Impact of Genetics on Neoadjuvant Therapy with Complete Pathological Response in Metastatic Colorectal Cancer: Case Report and Review of the Literature.

Treatment of colorectal metastatic cancer is still challenging, despite recent improvements in chemotherapy. A genetic cancer profile, such as the KRAS (Kirsten rat sarcoma) gene status, plays a key role in individualized tailored therapy. Molecular targeted therapy added to neo-adjuvant chemotherapy can achieve a better pathological response and prolong survival. Pathological complete response of colorectal cancer stage IV is rare. A 47-year-old female patient presented with rectal adenocarcinoma and three liver metastases (cT3d/4, N2, Ml). After seven cycles of Bevacizumab and CAPOX in neoadjuvant setting, we noted more than 70.0% regression of metastases and complete regression of the primary tumor. We performed low anterior resection of rectum and synchronous subsegmental resection of S3, because the other two lesions were not detectable. Pathology revealed complete response of the primary and also secondary tumors. After 8 months, diagnostic tests did not show any sign of recurrence and the remaining liver lesions disappeared. Colorectal cancer is a heterogeneous disease and it is necessary to identify patients who are at-risk of recurrence and suitable for neoadjuvant therapy. Genetic biomarkers play an important role in metastatic colorectal cancer treatment. Because of the mutated KRAS gene, Bevacizumab was added to cytotoxic therapy achieving a complete pathological response of primary tumor and metastasis. This case is unique because all reported cases with similar results, described staged surgery and one of reverse staged surgery, but with similar results. This neoadjuvant therapy has extraordinary results for colorectal cancer stage IV and can help disease-free and long-term survival.

Tailoring electronic and optical properties of hBN/InTe and hBN/GaTe heterostructures through biaxial strain engineering.

In this research study, we systematically investigate the electronic and optical properties of van der Waals heterostructures (HSs) consisting of InTe (GaTe) and hBN monolayers, subjected to controlled biaxial strain. Our analysis demonstrates that the application of strain induces noteworthy alterations in the electronic band structure, enabling precise manipulation of the band gap and augmentation of the absorption properties of these structures. Employing density functional theory, we conduct a comprehensive examination of the influence of strain on the electronic and optical characteristics of these HSs. Our investigation showcases the remarkable potential of strain engineering in rendering these heterostructures into efficient and robust wide-range absorbers, particularly optimised for the visible spectrum, underscoring their relevance in various photonic and optoelectronic applications, paving the way for integration into advanced nanodevices.

Novel wide spectrum light absorber heterostructures based on hBN/In(Ga)Te.

Two-dimensional group III monochalcogenides have recently attracted quite attention for their wide spectrum of optical and electric properties, being promising candidates for optoelectronic and novel electrical applications. However, in their pristine form they are extremely sensitive and vulnerable to oxygen in air and need good mechanical protection and passivization. In this work we modeled and studied two newly designed van der Waals (vdW) heterostructures based on layer of hexagonal boron nitride (hBN) and GaTe or InTe monolayer. Using density functional theory, we investigate electronic and optical properties of those structures. Their moderate band gap and excellent absorption coefficient makes them ideal candidate for broad spectrum absorbers, covering all from part of IR to far UV spectrum, with particularly good absorption of UV light. The hBN layer, which can be beneficial for protection of sensitive GaTe and InTe, does not only preserve their optical properties but also enhances it by changing the band gap width and enhancing absorption in low-energy part of spectrum. Calculated binding energies prove that all three stacking types are possible to obtain experimentally, with H-top as the preferable stacking position. Moreover, it is shown that type of stacking does not affect any relevant properties and bandstructure does not reveal any significant change for each stacking type.

Plasmon resonance-based optical trapping of single and multiple Au nanoparticles.

The plasmon resonance-based optical trapping (PREBOT) method is used to achieve stable trapping of metallic nanoparticles of different shapes and composition, including Au bipyramids and Au/Ag core/shell nanorods. In all cases the longitudinal plasmon mode of these anisotropic particles is used to enhance the gradient force of an optical trap, thereby increasing the strength of the trap potential. Specifically, the trapping laser is slightly detuned to the long-wavelength side of the longitudinal plasmon resonance where the sign of the real component of the polarizability leads to an attractive gradient force. A second (femtosecond pulsed) laser is used to excite two-photon fluorescence for detection of the trapped nanoparticles. Two-photon fluorescence time trajectories are recorded for up to 20 minutes for single and multiple particles in the trap. In the latter case, a stepwise increase reflects sequential loading of single Au bipyramids. The nonlinearity of the amplitude and noise with step number are interpreted as arising from interactions or enhanced local fields amongst the trapped particles and fluctuations in the arrangements thereof.

Dynamic ventilation 3He MRI for the quantification of disease in the rat lung.

Pulmonary diseases are known to be largely inhomogeneous. To evaluate such inhomogeneities, we are testing an image-based method to measure gas flow in the lung regionally. Dynamic, spin-density-weighted hyperpolarized (3)He MR images performed during slow inhalation of this gas were analyzed to quantify regional inflation rate. This parameter was measured in regions of interest (ROIs) that were defined by a rectangular grid that covered the entire rat lung and grew dynamically with it during its inflation. We used regional inflation rate to quantify elastase-induced emphysema and to differentiate healthy (n = 8) from elastase-treated (n = 9) rat lungs as well as healthy from elastase-treated areas of one rat unilaterally treated with elastase in the left lung. Emphysema was also assessed by gold standard morphological and well-established hyperpolarized (3)He MRI diffusion measurements. Mean values of regional inflation rates were significantly different for healthy and elastase-treated animals and correlated well with the apparent diffusion coefficient of (3)He and morphological measurements. The image-based biomarker inflation rate may be useful for the assessment of regional lung ventilation.

Brain injury activates microglia that induce neural stem cell proliferation ex vivo and promote differentiation of neurosphere-derived cells into neurons and oligodendrocytes.

Brain damage, such as ischemic stroke, enhances proliferation of neural stem/progenitor cells (NSPCs) in the subventricular zone (SVZ). To date, no reliable in vitro systems, which can be used to unravel the potential mechanisms underlying this lesion-induced effect, have been established. Here, we developed an ex vivo method to investigate how the proliferation of NSPCs changes over time after experimental stroke or excitotoxic striatal lesion in the adult rat brain by studying the effects of microglial cells derived from an injured brain on NSPCs. We isolated NSPCs from the SVZ of brains with lesions and analyzed their growth and differentiation when cultured as neurospheres. We found that NSPCs isolated from the brains 1-2 weeks following injury consistently generated more and larger neurospheres than those harvested from naive brains. We attributed these effects to the presence of microglial cells in NSPC cultures that originated from injured brains. We suggest that the effects are due to released factors because we observed increased proliferation of NSPCs isolated from non-injured brains when they were exposed to conditioned medium from cultures containing microglial cells derived from injured brains. Furthermore, we found that NSPCs derived from injured brains were more likely to differentiate into neurons and oligodendrocytes than astrocytes. Our ex vivo system reliably mimics what is observed in vivo following brain injury. It constitutes a powerful tool that could be used to identify factors that promote NSPC proliferation and differentiation in response to injury-induced activation of microglial cells, by using tools such as proteomics and gene array technology.