Robotic-assisted systems for the safe and reliable treatment of femoral neck fractures: retrospective cohort study

Abstract Background Robots are being used in a wide range of surgical procedures. However, in clinical practice, the efficacy of orthopedic robotic-assisted treatment of femoral neck fractures is still poorly reported, particularly in terms of screw placement accuracy, femoral neck fracture healing rates and postoperative functional recovery. Moreover, there is a lack of comparative analysis between robot-assisted surgery and traditional surgical approaches. Purpose The purpose of this study was to compare the clinical outcomes of patients with femoral neck fractures treated with TiRobot-assisted hollow screw fixation with those of patients with femoral neck fractures treated with traditional surgical approaches. Methods This study included 112 patients with femoral neck fracture who were treated from March 2017 to October 2021 with percutaneous hollow screw internal fixation. These included 56 cases in the TiRobot-assisted surgery group and 56 cases in the standard surgery group. After at least 1 year of follow-up, the treatment outcomes of the two groups were compared, including the amount of intraoperative bleeding, the duration of intraoperative fluoroscopy, the number of guide pin positioning adjustments, the length of hospital stay, the accuracy rate of screw placement, the final Harris Hip Score, the fracture healing rate, and the rate of femoral head necrosis. Statistical analysis software was used to process and analyze the result. Results The TiRobot-assisted group had a statistically significant improvement over the control group in terms of intraoperative bleeding, the duration of intraoperative fluoroscopy, the number of guide pin positioning adjustments, length of hospital stay, accuracy of screw placement and incidence of femoral head necrosis (P  0.05). Conclusion This study shows that TiRobot-assisted surgery has the advantages of short hospital stay, high safety, minimally invasive, high success rate of nail placement, and can reduce the amount of intraoperative radiation and the incidence of femoral head necrosis, thus achieving satisfactory clinical outcomes, and is worthy of clinical promotion

Highly sensitive light-induced thermoelastic spectroscopy oxygen sensor with co-coupling photoelectric and thermoelastic effect of quartz tuning fork

A light-induced thermoelastic spectroscopy (LITES) gas detection method based on CH3NH3PbI3 perovskite-coated quartz tuning fork (QTF) was proposed. By coating CH3NH3PbI3 thin film on the surface of ordinary QTF, a Schottky junction with silver electrodes was formed. The co-coupling of photoelectric effect and thermoelastic effect of CH3NH3PbI3-QTF results in a significant improvement in detection performance. The oxygen (O2) was select as the target analyte for measurement, and experimental results show that compared with the commercial standard QTF, the introduction of CH3NH3PbI3 perovskite Schottky junction increases the 2f signal amplitude and signal-to-noise ratio (SNR) by ∼106 times and ∼114 times, respectively. The minimum detection limit (MDL) of this LITES system is 260 ppm, and the corresponding normalized noise equivalent absorption coefficient (NNEA) is 9.21 × 10−13 cm−1·W·Hz−1/2. The Allan analysis of variance results indicate that when the average time is 564 s, the detection sensitivity can reach 83 ppm. This is the first time that QTF resonance detection has been combined with perovskite Schottky junctions for highly sensitive optical gas detection

Identification of serotonin 2A receptor as a novel HCV entry factor by a chemical biology strategy

ABSTRACT Hepatitis C virus (HCV) is a leading cause of liver disease worldwide. Although several HCV protease/polymerase inhibitors were recently approved by U.S. FDA, the combination of antivirals targeting multiple processes of HCV lifecycle would optimize anti-HCV therapy and against potential drug-resistance. Viral entry is an essential target step for antiviral development, but FDA-approved HCV entry inhibitor remains exclusive. Here we identify serotonin 2A receptor (5-HT2AR) is a HCV entry factor amendable to therapeutic intervention by a chemical biology strategy. The silencing of 5-HT2AR and clinically available 5-HT2AR antagonist suppress cell culture-derived HCV (HCVcc) in different liver cells and primary human hepatocytes at late endocytosis process. The mechanism is related to regulate the correct plasma membrane localization of claudin 1 (CLDN1). Moreover, phenoxybenzamine (PBZ), an FDA-approved 5-HT2AR antagonist, inhibits all major HCV genotypes in vitro and displays synergy in combination with clinical used anti-HCV drugs. The impact of PBZ on HCV genotype 2a is documented in immune-competent humanized transgenic mice. Our results not only expand the understanding of HCV entry, but also present a promising target for the invention of HCV entry inhibitor

RNF115/BCA2 deficiency alleviated acute liver injury in mice by promoting autophagy and inhibiting inflammatory response

Abstract The E3 ubiquitin ligase RING finger protein 115 (RNF115), also known as breast cancer-associated gene 2 (BCA2), has been linked with the growth of some cancers and immune regulation, which is negatively correlated with prognosis. Here, it is demonstrated that the RNF115 deletion can protect mice from acute liver injury (ALI) induced by the treatment of lipopolysaccharide (LPS)/D-galactosamine (D-GalN), as evidenced by decreased levels of alanine aminotransaminase, aspartate transaminase, inflammatory cytokines (e.g., tumor necrosis factor α and interleukin-6), chemokines (e.g., MCP1/CCL2) and inflammatory cell (e.g., monocytes and neutrophils) infiltration. Moreover, it was found that the autophagy activity in Rnf115 −/− livers was increased, which resulted in the removal of damaged mitochondria and hepatocyte apoptosis. However, the administration of adeno-associated virus Rnf115 or autophagy inhibitor 3-MA impaired autophagy and aggravated liver injury in Rnf115 −/− mice with ALI. Further experiments proved that RNF115 interacts with LC3B, downregulates LC3B protein levels and cell autophagy. Additionally, Rnf115 deletion inhibited M1 type macrophage activation via NF-κB and Jnk signaling pathways. Elimination of macrophages narrowed the difference in liver damage between Rnf115 +/+ and Rnf115 −/− mice, indicating that macrophages were linked in the ALI induced by LPS/D-GalN. Collectively, for the first time, we have proved that Rnf115 inactivation ameliorated LPS/D-GalN-induced ALI in mice by promoting autophagy and attenuating inflammatory responses. This study provides new evidence for the involvement of autophagy mechanisms in the protection against acute liver injury

Broadband microwave absorbing materials based on MWCNTs' electromagnetic wave filtering effect

Broadband microwave absorbing materials based on MWCNTs' electromagnetic wave filtering effec

Thin and broadband Ce2Fe17N3-delta/MWCNTs composite absorber with efficient microwave absorption

Thin and broadband Ce2Fe17N3-delta/MWCNTs composite absorber with efficient microwave absorptio

Spinal cord stimulation frequency influences the hemodynamic response in patients with disorders of consciousness

Spinal cord stimulation (SCS) is a promising technique for treating disorders of consciousness (DOCs). However, differences in the spatio-temporal responsiveness of the brain under varied SCS parameters remain unclear. In this pilot study, functional near-infrared spectroscopy was used to measure the hemodynamic responses of 10 DOC patients to different SCS frequencies (5 Hz, 10 Hz, 50 Hz, 70 Hz, and 100 Hz). In the prefrontal cortex, a key area in consciousness circuits, we found significantly increased hemodynamic responses at 70 Hz and 100 Hz, and significantly different hemodynamic responses between 50 Hz and 70 Hz/100 Hz. In addition, the functional connectivity between prefrontal and occipital areas was significantly improved with SCS at 70 Hz. These results demonstrated that SCS modulates the hemodynamic responses and long-range connectivity in a frequency-specific manner (with 70 Hz apparently better), perhaps by improving the cerebral blood volume and information transmission through the reticular formation-thalamus-cortex pathway

The effect of hyperthyroidism on cognitive function, neuroinflammation, and necroptosis in APP/PS1 mice

Abstract Background Increasing evidence has linked the thyroid dysfunction to the pathogenesis of dementia. Evidence from clinical studies has demonstrated that hypothyroidism is related to an increased risk of dementia. But the association of hyperthyroidism with dementia is largely unknown. Methods We used the adenovirus containing thyrotropin receptor (TSHR) amino acid residues 1-289 (Ad-TSHR289)-induced Graves’ disease (GD) phenotype in Alzheimer’s disease (AD) model mice (APP/PS1 mice) to evaluate the effect of hyperthyroidism on the cognitive function and β-amyloid (Aβ) accumulation. Results GD mice exhibited a stable long-term hyperthyroidism and cognitive deficits. Single Cell RNA-sequencing analysis indicated that microglia function played a critical role in the pathophysiological processes in GD mice. Neuroinflammation and polarization of microglia (M1/M2 phenotype) and activated receptor-interacting serine/threonine protein kinase 3 (RIPK3)/mixed lineage kinase domain–like pseudo-kinase (MLKL)-mediated necroptosis contributed to the pathological process, including Aβ deposition and neuronal loss. RIPK3 inhibitor could inhibit GD-mediated Aβ accumulation and neuronal loss. Conclusions Our findings reveal that GD hyperthyroidism aggravates cognitive deficits in AD mice and induces Aβ deposition and neuronal loss by inducing neuroinflammation and RIPK3/MLKL-mediated necroptosis