False Vision Graphics in Logo Design Based on Artificial Intelligence in the Visual Paradox Environment.

There are numerous fresh ways of thinking and creativity as a result of the ongoing development of art design. How do you create a fantastic logo that has extraordinary artistic effects? The incorrect interpretation of artistic graphics can cause a special visual phenomenon known as the contradiction between visual images and objective reality, which causes people's visual systems to produce points of interest. Wrong vision graphics, or visual paradox, can give people a wonderful experience that transcends time and space and reveals the enigmatic beauty that is concealed in the natural order, which is in line with the design goals of sign art. The integration of design and artificial intelligence has drawn a lot of attention as science and technology have advanced. Designing an intelligent and comfortable user experience is more important than ever, especially given the world's growing digital demand. The technical limitations of algorithm black boxes exacerbate the power disparity between humans and algorithms, which is inherent in artificial algorithms. According to its research, artificial intelligence's algorithm is responsible for roughly 60% of its calculations. Random forest technology's current benefits and drawbacks are contrasted with those of popular algorithms, and a clear vision of its potential applications in the future is presented. The artificial algorithm's recommended operation mechanism chooses the algorithm's nontechnical neutrality and value orientation.

Assessment of winter air pollution episodes using long-range transport modeling in Hangzhou, China, during World Internet Conference, 2015.

A winter air pollution episode was observed in Hangzhou, South China, during the Second World Internet Conference, 2015. To study the pollution characteristics and underlying causes, the Weather Research and Forecasting with Chemistry model was used to simulate the spatial and temporal evolution of the pollution episode from December 8 to 19, 2015. In addition to scenario simulations, analysis of the atmospheric trajectory and synoptic weather conditions were also performed. The results demonstrated that control measures implemented during the week preceding the conference reduced the fine particulate matter (PM2.5) pollution level to some extent, with a decline in the total PM2.5 concentration in Hangzhou of 15% (7%-25% daily). Pollutant long-range transport, which occurred due to a southward intrusion of strong cold air driven by the Siberia High, led to severe pollution in Hangzhou on December 15, 2015, accounting for 85% of the PM2.5 concentration. This study provides new insights into the challenge of winter pollution prevention in Hangzhou. For adequate pollution prevention, more regional collaborations should be fostered when creating policies for northern China.

Protective effects of allicin on streptozotocin-induced diabetic nephropathy in rats.

BACKGROUND: Studies in animal models have shown that allicin, a major biologically active component of garlic, can play a role in the prevention of tissue fibrosis in the liver, lung and heart, mainly related to the inhibition of fibroblast proliferation, fibrogenic cytokine secretion and extracellular matrix synthesis. This study aimed to investigate the protective effects of allicin on renal damage in streptozotocin (STZ)-induced diabetic rats. STZ-induced diabetic rats were administered allicin (15, 30 and 45 mg · kg-1 · day-1 ) via daily intra-gastric gavage for 12 weeks. The levels of fasting blood glucose (FBG), blood urea nitrogen (BUN), serum creatinine (sCr), lipid and 24 h urine albumin excretion (UAE) were measured at the end of weeks 4, 8 and 12. The renal histopathology and the expression levels of collagen I, transforming growth factor ß1 (TGF-ß1) and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) were measured using immunohistochemistry and/or western blotting. RESULTS: In 12 week STZ-induced diabetic rats, severe hyperglycemia and albuminuria were markedly developed. Treatment with allicin for 12 weeks ameliorated diabetes-induced morphological alterations of the kidney and decreased FBG, BUN, sCr, triglyceride (TG) and 24 h UAE in diabetic rats. The expression levels of collagen I, TGF-ß1 and p-ERK1/2 were significantly decreased by allicin treatment. CONCLUSION: These results suggested that allicin may play a protective role in diabetic nephropathy via the TGF-ß1/ERK pathway in diabetic rats. © 2016 Society of Chemical Industry.

Clinical diagnosis and mutation analysis of a Chinese family with Camurati-Engelmann disease.

Camurati-Engelmann disease (CED) is a rare autosomal dominant bone disorder caused by a mutation in transforming growth factor ß1 (TGFß1). The present study aimed to identify a Chinese family with suspected CED based on the clinical symptoms, including pain in extremities, waddling gait, muscle weakness, cortical thickening of the diaphysis of the long bones, and sclerosis of the skull, facial bone, and pelvis. Molecular analysis revealed the presence of the p.Glu169Lys (E169K) mutation in exon 2 of TGFß1 in patients when compared with the controls. Therefore, the Chinese family was diagnosed with CED due to the presence of the E169K mutation. The present study emphasized the importance of clinical and genetic evidence for the diagnosis of CED. The data presented in the present study are of significance to clinicians, as well as genetic counselors, in the prenatal screening of CED.

Clinical and genetic investigation of families with type II Waardenburg syndrome.

The present study aimed to investigate the molecular pathology of Waardenburg syndrome type II in three families, in order to provide genetic diagnosis and hereditary counseling for family members. Relevant clinical examinations were conducted on the probands of the three pedigrees. Peripheral blood samples of the probands and related family members were collected and genomic DNA was extracted. The coding sequences of paired box 3 (PAX3), microphthalmia­associated transcription factor (MITF), sex­determining region Y­box 10 (SOX10) and snail family zinc finger 2 (SNAI2) were analyzed by polymerase chain reaction and DNA sequencing. The heterozygous mutation, c.649_651delAGA in exon 7 of the MITF gene was detected in the proband and all patients of pedigree 1; however, no pathological mutation of the relevant genes (MITF, SNAI2, SOX10 or PAX3) was detected in pedigrees 2 and 3. The heterozygous mutation c.649_651delAGA in exon 7 of the MITF gene is therefore considered the disease­causing mutation in pedigree 1. However, there are novel disease­causing genes in Waardenburg syndrome type II, which require further research.

[Clinical classification and genetic mutation study of two pedigrees with type II Waardenburg syndrome].

OBJECTIVE: To explore the molecular etiology of two pedigrees affected with type II Waardenburg syndrome (WS2) and to provide genetic diagnosis and counseling. METHODS: Blood samples were collected from the proband and his family members. Following extraction of genomic DNA, the coding sequences of PAX3, MITF, SOX10 and SNAI2 genes were amplified with PCR and subjected to DNA sequencing to detect potential mutations. RESULTS: A heterozygous deletional mutation c.649_651delAGA in exon 7 of the MITF gene has been identified in all patients from the first family, while no mutation was found in the other WS2 related genes including PAX3, MITF, SOX10 and SNAI2. CONCLUSION: The heterozygous deletion mutation c.649_651delAGA in exon 7 of the MITF gene probably underlies the disease in the first family. It is expected that other genes may also underlie WS2.

HSF1 functions as a transcription regulator for Dp71 expression.

Heat shock factor 1 (HSF1) is one of the most important transcriptional molecules in the heat shock process; however, HSF1 can also regulate the expression of other proteins. Dystrophin Dp71 is one of the most widely expressed isoforms of the dystrophin gene family. In our experiments, we showed for the first time that HSF1 can function as a transcriptional factor for endogenous Dp71 expression in vivo and in vitro. We demonstrated that the messenger RNA (mRNA) and protein expression of Dp71 were significantly reduced in HSF1-knockout mice compared with wild-type mice in brain, lung, liver, spleen, and kidney. Overexpression of HSF1 significantly enhanced the mRNA and protein expression of Dp71 in HeLa cells. Inhibiting the expression of HSF1 in HeLa cells significantly reduced the expression of Dp71. By use of the EMSA technique, the chromatin immunoprecipitation assay, and the luciferase reporter system, we demonstrated that HSF1 can directly bind the HSE in the Dp71 promoter region. We concluded from our data that HSF1 functions as a transcriptional regulator of Dp71 expression.