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Objective:To explore the predictive value of the serum C-reactive protein (CRP)/albumin (ALB) ratio (CAR) for organ damage in tsutsugamushi disease.Methods:The clinical data of 166 patients with tsutsugamushi disease admitted to the First Affiliated Hospital of Wenzhou Medical University from January 1, 2010 to December 31, 2020 were retrospectively analyzed. The patients were divided into the organ damage group (72 cases) and non-organ damage group (94 cases) according to the organ damage criteria. The general data and laboratory test results of the two groups of patients were compared. The significant indicators of univariate analysis were analyzed by multivariate logistic regression analysis. The receiver operating characteristic (ROC) curve and area under the curve (AUC) were used to analyze the predictive value of CAR for organ damage in patients with tsutsugamushi disease.Results:There were no significant differences in age, sex, days of fever, and admission body temperature between the organ damage group and non-organ damage group ( P>0.05). However, the body mass index, acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ), sequential organ failure assessment (SOFA), length of hospital stay, hospitalization expense, percentage of neutrophils (NEUT), lymphocyte count, procalcitonin, CRP, and CAR in the organ damage group were significantly higher than those in the non-organ damage group ( P<0.05), and ALB was significantly lower than that in the non-organ damage group ( P<0.05). Multivariate logistic regression analysis showed that APACHEⅡ( P=0.039), NEUT ( P=0.003), and CAR ( P=0.011) were independent risk factors for tsutsugamushi disease complicated by organ damage. The ROC curve showed that the AUCs of APACHEⅡ, NEUT, and CAR were 0.655, 0.716, and 0.727, respectively. When the cut-off value of CAR was 2.86, the sensitivity was 55.6%, and the specificity was 79.8%. Conclusions:Elevated CAR is an independent risk factor for tsutsugamushi disease complicated with organ damage and can be used as an important indicator to evaluate the presence or absence of organ damage in patients with tsutsugamushi disease.
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Exosomes are cell-derived nanovesicles with diameters from 30 to 150 nm, released upon fusion of multivesicular bodies with the cell surface. They can transport nucleic acids, proteins, and lipids for intercellular communication and activate signaling pathways in target cells. In cancers, exosomes may participate in growth and metastasis of tumors by regulating the immune response, blocking the epithelial-mesenchymal transition, and promoting angiogenesis. They are also involved in the development of resistance to chemotherapeutic drugs. Exosomes in liquid biopsies can be used as non-invasive biomarkers for early detection and diagnosis of cancers. Because of their amphipathic structure, exosomes are natural drug delivery vehicles for cancer therapy.
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Glioblastoma multiforme (GBM) in the central nervous system is the most lethal advanced glioma and currently there is no effective treatment for it. Studies of sinomenine, an alkaloid from the Chinese medicinal plant,
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Glioblastoma is the most common and aggressive primary tumor in the central nervous system, accounting for 12%-15% of all brain tumors. 3--Acetyl-11-keto--boswellic acid (AKBA), one of the most active ingredients of gum resin from Birdw., was reported to inhibit the growth of glioblastoma cells and subcutaneous glioblastoma. However, whether AKBA has antitumor effects on orthotopic glioblastoma and the underlying mechanisms are still unclear. An orthotopic mouse model was used to evaluate the anti-glioblastoma effects of AKBA. The effects of AKBA on tumor growth were evaluated using MRI. The effects on the alteration of metabolic landscape were detected by MALDI-MSI. The underlying mechanisms of autophagy reducing by AKBA treatment were determined by immunoblotting and immunofluorescence, respectively. Transmission electron microscope was used to check morphology of cells treated by AKBA. Our results showed that AKBA (100 mg/kg) significantly inhibited the growth of orthotopic U87-MG gliomas. Results from MALDI-MSI showed that AKBA improved the metabolic profile of mice with glioblastoma, while immunoblot assays revealed that AKBA suppressed the expression of ATG5, p62, LC3B, p-ERK/ERK, and P53, and increased the ratio of p-mTOR/mTOR. Taken together, these results suggested that the antitumor effects of AKBA were related to the normalization of aberrant metabolism in the glioblastoma and the inhibition of autophagy. AKBA could be a promising chemotherapy drug for glioblastoma.
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Gangliosides are a class of important glycosphingolipids containing sialic acid that are widely distributed on the outer surface of cells and are abundantly distributed in brain tissue. Disialoganglioside with three glycosyl groups (GD3) and disialoganglioside with two glycosyl groups (GD2) are markedly increased in pathological conditions such as cancers and neurodegenerative diseases. GD3 and GD2 were found to play important roles in cancers by mediating cell proliferation, migration, invasion, adhesion, angiogenesis and in preventing immunosuppression of tumors. GD3 synthase (GD3S) is the regulatory enzyme of GD3 and GD2 synthesis, and is important in tumorigenesis and the development of cancers. The study of GD3S as a drug target may be of great significance for the discovery of new drugs for cancer treatment. This review will describe the gangliosides and their roles in physiological and pathological conditions; the roles of GD3 and GD2 in cancers; the expression, functions and mechanisms of GD3S, and its potential as a drug target in cancers.
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Objective To study the inhibitory effect of recombinant human interferon α1b (IFN-α1b) on enterovirus 71 (EV71) in vitro and to investigate the antiviral mechanism of IFN-α1b.Methods The cytotoxity of IFN-α1b and the inhibition of IFN-α1b on cytopathic effect before and after EV71 infection were measured in rhabdomyosarcoma (RD) cell line.The in vitro inhibition of IFN-α1b on EV71 RNA and VP1 protein,and the protection of IFN-α1b on EV71 infected cells were also investigated.Then the EV71 invasion prevention of IFN-α1b induced transmembrane protein IFITM3 was evaluated.Results When treated 12h before or 1h after EV71 infection,IFN-α1b presented a IC50 258.53IU/ml and 2113.58IU/ml with SI>16497 and >3271,respectively,suggesting that IFN-α1b had obvious anti EV71 activity,and IFN-α1b treatment before EV71 infection was more effective.This study also showed that IFN-α1b significantly inhibited EV71 RNA replication and protein synthesis,and delayed the progeny virus release,which might prevent EV71 invasion by inducing IFITM3 expression.Conclusion IFN-α1b has anti EV71 activity and can act as an antiviral agent by influencing the viral life cycle including invasion,replication,assembly and release.
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Objective To explore the effects of low load exercise on the gait and balance in patients with Parkinson's disease. Methods 12 inpatients with Parkinson's disease from May to August, 2015 accepted low load exercise on Power Rehabilitation System 14 times in 2 weeks, with the medication as before. They were assessed with 3D gait analysis and Berg Balance Scale before and after treatment. Results The step length, stride length and walking speed improved after treatment (P0.05). The scores of Berg Balance Scale improved after treatment (P<0.05). Conclusion The low load exercise can improve the gait and balance in patients with Parkinson's disease.
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Objective To explore whether hypermethylation in the promoter of p16 gene and protein of p16 were associated with development and clinicopathological characteristics of colorectal cancer. Methods Methylation-specific PCR ( MSP) and immunohistochemistry SP were used to detected hypermethylation of p16 gene and p16 protein in tumor tissues from 32 patients with colorectal cancer. Results The hypermethylation of p16 gene was detected in 40. 6% of tumor tissues. The protein of p16 promoter was detected in 75% of tumor tissues. The hypermethylation of p16 gene was detected in 63% in Dukes stages of C and D tumors. The protein of p16 promoter was detected in 69% of tumor tissues. The hypermethylation of p16 gene was detected in 25% in the stages of A and B tumors. The protein of p16 promoter was detected in 81% of tumor tissues. The hpermethylation of p16 gene was detected in 100% in low differentiated carcinomas. The protein of p16 promoter was detected in 20% , the hypermethylation of p16 gene was detected in 30% , in the high and mediate differentiated carcinomas, the protein of p16 promoter was detected in 85%. Furthermore, the hypermethylation of p16 gene was detected in 63% in the lymph node metastasis and 25% in without lymph node metastasis. The protein of p16 promoter was detected in 65% in rectum and 100% in colon. Conclusions Our study demonstrated that p16 hypermethylation and protein were associated with the development of colorectal cancer and could be used as a putative prognostic indicator for this malignancy.
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To explore whether aberrant methylation in the promoter of p16 gene was associated with development and clinicopathological characteristics of colorectal cancer. Methylation-specific PCR(MSP) was used to detect hypermethylation of p16 gene in tumor tissues obtained from 32 patients with colorectal cancer. The results showed that the hypermethylation of p16 promoter was detected in 40.6% of tumor tissues. p16 hypermethylation in patients with Dukes stages of C and D tumors (63%) was higher than that in the stages of A and B tumors (25%). The highly and intermediately differentiated carcinomas had lower positive rate (30%) than the poorly differentiated carcinoma. Furthermore, the hypermethylation of p16 gene in tumor tissue from patients with the lymph node metastasis was different from that without lymph node metastasis (P