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In response to the problems of small pressure monitoring range, low sensitivity, and high cost of existing fiber optic pressure sensors, an improved fiber optic pressure sensor is designed. A strain fiber optic grating is stuck on the cantilever beam and a temperature fiber optic grating is suspended (to make it stress free). The limit cover below the cantilever beam places the spring, corrugated pipe pressure cover, and corrugated pipe cover inside it. The inner upper plane of the limit cover contacts the upper plane of the spring, and the lower plane of the spring contacts the corrugated pipe pressure cover. When external pressure reaches the corrugated pipe through the pipeline at the bottom of the corrugated pipe, the high pressure causes it to undergo axial deformation. The deformation in turn compresses the spring. Finally, the spring undergoes deformation and transmits force to the cantilever beam, changing the stress situation of the strain grating. A spring with a larger stiffness coefficient is added to the single-layer corrugated pipe to limit its deformation when external pressure is generated, allowing the corrugated pipe and spring to jointly transmit pressure to the cantilever beam. The experimental test results show that the improved sensor has a pressure monitoring range of 0-5 MPa, which is 5 times higher than before. The sensitivity of the sensor is 0.379 98 nm/MPa, and the measurement error is within 0.02 MPa. The improved pressure sensor is validated in a water pipeline underground. The results show that compared with the measurement results of high-precision electronic pressure gauges, the pressure demodulation error of the sensor is within 0.02 MPa.

Background: Osteoporosis has influenced millions of people, especially postmenopausal women, which has become a big burden to the whole world. Although the diverse roles of casticin (CAS) on different diseases were identified, whether it was implicated with osteoporosis was unknown. Methods: A rat model of osteoporosis was established through dexamethasone (DEX) treatment and a cell model reflecting the osteogenic and osteoclast induction was constructed in bone marrow stromal cells (BMSCs). The calcification at the late stage of induction was measured via Alizarin Red S staining. Western blot was applied to evaluate the levels of proteins. Results: Hematoxylin and eosin staining revealed that the number of bone trabecular in DEX‐induced osteoporosis rats was decreased, while increased doses of CAS treatment elevated the number of bone trabecular. CAS treatment alleviated DEX‐induced osteoporosis in rats. Moreover, we found that CAS inhibited the nuclear factor‐κB/mitogen‐activated protein kinase (NF‐κB/MAPK) pathway. In addition, CAS promoted osteogenic differentiation of BMSCs and reduced osteoclastogenesis of bone marrow monocytes. Finally, CAS was observed to retard the receptor activator of NFκ‐B ligand‐induced NF‐κB/MAPK pathway. Conclusion: CAS promoted osteogenic differentiation of BMSCs and improved osteoporosis in rats by regulating the NF‐κB/MAPK pathway. This might shed a light into using CAS as a drug treating osteoporosis in the future. [ABSTRACT FROM AUTHOR]

The induction of pluripotent stem cells (iPSCs) by defined factors is poorly understood stepwise. Here, we show that histone H3 lysine 9 (H3K9) methylation is the primary epigenetic determinant for the intermediate pre-iPSC state, and its removal leads to fully reprogrammed iPSCs. We generated a panel of stable pre-iPSCs that exhibit pluripotent properties but do not activate the core pluripotency network, although they remain sensitive to vitamin C for conversion into iPSCs. Bone morphogenetic proteins (BMPs) were subsequently identified in serum as critical signaling molecules in arresting reprogramming at the pre-iPSC state. Mechanistically, we identified H3K9 methyltransferases as downstream targets of BMPs and showed that they function with their corresponding demethylases as the on/off switch for the pre-iPSC fate by regulating H3K9 methylation status at the core pluripotency loci. Our results not only establish pre-iPSCs as an epigenetically stable signpost along the reprogramming road map, but they also provide mechanistic insights into the epigenetic reprogramming of cell fate. [ABSTRACT FROM AUTHOR]

Type 2 diabetes mellitus (T2DM) is a metabolic disease accompanied by a series of diseases such as diabetic nephropathy. The drug pair (HS) of Astragalus Radix (HQ) and Dioscoreae Rhizoma (SY) was designed by Dr. Shi Jinmo to improve the treatment of T2DM. However, the exact mechanism involved requires further clarification. In this work, 1H-NMR–based metabonomics and network pharmacology were adopted. Metabolic profiling indicated that the metabolic perturbation was reduced after HS treatment. The results found 21 biomarkers. According to the network pharmacology, we found that the regulation of T2DM was primarily associated with 18 active compounds in HS. These active compounds mainly had an effect on 135 targets. Subsequently, combining network pharmacology and metabonomics, we found four target proteins, which indicated that HS has potential hypoglycemic effects through regulating monoamine oxidases B (MAOB), acetyl-CoA carboxylase 1 (ACACA), carbonic anhydrase 2 (CA2), and catalase (CAT). In conclusion, the result showed that these four targets might be the most relevant targets for the treatment of T2DM with HS. This study clarified the mechanism of HS in the treatment of T2DM and also confirmed the feasibility of combining metabonomics and network pharmacology to study the mechanisms of traditional Chinese medicine (TCM). In the future, this approach may be a potentially powerful tool to discovery active components of traditional Chinese medicines and elucidate their mechanisms. [ABSTRACT FROM AUTHOR]

Abstract: In the present work, poly(methyl methacrylate) (PMMA)/organically modified montmorillonite (O-MMT) composite microfibers were firstly prepared by emulsion polymerization combined with electrospinning, and then coated by nanosize titanium dioxide (TiO2) using RF magnetron sputter technique. The modified surfaces of PMMA/O-MMT composite microfibers were characterized by Fourier transform infrared spectroscopy (FTIR), scanning electron microscope (SEM), transmission electron microscope (TEM), X-ray diffraction (XRD), UV–vis spectroscopy and drop shape analyzer. Finally, the photocatalytic properties of TiO2 coated PMMA/O-MMT composite microfiber membranes were evaluated by degradation of methylene blue(MB) under UV illumination. The experimental results revealed that anatase-TiO2 and rutile-TiO2 nanoparticles were well spread and physically deposited on the surface of PMMA/O-MMT microfibers, and the wettability of the PMMA/O-MMT composite microfibers was improved after surface modification by sputter coating. Furthermore, the PMMA/O-MMT microfibers membrane coated with TiO2 performed well in photocatalytic degradation of MB. [Copyright &y& Elsevier]

Our previous studies have demonstrated that some male patients suffering from brachial plexus injury, particularly brachial plexus root avulsion, show erectile dysfunction to varying degrees. However, the underlying mechanism remains poorly understood. In this study, we evaluated the erectile function after establishing brachial plexus root avulsion models with or without spinal cord injury in rats. After these models were established, we administered apomorphine (via a subcutaneous injection in the neck) to observe changes in erectile function. Rats subjected to simple brachial plexus root avulsion or those subjected to brachial plexus root avulsion combined with spinal cord injury had significantly fewer erections than those subjected to the sham operation. Expression of neuronal nitric oxide synthase did not change in brachial plexus root avulsion rats. However, neuronal nitric oxide synthase expression was significantly decreased in brachial plexus root avulsion + spinal cord injury rats. These findings suggest that a decrease in neuronal nitric oxide synthase expression in the penis may play a role in erectile dysfunction caused by the combination of brachial plexus root avulsion and spinal cord injury.