72 polymorphism (C/G) is a high-risk factor for the development HPV-associated cervical carcinoma. However, it still was considered controversial in several studies of cervical and esophageal carcinoma. METHODS: In the current study, the authors used an allele specific polymerase chain reaction (PCR) method to analyze correlation between the p53 codon 72 (C/G) polymorphism and HPV-associated, noncancerous esophageal epithelium as well as esophageal, ovarian, and breast carcinoma in the Chinese population. Esophageal balloon cytology examination samples were obtained from high-incidence and low-incidence populations for esophageal carcinoma in Anyang (Henan Province). RESULTS: Thirty-six of 48 esophageal balloon samples from the high-incidence population were HPV positive, and 13 of 33 esophageal balloon samples from the low-incidence population were HPV positive. Thirty-nine of 62 esophageal carcinoma samples from Anyang Tumor Hospital were HPV positive. Twenty-six of 39 ovarian carcinoma samples from the Second Affiliated Hospital of Inner Mongolia Medical College were HPV positive. Nineteen of 82 breast carcinoma samples from Beijing Cancer Hospital were HPV positive. It is noteworthy that the distribution of the p53 codon 72 Arg homozygous genotype in HPV positive samples of esophageal epithelium, ovarian carcinoma, and breast carcinoma was significantly higher compared with HPV negative tumor samples. (P < 0.05). CONCLUSIONS: The current results suggest that the p53 codon 72 Arg homozygous genotype is one of the high-risk genetic factors for HPV-associated malignancies among the Chinese population.

Congenital expression of mdr-1 gene in tissues of carcinoma and its relation with pathomorphology and prognosis.

AIM:To detect the congenital expression patterns of mdr-1 gene in commonly encountered malignant tumors in clinic, and the relationship between the expression of mdr-1 gene and the prognostic morphology in esophageal carcinomas.METHODS:A total of 151 resected samples of malignant tumors without preoperative treatment were taken from Anyang City Tumor Hospital.The congenital expression of their mdr-1 gene was detected with reverse transcription polymerase chain reaction (RT-PCR) and was compared with each other.The positive incidence of mdr-1 gene in 46 samples of esophageal carcinoma was compared with their differentiated grades, TNM stages and macroscopic types, and the precautions and advantages of RT-PCR were evaluated.RESULTS:All the 151 samples were confirmed to be malignant histopathologically, including cancers of stomach and gastric cardia (n = 51), esophagus (n = 46), colorectum (n = 16),breast (n = 15), thyroid (n = 10), lung (n = 9) and uterine cervix (n = 24). The positive expression rate of their mdr-1 gene was 33.3%, 37%, 31.3%, 13.2%, 40%, 55%, and 0% respectively. All the 46 samples of esophageal carcinoma were pathologically confirmed to be squamous cell carcinoma. The total expression rate of their mdr-1 gene was 37% (17/46), 35% (6/17), 40% (8/20), and 33% (3/9) for differentiation grade I, II and III respectively. The expression rate of TNM classification was 33% (6/18), 40% (5/12) and 37% (6/16) in stage IIa, IIb andIII. The expression rate was 33% (3/9) in ulcerous type, 37% (3/8) in constrictive types, 33% (5/15) in fungoid types, and 40% (6/14) in medullary types.No statistically significant difference was found.CONCLUSION:Compared with other methods, RT-PCR is more simple, reliable and accurate in detecting mdr-1 gene expression in tissues of tumor. The overexpression of mdr-1 gene in these neoplasms suggested that cases should be handled differently for chemotherapy with rational use of drugs. Excision is the chief treatment for carcinoma of esophagus. The expression of mdr-1 gene in tissues of esophageal cancer is correlated with the parameters of tumor molecular biology which are independent of histopathological morphology.