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BACKGROUND: Accurate condition assessment is critical for improving the prognosis of neonatal respiratory distress syndrome (RDS), but current assessment methods for RDS pose a cumulative risk of harm to neonates. Thus, a less harmful method for assessing the health of neonates with RDS is needed. AIM: To analyze the relationships between pulmonary ultrasonography and respiratory distress scores, oxygenation index, and chest X-ray grade of neonatal RDS to identify predictors of neonatal RDS severity. METHODS: This retrospective study analyzed the medical information of 73 neonates with RDS admitted to the neonatal intensive care unit of Liupanshui Maternal and Child Care Service Center between April and December 2022. The pulmonary ultrasonography score, respiratory distress score, oxygenation index, and chest X-ray grade of each newborn before and after treatment were collected. Spearman correlation analysis was performed to determine the relationships among these values and neonatal RDS severity. RESULTS: The pulmonary ultrasonography score, respiratory distress score, oxygenation index, and chest X-ray RDS grade of the neonates were significantly lower after treatment than before treatment (P < 0.05). Spearman correlation analysis showed that before and after treatment, the pulmonary ultrasonography score of neonates with RDS was positively correlated with the respiratory distress score, oxygenation index, and chest X-ray grade (ρ = 0.429-0.859, P < 0.05). Receiver operating characteristic curve analysis indicated that pulmonary ultrasonography screening effectively predicted the severity of neonatal RDS (area under the curve = 0.805-1.000, P < 0.05). CONCLUSION: The pulmonary ultrasonography score was significantly associated with the neonatal RDS score, oxygenation index, and chest X-ray grade. The pulmonary ultrasonography score was an effective predictor of neonatal RDS severity.
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We established experimental models of manganese (Mn) and iron (Fe) exposure in vitro and in vivo, and addressed the effects of manganese and iron combined exposure on the synaptic function of pheochromocytoma derived cell line 12 (PC12) cells and rat cortex, respectively. We investigated the protective effect of sodium para-aminosalicylate (PAS-Na) on manganese and iron combined neurotoxicity, providing a scientific basis for the prevention and treatment of ferromanganese combined neurotoxicity. Western blot and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were performed to detect the expression levels of protein and mRNA related to synaptic damage. Y-maze novelty test and balance beam test were used to evaluate the motor and cognitive function of rats. Haematoxylin and eosin (H&E) and Nissl staining were performed to observe the cortical damage of rats. The results showed that the combined exposure of Mn and Fe in rats led to a synergistic effect, attenuating growth and development, and altering learning and memory as well as motor function. The combination of Mn and Fe also caused damage to the synaptic structure of PC12 cells, which is manifested as swelling of dendrites and axon terminals, and even lead to cell death. PAS-Na displayed some antagonistic effects against the Mn- and Fe-induced synaptic structural damage, growth, learning and memory impairment.
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Ácido Aminosalicílico , Manganeso , Sinapsis , Animales , Ratas , Células PC12 , Sinapsis/efectos de los fármacos , Masculino , Ácido Aminosalicílico/farmacología , Manganeso/toxicidad , Corteza Cerebral/efectos de los fármacos , Corteza Cerebral/patología , Corteza Cerebral/metabolismo , Ratas Sprague-Dawley , Hierro/metabolismo , Fármacos Neuroprotectores/farmacología , Aprendizaje por Laberinto/efectos de los fármacos , Síndromes de Neurotoxicidad/prevención & control , Síndromes de Neurotoxicidad/etiología , Síndromes de Neurotoxicidad/patología , Modelos Animales de EnfermedadRESUMEN
BACKGROUND: Lung cancer remains a major global health concern due to its high incidence and mortality rates. With advancements in medical treatments, an increasing number of early-stage lung cancer cases are being detected, making surgical treatment the primary option for such cases. However, this presents challenges to the physical and mental recovery of patients. Peplau known as the "mother of psychiatric associations" has formulated a theory of interpersonal relationships in nursing. Through effective communication between nurses and patients over four periods, she has established a good therapeutic nurse-patient relationship. Therefore, this study aimed to explore the effect of perioperative multimodal nursing based on Peplau's interpersonal relationship theory on the rehabilitation of patients with surgical lung cancer. METHODS: We retrospectively analyzed 106 patients with non-small cell lung cancer who underwent thoracoscopic lobectomy at our department between June 2021 and April 2022. Patients were categorized into two groups according to the different nursing intervention techniques. The Peplau's group comprised 53 patients who received targeted nursing interventions, and the control group comprised 53 patients who received conventional nursing care. We observed the patients' illness uncertainty, quality of life, and clinical symptoms in both groups. RESULTS: Patients in the Peplau's group had significantly lower illness uncertainty scores and a significantly higher quality of recovery than those in the control group. However, there were no significant differences in length of post-anesthesia care unit stay, complication rates, and visual analog scores between both groups. CONCLUSION: The multimodal perioperative nursing based on Peplau's interpersonal relationship theory not only reduces the illness uncertainty of patients with lung cancer surgery and improves their QoR but also expands the application of this theory in clinical practice, guiding perioperative nursing of patients with lung cancer. IMPLICATIONS: These findings provide practical information for standardized care in a hectic anesthetic care setting. IMPACT: The assessed anesthesia nursing model helps reduce uncertainty and promote early recovery in patients with cancer at various stages of their disease, which expands the scope of therapeutic practice and existing theories. It also serves as a guide for care in the anesthesia recovery room. REPORTING METHOD: We adhered to the relevant Equator guidelines and the checklist of items in the case-control study report. PATIENT OR PUBLIC CONTRIBUTION: Patients cooperated with medical staff to complete relevant scales.
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Carcinoma de Pulmón de Células no Pequeñas , Neoplasias Pulmonares , Femenino , Humanos , Teoría de Enfermería , Estudios Retrospectivos , Estudios de Casos y Controles , Neoplasias Pulmonares/cirugía , Carcinoma de Pulmón de Células no Pequeñas/cirugía , Calidad de VidaRESUMEN
Lead is one of the heavy metals that is toxic and widely distributed in the environment, and children are more sensitive to the toxic effects of lead because the blood-brain barrier and immune system are not yet well developed. The objective of the study was to investigate the clinical characteristics of lead poisoning in children aged 0â¼6 years in a hospital in Guangxi, and to provide scientific basis for the prevention and treatment of lead poisoning. We collected and analyzed the clinical data of 32 children with lead poisoning admitted to a hospital in Guangxi from 2010 to 2018. The results showed that most of the 32 cases presented with hyperactivity, irritability, poor appetite, abdominal pain, diarrhea, or constipation. The hemoglobin (HGB), mean corpusular volume (MCV), mean corpuscular hemoglobin (MCH), and hematocrit (HCT) of the lead-poisoned children were all decreased to different degrees and were below normal acceptable levels. Urinary ß2-microglobulin was increased. Blood lead levels (BLL) decreased significantly after intravenous injection of the lead chelator, calcium disodium edetate (CaNa2-EDTA). In addition, HGB returned to normal levels, while MCV, MCH, and HCT increased but remained below normal levels. Urinary ß2-microglobulin was reduced to normal levels. Therefore, in this cohort of children, the high-risk factors for lead poisoning are mainly Chinese medicines, such as baby powder. In conclusion, lead poisoning caused neurological damage and behavioral changes in children and decreased erythrocyte parameters, leading to digestive symptoms and renal impairment, which can be attenuated by CaNa2-EDTA treatment.
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Intoxicación por Plomo , Plomo , Niño , Lactante , Humanos , Plomo/toxicidad , China/epidemiología , Ácido Edético , Intoxicación por Plomo/epidemiología , Intoxicación por Plomo/etiología , Hematócrito , HemoglobinasRESUMEN
The aim of study was to address the effects of manganese and iron, alone and in combination, on apoptosis of BV2 microglia cells, and to determine if combined exposure to these metals augments their individual toxicity. We used a murine microglial BV2 cell line. Cell cytotoxicity was analyzed by propidium iodide (PI) exclusion assay. Cell ROS production was analyzed by 2', 7'-dichlorofluorescin diacetate (DCFH-DA) probe staining. Pro-inflammatory cytokine production was monitored by ELISA. Cell apoptosis was analyzed by PE Annexin V/7-AAD staining. Mitochondrial membrane integrity was analyzed by flow cytometry. We used immunoblotting to analyze the effect of manganese, iron alone, or their combined exposure on the activation of caspase9, P53, Bax, and Bcl2 apoptosis signaling pathways. Caspase3 activity was determined using a Colorimetric. Manganese, iron, and their combined exposure for 24 h induced the activation of BV2 microglia cells and increased ROS production and the expression of the inflammatory cytokines, IL-1ß and TNF-α. And we also found that the apoptosis rate increased, mitochondrial membrane potential decreased, apoptosis-related proteins caspase9, P53, Bax, and Bcl2 expression increased, and caspase3 activity increased. Furthermore, we found that combined manganese-iron cytotoxicity was lower than that induced by manganese exposure alone. Manganese, iron alone, or their combination exposure can induce apoptosis in glial cells. Iron can reduce the toxicity of manganese, and there is an antagonistic effect between manganese and iron.
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Hierro , Manganeso , Ratones , Animales , Manganeso/toxicidad , Manganeso/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Hierro/metabolismo , Proteína X Asociada a bcl-2/metabolismo , Proteína p53 Supresora de Tumor/metabolismo , Apoptosis , Proteínas Reguladoras de la Apoptosis/metabolismoRESUMEN
Bulblet initiation, including adventitious bud initiation and bulblet formation, is a crucial process for lily and other bulbous flowers that are commercially propagated by vegetative means. Here, by a hybrid strategy combining Pacific Biosciences (PacBio) full-length sequencing and Illumina RNA sequencing (RNA-seq), high-quality transcripts of L. brownii (Lb) and its variety, L. brownii var. giganteum (Lbg), during in vitro bulblet initiation were obtained. A total of 53,576 and 65,050 high-quality non-redundant full-length transcripts of Lbg and Lb were generated, respectively. Morphological observation showed that Lbg possessed a stronger capacity to generate bulblets in vitro than Lb, and 1 mg L-1 2,4-dichlorophenoxyacetic acid (2,4-D) significantly increased bulblet regeneration rate in two lilies. Screening of differentially expressed transcripts (DETs) between different stages and Mfuzz analysis showed 0 DAT to 1 DAT was the crucial stage with the most complex transcriptional change, with carbohydrate metabolism pathway was significantly enriched. In addition, 6,218 and 8,965 DETs were screened between the 2,4-D-treated group and the control group in Lbg and Lb, respectively. 2,4-D application had evident effects on the expression of genes involved in auxin signaling pathway, such as TIRs, ARFs, Aux/IAAs, GH3s and SAURs. Then, we compared the expression profiles of crucial genes of carbohydrate metabolism between different stages and different treatments. SUSs, SUTs, TPSs, AGPLs, GBSSs and SSs showed significant responses during bulblet initiation. The expression of CWINs, SUTs and SWEETs were significantly upregulated by 2,4-D in two lilies. In addition, 2,4-D increased the expression of starch degradation genes (AMYs and BAMs) and inhibited starch synthesis genes (AGPLs, GBSSs and SSs). SBEs were significantly upregulated in Lbg but not in Lb. Significant co-expression was showed between genes involved in carbohydrate metabolism and auxin signaling, together with transcription factors such as bHLHs, MYBs, ERFs and C3Hs. This study indicates the coordinate regulation of bulblet initiation by carbohydrate metabolism and auxin signaling, serving as a basis for further studies on the molecular mechanism of bulblet initiation in lily and other bulbous flowers.
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Heart Failure (HF) is a complex clinical syndrome in which the heart is unable to provide enough blood flow to meet metabolic needs and lacks efficient venous return. HF is a major risk factor for morbidity and mortality with cardiovascular diseases globally. Despite enormous research, the molecular markers relevant to disease prognosis and management remain not well understood. Here, we analyzed the whole transcriptomes of 18 failing hearts and 15 non-failing hearts (predominantly of Caucasian origin), by applying the standard in silico tools. The analyses revealed novel gene-markers including ALKBH5 of mRNA demethylation and KMT2E of histone modification processes, significantly over-expressed in the HF compared with the non-failing hearts (FDR < 0.05). To validate the over-expression of ALKBH5, we determined the global m6A level in hypoxic H9c2 cells using a dot blot assay. The global m6A level was found markedly lower in the hypoxic H9c2 cells than in the control cells. Additionally, the expression of ALKBH5 in the H9c2 cells was quantified by the qPCR and found to be 1.18 times higher at 12â h (p < 0.05), and 1.67 times higher at 24â h of hypoxia (p < 0.01) compared with the control cells, indicating a likely role of ALKBH5 in the failing cardiac cells. Furthermore, we identified several compounds through the virtual screening of 11,272 drug-like molecules of the ZINC15 database to inhibit the ALKBH5 in a molecular docking process. Collectively, the study revealed novel markers potentially involved in the pathophysiology of HF and suggested plausible therapeutic molecules for the management of the disease.
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PURPOSE: To take a systematic bibliometric analysis and generate the knowledge mapping of diabetic foot research, basing on big data from Web of Science Core Collection (WoSCC) database. METHODS: Two authors retrieved the WoSCC independently, to obtain publications in field of diabetic foot. CiteSpace was used to detect the co-occurrence relationships of authors, keywords, institutions, and countries/regions, co-citation relationships of authors, references, and journals, and distribution of WoS category. RESULTS: A total of 10,822 documents were included, with 39,541 authors contributed to this field. "Armstrong DG," "Lavery LA," and "Lipsky BA" are the top 3 productive authors, and "Armstrong DG," "Boulton AJM," and "Lavery LA" were most commonly cited. The United States, England and China are the most productive countries, and Univ Washington, Univ Manchester and Harvard Univ published the largest quantity of articles. "Diabetes Care," "Diabetic Med," and "Diabetologia" are the most frequently cited journals, providing the greatest knowledge base. Clustering analysis of keywords co-occurrence map presented the following hotspots: #1 diabetic wound healing, #2 diabetic polyneuropathy, #3 plantar pressure, #4 diabetic foot infection, #5 endovascular treatment, and #6 hyperbaric oxygen therapy. CONCLUSION: This study performed a global overview of diabetic foot research using bibliometric and visualization methods, which would provide helpful references for researchers focusing on this area to capture the future trend.
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Diabetes Mellitus , Pie Diabético , Neuropatías Diabéticas , Humanos , Bibliometría , Macrodatos , ChinaRESUMEN
Background Different T-lymphocyte subsets, including CD1d-dependent natural killer T (NKT) cells, play distinct roles in hypertension, highlighting the importance of identifying key immune cells for its treatment. This study aimed to determine the unknown effects of CD1d-dependent NKT cells on hypertension and vascular injury. Methods and Results Hypertension models were induced in male CD1d knockout (CD1dko), wild-type, and adoptive bone marrow transfer mice by angiotensin II (Ang II) or deoxycorticosterone acetate salt. Blood pressure was measured by the tail-cuff system and radiotelemetry. Vascular injury was assessed by histologic studies or aortic ring assay. Inflammation was detected by flow cytometry, quantitative real-time polymerase chain reaction, or ELISA. Results showed that Ang II infusion significantly reduced CD1d expression and NKT cell numbers in the aorta of mice. CD1dko mice exhibited worsened blood pressure elevation, vascular injury, and inflammatory response induced by Ang II or deoxycorticosterone acetate salt. However, these effects were markedly reversed in wild-type mice treated with NKT cell-specific activator. Adoptive transfer of CD1dko bone marrow cells to wild-type mice also significantly worsened Ang II-induced responses. Mechanistically, CD1dko increased Ang II-induced interleukin-6 production and activated signal transducer and activator of transcription 3 and orphan nuclear receptor γ, subsequently inducing interleukin-17A production. Neutralizing interleukin-17A partially reversed Ang II-induced hypertension and vascular injury in CD1dko mice. In addition, levels of NKT cells were lower in the blood of patients with hypertension (n=57) compared with normotensive individuals (n=87). Conclusions These findings reveal a previously unknown role for CD1d-dependent NKT cells in hypertension and vascular injury, indicating that NKT cell activation could be a promising therapeutic target for hypertension.
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Hipertensión , Células T Asesinas Naturales , Lesiones del Sistema Vascular , Animales , Masculino , Ratones , Acetatos/efectos adversos , Acetatos/metabolismo , Desoxicorticosterona/efectos adversos , Desoxicorticosterona/metabolismo , Hipertensión/inducido químicamente , Hipertensión/metabolismo , Interleucina-17/metabolismo , Ratones Endogámicos C57BL , Ratones Noqueados , Células T Asesinas Naturales/metabolismo , Lesiones del Sistema Vascular/metabolismoRESUMEN
Cardiovascular diseases (CVDs) are the leading cause of hospitalization and death worldwide, especially in developing countries. The increased prevalence rate and mortality due to CVDs, despite the development of several approaches for prevention and treatment, are alarming trends in global health. Chronic inflammation and macrophage infiltration are key regulators of the initiation and progression of CVDs. Recent data suggest that epigenetic modifications, such as DNA methylation, posttranslational histone modifications, and RNA modifications, regulate cell development, DNA damage repair, apoptosis, immunity, calcium signaling, and aging in cardiomyocytes; and are involved in macrophage polarization and contribute significantly to cardiac disease development. Cardiac macrophages not only trigger damaging inflammatory responses during atherosclerotic plaque formation, myocardial injury, and heart failure but are also involved in tissue repair, remodeling, and regeneration. In this review, we summarize the key epigenetic modifications that influence macrophage polarization and contribute to the pathophysiology of CVDs, and highlight their potential for the development of advanced epigenetic therapies.
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Stimulus-responsive nanomaterials have become a hot spot in controllable drug delivery systems researches owing to their spatiotemporal controllable properties based on the differences between tumor microenvironment and normal tissue. Herein, iron (III) carboxylate metal-organic framework nanoparticles coated with glycyrrhetinic acid-chitosan conjugate (MIL-101/GA-CS) were successfully fabricated and acted as the pH-responsive and target-selective system to deliver doxorubicin (DOX) for hepatocellular carcinoma (HCC) therapy. The prepared nanocarrier possess the advantages of uniform size, comparable drug loading efficiency (28.89%), and superior pH-dependent controlled drug release (DOX release of 2.74% and 89.18% within 72 h at pH 7.4 and 5.5, respectively). In vitro cytotoxicity assays showed that the drug-loaded nanocarriers exhibited excellent inhibitory effects on HepG2 cells due to the sustained release of DOX, while the nanocarriers showed no significant toxicity. Furthermore, cell uptake experiments demonstrated that MIL-101-DOX/GA-CS could target HepG2 cells based on receptor-dependent internalization of glycyrrhetinic acid receptors mediated. In vitro 3D hepatoma cell microspheres experiments showed that MIL-101-DOX/GA-CS had excellent penetration and tumor killing ability. Therefore, MIL-101-DOX/GA-CS nanoparticles have a prospective application in cancer therapy as a pH-responsive controlled drug delivery system.
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Carcinoma Hepatocelular , Quitosano , Ácido Glicirretínico , Neoplasias Hepáticas , Estructuras Metalorgánicas , Nanopartículas , Humanos , Quitosano/química , Carcinoma Hepatocelular/tratamiento farmacológico , Carcinoma Hepatocelular/patología , Ácido Glicirretínico/química , Neoplasias Hepáticas/tratamiento farmacológico , Neoplasias Hepáticas/patología , Sistemas de Liberación de Medicamentos , Doxorrubicina/química , Nanopartículas/química , Concentración de Iones de Hidrógeno , Liberación de Fármacos , Portadores de Fármacos/uso terapéutico , Microambiente TumoralRESUMEN
BACKGROUND: Combined exposure to lead and cadmium is common in occupational environments. However, the effects of co-exposure to Pb-Cd on neurotoxicity have not been fully clarified. Sodium para-aminosalicylic acid (PAS-Na) has previously been shown to protect neurons from Pb-induced toxicity. This study aimed to investigate the beneficial effect of PAS-Na against co-exposure to Pb-Cd-induced neurodegeneration in SH-SY5Y cells. METHODS: The MTT assay was used to detect the effects of Pb and Cd alone, or in combination, on SH-SY5Y cell survival. The effects of Pb and Cd alone or in combination on oxidative stress were assessed by reactive oxygen species (ROS) level. Nrf2, the master switch for antioxidant responses, was detected by immunofluorescence. Protein expression levels of PI3K, Akt, p-Akt, Nrf2 and HO-1 were determined by Western blot analysis. RESULTS: MTT assay results established that the survival rate of SH-SY5Y cells was not significantly affected by exposure to 1 µmol/L lead, 0.25 µmol/L cadmium, and 1-fold Pb-Cd mixture (1 µmol/L Pb + 0.25 µmol/L Cd), while 10-fold Pb-Cd combined exposure (10 µmol/L Pb + 2.5 µmol/L Cd) significantly reduced the survival rate of SH-SY5Y cells. Combined Pb-Cd exposure significantly increased intracellular ROS levels, and N-Acetyl-L-cysteine (NAC) treatment in the 10 µmol/L Pb + 2.5 µmol/L Cd group significantly decreased ROS expression levels, attenuating the levels of oxidative stress. Protein expression of PI3K and p-Akt significantly decreased in the 10 µmol/L Pb + 2.5 µmol/L Cd group, while the expression of PI3K and p-Akt protein increased after PAS-Na intervention. Immunofluorescence analysis showed that levels of Nrf2 in the nucleus increased in the 10 µmol/L Pb + 2.5 µmol/L Cd group, along with Nrf2 protein levels, suggesting that Nrf2 was translocated from the cytoplasm into the nucleus upon combined Pb-Cd exposure. In addition, HO-1 protein expression level, a downstream gene product of Nrf2, was increased. In response to NAC intervention, HO-1 protein expression levels significantly decreased. PAS-Na had the same intervention effect as NAC. CONCLUSION: Combined exposure to Pb-Cd induced oxidative stress and cytotoxicity in SH-SY5Y cells. PAS-Na displayed antagonistic effects on neurodegenerative changes induced by combined Pb-Cd exposure; hence, it may afford a novel treatment modality for exposure to these metals.
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Lead (Pb) is a common heavy metal contaminant in the environment, and it may perturb autophagy and cause neurodegeneration. Although sodium para-aminosalicylic (PAS-Na) has been shown to protect the brain from lead-induced toxicity, the mechanisms associated with its efficacy have yet to be fully understood. In this study, we evaluated the efficacy of PAS-Na in attenuating the neurotoxic effects of lead, as well as the specific mechanisms that mediate such protection. Lead exposure resulted in weight loss and injury to the liver and kidney, and PAS-Na had a protective effect against this damage. Both short-term and subchronic lead exposure impaired learning ability, and this effect was reversed by PAS-Na intervention. Lead exposure also perturbed autophagic processes through the modulation of autophagy-related factors. Short-term lead exposure downregulated LC3 and beclin1 and upregulated the expression of p62; subchronic lead exposure upregulated the expression of LC3, beclin1, and P62. It follows that PAS-Na had an antagonistic effect on the activation of the above autophagy-related factors. Overall, our novel findings suggest that PAS-Na can protect the rat cortex from lead-induced toxicity by regulating autophagic processes. (1) Short-term lead exposure inhibits autophagy, whereas subchronic lead exposure promotes autophagy. (2) PAS-NA ameliorated the abnormal process of lead-induced autophagy, which had a protective effect on the cerebral cortex.
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Ácido Aminosalicílico , Autofagia , Corteza Cerebral , Animales , Ratas , Ácido Aminosalicílico/farmacología , Autofagia/efectos de los fármacos , Beclina-1 , Plomo/toxicidad , Ratas Sprague-Dawley , Sodio , Corteza Cerebral/patología , Enfermedades Neurodegenerativas/inducido químicamente , Enfermedades Neurodegenerativas/patologíaRESUMEN
Lead (Pb) is a developmental neurotoxin that can disrupt brain development and damage the brain regions responsible for executive function, behavioral regulation and fine motor control. Sodium para-aminosalicylic acid (PAS-Na) is a non-steroidal anti-inflammatory drug that can cross the blood-brain barrier. The purpose of this study was to examine the effects of juvenile rat Pb exposure on behavioral changes and brain inflammation, and the efficacy of PAS-Na in ameliorating these effects. The results showed that Pb exposure during the juvenile period (from weaning to adult period) delayed rats' growth development and impaired their motor learning. Pb exposure not only increased Pb concentrations in several brain regions (including hippocampus, striatum and substantia nigra), but also disrupted metal-homeostasis in the brain, as higher levels of iron (Fe) and calcium (Ca) were observed in the substantia nigra. Moreover, Pb activated the MAPK pathway and increased levels of inflammatory factors such as IL-1ß, TNF-α and IL-6 in the hippocampus, striatum and substantia nigra. Furthermore, Pb increased the levels of alpha-synuclein (α-syn) in these brain sites. PAS-Na improved the motor deficits and brain inflammation in the Pb-exposed rats. Moreover, the elevated Pb, Fe and Ca concentrations in the brain were significantly reduced by PAS-Na, which contains amino, carboxyl and hydroxyl functional groups, suggesting that it may act as a chelator of brain metals. In addition, PAS-Na inhibited the Pb-induced MAPK pathway activation and α-syn accumulation in the same brain regions. Taken together, our novel study suggest that PAS-Na shows efficacy in improving the Pb-induced behavioral changes in rats by inhibiting MAPK-dependent inflammatory pathways and reducing α-syn accumulation.
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Ácido Aminosalicílico , Encefalitis , Ratas , Animales , Ácido Aminosalicílico/farmacología , Ácido Aminosalicílico/uso terapéutico , alfa-Sinucleína , Plomo/toxicidad , Enfermedades Neuroinflamatorias , Sodio , Encéfalo , Encefalitis/inducido químicamente , Encefalitis/tratamiento farmacológico , Sistema de Señalización de MAP QuinasasRESUMEN
In recent years, using magnetic nanocomposites for controlled release of drugs and target-specific drug delivery has great potential in exploring a new method for cancer chemotherapy. Nevertheless, the low loading rate of insoluble drugs greatly restricts their efficacy and clinical application. Here, an efficient magnetic nanostructure combining Fe3O4 nanoparticles and layered double hydroxide (LDH) was developed and used for tumor cell inhibition. LDH was first deposited on Fe3O4 nanoparticles (Fe3O4@LDH), curcumin (Cur) was then loaded and polydopamine (PDA) eventually formed a PDA-coating on Fe3O4@Cur-LDH via self-polymerization. The Fe3O4@Cur-LDH/PDA nanostructure showed a suitable nano-meter size, excellent magnetic property, and high drug loading rate (up to 38 %). In vitro release results implied that Fe3O4@Cur-LDH/PDA nanostructure had good pH-responsive performance and excellent controlled-release behaviors due to the introduction of PDA. The cellular experiments demonstrated that Fe3O4@Cur-LDH/PDA nanostructure had good biocompatibility. In addition, Fe3O4@Cur-LDH/PDA entered into the cells mainly through endocytosis and had excellent inhibition on HepG2 cell viability in a concentration-dependent manner. Therefore, Fe3O4@Cur-LDH/PDA nanostructure has a prospective application in cancer therapy as a controlled drug delivery system.
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Curcumina , Nanocompuestos , Sistemas de Liberación de Medicamentos , Curcumina/química , Nanocompuestos/química , Fenómenos Magnéticos , Hidróxidos/química , Concentración de Iones de HidrógenoRESUMEN
Lead (Pb) is considered to be a major environmental pollutant and occupational health hazard worldwide which may lead to neuroinflammation. However, an effective treatment for Pb-induced neuroinflammation remains elusive. The aim of this study was to investigate the mechanisms of Pb-induced neuroinflammation, and the therapeutic effect of sodium para-aminosalicylic acid (PAS-Na, a non-steroidal anti-inflammatory drug) in rat cerebral cortex. The results indicated that Pb exposure induced pathological damage in cerebral cortex, accompanied by increased levels of inflammatory factors tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1ß). Moreover, Pb decreased the expression of silencing information regulator 2 related enzyme 1 (SIRT1) and brain-derived neurotrophic factor (BDNF), and increased the levels of high mobile group box 1 (HMGB1) expression and p65 nuclear factor-κB (NF-κB) phosphorylation. PAS-Na treatment ameliorated Pb-induced histopathological changes in rat cerebral cortex. Moreover, PAS-Na reduced the Pb-induced increase of TNF-α and IL-1ß levels concomitant with a significant increase in SIRT1 and BDNF levels, and a decrease in HMGB1 and the phosphorylation of p65 NF-κB expression. Thus, PAS-Na may exert anti-inflammatory effects by mediating the SIRT1/HMGB1/NF-κB pathway and BDNF expression. In conclusion, in this novel study PAS-Na was shown to possess an anti-inflammatory effect on cortical neuroinflammation, establishing its efficacy as a potential treatment for Pb exposures.
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Ácido Aminosalicílico , Proteína HMGB1 , Ratas , Animales , FN-kappa B/metabolismo , Factor Neurotrófico Derivado del Encéfalo/metabolismo , Proteína HMGB1/metabolismo , Ratas Sprague-Dawley , Factor de Necrosis Tumoral alfa/metabolismo , Enfermedades Neuroinflamatorias , Sodio , Sirtuina 1/metabolismo , Plomo/toxicidad , Encéfalo/metabolismo , Corteza Cerebral/metabolismo , AntiinflamatoriosRESUMEN
Nonsmall cell lung cancer (NSCLC) accounts for ~85% of lung cancer cases and has high morbidity and mortality rates. Over the past decade, treatment strategies for NSCLC have progressed rapidly, particularly with the increasing use of screening programs, leading to improvements in the initial diagnosis and treatment of earlystage and preinvasive tumors. Surgical intervention remains the primary treatment for earlystage NSCLC. Thoracoscopic lobectomy has become the main treatment for earlystage NSCLC, as it results in less postoperative bleeding and pain and fewer complications. However, the complication rate for thoracoscopic lobectomy due to sputum retention and weakened respiratory muscle strength remains as high as 1959%. Treating NSCLC remains challenging in terms of postoperative pulmonary rehabilitation. In the present review, recent advances in postoperative pulmonary rehabilitation for patients with NSCLC were presented in order to assist researchers in developing improved treatments to enhance postoperative pulmonary rehabilitation for such patients.
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Carcinoma de Pulmón de Células no Pequeñas , Neoplasias Pulmonares , Humanos , Carcinoma de Pulmón de Células no Pequeñas/patología , Neoplasias Pulmonares/patología , Neumonectomía/efectos adversos , Neumonectomía/métodos , Cirugía Torácica Asistida por Video/efectos adversos , Cirugía Torácica Asistida por Video/métodos , Tiempo de Internación , Complicaciones Posoperatorias/etiología , Complicaciones Posoperatorias/cirugía , Estudios RetrospectivosRESUMEN
Rheumatoid arthritis is an autoimmune disease characterized by chronic symmetric synovial inflammation and erosive bone destruction. Mitochondria are the main site of cellular energy supply and play a key role in the process of energy metabolism. They possess certain self-regulatory and repair capabilities. Mitochondria maintain relative stability in number, morphology, and spatial structure through biological processes, such as biogenesis, fission, fusion, and autophagy, which are collectively called mitochondrial homeostasis. An imbalance in the mitochondrial homeostatic environment will affect immune cell energy metabolism, synovial cell proliferation, apoptosis, and inflammatory signaling. These biological processes are involved in the onset and development of rheumatoid arthritis. In this review, we found that in rheumatoid arthritis, abnormal mitochondrial homeostasis can mediate various immune cell metabolic disorders, and the reprogramming of immune cell metabolism is closely related to their inflammatory activation. In turn, mitochondrial damage and homeostatic imbalance can lead to mtDNA leakage and increased mtROS production. mtDNA and mtROS are active substances mediating multiple inflammatory pathways. Several rheumatoid arthritis therapeutic agents regulate mitochondrial homeostasis and repair mitochondrial damage. Therefore, modulation of mitochondrial homeostasis would be one of the most attractive targets for the treatment of rheumatoid arthritis.
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In this study, docosanoic acid, a very long chain fatty acid, was used to modify pectin, and the products were incorporated with carboxylmethyl cellulose (CMC) to prepare a hydrophobic composite. Results of structural characterisation showed that docosanoic acid was grafted to pectin through the esterification reaction, and the highest grafting ratio was 7.89 %. After grafting with docosanoic acid, the emulsifying activity and stability of pectin were significantly enhanced from 1.23 × 10-2 and 9.27 % to 4.78 × 10-2 and 26.73 %. Moreover, when modified pectin was blended with CMC instead of native pectin, the hydrophobicity of the composite membranes increased significantly. In detail, the highest contact angle of the composite membrane incorporated with modified pectin was 97.6°, which was much higher than that with native pectin (68.9°). As the grafting ratio of pectin increased, the water vapor permeability of the composite membranes significantly increased, while the water absorption decreased. Furthermore, the mechanical properties and transparency of the composite membranes could be improved by grafting docosanoic acid into pectin. All the results indicated that incorporating docosanoic acid possibly helped improve the comprehensive properties of the composite membranes based on polysaccharides and expand their application in food packaging.