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Laser has been demonstrated to be a mature and versatile tool that presents great flexibility and applicability for the precision engineering of a wide range of materials over other established micromachining techniques. Past decades have witnessed its rapid development and extensive applications ranging from scientific researches to industrial manufacturing. Transparent hard materials remain several major technical challenges for conventional laser processing techniques due to their high hardness, great brittleness, and low optical absorption. A variety of hybrid laser processing technologies, such as laser-induced plasma-assisted ablation, laser-induced backside wet etching, and etching assisted laser micromachining, have been developed to overcome these barriers by introducing additional medium assistance or combining different process steps. This article reviews the basic principles and characteristics of these hybrid technologies. How these technologies are used to precisely process transparent hard materials and their recent advancements are introduced. These hybrid technologies show remarkable benefits in terms of efficiency, accuracy, and quality for the fabrication of microstructures and functional devices on the surface of or inside the transparent hard substrates, thus enabling widespread applications in the fields of microelectronics, bio-medicine, photonics, and microfluidics. A summary and outlook of the hybrid laser technologies are also highlighted.Schematic of the dynamic process of the laser-induced plasma assisted ablation. The process consists of laser heating, plasma generation, absorption enhancement and material removal.

The gene expression profile of abdominal aortic aneurysm (AAA) neck is not fully understood. The etiology of AAA is considered to be related to atherosclerosis and the inflammatory response, involving congenital, genetic, metabolic, and other factors. The level of proprotein convertase subtilisin/kexin type 9 (PCSK9) is related to those of cholesterol, oxidized low-density lipoprotein, and triglycerides. PCSK9 inhibitors have significant effects on lowering LDL-cholesterol, reversing atherosclerotic plaques, and reducing the risk of cardiovascular events and have been approved by several lipid-lowering guidelines. This work was aimed to investigate the potential role of PCSK9 in the neck of AAA. We extracted the expression dataset (GSE47472) containing 14 AAA patients and 8 donors and single-cell RNAseq (scRNA-seq) data (GSE164678) of CaCl 2 -induced (AAA) samples from the Gene Expression Omnibus dataset. Through bioinformatics methods, we found that PCSK9 was up-regulated in the proximal neck of human AAA. In AAA, PCSK9 was mainly expressed in fibroblasts. Additionally, immune check-point PDCD1LG2 was also expressed higher in AAA neck than donor, while CTLA4, PDCD1, and SIGLEC15 were down-regulated in AAA neck. The expression of PCSK was correlated with PDCD1LG2, LAG3, and CTLA4 in AAA neck. Additionally, some ferroptosis-related genes were also down-regulated in AAA neck. PCSK9 was also correlated with ferroptosis-related genes in AAA neck. In conclusion, PCSK9 was highly expressed in AAA neck, and may exert its role through interacting with immune check-points and ferroptosis-related genes.

Tungsten's ultrahigh melting point and thermal stress‐induced cracking pose significant challenges for additive manufacturing. To address this, we propose a novel strategy combining low‐temperature spray drying with optimized heat treatment to fabricate spherical tungsten (W) powders with high sphericity (≥ 95%), narrow particle size distribution (10–50 μm), and excellent flowability (28 s/50 g). Compared to conventional plasma‐spheroidized powders, our method reduces production costs and enables selective laser melting (SLM) at remarkably low energy densities (200–600 J/mm3), far below the typical range of 500–1500 J/mm3. Mechanistic analysis reveals that the tailored powder structure suppresses thermal shrinkage cracks by lowering the critical ratio of laser energy density to scanning speed (E/v ≤ 2). At E/v = 1.7 (170 W, 300 mm/s, 0.08 mm spacing), the printed components achieve a relative density of 94.1% (vs. 96% for high‐energy SLM) and microhardness of 488 kg/mm2, surpassing commercial cast tungsten (423 kg/mm2). Notably, nanoindentation tests demonstrate exceptional plasticity (indentation work: 0.204 kN·m/m2), comparable to single‐crystal tungsten. This work not only establishes a low‐cost pathway for refractory metal additive manufacturing but also provides a universal parameter framework (E/v threshold) to mitigate defects in high‐melting‐point alloys and improves the issues of element evaporation and combustion in additive manufacturing of refractory alloys. This study combines low‐temperature spray drying with low‐energy SLM technology to produce high‐sphericity tungsten powder, enabling low‐energy consumption printing. It proposes the E/v ≤ 2 parameter framework to suppress cracks, with the components exhibiting excellent performance, providing a universal solution for additive manufacturing of high‐melting‐point alloys.

We explored Q-switching mechanism for the newly proposed Tm/Ho composite laser via developing a hybrid resonator for separating the intra-cavity Tm laser modulated by the saturable absorber (SA). With a Cr:ZnSe SA, successful passively Q-Switching process with the maximum average output power of 474 mW and the shortest pulse width of 145 ns were obtained at the pulse repetition frequency of 7.14 kHz, where dual wavelength oscillation in both 2090 nm and 2097 nm was observed. This work provides an effective way for a direct laser diode (LD) pumped Q-switched Ho laser, which is compact and accessible. Furthermore, the current SA could be replaced by the 2D materials with broadband saturable absorption such as topological insulators or transition-metal dichalcogenides for seeking novel PQS lasers.

We present a high-brightness, nanosecond pulsed blue laser source at 476.8 nm through efficient quadruple-harmonic generation from a thulium-doped yttrium lithium fluoride (Tm:YLF) master oscillator power amplifier operating at 1.9 μm. The fundamental-frequency stage produces 42 mJ pulses at 1907.3 nm with a narrow linewidth of 0.19 nm at 1 kHz. Through cascade second-harmonic generation using low-walk-off lithium triborate crystals, we achieve 10.52 mJ blue laser pulses with 16.1 ns duration, corresponding to a peak power of 0.65 MW and exhibiting excellent energy stability of 0.47%. The system maintains exceptional beam quality (M 2 x = 1.46, M 2 y = 1.27) at maximum output power, attributed to the negative thermal-optical properties of the Tm:YLF crystal, end-pumped amplification architecture and optimized nonlinear conversion. This work demonstrates a compact and efficient route to high-brightness (~2.49 GW·cm–2·sr–1) pulsed blue laser emission, which is particularly suitable for advanced marine scientific applications including underwater LiDAR and communication systems.

Apoptosis of pulmonary microvascular endothelial cells (PMVECs) was considered to be closely related to the pathogenesis of acute lung injury (ALI). We aim to investigate whether IL-22 plays protective roles in lung injury through inhibiting the apoptosis of PMVECs. ALI model was induced through subcutaneous infusion of angiotensin II (Ang II). Lung injury and infiltration of inflammatory cells were evaluated by determining the PaO 2 /FiO 2 , calculation of dry to weight ratio in lung, and immunohistochemisty analysis. Apoptosis of PMVECs was determined using TUNEL assay and flow cytometry, respectively. Immunofluorescence and Western blot analysis were used to determine the expression and localization of STAT3, as well as the nucleus transmission of STAT3 from cytoplasm after IL22 treatment. Pathological findings showed ALI was induced 1 week after AngII infusion. IL22 inhibited the AngII-induced ALI, attenuated the edema in lung and the infiltration of inflammatory cells. Also, it contributed to the apoptosis of PMVECs induced by AngII. Meanwhile, significant increase was noticed in the expression of STAT3, phosphorylation of Y705-STAT3, and migration from cytoplasm to the nucleus after IL-22 treatment (P < 0.05). The activation of STAT3 by IL22 showed significant attenuation after AG490 treatment. Our data indicated that IL22 showed protective effects on lung injury through inhibiting the AngII-induced PMVECs apoptosis and PMVEC barrier injury by activating the JAK2/STAT3 signaling pathway.

Numerous studies have demonstrated promising application of single-walled carbon nanotubes (SWNTs) in drug delivery, diagnosis, and targeted therapy. However, the adverse health effects resulting from intravenous injection of SWNTs are not completely understood. Studies have shown that levels of \"pristine\" or carboxylated carbon nanotubes are very high in mouse lungs after intravenous injection. We hypothesized that long-term and repeated intravenous administration of carboxylated SWNTs (c-SWNTs) can result in persistent accumulation and induce histopathologic changes in rat lungs. Here, c-SWNTs were administered repeatedly to rats via tail-vein injection for 90 days. Long-term intravenous injection of c-SWNTs caused sustained embolization in lung capillaries and granuloma formation. It also induced a persistent inflammatory response that was regulated by the nuclear factor-kappa B signaling pathway, and which resulted in pulmonary fibrogenesis. c-SWNTs trapped within lung capillaries traversed capillary walls and injured alveolar epithelial cells, thereby stimulating production of pro-inflammatory cytokines (tumor necrosis factor-alpha and interleukin-1 beta) and pro-fibrotic growth factors (transforming growth factor-beta 1). Protein levels of type-I and type-III collagens, matrix metalloproteinase-2, and the tissue inhibitor of metalloproteinase-2 were upregulated after intravenous exposure to c-SWNTs as determined by immunohistochemical assays and Western blotting, which suggested collagen deposition and remodeling of the extracellular matrix. These data suggest that chronic and cumulative toxicity of nanomaterials to organs with abundant capillaries should be assessed if such nanomaterials are applied via intravenous administration.

Angiotensin II (AngII) caused pulmonary microvascular endothelial barrier injury, which induced acute aortic dissection (AAD) combined with acute lung injury (ALI). However, the exact mechanism is unclear. We investigated the role of dephosphorylation of Y685-VE-cadherin in the AngII induced pulmonary microvascular endothelial barrier injury. Mice or pulmonary microvascular endothelial cells (PMVECs) were divided into control group, AngII group, AngII+PP2 (Src kinase inhibitor) group, and PP2 group. PP2 was used to inhibit the phosphorylation of Y685-VE-cadherin. Pathological changes, infiltration of macrophages and neutrophils, and pulmonary microvascular permeability were used to determine the pulmonary microvascular endothelial barrier function. Flow cytometry was used to determine the apoptosis of PMVECs, and immunofluorescence was used to determine the skeletal arrangement. Transendothelial resistance was used to detect the permeability of endothelial barrier. Phosphorylation of Y685-VE-cadherin was significantly reduced after AngII stimulation (P<0.05), together with skeletal rearrangement, and elevation of endothelial permeability which finally induced endothelial barrier injury. After PP2 interference, the phosphorylation of Y685-VE-cadherin was further reduced and the endothelial permeability was further elevated. These data indicated that AngII could induce pulmonary injury by triggering endothelial barrier injury, and such process may be related to the dephosphorylation of Y685-VE-cadherin and the endothelial skeletal rearrangement.

Complexes of copper (II) with hesperetin, naringenin, and apigenin of general composition [CuL2(H2O)2]⋅nH2O (1–3) have been synthesized and characterized by elemental analysis, UV-Vis, FT-IR, ESI-MS, and TG-DTG thermal analysis. The free ligands and the metal complexes have been tested in vitro against human cancer cell lines hepatocellular carcinoma (HepG-2), gastric carcinomas (SGC-7901), and cervical carcinoma (HeLa). Complexes 1 and 3 were found to exhibit growth inhibition of SGC-7901 and HepG2 cell lines with respect to the free ligands; the inhibitory rate of complex 1 is 43.2% and 43.8%, while complex 3 is 46% and 36%, respectively. The interactions of complex 1 and its ligand Hsp with calf thymus DNA were investigated by UV-Vis, fluorescence, and CD spectra. Both complex 1 and Hsp were found to bind DNA in intercalation modes, and the binding affinity of complex 1 was stronger than that of free ligand.

263-277.Page 266. In the right column the data range \"6 to 15 nm\" should be \"5 to 15 nm\".Page 267. In Figure 1 Notes \"wt%\" should be \"wt‰ in SWNTs powder\".Page 268. In Figure 2 Notes \"1 mL per rat\" should be \"1 mL/kg body weight\".Read the original article.