Influence of the atmospheric environment on spatial variation of lung cancer incidence in China.

Conducting this research contributes to a deeper understanding of the correlation between atmospheric environmental quality and lung cancer incidence, and provides the scientific basis for formulating effective environmental protection and lung cancer prevention and control strategies. Lung cancer incidence in China has strong spatial variation. However, few studies have systematically revealed the characteristics of the spatial variation in lung cancer incidence, and have explained the causes of this spatial variation in lung cancer incidence from the perspectives of multiple components of the atmospheric environment to explain this spatial variation in lung cancer incidence. To address research limitations, we first analyze the spatial variation and spatial correlation characteristics of lung cancer incidence in China. Then, we build a spatial regression model using GeoDa software with lung cancer incidence as the dependent variable, five atmospheric environment factors-particulate matter 2.5 (PM2.5) concentration, temperature, atmospheric pressure, and elevation as explanatory variables, and four socio-economic characteristics as control variables to systematically analyze the influence and intensity of these factors on lung cancer incidence. The results show that lung cancer incidence in China has apparent changes in geographical and spatial unevenness, and spatial autocorrelation characteristics. In China, the lung cancer incidence is relatively high in Northeast China, while some areas of high lung cancer incidence still exist in Central China, Southwest China and South China, although the overall lung cancer incidence is relatively low. The atmospheric environment significantly affects lung cancer incidence. Different elements of the atmospheric environment vary in the direction and extent of their influence on the development of lung cancer. A 1% increase in PM2.5 concentration is associated with a level of 0.002975 increase in lung cancer incidence. Atmospheric pressure positively affects lung cancer incidence, and an increase in atmospheric pressure by 1% increases lung cancer incidence by a level of 0.026061. Conversely, a 1% increase in temperature is linked to a level of 0.006443 decreases in lung cancer incidence, and a negative correlation exists between elevation and lung cancer incidence, where an increase in elevation by 1% correlates with a decrease in lung cancer incidence by a level of 0.000934. The core influencing factors of lung cancer incidence in the seven geographical divisions of China exhibit variations. This study facilitates our understanding of the spatial variation characteristics of lung cancer incidence in China on a finer scale, while also offering a more diverse perspective on the impact of the atmospheric environment on lung cancer incidence.

Automated tooth crown design with optimized shape and biomechanics properties.

Despite the large demand for dental restoration each year, the design of crown restorations is mainly performed via manual software operation, which is tedious and subjective. Moreover, the current design process lacks biomechanics optimization, leading to localized stress concentration and reduced working life. To tackle these challenges, we develop a fully automated algorithm for crown restoration based on deformable model fitting and biomechanical optimization. From a library of dental oral scans, a conditional shape model (CSM) is constructed to represent the inter-teeth shape correlation. By matching the CSM to the patient's oral scan, the optimal crown shape is estimated to coincide with the surrounding teeth. Next, the crown is seamlessly integrated into the finish line of preparation via a surface warping step. Finally, porous internal supporting structures of the crown are generated to avoid excessive localized stresses. This algorithm is validated on clinical oral scan data and achieved less than 2 mm mean surface distance as compared to the manual designs of experienced human operators. The mechanical simulation was conducted to prove that the internal supporting structures lead to uniform stress distribution all over the model.

Berberine attenuates cardiac dysfunction in hyperglycemic and hypercholesterolemic rats.

The positive effects of berberine (30 mg/kg/day, i.g. for 6 weeks) on cardiac dysfunction were evaluated in the rat model of hyperglycemia and hypercholesterolemia. Hyperglycemia and hypercholesterolemia were induced by feeding high-sucrose/fat diet (HSFD) consisting of 20% sucrose, 10% lard, 2.5% cholesterol, 1% bile salt for 12 weeks and streptozotocin (30 mg/kg, i.p.). The plasma sugar, total cholesterol, and triglyceride levels were significantly increased (422, 194 and 82%, respectively) in the HSFD/streptozotocin-treated rats, when compared with control animals receiving normal diet and vehicle. Berberine treatment reduced the plasma sugar and lipid levels by 24-69% in the rat model of hyperglycemia and hypercholesterolemia. Cardiac functions signed as values of cardiac output, left ventricular systolic pressure, the maximum rate of myocardial contraction (+dp/dtmax), left ventricular end diastolic pressure and the maximum rate of myocardial diastole (-dp/dtmax) were injured by 16-55% in the hyperglycemic/hypercholesterolemic rats. Berberine increased cardiac output, left ventricular systolic pressure and +dp/dtmax by 64, 16 and 79%, but decreased left ventricular end diastolic pressure and -dp/dtmax by 121 and 61% in the rats receiving HSFD/streptozotocin, respectively, when compared with the drug-untreated rats of hyperglycemia and hypercholesterolemia. Berberine caused significant increase in cardiac fatty acid transport protein-1 (159%), fatty acid transport proteins (56%), fatty acid beta-oxidase (52%), as well as glucose transporter-4 and peroxisome proliferator-activated receptor-γ (PPARγ), but decrease in PPARα mRNA and protein expression in hyperglycemic/hypercholesterolemic rats. These results indicated that berberine exerted protective effects on cardiac dysfunction induced by hyperglycemia/hypercholesterolemia through alleviating cardiac lipid accumulation and promoting glucose transport.