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Lung cancer is one of the common types of malignant disorders and the most prevalent cause of cancer-related mortality in the world. Although a wide range of approaches has been examined, strategies in prevention and treatment of lung cancer are still inadequate. Studies show that Vitamin D (VitD) is involved in various biological pathways and has been associated with the etiopathogenesis of several diseases, like cancers. In Vitro and In Vivo experiments have disclosed that VitD plays immunomodulatory and anti-tumor functions. Several lines of evidence have indicated that VitD is involved in the inflammatory settings of the lung. Epidemiological studies have reported that sufficient levels of VitD might be critical in the prevention of lung cancer. Polymorphisms in the genes encoding the different molecules involved in the signaling of VitD might affect the lung cancer risk as well as the quality and quantity of responses to different treatments. In this review article, we intended to clarify the implications of VitD in the normal biology and physiology of the lung and discuss diverse line of evidence about the possible role of VitD in the prevention or treatment of lung cancer. [ABSTRACT FROM AUTHOR]

Pneumonitis is a rare but severe and potentially fatal adverse effect in chemotherapy of lymphoma. This study is aimed to investigate the incidence of interstitial pneumonitis in non-Hodgkin's lymphoma (NHL) patients receiving immunochemotherapy with pegylated liposomal doxorubicin and rituximab. Lymphoma patients were retrospectively reviewed, and eligible patients were included in this study. According to the chemotherapy regimens, patients were classified in four groups: combination of vincristine, cyclophosphamide, doxorubicin, and prednisone (CHOP group) with rituximab (RCHOP group) and combination of vincristine, cyclophosphamide, pegylated liposomal doxorubicin and prednisone (CDOP group) with rituximab (RCDOP group). Incidence and severity of interstitial pneumonitis were compared among the four groups. Among 757 patients reviewed, 207 patients were included in final analysis. Thirteen patients developed chemotherapy-induced interstitial pneumonitis, and the mean cycle of chemotherapy before the onset of pneumonitis was 4. Incidence rates of pneumonitis were 0, 1.8, 17.4, and 21.1% in CHOP, RCHOP, CDOP, and RCDOP groups, respectively (p < 0.001). The mean grades of pneumonitis were 0, 2, 2.5, and 3 in four groups, respectively (p < 0.001). After adjustment of confounders, chemotherapy regimens (OR 3.491, 95% CI 1.527-7.981, p = 0.003) and neutropenia in previous cycles (OR 2.186, 95% CI 1.281-3.731, p = 0.004) were independently associated with the incidence of pneumonitis. Interstitial pneumonitis should be highlighted in NHL patients who received more than 4 cycles of RCDOP chemotherapy regimen, especially in those who had grade 4 neutropenia in the previous cycles of chemotherapy. [ABSTRACT FROM AUTHOR]

To understand multidrug resistance gene expression in reactive astrocytes, the present study involved stimulated astrocytes with tumor necrosis factor (TNF)-α and determined gene expression by reverse transcription-quantitative polymerase chain reaction and western blot analysis. Stimulation induced P-glycoprotein (gp) and multidrug resistance-associated protein (MRP0) 1 expression, which peaked by 24 h. Interestingly, the expression of P-gp and Mrp1 correlated with cell proliferation. Therefore, reactivation of astrocytes may increase P-gp and Mrp1 expression through TNF-α and nuclear factor (NF)-κB signaling. To the best of the authors' knowledge, the present study is the first to demonstrate that in vitro activated astrocytes likely induced P-gp and Mrp1 expression by increasing NF-κB expression. The results of the present study provide a novel insight into the mechanism of refractory epilepsy and suggest inhibiting cytokine signaling may block multidrug resistance. [ABSTRACT FROM AUTHOR]

The molecular mechanism underlying cancer invasiveness and metastasis of colorectal cancer (CRC) remains elusive. Here we reported a strong correlation of the levels of neuregulin receptor degradation protein-1 (Nrdp1) and matrix metalloproteinase-7 (MMP7) in CRC from the patients. We then used a human CRC line, Caco-2, to study the underlying molecular basis. We found that Nrdp1 inhibited the phosphorylation of ErB3, a key player in epidermal growth factor receptor (EGFR) signaling in Caco-2 cells, which is required for activation of MMP7 to promote cell invasion. Our findings thus reveal Nrdp1, EGFR signaling, and MMP7 as promising therapeutic targets for preventing the metastasis of CRC. [ABSTRACT FROM AUTHOR]

Multifunctional type-I photosensitizers (PSs) for hydrogen sulfide (H 2 S) detection and photodynamic therapy (PDT) of hypoxia tumors exhibits attractive curative effect but remains a challenging task. Herein, a mitochondria targeted aggregation-induced emission (AIE) photosensitizer TSPy-SS-P was designed and synthesized, which could be used for H 2 S detection and simultaneously type I and type II PDT. TSPy-SS-P had excellent selectivity and anti-interference abilities for endogenous and exogenous H 2 S detection in tumor cells. TSPy-SS-P was able to distinguish tumor cells with high level of H 2 S from normal cells by fluorescence "turn off" response to H 2 S. In addition, TSPy-SS-P showed type Ⅰ and type Ⅱ reactive oxygen species (ROS) generation ability to effectively ablate hypoxic tumor cells. TSPy-SS-P showed mitochondria targeting capacity which could produce ROS in situ to disrupt mitochondria and promote cell apoptosis. In vivo PDT experiments showcased that TSPy-SS-P had excellent tumor retention capability, effective tumor ablation ability and good biocompatibility. This work provided a two-pronged strategy to design organelles targeted photosensitizers for H 2 S detection and effective PDT of tumors., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

In recent years, the incidence of neurodegenerative diseases (NDs) has gradually increased over the past decades due to the rapid aging of the global population. Traditional research has had difficulty explaining the relationship between its etiology and unhealthy lifestyle and diets. Emerging evidence had proved that the pathogenesis of neurodegenerative diseases may be related to changes of the gut microbiota's composition. Metabolism of gut microbiota has insidious and far-reaching effects on neurodegenerative diseases and provides new directions for disease intervention. Here, we delineated the basic relationship between gut microbiota and neurodegenerative diseases, highlighting the metabolism of gut microbiota in neurodegenerative diseases and also focusing on treatments for NDs based on gut microbiota. Our review may provide novel insights for neurodegeneration and approach a broadly applicable basis for the clinical therapies for neurodegenerative diseases., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Author Contributions, (Copyright © 2024 Fu, Gu, Cao, Zuo, Huang, Song, Jiang and Wang.)

The purpose of the article is to investigate Dirichlet boundary-value problems of the fractional p-Laplacian equation with impulsive effects. By using the Nehari manifold method, mountain pass theorem and three critical points theorem, some new results are achieved under more general growth conditions. In addition, this paper weakens the commonly used p-suplinear and p-sublinear growth conditions.

Objective: Oxytocin (OT) is primarily synthesized in the paraventricular nucleus of the hypothalamus and supraoptic nucleus of the hypothalamus in the central nervous system and exhibits a wide spectrum of central and peripheral activities. OT is involved in lipid metabolism and glucose homeostasis and plays a protective role against liver damage., Methods: In this study, we investigated whether CSF OT levels correlates with peripheral glucose, lipid profiles, and/or liver enzymes in Chinese subjects. Sixty-nine subjects (n=36 males; n=33 females) who were recruited from Beijing Jishuitan Hospital participated in the study. Their levels of CSF OT and peripheral parameters were assayed by radioimmunoassay and continuous monitoring assay, respectively., Results: There was no significant difference in CSF OT levels between males (53.09±6.88 nmol/mL) and females (52.34±6.87 nmol/mL), and no correlation found between CSF OT levels and peripheral glucose and lipid profiles. Significant negative correlation was observed between CSF OT levels and peripheral ALT and AST concentration in females but not in males., Conclusion: Our results support the physiological role of neuropeptides acting on brain sites to regulate liver enzymes, and shed new light on the brain-liver interaction.

Nonalcoholic fatty liver disease (NAFLD) is often associated with dyslipidemia. Metabolic disequilibrium, resulting from being overweight and obesity, increases risk to cardiovascular system and chronic liver disease. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transferase (GGT) are standard clinical markers for liver injury. In this study, we examined association of body mass index (BMI) and metabolic markers with serum ALT, AST and GGT activity in an overweight and obese Chinese population. A total of 421 overweight and obese Chinese adults (211 males and 210 females) from The First Affiliated Hospital of Wenzhou Medical University were recruited in this study in 2014. All participants underwent anthropometric measures and phlebotomy after an overnight fast. Elevated ALT, AST and GGT levels were found in 17%, 5% and 24%, respectively. There were significant correlations between ALT and BMI, plasma triglycerides (TG), cholesterol, HDL and glucose, and between AST and plasma TG and cholesterol. GGT also correlated with plasma TG, cholesterol and glucose. The levels of ALT, AST and GGT could be predicted by BMI, plasma TG, cholesterol, HDL and glucose using the back propagation artificial neural network model (BP-ANN). These data suggest that abnormal metabolic markers could be used to monitor liver function to determine whether liver damage has occurred in overweight and obese individuals. This approach has clinical utility with respect to early scanning of liver injury or NAFLD based on routinely available metabolic data in overweight and obese population.

The molecular mechanism underlying cancer invasiveness and metastasis of colorectal cancer (CRC) remains elusive. Here we reported a strong correlation of the levels of neuregulin receptor degradation protein-1 (Nrdp1) and matrix metalloproteinase-7 (MMP7) in CRC from the patients. We then used a human CRC line, Caco-2, to study the underlying molecular basis. We found that Nrdp1 inhibited the phosphorylation of ErB3, a key player in epidermal growth factor receptor (EGFR) signaling in Caco-2 cells, which is required for activation of MMP7 to promote cell invasion. Our findings thus reveal Nrdp1, EGFR signaling, and MMP7 as promising therapeutic targets for preventing the metastasis of CRC.