Search

Background The relationship between cancer and COVID‐19 has been revealed during the pandemic. Some anticancer treatments have been reported to have negative influences on COVID‐19‐infected patients while other studies did not support this hypothesis. Methods A literature search was conducted in WOS, PubMed, Embase, Cochrane Library, CNKI and VIP between Dec 1, 2019 and Sept 23, 2020 for studies on anticancer treatments in patients with COVID‐19. Cohort studies involving over 20 patients with cancer were included. The characteristics of the patients and studies, treatment types, mortality, and other additional outcomes were extracted and pooled for synthesis. RRs and forest plots were adopted to present the results. The literature quality and publication bias were assessed using NOS and Egger's test, respectively. Results We analyzed the data from 29 studies, with 5121 cancer patients with COVID‐19 meeting the inclusion criteria. There were no significant differences in mortality between patients receiving anticancer treatment and those not (RR 1.17, 95%CI: 0.96–1.43, I2=66%, p = 0.12). Importantly, in patients with hematological malignancies, chemotherapy could markedly increase the mortality (RR 2.68, 95% CI: 1.90–3.78, I2=0%, p, No significant difference was seen in any anticancer treatments in solid tumor subgroup. Chemotherapy, however, will lead to a higher mortality in patients with hematological malignancies.

Highlights • Self-reported depression appeared in the early stage of recovery even when COVID-19 patients discharged from hospital. • Self-reported depression has no significant correlation with gender, age, comorbidities, severity of initial infection, duration of initial illness of SARS-CoV-2. • Patients with self-reported depression exhibited increased immune response, as indicated by increased white blood cell and neutrophil counts, as well as neutrophil-to-lymphocyte ratio. • Appropriate psychological interventions are necessary, and changes in immune function should be emphasized during long-term follow up of these patients., Self-reported depression has been observed in coronavirus disease-2019 (COVID-19) patients, infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), during discharge from the hospital. However, the cause of this self-reported depression during the convalescent period remains unclear. Here, we report the mental health status of 96 convalescent COVID-19 patients who were surveyed using an online questionnaire at the Shenzhen Samii Medical Center from March 2 to March 12, 2020 in Shenzhen, China. After obtaining their informed consent, we retrospectively analyzed the clinical characteristics of patients, including routine blood and biochemical data. The results suggested that patients with self-reported depression exhibited increased immune response, as indicated by increased white blood cell and neutrophil counts, as well as neutrophil-to-lymphocyte ratio. However, the mechanism linking self-reported depression to these cellular changes needs further study. In conclusion, self-reported depression occurred at an early stage in convalescent COVID-19 patients, and changes in immune function were apparent during short-term follow-up of these patients after discharge. Appropriate psychological interventions are necessary, and changes in immune function should be emphasized during long-term follow up of these patients.

This study aimed to reveal potential roles of the phosphatidylinositol 3 kinase (PI3K)-protein kinase B (Akt)-mammalian target of rapamycin (mTOR) signaling pathway in apoptosis and autophagy of astrocytes induced by methamphetamine (METH). A Cell Counting Kit-8 (CCK-8) was used to determine the reduction in proliferation of U-118 MG cells induced by METH. Hoechst 33258 and flow cytometry were used to observe the astrocytes. Western blot analysis was performed to evaluate protein expression and phosphorylation levels. METH inhibited the proliferation of U-118 MG cells and induced apoptosis and autophagy. Western blot analysis showed that the ratio of LC3-II/I was increased, whereas the expression of Bcl-2 was decreased. The phosphorylation cascade of kinases in the PI3K-Akt-mTOR signaling pathway was significantly inhibited by METH exposure, as were proteins downstream of mTORC1, such as p70s6k, rps6, 4EBP1 and eIF4E. METH inhibited proliferation of U-118 MG cells and induced apoptosis and autophagy. The PI3K-Akt-mTOR signaling pathway likely plays a critical role in these effects.

Berberine (BBR) is a plant secondary metabolite that has been used in photodynamic therapy (PDT) in the last few decades. The present review aimed to discuss the research progress of BBR-mediated photodynamic actions. The following key words were searched in several databases: 'Berberine' combined with 'photodynamic therapy', 'sonodynamic therapy (SDT)', 'ultraviolet', 'reactive oxygen' and 'singlet oxygen'. The results demonstrated that both type I and type II reactions participated in the photodynamic progression of BBR derivatives. In addition, the photochemical characteristics of BBR derivatives were affected by the polarity, pH and O2 content of solvents. DNA binding increases the lifespan of the photoexcited BBR state and generation of singlet oxygen (1O2). The chemical properties of substituents in different positions of the BBR skeleton are pivotal for its photochemical properties, particularly the methylenedioxy group at the C-2 and C-3 positions. BBR is a promising agent for mediating both PDT- and SDT-treated diseases, particularly in tumors. However, further studies are required to validate their biological effects. In addition, the molecular mechanisms underlying the antitumor effects of BBR-PDT remain unclear and warrant further investigation. The structural modification and targeted delivery of BBR have made it possible to broaden its applications; however, experimental verification is required. Overall, BBR acts as a sensitizer for PDT and has promising development prospects.

Thyroid cancers (TC) have increasingly been detected following advances in diagnostic methods. Risk stratification guided by refined information becomes a crucial step toward the goal of personalized medicine. The diagnosis of TC mainly relies on imaging analysis, but visual examination may not reveal much information and not enable comprehensive analysis. Artificial intelligence (AI) is a technology used to extract and quantify key image information by simulating complex human functions. This latent, precise information contributes to stratify TC on the distinct risk and drives tailored management to transit from the surface (population-based) to a point (individual-based). In this review, we started with several challenges regarding personalized care in TC, for example, inconsistent rating ability of ultrasound physicians, uncertainty in cytopathological diagnosis, difficulty in discriminating follicular neoplasms, and inaccurate prognostication. We then analyzed and summarized the advances of AI to extract and analyze morphological, textural, and molecular features to reveal the ground truth of TC. Consequently, their combination with AI technology will make individual medical strategies possible.

The BMI1 protein, a member of the PRC1 family, is a well recognised transcriptional suppressor and has the capability of maintaining the self-renewal and proliferation of tissue-specific stem cells. Numerous studies have established that BMI1 is highly expressed in a variety of malignant cancers and serves as a key regulator in the tumorigenesis process. However, our understanding of BMI1 in terminally differentiated organs, such as the heart, is relatively nascent. Importantly, emerging data support that, beyond the tumor, BMI1 is also expressed in the heart tissue and indeed exerts profound effects in various cardiac pathological conditions. This review gives a summary of the novel functions of BMI1 in the heart, including BMI1-positive cardiac stem cells and BMI1-mediated signaling pathways, which are involved in the response to various cardiac pathological stimuli. Besides, we summarize the recent progress of BMI1 in some novel and rapidly developing cardiovascular therapies. Furtherly, we highlight the properties of BMI1, a therapeutic target proved effective in cancer treatment, as a promising target to alleviate cardiovascular diseases.

The aim of the present study was to explore the antitumor effects of sinoporphyrin sodium (DVDMS)-mediated photodynamic therapy (PDT) and sonodynamic therapy (SDT) in glioma, and to reveal the underlying mechanisms. The uptake of DVDMS by U-118 MG cells was detected by flow cytometry (FCM). A 630-nm semiconductor laser and 1-MHz ultrasound were used to perform PDT and SDT, respectively. Cell proliferation and apoptosis were evaluated using the Cell Counting Kit-8 assay, FCM and Hoechst 33258 staining, respectively. Western blot analysis was used to detect protein expression and phosphorylation levels. BALB/c nude mice were used to establish a xenograft model of U-118 MG cells. DVDMS was injected intravenously and PDT and SDT were performed 24 h later. An in vivo imaging system was used to evaluate the fluorescence of DVDMS, to measure tumor sizes, and to evaluate the therapeutic effects. The uptake of DVDMS by U-118 MG cells was optimal after 4 h. PDT and SDT following DVDMS injection significantly inhibited the proliferation and increased apoptosis of glioma cells in vitro (P

Recently, the recurrence of positive SARS-CoV-2 viral RNA in recovered COVID-19 patients is receiving more attention. Herein we report a cohort study on the follow-up of 182 recovered patients under medical isolation observation. Twenty (10.99%) patients out of the 182 were detected to be SARS-CoV-2 RNA positive (re-positives), although none showed any clinical symptomatic recurrence, indicating that COVID-19 responds well to treatment. Patients aged under 18 years had higher re-positive rates than average, and none of the severely ill patients re-tested positive. There were no significant differences in sex between re-positives and non-re-positives. Notably, most of the re-positives turned negative in the following tests, and all of them carried antibodies against SARS-CoV-2. This indicates that they might not be infectious, although it is still important to perform regular SARS-CoV-2 RNA testing and follow-up for assessment of infectivity. The findings of this study provide information for improving the management of recovered patients, and for differentiating the follow-up of recovered patients with different risk levels.

The aim of this study was to determine the effects of Jinniu Capsule on methamphetamine (METH)-induced conditioned place preference (CPP) in rats and identify the underlying mechanisms. An intraperitoneal injection of 3 mg/kg METH was used for CPP training in rats. The effects of Jinniu Capsule following a single dose on rat CPP and repeat dosing on METH withdrawal were evaluated. Western Blot analysis was used to measure protein expression of the PI3K-AKT-mTOR signaling pathway to determine the mechanisms of Jinniu Capsule. A single dose of Jinniu Capsule did not influence METH-induced CPP in rats. However, repeat dosing for 7 days significantly promoted METH withdrawal. Furthermore, METH withdrawal activated the PI3K-AKT-mTOR signaling pathway phosphorylation cascade, and Jinniu Capsule partly blocked this cascade. Jinniu Capsule demonstrated potential in promoting METH withdrawal in a rat CPP model, which may be related to its influence on the PI3K-AKT-mTOR signaling pathway.

Background/Aims: This study aimed to investigate the anti-inflammatory activity of Berbamine (BER), a bisbenzylisoquinoline alkaloid extracted from Berberis amurensis (Xiao Bo An), and the underlying mechanisms. Methods: Macrophages and neutrophils were treated with BER in vitro and stimulated with LPS and fMLP. The effects of BER on the expression of pro-inflammatory mediators in macrophages were evaluated with quantitative RT-PCR and ELISA. The effects of BER on the activation and superoxide release of neutrophils were determined with flow cytometry and WST-1 reduction test. The inhibitory effects of BER on the activation of signaling pathways related to inflammatory response in macrophages were evaluated by western blot analysis. In addition, a mouse peritonitis model was made by peritoneal injection of thioglycollate medium and anti-inflammatory effects of BER were investigated in vivo by quantitative analysis of pro-inflammatory factor production and leukocyte exudation. Results: BER significantly inhibited inflammatory factor expression by LPS-stimulated macrophages and suppressed activation and superoxide release of fMLP-stimulated neutrophils. In the mouse peritonitis model, BER significantly inhibited the activation of macrophages and exudation of neutrophils. According to analysis, BER significantly suppressed phosphorylation of NF-κB and MAPK (JNK and ERK1/2) signaling pathways in LPS-stimulated macrophages. Conclusions: Collectively, data from this study suggest that BER has anti-inflammatory potential, which is effected via inhibition of NF-κB and MAPK signaling pathways, and thus holds promise for treatment of inflammatory disease.