An Li 2 B 4 O 7 cladded carbon nanofiber membrane has been designed as an interlayer for Li–S batteries. Due to abundant electronic deficiencies [BO 3 ] in Li 2 B 4 O 7 , the enhanced electrochemical performance of Li–S batteries was achieved.
The purpose of this study is to develop an innovative solution for chronic wounds in high-mobility areas, such as joints, where conventional treatments are hindered by passive healing mechanisms and the need for immobilization. By designing a micro-electro-Nanofiber dressing composed of piezoelectric polyvinylidene fluoride (PVDF) integrated with antimicrobial silver nanoparticles (AgNPs), this research aims to address the dual challenges of promoting effective wound healing and maintaining joint mobility. Herein, we developed a novel micro-electro-Nanofiber dressing using electrospinning technology, incorporating polyvinylidene fluoride (PVDF) with silver nanoparticles (AgNPs). The optimized PVDF-AgNPs Nanofiber dressings exhibited strong piezoelectric effects suitable for joint wounds. In vitro experiments demonstrated that the dressing effectively promoted fibroblast migration and collagen synthesis. In vivo, the dressing exhibited a trend of rapid healing in infected wounds within 12 days while modulating macrophage differentiation toward the anti-inflammatory M2 phenotype. Additionally, the incorporation of antimicrobial nanosilver effectively controlled local infections, further facilitating the healing process. To sum up, by harnessing the piezoelectric effect to stimulate endogenous healing mechanisms without restricting joint mobility, the developed PVDF-AgNPs Nanofiber dressings represent a transformative approach for the treatment of wounds in highly mobile body areas.
Patients who are bedridden are for a long-time prone to develop bedsores, especially in the hip and sacral areas and limbs, which causes eczema, ulcers, infection and other complications, resulting in pain and more medical costs. Therefore, the medical staff of the Second Affiliated Hospital of Zunyi Medical University designed and developed a kind of anti-bedsore turning pad, and has obtained the national utility model patent (ZL 2021 2 3004923.9), which is suitable for various long-term bedridden patients. The anti-bedsore turning pad includes the center axis of the turning pad, and ventilation pad 1 and ventilation pad 2 designed on the left and right of turning pad center axis. Under the ventilation pad 1 and the ventilation pad 2, the air pad 1 and the air pad 2 are respectively designed. There is a bedspread connected with ventilation pad 1 and ventilation pad 2 on the inflatable pad 1 and the inflatable pad 2. Through the design of inflatable pad 1 and inflatable pad 2, the left and right of the anti-bedsore turning pad can be lowered or raised independently, which is convenient for the patient's body to tilt and turn over, and can significantly reduce the number of nursing staff and the burden of nursing staff when turning over. In addition, it is convenient to replace the force site at any time and reduce the occurrence of pressure ulcers caused by long-term pressure on the force site. Through the design of ventilation cushion 1 and ventilation cushion 2, the internal gas flow of the turning pad can be made, and the ventilation between the patient and the turning pad can be kept dry, so as to reduce the occurrence of eczema, ulcers or infection and other complications, and ultimately reduce the occurrence of bedsores. In addition, through the design of the most superficial limb pad, the patient's limb can be appropriately elevated or massaged, which increases the comfort of the patient. The anti-bedsore turning pad is simple and effective, and can be widely used in long-term bedridden patients.
Abstract Background Human enterovirus 71 (EV-A71) is a non-enveloped virus that has a single stranded positive sense RNA genome. In a previous study, we showed that miR-876-5p upregulation was observed in the serum of patients with severe EV-A71 infection. Micro-876-5p (miR-876-5p) is a circulating miRNA that can be identified to modulate EV-A71 infections through both in vitro and in vivo studies. However, the regulatory mechanisms that involve miR-876-5p in the EV-A71 infection cycle remain unclear. Methods We demonstrated that miR-876-5p facilitated EV-A71 replication and expression by overexpression and knocking-down of miR-876-5p through the transfection of miR-876-5p plasmid and miR-876-5p inhibitor. Although miR-876-5p suppressed CREB5 expression, luciferase reporter assay confirmed this. We also evaluated the role of miR-876-5p in the EV-A71 infection cycle by CREB5 mediated by transfection with an anti-miR-876-5P inhibitor or in combination with an si-CREB5 plasmid. Results MicroR-876-5p was upregulated in EV-A71-infected neuroblastoma cells. Overexpression of miR-876-5p or knockdown of cyclic-AMP responsive element binding protein 5 (CREB5) promoted EV-A71 replication. The downregulation of miR-876-5p inhibited the accumulation of viral RNA and the production of viral proteins. Interestingly, CREB5 overexpression also suppressed EV-A71 replication. Our in vitro studies reveal that miR-876-5p directly targets CREB5. Finally, downregulation of CREB5 protein abated the inhibitory effect of anti-miR-876-5p and induced inhibitory effect of EV-A71 replication. Conclusions Our results suggest that intracellular miR-876-5p promotes EV-A71 replication indirectly by targeting the host CREB5 protein.
To study the correlations between loss of activity and/or amont of serum 1,25-dihydroxyvitamin D(1,25(OH)2D) and 25-dihydroxyvitamin D(1,25(OH)2D) and bone loss in postmenopausal women, in order to reveal the possible pathophysiology of postmenopausal osteoporosis.The serum levels of 1,25 (OH)2D, 25 (OH) D, PTH, and E2 in 57 postmenopausal women with osteoporosis and 37 postmenopausal women without osteoporosis were measured by radioimmunology. Their Dpd/Cr in urine was measured by ELISA. The bone mineral density (BMD) at lumbar spine (L2-4) was measured in each subject by DEXA.The serum 1,25(OH)2D in postmenopausal oeteoporotic women and non-osteoporotic women were 18 pg/ml +/- 6 pg/ml and 31 pg/ml +/- 14 pg/ml respectively (P < 0.01) The serum 25 (OH)2D in postmenopausal oeteoporotic women and non-osteoporotic women were 32 ng/ml +/- 9 ng/ml and 46 ng/ml +/- 17 ng/ml respectively (P < 0.01). Postmenopausal osteoporotic women had a lower estrogen concentration (P < 0.01), higher serum parathyroid hormone (PTH) (P < 0.01) and higher urinary Dpd/Cr level (P < 0.01). The level of serum 1,25(OH)2D was highly correlated with BMD in L2-4 for postmenopausal women (r = 0.693, P < 0.001). There was a close relationship between the serum level of 1,25(OH)2D and serum level of 25(OH)2D, suggesting an association between the two factors.The lower bone mass density was associated with lower level of serum 1,25-dihydroxyvitamin D, accompanied by reduced serum estrogen and elevated serum PTH in postmenopausal women. Those may be among the important pathphysiological changes of postmenopausal osteoporosis.
Assembly of a high-quality genome is important for downstream comparative and functional genomic studies. However, most tools for genome assembly assessment only give qualitative reports, which do not pinpoint assembly errors at specific regions. Here, we develop a new reference-free tool, Clipping information for Revealing Assembly Quality (CRAQ), which maps raw reads back to assembled sequences to identify regional and structural assembly errors based on effective clipped alignment information. Error counts are transformed into corresponding assembly evaluation indexes to reflect the assembly quality at single-nucleotide resolution. Notably, CRAQ distinguishes assembly errors from heterozygous sites or structural differences between haplotypes. This tool can clearly indicate low-quality regions and potential structural error breakpoints; thus, it can identify misjoined regions that should be split for further scaffold building and improvement of the assembly. We have benchmarked CRAQ on multiple genomes assembled using different strategies, and demonstrated the misjoin correction for improving the constructed pseudomolecules.
Objective
To investigate whether the combination of oral propranolol and topical 0.5% timolol maleate cream is more effective than oral propranolol alone for treating infantile hemangioma (IH).
Methods
From September 2015 to July 2016, 14 patients with proliferative IH, visited the infantile hemangioma outpatient clinic of the Department of Plastic and Reconstructive Surgery of Shanghai 9th People′s Hospital, were enrolled in this study. All patients took oral propranolol. Half of each IH lesion was treated with 0.5% timolol maleate cream. There were 5 male patients and 9 female patients, aged from 1.5 to 5.0 months. After 4 months of treatment, the color, size, extent, volume and the overall clinical outcomes of each lesion were measured, and the side effects were recorded. The therapeutic outcomes of oral propranolol alone and the combination of propranolol and timolol were analyzed and compared using Wilcoxon matched-pair signed-rank nonparametric tests.
Results
Both oral propranolol alone and oral propranolol combined with topical 0.5% timolol maleate cream were proved to effectively improve the regression of IH with minor side effects. The color VAS score of oral propranolol alone group was 6.92±2.63, while the combination group was 6.88±2.33 (Z=0.043, P=0.966). The volume VAS score of oral propranolol alone group was 6.94±2.00, while the combination group was 6.98±2.11(Z=-0.051, P=0.959).
Conclusions
Oral propranolol combined with topical application of 0.5% timolol maleate could not increase the efficacy in the treatment of IH, compared with oral propranolol alone in the short-term observation.
Key words:
Infantile hemangioma; Propranolol; Timolol
Abstract Osteoarthritis (OA) is the most common form of arthritis involving major structural changes of peripheral joints and local or systemic inflammation and in lack of therapeutic approaches because of complexity of underlying molecular basis. Our previous work showed that HS6ST2, an enzyme involved in the transfer of sulfate, is downregulated in cartilage tissues of OA patients compared with normal donors, but little is known about its regulatory mechanism. In this study, we demonstrated that the expression of HS6ST2 was lower in OA-damaged cartilage than smooth cartilage from the same patient. In chondrocytes, HS6ST2 could be targeted by miR-23b-3p, which was higher expressed in OA-damaged cartilage. Under TNF-α stimulation, the expression of HS6ST2 was found inversely correlated with the expression of miR-23b-3p. Downregulation of HS6ST2 regulated by overexpression of miR-23b-3p and siRNAs against HS6ST2 could enhance the protein level of MMP13 and aggravate the matrix degradation in chondrocytes. Increased expression of MMP13 depended on activity of p38 MAPK rather than total p38 MAPK level and was abrogated by HS6ST2 overexpression. Together, the results indicated that downregulated HS6ST2 targeted by miR-23b-3p promotes matrix degradation by activating p38 MAPK in chondrocytes and OA cartilage.
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