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Background Breast cancer is one of the most commonly diagnosed cancers in women, with high morbidity and mortality. Tumor metastasis is implicated in most breast cancer deaths; thus, inhibiting metastasis may provide a therapeutic direction for breast cancer. In the present study, pyropheophorbide-α methyl ester-mediated photodynamic therapy (MPPa-PDT) was used to inhibit metastasis in MCF-7 breast cancer cells. Methods Uptake of MPPa was detected by fluorescence microscopy. Cell viability was evaluated by the Cell Counting Kit-8 (CCK-8). ROS generation was detected by 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA). The migration of cells was assessed by wound healing assay, and invasion ability was assessed by Matrigel invasion assay. Levels of MMP2 and MMP9 were measured by PCR. Akt, phospho-Akt (Ser473), phospho-NF-κB p65 (Ser536) and NF-κB p65 were measured by western blotting. The F-actin cytoskeleton was observed by immunofluorescence. Lung tissue was visualized by hematoxylin and eosin staining. Results Following MPPa-PDT, migration and invasion were decreased in the MCF-7 cells. MPPa-PDT downregulated the expression of MMP2 and MMP9, which are responsible for the initiation of metastasis. MPPa-PDT reduced the phosphorylation of Akt and NF-κB. MPPa-PDT also reduced the expression of F-actin in cytoskeleton in MCF-7 cells. These effects were blocked by the reactive oxygen species scavenger NAC or the Akt activator SC79, while the PI3K inhibitor LY294002 or the Akt inhibitor triciribine enhanced these effects. Moreover, MPPa-PDT inhibited tumor metastasis and destroyed F-actin in vivo. Conclusion Taken together, these results demonstrate that MPPa-PDT inhibits the metastasis of MCF-7 cells both in vitro and in vivo and may be involved in the Akt/NF-κB-dependent MMP-9 signaling pathway. Thus, MPPa-PDT may be a promising treatment to inhibit metastasis.

Enhanced external counterpulsation (EECP) is currently applied for treating coronary artery disease (CAD) patients. However, the mechanism(s) by which EECP ameliorates angina pectoris and long-term left ventricular function remain largely unknown. The aim of this study will be to assess whether EECP significantly affects myocardial perfusion in CAD patients through a systematic review and meta-analysis of the available literature. MEDLINE, EMBASE, and Cochrane CENTRAL databases were searched for prospective studies on CAD patients that underwent EECP and reported myocardial perfusion data pre- and post-EECP. The impact of EECP was assessed based on the weighted mean difference (WMD) in myocardial perfusion from pre-EECP to post-EECP. Statistical heterogeneity was assessed by the I2 index. Publication bias was assessed through visual inspection of the funnel plot as well as Begg's and Egger's testing. Standard EECP therapy (i.e., 35-36 one-hour sessions within a seven-week period) significantly increased myocardial perfusion in CAD patients (pooled WMD: -0.19, 95% CI: -0.38 to 0.00, p = 0.049). A random effects analysis was applied on account of significant heterogeneity (I2 = 89.1%, p = 0.000). There was no evidence of significant publication bias (Begg's p = 0.091; Egger's p = 0.282). Standard EECP therapy significantly increases myocardial perfusion in CAD patients. This study's findings support the continued use of standard EECP therapy in CAD patients and provides one putative physiological mechanism to help explain the improvements in angina pectoris and long-term left ventricular function observed in CAD patients after EECP therapy.

The optimal treatment methods for delayed encephalopathy after acute carbon monoxide (CO) poisoning (DEACMP) were not identified. Thus, this study was conducted to compare the efficacies of intermittent theta burst stimulation (iTBS) and short-chain fatty acids (SCFAs) in treating cognitive dysfunction and anxiety symptoms of DEACMP rat. In phase I, a DEACMP rat model was built to assess the inflammation levels in the hippocampus and levels of SCFAs in the serum of DEACMP rats. In phase II, DEACMP rats were randomly assigned into four groups: DEACMP + placebo, DEACMP + SCFAs, DEACMP + sham iTBS, and DEACMP + iTBS. The intervention was continued for 2 weeks. A Morris water maze and open field tests were used to assess cognitive function and anxiety symptoms, respectively. The levels of three inflammatory factors (IL-1β, IL-6, and TNF-α) and two SCFAs (acetate and propionate) were significantly increased and decreased, respectively, in DEACMP rats. After treatment, cognitive dysfunction and anxiety symptoms were significantly improved in the DEACMP + iTBS group and the DEACMP + SCFAs (consisting of acetate and propionate) group. Both SCFAs and iTBS could significantly improve the increased levels of IL-1β, IL-6, and TNF-α in the hippocampus, and SCFAs could also improve the decreased levels of GPR41, GPR43, dopamine, and norepinephrine in the hippocampus of DEACMP rats. These results indicate that both iTBS and SCFA solutions consisting of acetate and propionate produced good effects on DEACMP rats by regulating inflammation levels in the hippocampus, and acetate/propionate-GPR41/GPR43-IL-1β/IL-6/TNF-α-dopamine/norepinephrine may be a potential pathway in SCFAs for the treatment of DEACMP.

This study aimed to investigate the prevalence of and risk factors for multidrug-resistant organism (MDRO) infection in the rehabilitation ward of a general hospital in Southwest China. We analyzed rehabilitation patients with nosocomial infections caused by MDROs from June 2016 to June 2020. MDRO infection pathogens and associated antibiotic resistance were calculated. Possible risk factors for MDRO-related infection in the neurorehabilitation ward were analyzed using chi-square, and logistic regression. A total of 112 strains of MDRO were found positive from 96 patients. The MDRO test-positive rate was 16.70% (96/575). Ninety-five MDRO strains were detected in sputum, of which 84.82% (95/112) were gram-negative bacteria. Acinetobacter baumannii ( A. Baumannii ), Pseudomonas aeruginosa ( P. aeruginosa ), and Klebsiella pneumonia ( K. pneumonia ) were the most frequently isolated MDRO strains. The logistic regression model and multifactorial analysis showed that long-term (≥ 7 days) antibiotic use (OR 6.901), history of tracheotomy (OR 4.458), and a low albumin level (< 40 g/L) (OR 2.749) were independent risk factors for the development of MDRO infection in patients in the rehabilitation ward (all P  < 0.05). Gram-negative MRDOs were dominant in rehabilitation ward patients. Low albumin, history of a tracheostomy, and long-term use of antibiotics were independent risk factors for MRDO infection and are worthy of attention.

Objective C1qTNF-related protein 4 (CTRP4) acts in the hypothalamus to modulate food intake in diet-induced obese mice and has been shown to exert an anti-inflammatory effect on macrophages. Since high-fat diet-induced microglial activation and hypothalamic inflammation impair leptin signaling and increase food intake, we aimed to explore the potential connection between the anorexigenic effect of CTRP4 and the suppression of hypothalamic inflammation in mice with DIO. Methods Using an adenovirus-mediated hypothalamic CTRP4 overexpression model, we investigated the impact of CTRP4 on food intake and the hypothalamic leptin signaling pathway in diet-induced obese mice. Furthermore, central and plasma proinflammatory cytokines, including TNF-α and IL-6, were measured by Western blotting and ELISA. Changes in the hypothalamic NF-κB signaling cascade and microglial activation were also examined in vivo. In addition, NF-κB signaling and proinflammatory factors were investigated in BV-2 cells after CTRP4 intervention. Results We found that food intake was decreased, while leptin signaling was significantly improved in mice with DIO after CTRP4 overexpression. Central and peripheral TNF-α and IL-6 levels were reduced by central Ad-CTRP4 administration. Hypothalamic NF-κB signaling and microglial activation were also significantly suppressed in vivo. In addition, NF-κB signaling was inhibited in BV-2 cells following CTRP4 intervention, which was consistent with the decreased production of TNF-α and IL-6. Conclusions Our data indicate that CTRP4 reverses leptin resistance by inhibiting NF-κB-dependent microglial activation and hypothalamic inflammation.

Urinary incontinence is a common complication in stroke survivors for whom new interventions are needed. This study investigated the therapeutic effect of low-frequency (LF) repeated transcranial magnetic stimulation (rTMS) on the contralesional primary motor cortex (M1) in patients with poststroke urinary incontinence (PSI). A total of 100 patients were randomly assigned to the rTMS group or sham-rTMS group on basis of the intervention they received. Both groups underwent five treatment sessions per week for 4 weeks. Data from the urodynamic examination were used as the primary outcome. The secondary outcome measures were questionnaires and pelvic floor surface electromyography. After 4 weeks of intervention, the maximum cystometric capacity (MCC), maximum detrusor pressure (Pdet.max), residual urine output, overactive bladder score (OABSS) (including frequency, urgency, and urgency urinary incontinence), and the ICIQ-UI SF improved significantly in the rTMS group compared with those in the sham-rTMS group (P < 0.05). However, no changes in pelvic floor muscle EMG were detected in patients with PSI (both P > 0.05). Our data confirmed that 4 weeks of LF-rTMS stimulation on the contralateral M1 positively affects poststroke urinary incontinence in several aspects, such as frequency, urgency urinary incontinence, MCC, end-filling Pdet, OABSS, and ICIQ-UI SF scores.

Abstract Background: Clinical and animal studies have shown that transcutaneous auricular vagus nerve stimulation (ta-VNS) exerts neuroprotection following cerebral ischaemia. Studies have revealed that white matter damage after ischemia is related to swallowing defects, and the degree of white matter damage is related to the severity of dysphagia. However, the effect of ta-VNS on dysphagia symptoms and white matter damage in dysphagic animals after ischaemic stroke has not been investigated. Methods: Middle cerebral artery occlusion (MCAO) rats were randomly divided into the sham, control and vagus nerve stimulation (VNS) group, which subsequently received ta-VNS for three weeks. The swallowing reflexes were measured once weekly by electromyography (EMG). White matter remyelination, volume, angiogenesis and the inflammatory response in the white matter were assessed by electron microscopy, immunohistochemistry, stereology, enzyme-linked immunosorbent assay (ELISA) and western blotting. Results: Ta-VNS significantly increased the number of swallows within 20 s and reduced the onset latency to the first swallow. ta-VNS significantly improved remyelination but did not alleviate white matter shrinkage after MCAO. Stereology revealed that ta-VNS significantly increased the density of capillaries and increased vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (FGF2) expression in the white matter. ta-VNS significantly alleviated the increase in TLR4, MyD88, phosphorylated MAPK and NF-κB protein levels and suppressed the expression of the proinflammatory factors IL-1β and TNF-α. Conclusion: These results indicated ta-VNS slightly improved dysphagia symptoms after ischaemic stroke, possibly by increasing remyelination, inducing angiogenesis and inhibiting the inflammatory response in the white matter of cerebral ischaemia model rats, implying that ta-VNS may be an effective therapeutic strategy for the treatment of dysphagia after ischaemic stroke.

The pathogenesis of Alzheimer’s disease (AD) involves activation of many NLRP3 inflammatory bodies, which may be related to amyloid β peptide and aggregation of misfolded proteins. Autophagy is an important regulator of inflammatory bodies. However, autophagy shows dynamic changes in the development of AD, and its role in inflammation remains controversial. In this study, the key link between autophagic disorders and the NLRP3 inflammasome in AD was investigated. APP/PS1 double transgenic mice and C57 mice with Aβ 25–35 injected into the lateral ventricle were used as two animal models of AD. Immunofluorescence staining and Western blot analysis showed that NLRP3 inflammasome-related proteins and inflammatory cytokines, such as IL-1α, IL-1β, IL-6, IL-12, and TNF-α, were increased and microglia were activated in the brains of both AD animal models. Endogenous overexpression of the APPswe gene and exogenous addition of Aβ 25–35 increased the expression of NLRP3 inflammasome-related proteins, while exogenous Aβ 25–35 intervention more significantly activated inflammation. Furthermore, LC3 was increased in the AD animal and cell models, and the level of Lamp1 decreased. After overexpression of the primary regulator of lysosomal biogenesis, TFEB, the lysosome protein Lamp1 was increased, and LC3 and inflammatory protein expression were decreased. These results suggest that the NLRP3 inflammasome-mediated inflammatory response is activated in AD animal and cell models, which may be related to the decline in autolysosome function. Overexpression of the TFEB protein can reduce the inflammatory response by improving autolysosome function in AD model cells.

This paper presents a passive wireless humidity sensor for concrete monitoring. After discussing the transmission of electromagnetic wave in concrete, a novel architecture of wireless humidity sensor, based on Ultra-High Frequency (UHF) Radio Frequency Identification (RFID) technology, is proposed for low-power application. The humidity sensor utilizes the top metal layer to form the interdigitated electrodes, which were then filled with polyimide as the humidity sensing layer. The sensor interface converts the humidity capacitance into a digital signal in the frequency domain. A two-stage rectifier adopts a dynamic bias-voltage generator to boost the effective gate-source voltage of the switches in differential-drive architecture. The clock generator employs a novel structure to reduce the internal voltage swing. The measurement results show that our proposed wireless humidity can achieve a high linearity with a normalized sensitivity of 0.55% %RH at 20 °C. Despite the high losses of concrete, the proposed wireless humidity sensor achieves reliable communication performances in passive mode. The maximum operating distance is 0.52 m when the proposed wireless sensor is embedded into the concrete at the depth of 8 cm. The measured results are highly consistent with the results measured by traditional methods.

Activation of peroxisome proliferator-activated receptor gamma (PPARγ) in the cerebrovascular endothelium is a key suppressor of post-stroke brain damage. However, the role of PPARγ’s co-regulators during cerebral ischemia remains largely unknown. Here, we show that the transcription factor IRF6 is a novel PPARγ co-regulator that directly binds to and suppresses PPARγ activity in murine cerebrovascular endothelial cells. Moreover, IRF6 was also revealed to be a transcriptional target of PPARγ suppression, with PPARγ silencing significantly promoting IRF6 expression in cerebrovascular endothelial cells. In addition, IRF6 silencing significantly promoted pioglitazone’s cytoprotective effects in ischemic murine cerebrovascular endothelial cells. Mechanistically, IRF6 significantly suppressed PPARγ’s transcriptional inhibition of the ischemia-induced, pro-apoptotic microRNA miR-106a. In conclusion, we identified IRF6 as a novel PPARγ co-suppressor that serves a key role in suppressing PPARγ-mediated cerebrovascular endothelial cytoprotection following ischemia. Further investigation into IRF6 and other PPARγ co-regulators should provide additional insights into PPARγ’s cytoprotective role in the cerebrovascular endothelium following stroke.