Maternal tobacco exposure during pregnancy and atopic dermatitis in offspring: A systematic review and meta-analysis.

The main purpose of this review was to examine the evidence of the relationship between active smoking or passive smoking during pregnancy and atopic dermatitis in offspring. The protocol was written following the PRISMA Checklist and was registered in the PROSPERO database (registration number CRD42022381136). We implemented a comprehensive search in PubMed, Embase and Web of Science databases to identify all potentially related articles from inception through 1 December 2022. We assessed cohort studies and case-control studies using the Newcastle-Ottawa Scale (NOS), and the Joanna Briggs Institute (JBI) critical appraisal tool to assess the quality of cross-sectional studies. Heterogeneity was investigated by using Cochrane Q tests and I2 statistics. In addition, according to the research design, population source and population size, the reasons for the heterogeneity were analysed. A total of 15 observational studies were included in this analysis. Our meta-analysis suggests that atopic dermatitis in offspring is not associated with active smoking during pregnancy (pooled OR, 0.96 [95% CI 0.86-1.07]); however, it is related to passive smoking (OR, 1.52 [95% CI 1.36-1.70]). Passive smoking during pregnancy is associated with an increased risk of eczema development in offspring. More research is needed to explore the risk of active smoking and eczema development in offspring, especially the association between measurements of pregnancy cotinine levels in maternal body fluids and AD in offspring.

Intraoperative analgesic effect of intravertebral lidocaine injection during percutaneous kyphoplasty in the treatment of thoracolumbar compression fractures in elderly patients.

BACKGROUND: In recent years, percutaneous kyphoplasty (PKP) has been increasingly used in clinical settings. OBJECTIVE: In this study, we aimed to determine the analgesic effect of intravertebral lidocaine injections in PKP. METHODS: A total of 60 patients who were treated with PKP were enrolled in this study. Lidocaine hydrochloride was chosen as the medication for the experimental group. Patients were randomly assigned into three groups using a double-blind study design: In group A (20 cases), no drugs were injected into the vertebral body during surgery; group B (20 cases) received intravertebral injection of normal saline; and in group C (20 cases), lidocaine hydrochloride was administered into the vertebral body during surgery. The age of patients, operation time, balloon dilatation pressure, balloon dilatation volume, and amount of bone cement injected were compared across the three groups. A pain visual analog scale (VAS) was used to assess pain suffered by the patients before, during, and 24 hours after the surgery. RESULTS: Age, operation time, balloon dilatation pressure, balloon dilatation volume, and amount of bone cement injected did not differ significantly among the three groups (P> 0.05). The differences in VAS scores 24 hours before and after surgery were not statistically significant (P> 0.05). Group C had lower intraoperative VAS scores than groups A and B, and the difference was statistically significant (P< 0.01). There was no statistically significant difference between group A and group B (P> 0.05). CONCLUSION: Intravertebral injections of lidocaine during PKP can successfully reduce intraoperative pain.

Association of bone mineral density with lung function in a Chinese general population: the Xinxiang rural cohort study.

BACKGROUND: Bone mineral density (BMD) has been positively associated with lung function in patients diagnosed with respiratory diseases such as chronic obstructive pulmonary disease (COPD) and cystic fibrosis. However, the relationship between BMD and lung function is inconsistent in the general population. METHODS: To investigate the association between BMD and lung function in a Chinese general population, a total of 1024 adults aged 40-70 years old from Qiliying (an industrial polluted exposure area) and Langgongmiao (the reference area with non-industrial pollution) were recruited and underwent BMD and spirometry tests. RESULTS: Both BMD and lung function levels were lower in the exposed area compared to the reference area. In addition, BMD and lung function levels were also lower in females compared to males. Both Spearman and partial correlation analyses showed that BMD was positively correlated with FVC and FEV1. After adjusting linear regression analyses for potential confounding factors, every 0.1 g/cm2 drop in BMD was associated with 53.0 mL decrease in FVC and 33.5 mL decrease in FEV1. CONCLUSIONS: A reduction of BMD is associated with lower lung function in a general population from China.

Spin switching in tris(8-aminoquinoline)iron(ii)(BPh4)2: quantitative guest-losing dependent spin crossover properties and single-crystal-to-single-crystal transformation.

As a derivative of 2-picolylamine, which contains rich protons favouring hydrogen bond formation to assemble a variety of valuable spin crossover (SCO) compounds, 8-aminoquinoline (aqin) will be a good candidate for constructing new mononuclear bistable state compounds. With the guidance of this view, two solvated compounds [Fe(aqin)3](BPh4)2·2(CH3CN) (1·2CH3CN) and [Fe(aqin)3](BPh4)2·1.5(CH3COCH3) (2·1.5CH3COCH3) were synthesized. The structural characterization and magnetic studies demonstrate that this strategy has been successful. Single-crystal diffraction reveals that both the mononuclear compounds have facial (fac-)-configuration cations, which form hydrogen bonds using -NH2 groups with solvent molecules (acetonitrile or acetone). Subsequent magnetic measurement shows the highly sensitive solvent-dependent occurrence of a spin transition above room temperature for both compounds. Interestingly, for compound 1·2CH3CN, in the successively repeated heating and cooling process, by monitoring the loss of solvent molecules by TGA, the shifting of the spin transition curve is found to be linearly dependent on the fraction of the residual solvent content. Additionally, the desolvated sample can re-solvate with CH3CN and recover the magnetic response reproducibly. Furthermore, after losing the acetonitrile molecules, the single-crystal-to-single-crystal transformation occurred to give 1.

Targeting intracellular MMPs efficiently inhibits tumor metastasis and angiogenesis.

Treatment for metastatic cancer is a great challenge throughout the world. Commonly, directed inhibition of extracellular matrix metalloproteinases (MMPs) secreted by cancer cells can reduce metastasis. Here, a novel nanoplatform (HPMC NPs) assembled from hyaluronic acid (HA)-paclitaxel (PTX) prodrug and marimastat (MATT)/ß-casein (CN) complexes was established to cure a 4T1 metastatic cancer model via targeting CD44 and intracellular, rather than extracellular, MMPs. Methods: HPMC NPs were prepared by assembling the complexes and prodrug under ultrasonic treatment, which the interaction between them was evaluated by förster resonance energy transfer, circular dichroism and fluorescence spectra. The developed nanoplatform was characterized via dynamic light scattering and transmission electron microscopy, and was evaluated in terms of MMP-sensitive release and stability. Subsequently, the cellular uptake, trafficking, and in vitro invasion were studied by flow cytometry, confocal laser microscopy and transwell assay. MMP expression and activity was determined by western blotting and gelatin zymography. Finally, the studies of biodistribution and antitumor efficacy in vivo were performed in a mouse 4T1 tumor breast model, followed by in vivo safety study in normal mouse. Results: The interaction between the prodrug and complexes is strong with a high affinity, resulting in the assembly of these two components into hybrid nanoparticles (250 nm). Compared with extracellular incubation with MATT, HPMC NP treatment markedly reduced the expression (100%) and activity (50%) of MMPs in 4T1 cells and in the tumor. HPMC NPs exhibited 1.4-fold tumor accumulation, inhibited tumor-growth by >8-fold in volume with efficient apoptosis and proliferation, and suppressed metastasis (>5-fold) and angiogenesis (>3-fold). Overall, HPMC NPs were efficient in metastatic cancer therapy. Conclusions: According to the assembly of polymer prodrug and protein-drug complexes, this study offers a new strategy for constructing nanoparticles for targeted drug delivery, biomedical imaging, and combinatorial treatment. Importantly, via inhibition of intracellular MMPs, metastasis and angiogenesis can be potently blocked, benefiting the rational design of nanomedicine for cancer treatment.

Nanoplatform Assembled from a CD44-Targeted Prodrug and Smart Liposomes for Dual Targeting of Tumor Microenvironment and Cancer Cells.

The tumor microenvironment (TME) plays a critical role in tumor initiation, progression, invasion, and metastasis. Therefore, a therapy that combines chemotherapeutic drugs with a TME modulator could be a promising route for cancer treatment. This paper reports a nanoplatform self-assembled from a hyaluronic acid (HA)-paclitaxel (PTX) (HA-PTX) prodrug and marimastat (MATT)-loaded thermosensitive liposomes (LTSLs) (MATT-LTSLs) for the dual targeting of the TME and cancer cells. Interestingly, the prodrug HA-PTX can self-assemble on both positively and negatively charged liposomes, forming hybrid nanoparticles (HNPs, 100 nm). Triggered by mild hyperthermia, HA-PTX/MATT-LTSLs HNPs rapidly release their payloads into the extracellular environment, and the released HA-PTX quickly enters 4T1 cells through a CD44-HA affinity. The HNPs possess promoted tumor accumulation (1.6-fold), exhibit deep tumor penetration, and significantly inhibit the tumor growth (10-fold), metastasis (100%), and angiogenesis (10-fold). Importantly, by targeting the TME and maintaining its integrity via inhibiting the expression and activity of matrix metalloproteinases (>5-fold), blocking the fibroblast activation by downregulating the TGF-ß1 expression (5-fold) and suppressing the degradation of extracellular matrix, the HNPs allow for significant metastasis inhibition. Overall, these findings indicate that a prodrug of an HA-hydrophobic-active compound and liposomes can be self-assembled into a smart nanoplatform for the dual targeting of the TME and tumor cells and efficient combined treatment; additionally, the co-delivery of MATT and HA-PTX with the HNPs is a promising approach for the treatment of metastatic cancer. This study creates opportunities for fabricating multifunctional nanodevices and offers an efficient strategy for disease therapy.

Resveratrol and caloric restriction prevent hepatic steatosis by regulating SIRT1-autophagy pathway and alleviating endoplasmic reticulum stress in high-fat diet-fed rats.

BACKGROUND: Studies have demonstrated that resveratrol (a natural polyphenol) and caloric restriction activate Sirtuin-1 (SIRT1) and induce autophagy. Furthermore, autophagy is induced by the SIRT1-FoxO signaling pathway and was recently shown to be a critical protective mechanism against non-alcoholic fatty liver disease (NAFLD) development. We aimed to compare the effects of resveratrol and caloric restriction on hepatic lipid metabolism and elucidate the mechanism by which resveratrol supplementation and caloric restriction alleviate hepatosteatosis by examining the molecular interplay between SIRT1 and autophagy. METHODS AND RESULTS: Eight-week-old male Wistar rats (40) were divided into four groups: the STD group, which was fed a standard chow diet; the HFD group, which was fed a high-fat diet; HFD-RES group, which was fed a high-fat diet plus resveratrol (200 mg/kg.bw); and the HFD-CR group, which was fed a high-fat diet in portions containing 70% of the mean intake of the HFD group rats. The groups were maintained for 18 weeks. Metabolic parameters, Oil Red O and hematoxylin-eosin staining of the liver, and the mRNA and protein expression of SIRT1, autophagy markers and endoplasmic reticulum(ER) stress-associated genes in the liver were assessed after the 18-week treatment. We found that resveratrol (200 mg/kg bw) and caloric restriction (30%) partially prevented hepatic steatosis and hepatocyte ballooning, increased the expression of SIRT1 and autophagy markers while decreasing ER stress markers in the liver and alleviated lipid metabolism disorder. Moreover, caloric restriction provided superior protection against HFD-induced hepatic fatty accumulation compared with resveratrol and the effects were associated with decreased total energy intake and body weight. CONCLUSION: We conclude that the SIRT1-autophagy pathway and decreased ER stress are universally required for the protective effects of moderate caloric restriction (30%) and resveratrol (a pharmacological SIRT1 activator) supplementation against HFD-induced hepatic steatosis.

Overexpression of CRY1 protects against the development of atherosclerosis via the TLR/NF-κB pathway.

It has been demonstrated that the circadian clock system could be a potential factor involved in inflammation and the progression of atherosclerosis. A previous study has reported that cryptochrome 1 (CRY1), which is a core clock component, is associated with regulating proinflammation. However, whether CRY1 is involved in atherosclerosis is currently unknown. In the present study, we aimed to explore the role of CRY1 in regulating atherosclerosis in apolipoprotein E (ApoE)-deficient mice and the underlying molecular mechanism. We found that CRY1 mRNA expression was significantly decreased in atherosclerotic patients compared to the healthy subjects. Overexpression of CRY1 in the mouse model of atherosclerosis by adenovirus-mediated gene transfer significantly decreased the expression of proinflammatory factors including tumor necrosis factor-α (TNF-α), interleukin (IL)-1, IL-6, and macrophage inflammatory protein-1α (MIP-1α). In addition, the adhesion molecules including vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin, were also downregulated by CRY1 overexpression. Furthermore, the plaque area of the aortic sinus and the concentrations of total cholesterol (TC), triglyceride (TG), and low density lipoprotein cholesterol (LDL-C) were also decreased in the atherosclerotic mice by CRY1 overexpression. Moreover, overexpression of CRY1 significantly decreased the protein levels of toll-like receptor (TLR) 2, TLR4 and phosphorylated p65 (p-p65). Additionally, the results of luciferase reporter assay exhibited that CRY1 overexpression was capable of inhibiting the activation of nuclear factor-kappa B (NF-κB). Taken together, our results suggest that overexpression of CYR1 relieves the development of atherosclerosis that may be associated with regulating the TLR/NF-κB pathway.

Kanglaite injection combined with chemotherapy versus chemotherapy alone in the treatment of advanced non-small cell lung carcinoma.

OBJECTIVE: To evaluate the clinical efficacy of Kanglaite (KLT) injection combined with chemotherapy versus chemotherapy alone in the treatment of advanced non-small cell lung carcinoma (NSCLC) by meta-analysis. MATERIALS AND METHODS: Electronic search of PubMed, EMBASE, Chinese National Knowledge Infrastructure (CNKI) and Wanfang databases was conducted to select studies about KLT injection combined with chemotherapy versus chemotherapy alone in the treatment of advanced NSCLC. The pooled risk ratio (RR) and its 95% confidence interval (95% CI) for objective response rate (ORR), Karnofsky (KPS) score improvement and nausea and vomiting were calculated by Stata11.0 statistical software. RESULT: Finally, we included 34 clinical trials in this meta-analysis. The pooled results suggested that KLT injection combined with systematic chemotherapy can significantly increase the objective response rate (ORR) [RR = 1.35, 95% CI: 1.23-1.48, (Z = 6.43, P = 0.000)], the quality of patients' life (KSP improvement) [RR = 2.04, 95% CI: 1.79-2.33, (Z = 10.57, P = 0.000)] and decrease the risk ratio of gastrointestinal reaction [RR = 0.53, 95% CI: 0.42-0.66, (Z = 5.53, P = 0.000)] compared with chemotherapy alone. CONCLUSION: KLT injection combined with chemotherapy can improve the short-term efficacy, performance status and decrease the risk of gastrointestinal reaction compared with systematic chemotherapy alone.

siRNA-mediated silencing of Wnt5a regulates inflammatory responses in atherosclerosis through the MAPK/NF-κB pathways.

Previous studies have demonstrated that the aberrant expression of Wnt5a occurs in atherosclerotic lesions. However, the precise role of Wnt5a in the pathogenesis of atherosclerosis remains largely unknown. The present study was undertaken to determine whether the RNA interference of Wnt5a in vivo by adenovirus (Ad)-mediated small interfering RNA (siRNA) transfection is capable of inhibiting the progression of atherosclerosis. Recombinant adenovirus carrying siRNA targeting Wnt5a (Ad-Wnt5a siRNA) was designed. Male apolipoprotein E-deficient (ApoE(-/-)) mice were fed a high-fat diet to induce the pathogenesis of atherosclerosis. Mice were randomly divided into 3 groups (n=15 in each group): the mock group, which received treatment with phosphate-buffered saline (PBS); the Ad-NC group, which received treatment with Ad-non-specific siRNA; and the Ad-Wnt5a siRNA group, which received treatment with Ad-Wnt5a siRNA. Treatment with Ad-Wnt5a siRNA markedly inhibited the mRNA and protein expression of Wnt5a in the aortic tissues. The knockdown of Wnt5a had no significant effect on blood lipid levels, but it suppressed atherosclerotic development and increased plaque stability, which was determined by hematoxylin and eosin staining, picrosirius red staining and Oil Red O staining. Furthermore, the mRNA and protein expression of inflammatory cytokines, including monocyte chemotactic protein-1 (MCP-1), cyclooxygenase-2 (COX-2), matrix metalloproteinase (MMP)-2 and MMP-9 was significantly downregulated in the Ad-Wnt5a siRNA group. In addition, the knockdown of Wnt5a inhibited the nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. These results demonstrate that Ad-mediated Wnt5a silencing in vivo attenuates the development of atherosclerotic disease by reducing inflammatory mediators involved in the MAPK/NF-κB pathways.