3D Scene Creation and Rendering Via Rough Meshes: A Lighting Transfer Avenue.

This paper studies how to flexibly integrate reconstructed 3D models into practical 3D modeling pipelines such as 3D scene creation and rendering. Due to the technical difficulty, one can only obtain rough 3D models (R3DMs) for most real objects using existing 3D reconstruction techniques. As a result, physically-based rendering (PBR) would render low-quality images or videos for scenes that are constructed by R3DMs. One promising solution would be representing real-world objects as Neural Fields such as NeRFs, which are able to generate photo-realistic renderings of an object under desired viewpoints. However, a drawback is that the synthesized views through Neural Fields Rendering (NFR) cannot reflect the simulated lighting details on R3DMs in PBR pipelines, especially when object interactions in the 3D scene creation cause local shadows. To solve this dilemma, we propose a lighting transfer network (LighTNet) to bridge NFR and PBR, such that they can benefit from each other. LighTNet reasons about a simplified image composition model, remedies the uneven surface issue caused by R3DMs, and is empowered by several perceptual-motivated constraints and a new Lab angle loss which enhances the contrast between lighting strength and colors. Comparisons demonstrate that LighTNet is superior in synthesizing impressive lighting, and is promising in pushing NFR further in practical 3D modeling workflows.

Interactive NeRF Geometry Editing With Shape Priors.

Neural Radiance Fields (NeRFs) have shown great potential for tasks like novel view synthesis of static 3D scenes. Since NeRFs are trained on a large number of input images, it is not trivial to change their content afterwards. Previous methods to modify NeRFs provide some control but they do not support direct shape deformation which is common for geometry representations like triangle meshes. In this paper, we present a NeRF geometry editing method that first extracts a triangle mesh representation of the geometry inside a NeRF. This mesh can be modified by any 3D modeling tool (we use ARAP mesh deformation). The mesh deformation is then extended into a volume deformation around the shape which establishes a mapping between ray queries to the deformed NeRF and the corresponding queries to the original NeRF. The basic shape editing mechanism is extended towards more powerful and more meaningful editing handles by generating box abstractions of the NeRF shapes which provide an intuitive interface to the user. By additionally assigning semantic labels, we can even identify and combine parts from different objects. We demonstrate the performance and quality of our method in a number of experiments on synthetic data as well as real captured scenes.

Clinical features of 18 perivascular epithelioid cell tumor cases.

To investigate the biological behavior and clinical characteristics of perivascular epithelioid cell tumor (PEComa).Eighteen PEComa patients admitted to Zhongshan Hospital and the Central Hospital of Xuhui District in China from January 2006 to October 2018 were included. All patients were diagnosed based on pathological findings and treated with surgical resection or medication.Among the 18 patients, 1 underwent lymph node biopsy for multiple enlarged lymph nodes and 17 underwent mass resection. The median disease-free survival was 22 months after the first resection and over 12 months following a second resection. Treatment with mechanistic target of rapamycin (mTOR) inhibitors was effective for patients with unresectable or metastatic lesions. The median progression-free survival was approximately 13 months.Surgery is the predominant treatment approach for PEComa and patients can benefit from multiple operations. mTOR inhibitors are considered for patients with multiple lesions or intolerance to surgery. Anti-angiogenetic drugs can be selected when mTOR inhibitors fail to control the illness.

The Levels of Tumor Markers in Pancreatic Neuroendocrine Carcinoma and Their Values in Differentiation Between Pancreatic Neuroendocrine Carcinoma and Pancreatic Ductal Adenocarcinoma.

OBJECTIVES: The levels of tumor markers in pancreatic neuroendocrine carcinoma (PNEC) are unknown, and imaging findings of PNEC and pancreatic ductal adenocarcinoma (PDAC) have overlaps. In this study, we show the tumor markers in PNEC and evaluate their values for distinguishing PNEC from PDAC. METHODS: Thirty-three cases of PDAC and 21 cases of PNEC were retrospectively evaluated. The demographic information and clinical data were reviewed. RESULTS: Pancreatic neuroendocrine carcinoma was usually misdiagnosed (57.1%) as PDAC based on imaging findings. Abnormal carbohydrate antigen (CA) 19-9, carcinoembryonic antigen (CEA), and α-fetoprotein (AFP) were observed in 19.0% to 28.6% of PNECs. Abnormal CA 19-9 and CA 125 levels were more common in PDAC than in PNEC (P < 0.05). Higher level of AFP was more common in PNEC than in PDAC (33.3% vs 3.0%, P < 0.05). The cutoff value of CA 19-9 for detecting PNEC was calculated as 38.5 U/mL or less with 0.788 sensitivity and 0.800 specificity. Carbohydrate antigen 19-9 (odds ratio [OR], 22.9; 95% confidence interval [CI], 2.94-179.3), AFP (OR, 0.08; 95% CI, 0.012-0.564), and CA 125 (OR, 17.4; 95% CI, 1.13-267.3) were predictors in differentiating PDAC from PNEC. CONCLUSIONS: Carbohydrate antigen 19-9, AFP, and CA 125 have potential for distinguishing hypovascularized PNEC from PDAC.

Treatment of grey zone lymphoma using the R-CODOX-M/R-IVAC protocol: Two case reports.

RATIONALE: We report our experience with 2 patients diagnosed with grey zone lymphoma (GZL). The histopathological characteristics of lymphomatous tissues in these patients ranged between those of diffuse large B-cell lymphoma (DLBCL) and the classical Hodgkin lymphoma. PATIENT CONCERNS: A 52-year-old female presented to the hospital with a history of lower abdominal pain of metastatic origin for 2 days. She was diagnosed with acute appendicitis and had undergone emergency surgery. A 17-year-old male was admitted to the hospital because of acute left upper abdomen pain. DIAGNOSES: Both patients are diagnosed of GZL primarily based on histopathology. INTERVENTIONS: Both patients were treated with R-CODOX-M/R-IVAC regimen for 4 to 6 cycles. OUTCOMES: The short-term curative effect was complete response; no recurrence was observed as of 32-month follow-up. LESSONS: R-CODOX-M/IVAC regimen exhibited relatively good curative effect. International Prognostic Index score and lactate dehydrogenase level may correlate with prognosis of these patients.

Targeting Cellular Metabolism Chemosensitizes the Doxorubicin-Resistant Human Breast Adenocarcinoma Cells.

Metabolic energy preferentially produced by glycolysis was an advantageous metabolic phenotype of cancer cells. It is also an essential contributor to the progression of multidrug resistance in cancer cells. By developing human breast cancer MCF-7 cells resistant to doxorubicin (DOX) (MCF-7/MDR cells), the effects and mechanisms of 2-deoxy-D-glucose (2DG), a glucose analogue, on reversing multidrug resistance were investigated. 2DG significantly inhibited the viability of MCF-7/MDR cells and enhanced DOX-induced apoptosis by upregulating protein expression of AMPKα, P53, and caspase-3. The study demonstrated that energy restriction induced by 2DG was relevant to the synergistic effect of 2DG and DOX. The proteins of multidrug gene (the MDR-related protein, MRP1) and P-glycoprotein (P-gp) in MCF-7/MDR cells were downregulated after exposure to 2DG, accompanied with the suppression of the activity of ATP-dependent drug-efflux pump and transmembrane transporter, increasing the intracellular accumulation of DOX to reverse the chemoresistance in multidrug cancer cells.

Comparison of cellular damage response to low-dose-rate 125I seed irradiation and high-dose-rate gamma irradiation in human lung cancer cells.

PURPOSE: To investigate the difference of cellular response between low-dose-rate (LDR) 125I seed irradiation and high-dose-rate (HDR) γ-irradiation in human lung cancer cells. METHODS AND MATERIALS: A549 and NCI-H446 cells with or without wortmannin (WM) treatment were exposed to 125I seeds and γ-rays, respectively. Cell survival, micronuclei (MN) formation, and the expressions of Ku70/Ku80 proteins were measured. RESULTS: There was a strong negative correlation between survival and MN formation for both irradiations, and the MN inductions of NCI-H446 were about twofolds of those of A549, and the survival of NCI-H446 was lower than that of A549, indicating the radiosensitivity of NCI-H446 cells was greater than that of A549 cells. Interestingly, at 4-Gy radiation, NCI-H446 cells were more sensitive to LDR irradiation than HDR irradiation. WM treatment enhanced the radiosensitivity of A549 cells evenly to (125I seed and γ-irradiation, but this treatment led NCI-H446 cells to be more sensitive to LDR 125I. Further results revealed that the expression of phosphorylated Ku80 protein was enhanced in irradiated A549, but in contrast, it was markedly decreased in NCI-H446 cells after 4-Gy LDR 125I irradiation as that compared with γ-irradiated and nonirradiated cells. CONCLUSION: NCI-H446 cells were more sensitive to LDR 125I irradiation than HDR irradiation, and this sensitivity could be further enhanced by WM treatment. But no obvious differences of cellular response to both irradiations were observed in A549. Ku as molecular markers together with cell proliferation rate can be used to predict the radiosensitivity of tumor cells to LDR 125I seed irradiation.

The role of nucleophosmin/B23 in radiation-induced chromosomal instability in human lymphoblastoid cells of different p53 genotypes.

PURPOSE: To investigate the role of nucleophosmin (NPM/B23) in radiation-induced chromosomal instability and apoptosis in human lymphoblastoid cells with different protein 53 (p53) status. MATERIALS AND METHODS: Wild type (wt) p53 TK6 and mutant type (mt) p53 WTK1 with or without short hairpin RNA (shRNA)-mediated silencing of NPM, TK6 with or without short interfering RNA (siRNA)-mediated silencing of p53 (p53i and NEGi) were irradiated with 4 Gy gamma-rays. Six to 48 h after irradiation, the index of apoptosis, chromosome aberration, cell cycle distribution and the levels of total NPM and phosphorylated-threonine 199 (pThr¹99) NPM proteins were measured. Cells in some dishes were treated with 10 µM Olomoucine (OLO) for 3 h before irradiation and remained in the medium after irradiation. RESULTS: The rates of radiation-induced apoptosis in TK6 and TK6/NEGi were about 2-fold of those in WTK1 and TK6/p53i, while the frequencies of polyploidy in TK6 and TK6/NEGi were obviously lower than those in WTK1 and TK6/p53i. Moreover, after irradiation, pThr¹99 NPM levels increased significantly in WTK1 and TK6/p53i, and slightly increased in TK6 and TK6/NEGi, indicating that the increased level of pThr¹99 NPM was related to p53 status. When Thr¹99 hyperphosphorylation of NPM was inhibited by OLO or when NPM was knocked down, we found that radiation-induced apoptosis was more pronounced and polyploidy formation was reduced as compared with negative control while the magnitude of these changes in TK6 was obviously higher than that in WTK1, indicating that NPM has an antagonistic interaction with wt p53. CONCLUSIONS: NPM/B23 plays an important role in protecting cells from radiation-induced apoptosis and increasing polyploidy formation via either a p53 or non-p53 pathway.