Association between C-reactive protein-albumin ratio and overall survival in Parkinson's disease using publicly available data: A retrospective cohort study.

Background: At present, many studies have confirmed that inflammation plays a central role in Parkinson's disease (PD). The inflammatory index is related to the prognosis of the disease, but a single inflammatory index has some limitations. The C-reactive protein-albumin ratio (CAR) is a better marker of inflammation or nutritional status than C-reactive protein (CRP) or albumin (Alb), but there is limited study on the association between CAR and the overall survival (OS) of PD. Object: To study the association between CAR and OS in PD patients. Methods: All of these data were obtained from the Dryad Digital Repository, based on which we conducted a secondary analysis. The study was conducted by the Department of Neurology, the National Regional Center for Neurological Disorders, and the National Hospital of Utano study between March 2004 to November 2007. The final analytic sample included 235 PD patients with the outcome of survival or all-cause death from the study registration to the endpoint. In this study, univariate and multivariate COX regression analyses were used to calculate the adjusted hazard ratio (HR), with a 95% confidence interval (CI). In addition, the association between CAR and OS in PD patients was explored by Kaplan-Meier curve and subgroup analysis. Results: This study included 235 PD patients with an average age of 62.25 years, including 135 females and 100 males, and 45 died during the follow-up period. CAR was associated with gender, modified Hoehn-Yahr stages (mH-Y), and Mini-Mental State Examination (MMSE) of PD patients. In the COX multivariate regression model, after adjusting the age, gender, PD duration, mH-Y, MMSE, and the non-steroidal anti-inflammatory drugs, CAR was found to be associated with the OS in PD (HR = 1.54, 95% CI = 1.01-2.34, p = 0.044). Subgroup analysis showed that the subgroup did not play an interactive role in the association between the prognosis of patients with CAR and PD (p for interaction >0.05), and the results remained stable. Conclusions: The all-cause mortality of PD patients with a high level of CAR is higher, which indicates that the poor overall survival of PD patients is associated with the increase of CAR. The CAR may be a reliable prognostic biomarker for PD patients.

PD-1/L1 inhibitors may increase the risk of pericardial disease in non-small-cell lung cancer patients: a meta-analysis and systematic review.

Background: The advent of PD-1/L1 inhibitors has changed the landscape for patients with non-small-cell lung cancer (NSCLC). Meanwhile, the adverse events of PD-1/L1 inhibitors have been focused. Methods: The Cochrane Central Register of Controlled Trials, PubMed and Embase databases and ClinicalTrials.gov were searched from inception to February 2021. Results: 18 studies involving 11,394 patients with NSCLC were included. PD-1/L1 inhibitor monotherapy was associated (relative risk, 95% confidence interval) with an increased risk of pericardial effusion (2.72 [1.45-5.12]; p = 0.002) and cardiac tamponade (2.76 [1.15-6.62]; p = 0.023), whereas PD-1/L1 inhibitors combined with chemotherapy did not increase the risk of pericardial effusion and cardiac tamponade (3.08 [0.93-10.21]; p = 0.066 and 3.27 [0.37-28.94]; p = 0.288, respectively). Conclusion: For patients with NSCLC, treatment with PD-1/L1 inhibitor monotherapy increases the risk of pericardial effusion and cardiac tamponade, but PD-1/L1 inhibitors combined with chemotherapy do not.

In this study, the authors found that the incidence of pericardial effusion and cardiac tamponade in non-small-cell lung cancer patients treated with PD-1/L1 inhibitors was 0.63% and 0.35%, respectively, and in chemotherapy was 0.07% and less than 0.01%, respectively. The authors found that PD-1/L1 inhibitors combined with chemotherapy did not increase the risk of cardiac adverse events (AEs); however, the risk of cardiac AEs with PD-1/L1 inhibitor monotherapy should be considered, and the damage of pembrolizumab to the pericardium needs further attention. The mechanism of pericardial effusion and cardiac tamponade is not well understood, and pseudoprogression cannot be ruled out. Although the incidence of cardiac AEs is low, the prevention and management of immunotherapy should be paid attention to.

Wrist pulse diagnosis of stable coronary heart disease based on acoustics waveforms.

BACKGROUND AND OBJECTIVE: As a common pathological pulse, unsmooth pulse has important diagnostic value in traditional Chinese medicine (TCM). In modern pulse diagnosis, unsmooth pulse plays an important role in the diagnosis of disease location and nature, but there are few studies on it. In this paper, a pulse diagnosis approach based on acoustic waveforms was proposed, the wrist pulse was divided into five layers vertically for the first time. Five layers acoustic waves of the radial artery in stable coronary heart disease (CHD) patients and relatively healthy people were compared to explore whether there are abnormal changes in acoustic pulse in stable CHD patients. METHODS: The acoustic features of unsmooth pulse in patients with stable CHD were analyzed in time domain, frequency domain and empirical mode decomposition, combined with shannon entropy and multi-scale entropy. Sixteen pulse characteristics were discovered, and one-way analysis of variance were performed. The characteristics of the two groups were tested by T test. 13 features were used to identify patients with stable CHD by support vector machine (SVM). RESULTS: Compared to healthy people, all parameters of the third layer of the stable CHD left Cun pulse were significantly different from those of the healthy people. The identification rates of the fourth and third layer of the left Cun pulse were the first (90.79%) and the second (88.16%), respectively. CONCLUSION: Abnormal acoustic pulse appeared in the radial artery in patients with stable CHD. According to these changes, patients with stable CHD can be effectively identified from the perspective of pulse.

Adverse cardiac events in the treatment of non-small cell lung cancer with programmed death-1and programmed death-ligand 1 inhibitors: A protocol for systematic review and meta-analysis.

BACKGROUND: Programmed death-1 (PD-1) and programmed death ligand-1 (PD-L1) inhibitors are immune therapies that have shown great promise in the treatment of multiple cancers. However, immune-related adverse events of PD-1 and PD-L1 inhibitors may limit their use in non-small cell lung cancer (NSCLC). Given the rising number of clinical trials in recent years, it is essential to perform a meta-analysis to provide assess the cardiotoxicity of PD-1/ PD-L1 inhibitors in NSCLC therapy. METHOD AND ANALYSIS: The ClinicalTrials.gov, Embase, PubMed, and Cochrane Central Register of Controlled Trials repositories will be searched from their inception to December 2019. The bibliography of the searching process will be imported into Endnote X9 software. Two reviewers independently will screen the literature, extract data, and conduct the risk of bias for every added study. The data analysis will be analyzed using Stata15.0 software. Specific adverse cardiac events will be identified, with particular attention on atrial fibrillation, cardiac arrest, cardiac failure, and pericarditis. This review will be performed as per the Preferred Reporting Item for Systematic Review and meta-analysis statement recommendations. ETHICS AND DISSEMINATION: This study will provide support for the cardiotoxicity linked to the treatment of NSCLC using PD-1/PD-L1 inhibitors. The data in the meta-analysis will be retrieved from completed and published clinical trials; therefore, ethical review and patient informed consent will not be required. PROSPERO NUMBER: CRD42020156397.

Cardiac adverse events of PD-1 and PD-L1 inhibitors in cancer protocol for a systematic review and network meta-analysis: A protocol for systematic review.

INTRODUCTION: Programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) inhibitors have been increasingly used in the treatment of cancer. Immunosuppressive therapy can control the cancer well and is suitable for the moderate to severe diseases. However, according to clinical observation, immune-related cardiac adverse events against PD-1or/and PD-L1 are inevitable, but generally reversible. Understanding the cardiac adverse events of PD-1 or/and PD-L1 inhibitors is crucial to improve the anti-cancer efficacy and ensure the life safety of patients. The variability of cardiac adverse events between different immunosuppressants and different cancers is not clear. METHODS AND ANALYSIS: This protocol established in this study has been reported following the Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols. We will search the following electronic bibliographic databases: PubMed, Cochrane Library, EMBASE databases and ClinicalTrials.gov from their inception to December 2019. We will use a combination of Medical Subject Heading, and free-text terms with various synonyms to search based on the Eligibility criteria. We will include RCTs on PD-1 or/and PD-L1 inhibitors therapy to analyze. In addition, our study will include some clinical trials. All relevant RCTs will be included, such as early phase I/II, phase III experimental trials, prospective and retrospective observational studies. According to the inclusion and exclusion criteria outlined above, the full texts of each eligible study will be retrieved for further identification by one reviewer. Two authors will screen the titles and abstracts of all records retrieved in above electronic databases independently to find potentially eligible reviews. Data will be extracted by 2 reviewers independently using a pre-designed data extraction form. The other reviewer will validate data. I-square (I) test, substantial heterogeneity, sensitivity analysis and publication bias assessment will be performed accordingly. For our network meta-analysis, we will use Stata 15.0 and WinBUGS 1.4.3. ETHICS AND DISSEMINATION: Ethics approval and patient consent would be not required because the data of this network meta-analysis mainly are obtained from existing resources. This network meta-analysis will be published in a peer-reviewed journal. PROSPERO NUMBER: CRD42019142865.

Screening and Identification of Molecular Targets Involved in Preventing Gastric Precancerous Lesions in Chronic Atrophic Gastritis by Qilianshupi Decoction.

Chronic atrophic gastritis (CAG) is a common and possibly precancerous digestive tract disease. Development of drugs with effect of preventing precancerous lesions draws the eyes of global researchers. Qilianshupi decoction (QLSP) is a Traditional Chinese Medicine (TCM) that is commonly used to treat CAG, but few studies have explored the mechanism of QLSP on treating CAG. This study investigated the molecular targets of the component herbs of QLSP in preventing precancerous lesions based on network pharmacology. Network pharmacology analysis revealed that the 6 herbs regulated multiple CAG-related genes, among which the most important were cancer-related pathway (apoptosis, p53, and VEGF) and epithelial cell signaling in Helicobacter pylori infection. Further animal experiments showed that the expression of survivin and p53 in precancerous lesions of CAG rats was significantly increased which was suppressed by QLSP. Moreover, telomerase activity was inhibited in precancerous lesions of CAG rats, and telomere length of gastric mucosa was increased, which was reversed by QLSP. Our results suggest that the components of QLSP prevents gastric precancerous lesions through decreasing the expression of survivin and p53 and regulating telomerase activity and telomere length in CAG.

Coupling Factor 6 Is Upregulated in Monocrotaline-induced Pulmonary Arterial Hypertension in Rats.

BACKGROUND: Pulmonary arterial hypertension (PAH) is a rare and fatal disease. The prostacyclin (PGI2) pathway is a well-known therapeutic target for PAH. As a novel vasoconstrictive peptide, coupling factor 6 (CF6) has been recognized as the only endogenous inhibitor of PGI2. However, the relationship between CF6 and PAH is still unknown. In this study, we investigated the involvement of CF6 in PAH in rats. METHODS: A total of 80 Sprague-Dawley rats were randomly divided into 2 groups: a control group (with saline intraperitoneally) and a monocrotaline (MCT)-treated group (with MCT 60mg/kg intraperitoneal injection). The expression level of CF6 was measured by immunohistochemistry, reverse transcription polymerase chain reaction, and enzyme-linked immunosorbent assay. The plasma level of 6-keto-PGF1α, a stable metabolite of PGI2, was measured by enzyme-linked immunosorbent assay. RESULTS: After MCT injection, although the plasma level of CF6 was markedly increased in a time-dependent manner, the level of 6-keto-PGF1α was decreased in the MCT rats as compared to that in the controls (P < 0.05). Reverse transcription polymerase chain reaction indicated that the lung tissue level of CF6 messenger RNA (mRNA) in the MCT rats was significantly upregulated compared to the level in the controls. There was an intense CF6 immunostain concentrated on the lung tissue of the MCT rats compared with the controls. Univariate analysis indicated that the plasma level of CF6 was not correlated with blood pressure, fasting blood glucose, cholesterol (high-density lipoprotein, triglycerides and total cholesterol) or C-reactive protein level. CONCLUSIONS: These results demonstrated that CF6 was elevated in MCT-induced PAH rats and may play an important role in the development of PAH.