With the rapid development of 5th Generation Mobile Communication Technology (5G), late-model electromagnetic wave absorbing and shielding (EMAS) materials have proven to be the research emphasis of electromagnetic (EM) wave shelter. Great efforts have been made to optimize EMAS functional materials for diverse EM wavebands. [1] Each range of EM wave bands has a specific application in communication, electrical engineering, or information transmission. [2] For instance, ultrahigh frequency (UHF) EM wave of 0.3 < f < 3 GHz, also known as P/L/S or B/C/D/E band, is applied to television radar air navigation and mobile communication as well as microwave relay systems; the superhigh frequency (SHF) EM wave of 3 < f < 30 GHz, including S/C/X/Ku/K/ Ka-band or F/G/H/I/J/K band, is customarily adopted in digital telecommunication and satellite communication as well as waveguide communication. Moreover, EM waves in other frequency ranges, like terahertz wave and gamma ray, have been widely used in label-free DNA detection, high-temperature superconducting material research, radiographic testing, and even oncotherapy. In these cases, each specific application scenario requires specific EM waves in a specific frequency range, illustrating that EM wave clutters should be absorbed or otherwise shielded. Under these circumstances, developing novel and practical EMAS materials may meet the demands of EM wave science, especially in multifunctional fields.Traditional EMAS materials consist of resistance absorber, [3] dielectric absorber, [4] magnetic medium absorber, [5] and composites based on monomaterials as mentioned earlier, [6] including CuS, [7] MoSe 2 , [8] ferrites and alloys (Co x Fe 3Àx O 4 @C), [9] modified carbons (hollow carbon spheres), [10] etc. In the past decade, 2D transition metal carbides or nitrides, or MXenes, have been prefabricated and naturally applied to EMAS materials synthesis due to their outstanding EM wave loss capacity. [11] Many scholars have devoted themselves to MXene materials and structure design. The electrical conductivity of MXenes can reach 10 3 S cm À1 , leading to extraordinary EM wave shielding property. [12] Many reported MXene absorbers are monolayers, [13] whereas macrostructure design is introduced. Thus, macrodevices, like hollow MXene sphere foam, [14] are synthesized. It is

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Pulpotomy is the typical treatment for keeping deciduous teeth until exfoliation. Formocresol is one of the most common materials used in dental pulpotomy. Due to the side effects of this drug, its replacement with other substances seems necessary. Therefore, this study compared clinical and histopathological evaluations of primary pulpotomy molars with formocresol and biodentine. In this clinical trial, 66 second-mandibular deciduous molars of children aged 6 to 9 years who met the criteria for pulpotomy were selected. Pulpotomy of the teeth was performed using formocresol and biodentine.For each patient, one tooth was randomly placed in the pulpotomy group with formocresol. The other tooth was placed in the pulpotomy group with biodentine. Then the crowns of the teeth were restored with stainless steel veneer. We recorded clinical and radiographic results of these teeth over six months and one year. The teeth were then extracted after 12 months, and hematoxylin-eosin staining was performed for histopathological evaluations. The obtained data were analyzed by Fisher test and SPSS software version 22. The results showed that clinical success of 6 and 12 months of pulpotomy in both groups was 100%. The 6-month radiographic evaluation of the formocresol group was 84.8%, and the biodentine group was 93.9% (p = 0.21). The success of 12-month radiographs of the formocresol group and the biodentine group were 81.8 and 93.9, respectively (p = 0.13). Also, the histopathological evaluation showed that in the biodentine group, there was mild inflammation in two teeth, two teeth showed moderate inflammation, and two teeth showed severe inflammation. In the formocresol group, severe inflammation was seen in two cases. Mild inflammation was not seen in any of the teeth. Moderate inflammation was seen in one tooth. It was found that there was no significant difference between the two groups in terms of inflammation (P >0.05). No necrosis was seen in any of the biodentine group teeth, and there was necrosis in four teeth of the formocresol group. There was a significant difference between the two groups regarding necrosis (P = 0.032). There was no significant difference between the two groups regarding abscess (P> 0.05). According to the obtained results, biodentine could be a suitable alternative for mandibular second molar pulpotomy.

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This study aimed to explore PINK1/Parkin's role in methanol metabolite formic acid‐induced autophagy in PC12 cells and provide a theoretical basis for elucidating methanol‐induced neurotoxicity. After treatment with different formic acid concentrations, we observed the morphology and mitochondria of PC12 cells. We used an ultra‐micro enzyme kit to detect the mitochondrial Na+‐K+‐ATPase and Ca2+‐Mg2+‐ATPase activities; a JC‐1 kit to detect changes in the mitochondrial membrane potential (MMP); MDC staining to detect the autophagy levels; and western blotting to measure the expression levels of the mitochondrial marker protein COX IV and the autophagy‐related proteins Beclin1, P62 and LC3II/LC3I, and the mitochondrial and cytoplasmic levels of PINK1, Parkin and P‐Parkin. Compared with the control group, the mitochondrial diameters, the mitochondrial Na+‐K+‐ATP and Ca2+‐Mg2+‐ATPase activities, the MMP, and the COX IV expression levels decreased significantly (P < 0.05). The fluorescence signal intensity (indicating autophagy); relative Beclin1 and LC3II/LC3I protein expression levels; and relative mitochondrial PINK1, Parkin and P‐Parkin levels increased significantly, and the relative P62 protein expression levels and relative cytoplasmic PINK1, Parkin and P‐Parkin levels decreased significantly (P < 0.05) compared with the control group. Thus, formic acid alters mitochondrial morphology, causes mitochondrial dysfunction, affects the PINK/Parkin pathway and, thus, activates the process of mitochondrial autophagy.