scholarly journals Effect of vitiligo treatment by compound Glycyrrhizin combined with fractional laser and Triamcinolone Acetonide injection on T Lymphocyte subpopulation

2021 ◽  
Vol 38 (1) ◽  
Author(s):  
Ling Li ◽  
Lei Gao ◽  
Yifan Zhao

Objectives: To discuss the effective mechanism of vitiligo treatment by compound glycyrrhizin combined with fractional laser and triamcinolone acetonide injection. Methods: Forty-two patients with vitiligo vulgaris in the stable phase were classified into combined group (19 cases) and medicine group (23) admitted in dermatology department, Baoding First Central Hospital from January 2017 to July 2018. Both groups took 50mg compound glycyrrhizin orally three times per day, and applied halometasone cream externally once per day. Based on this treatment method, after the combined group adopted fractional laser, triamcinolone acetonide injection encapsulation was used immediately. After the treatment for six months, the curative effect was judged for both groups. Flow cytometry was used to test the changes of T lymphocyte subpopulation in peripheral blood before and after treatment. Meanwhile, immunohistochemical method was adopted to determine CD4+ and CD8+ T lymphocyte expression level. Besides, the normal control group was set up. Results: The efficacy of combined group and medicine group were 73.68% and 56.52% respectively, P<0.05. The comparison of CD3+, CD4+, CD8+ and CD4+/CD8+ T lymphocyte level in serum and skin damage before and after treatment had no statistical significance (P>0.05). Serum CD4+ T cells of vitiligo patients reduced, compared with the normal control group (P<0.05), and CD4+/CD8+ declined (P<0.05). CD4+ and CD8+ T lymphocytes at the skin damage of patients increased, compared with normal control group (P<0.05). Conclusions: Compound glycyrrhizin combined with fractional laser and triamcinolone acetonide injection has good clinical effect in the treatment of vitiligo vulgaris in the stable phase, and its effective mechanism may have nothing to do with T lymphocyte subpopulation. doi: https://doi.org/10.12669/pjms.38.1.4412 How to cite this:Li L, Gao L, Zhao Y. Effect of vitiligo treatment by compound Glycyrrhizin combined with fractional laser and Triamcinolone Acetonide injection on T Lymphocyte subpopulation. Pak J Med Sci. 2022;38(1):---------. doi: https://doi.org/10.12669/pjms.38.1.4412 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Author(s):  
Xitong Yang ◽  
Pengyu Wang ◽  
Shanquan Yan ◽  
Guangming Wang

AbstractStroke is a sudden cerebrovascular circulatory disorder with high morbidity, disability, mortality, and recurrence rate, but its pathogenesis and key genes are still unclear. In this study, bioinformatics was used to deeply analyze the pathogenesis of stroke and related key genes, so as to study the potential pathogenesis of stroke and provide guidance for clinical treatment. Gene Expression profiles of GSE58294 and GSE16561 were obtained from Gene Expression Omnibus (GEO), the differentially expressed genes (DEGs) were identified between IS and normal control group. The different expression genes (DEGs) between IS and normal control group were screened with the GEO2R online tool. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the DEGs were performed. Using the Database for Annotation, Visualization and Integrated Discovery (DAVID) and gene set enrichment analysis (GSEA), the function and pathway enrichment analysis of DEGS were performed. Then, a protein–protein interaction (PPI) network was constructed via the Search Tool for the Retrieval of Interacting Genes (STRING) database. Cytoscape with CytoHubba were used to identify the hub genes. Finally, NetworkAnalyst was used to construct the targeted microRNAs (miRNAs) of the hub genes. A total of 85 DEGs were screened out in this study, including 65 upward genes and 20 downward genes. In addition, 3 KEGG pathways, cytokine − cytokine receptor interaction, hematopoietic cell lineage, B cell receptor signaling pathway, were significantly enriched using a database for labeling, visualization, and synthetic discovery. In combination with the results of the PPI network and CytoHubba, 10 hub genes including CEACAM8, CD19, MMP9, ARG1, CKAP4, CCR7, MGAM, CD79A, CD79B, and CLEC4D were selected. Combined with DEG-miRNAs visualization, 5 miRNAs, including hsa-mir-146a-5p, hsa-mir-7-5p, hsa-mir-335-5p, and hsa-mir-27a- 3p, were predicted as possibly the key miRNAs. Our findings will contribute to identification of potential biomarkers and novel strategies for the treatment of ischemic stroke, and provide a new strategy for clinical therapy.


2014 ◽  
Vol 1033-1034 ◽  
pp. 220-223
Author(s):  
Xue Mei Han ◽  
Li Bo Wang ◽  
Ni Ni Li ◽  
Song Yan Liu

To examine the effect of GDM on the expression of MT1-MMP and u-PA genes in glioma cells. Glioma cell lines U251 and U87 were cultured in DMEM medium supplemented with 10% fetal bovine serum. RT-PCR was used to identify gene expression level. The level of u-PA mRNA was up-regulated significantly in the HGF group compared with the normal control group (P<0.05). The expression of MT1-MMP and u-PA was significantly lower in the GDM group than in the normal control and HGF groups (P<0.05). The expression of u-PA in the HGF+GDM group was down-regulated significantly compared with the normal control and HGF groups (P<0.05).GDM can inhibit expression of both MT1-MMP and u-PA in glioma cells.


2021 ◽  
Author(s):  
Jinglei Li ◽  
Wei Hou

Abstract Purpose: Lung adenocarcinoma (LUAD) has high heterogeneity and poor prognosis, posing a major challenge to human health worldwide. Therefore, it is necessary to improve our understanding of the molecular mechanism of LUAD in order to be able to better predict its prognosis and develop new therapeutic strategies for target genes.Methods: The Cancer Genome Atlas and Gene Expression Omnibus, were selected to comprehensively analyze and explore the differences between LUAD tumors and adjacent normal tissues. Critical gene information was obtained through weighted gene co-expression network analysis (WGCNA), differential gene expression analysis, and survival analysis.Results: Using WGCNA and differential gene expression analysis, 29 differentially expressed genes were screened. The functional annotation analysis showed these genes to be mainly concentrated in heart trabecula formation, regulation of inflammatory response, collagen-containing extracellular matrix, and metalloendopeptidase inhibitor activity. Also, in the protein–protein interaction network analysis, 10 central genes were identified using Cytoscape's CytoHubba plug-in. The expression of CDH5, TEK, TIMP3, EDNRB, EPAS1, MYL9, SPARCL1, KLF4, and TGFBR3 in LUAD tissue was found to be lower than that in the normal control group, while the expression of MMP1 in LUAD tissue was higher than that in the normal control group. According to survival analysis, the low expression of MYL9 and SPARCL1 was correlated with poor overall survival in patients with LUAD. Finally, through the verification of the Oncomine database, it was found that the expression levels of MYL9 and SPARCL1 were consistent with the mRNA levels in LUAD samples, and both were downregulated.Conclusion: Two survival-related genes, MYL9 and SPARCL1, were determined to be highly correlated with the development of LUAD. Both may play an essential role in the development LUAD and may be potential biomarkers for its diagnosis and treatment in the future.


2019 ◽  
Vol 1 (2) ◽  
pp. p42
Author(s):  
Service @ Ideasspread.org ◽  
Okafor I. J. ◽  
Nweke E. O. ◽  
Ewa O.

This study was carried out to ascertain the hepatotoxic potential of T.daniellii (T.d) and A. cordifolia (A.c). Investigations were conducted using standard methods. Oral administration of 200mg/kg aqueous leaf extracts of T.daniellii caused a non-significant increase in the activity of ALT (5.43±0.60IU/L), AST (16.93±0.26 IU/L) and ALP (160.70±1.04 IU/L) compared to the values recorded on the normal control (group I) ALT (3.84±0.16 IU/L), AST (14.19±0.52 IU/L) and ALP (157.26±0.64 IU/L). Group III administered with 200mg/kg methanolic leaf extract of T. daniellii manifested a significant elevation in the activity of ALT (13.15±0.89 IU/L), AST (22.84±0.38 IU/L) and ALP (170.40±0.44 IU/L) compared to the normal control. Similarly, groups IV and V which were orally administered with 200mg/kg aqueous and methanolic leaf extracts of A. cordifolia showed significant increase in the activity of ALT (6.32±0.33U/L), AST (17.70±0.030U/L) and ALP (161.13±0.09U/L) and ALT (7.55±0.59U/L), AST (19.35±0.26U/L) and ALP (165.38±0.35U/L) respectively compared to the values recorded on the control (group I). In conclusion, drug development protocols involving T. daniellii leaf should preferably use water as an ideal solvent. On the other hand, the hepatotocity associated with both aqueous and methanolic extracts of A. cordifolia could imply the presence of hepatotoxins in the leaf of the said plant.


Author(s):  
NITIN DWIVEDI ◽  
DUSHYANT KUMAR PARMAR ◽  
PRASHANT KESHARWANI ◽  
JIGNA SHAH

Objective: The aim of the present study leads a comparative assessment of the toxicological profile of PEGylated fourth and fifth-generation poly (propylene imine) dendrimers (PPI). Methods: 4.0G and 5.0G generations of PPI dendrimer were synthesized and PEGylated with Mono polyethylene glycol 5000 (MPEG-5000). Each PEGylated 4.0G and 5.0G dendrimeric generation were administered in three different doses: 2.5 mg/kg, 25 mg/kg and 250 mg/kg (i.e., low, intermediate and high dose) to wister rats. After the dose administration, the blood and tissue samples of wister rats were collected after 24 h and 15 d after. All the collected samples were proceeded for hematological, biochemical and histopathological studies. Results: After 24 h of (250 mg/kg) dose administration PEGylated 5.0G PPI dendrimer the RBC count, hemoglobin content and WBC count were found 7.873±0.129 mill/cmm, 13.833±0.491g/dl and 9033.33±2384.906 mill/cmm, while PEGylated 4.0G PPI dendrimer indicated RBC count, hemoglobin content and WBC count 8.733±0.239 mill/cmm, 14.033±0.12 g/dl and 9666.667±2567.316 mill/cmm, in blood samples as compare to RBC count 9.346±0.037 mill/cmm, hemoglobin content 15.35±0.15 g/dl and WBC count 8500±286.675 mill/cmm of the animals of normal control group. Thus there are no remarkable changes (p>0.05) in RBC count, hemoglobin content and other hematological profile after 24 h in comparison of normal control group of animals. Similarily insignificant changes (p>0.05) in serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), lactate dehydrogenase (LDH) and sections of different organs indicate inoffensive nature of both generations of PEGylated 4.0G and 5.0 G PPI dendrimers. Conclusion: It can be concluded that fifth-generation PPI dendrimers are more suitable as compared to fourth generation of PPI dendrimer, while both dendrimers are not generating any severe toxicity.


1989 ◽  
Vol 154 (5) ◽  
pp. 677-682 ◽  
Author(s):  
Elsa Bernardi ◽  
Michael Jones ◽  
Chris Tennant

Alcoholics and heroin addicts were compared with a normal control group to determine whether there were differences in quality of parenting during childhood, assessed using the Parental Bonding Instrument. Maternal and paternal overprotection were reported more commonly by narcotic addicts. Maternal overprotection alone was implicated in alcoholics. Narcotic addicts seem to have more disturbed parenting than alcoholics, especially paternal parenting.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 709-709 ◽  
Author(s):  
Daniel B. Bellissimo ◽  
P.A. Christopherson ◽  
S.L. Haberichter ◽  
V.H. Flood ◽  
J.C. Gill ◽  
...  

Abstract Von Willebrand disease (VWD) is caused by quantitative (types 1 and 3) and qualitative (type 2) defects in von Willebrand factor (VWF). The TS Zimmerman Program for the Molecular and Clinical Biology of VWD is a multinational Program Project established to further the study of VWD in the United States and to contrast these studies with the studies initiated previously in the EU and Canada. As one of the components of this study we sought further insight into the clinical expression and penetrance of established types of VWD by performing full gene DNA sequence analysis in VWD patients and normal controls. This report is an interim report of the first 50 index cases and 113 normal individuals recruited into this study. Twenty four of these index cases were found to have known mutations, four of which had a second new mutation, and 11 cases had 1 or 2 new mutations. In cases where mutations were identified, 46% of the identified mutations were new mutations that have not been reported in the Sheffield VWF Mutation Database. In 15 patients, no mutations were identified in the coding region, although analysis of the non-coding regions is still in progress. Five of the mutations were deletions, insertions, or nonsense mutations that have clear functional consequences. The other 12 mutations were missense mutations. Since VWF polymorphisms are not well characterized in all exons, we have also completed studies of the first 113 normal control individuals in our study. These are individuals without a bleeding history and in whom full VWF laboratory testing and VWF sequencing was also undertaken. Since some estimates in the EU and Canadian studies have determined the prevalence of VWF mutations varies by the severity of type 1 VWD patients, we wanted to determine the frequency of VWF variation in a normal population and determine if sequence variations correlate with VWF levels. There were three linked common polymorphims identified in normal African Americans that are discussed elsewhere and are not included in this present analysis. We found 19 new sequence variations in the normal control group of which three (2900G>A, 6554G>A, 7997C>T) were found individually in 4–6% of the normal control samples. In addition, in 12 normal control samples we identified 6 sequence variations that were previously reported as VWF mutations. Four were reported as type 1 mutations (2220 G>A, 3686T>G, 3692A>C, 6859C>T) and two as type 2N mutations (2451T>A, 2771G>A). The 2220G>A and 2451T>A mutations were seen in 6 normal controls (5%) and 5 of these 6 normal controls had both mutations. In another normal control, both 3686T>G and 3692A>C were identified. Although the reported prevalence of VWD is 1% or greater, the frequency of these mutations in our normal controls is higher than expected (as high as 5%). In our normal control group, the mean VWF:Ag concentration in the patients with polymorphisms/mutations did not differ from the normal control group as a whole and did not cluster on the lower end of the normal range. Thus, the data on our normal individuals suggest that VWF gene variation is considerable and that many mutations and polymorphisms remain to be identified. Differentiation of those that affect the diagnosis of VWD and/or hemorrhagic risk continues to be difficult.


Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3362-3362 ◽  
Author(s):  
Annick Ankri ◽  
Anne Baranger ◽  
Isabelle Martin-Toutain ◽  
Yves Samson ◽  
Jean-Philippe Collet ◽  
...  

Abstract Abstract 3362 The five channel computerized Whole Blood Aggregation instrument (Multiple Platelet Function Analyzer or Multiplate®), assesses platelet aggregation based on a modified whole blood impedance aggregation method. It permits platelet aggregation to be measured after adding commonly used agonists as arachidonic acid (ASPItest), ADP (ADPtest), collagen (COLtest), ristocetin (RISTOtest) and TRAP (TRAPtest), by detecting changes in electrical resistance in whole blood. Instrument handling is easy. Results are available within 9 minutes. Our objective was to evaluate the effect of aspirin (irreversible inhibitor of COX-1) and/or clopidogrel (irreversible inhibitor of the platelet P2Y12 receptor) on whole blood platelet aggregations induced by the 5 agonists using the Multiplate® in patients treated by aspirin and/or clopidogrel. Patients and controls. Two hundred and twenty two consecutive patients were recruited: 83 treated daily by 75 or 100 mg aspirin (group A); 42 treated daily by 75 mg clopidogrel (group C); 70 treated daily by 75 or 100 mg aspirin plus 75mg clopidogrel (group AC) and 27 who were daily on 100 mg aspirin before coronary intervention were tested 12 h after dual loading dose of aspirin between 75 et 500 mg and 75 to 900 mg clopidogrel according to cardiologists' recommendations: group loading aspirin-clopidogrel (LAC). Among group AC, 23 consecutive patients requiring intracranial stent placement of supra-aortic vessel were tested first at preoperative, without antiplatelet therapy, then 1 month after initiation of daily continuous dual antiplatelet therapy by 100 mg aspirin + 75mg clopidogrel. Ninety six volunteers without pathology or drugs influencing platelet functions constitute the normal control group (N). Blood samples. All patient and controls gave informed consent prior to blood sampling. Blood samples were collected by venipuncture or obtained from the arterial sheath directly into vacutainer Becton Dickinson tube containing 0.129M sodium citrate. Results. Patients under medication showing lower aggregation values than the arbitrary cutoff (fifth percentile of the aggregation in the normal control group was selected for each agonist) were classified as abnormal and having biological sensitivity to the agonist tested. Aggregation values above the cutoff with ASPItest or ADPtest for patients on antiplatelet agents were considered as a persistent platelet aggregation and as a biological resistance. According to the literature, resistance to aspirin was found in 8.6% of patients under aspirin alone or in combination and in 25.1% of patients under clopidogrel alone or in combination. Our main result shows an inhibition in platelet aggregation using ristocetin as agonist for 73.9% of patients taking aspirin alone, for 27.8% on clopidogrel and in 94% of patients receiving combination of the 2 drugs. This inhibition appears after aspirin + clopidogrel intake as we could observe it among patients candidates for intracranial stent placement tested before and after one month of treatment by dual antiplatelet therapy. This effect is not related to von Willebrand Factor (vWF) deficiency since the measurement of ristocetin cofactor activity, and vWF antigen carried out among 14 patients exhibiting an inhibition in whole blood platelet aggregation using RISTOtest were normal and unchanged before and after antiplatelet treatment. VWF is essential platelet-to-platelet interactions which is promoted by the binding of VWF with platelet-receptor glycoprotein IbIX (GPIbIX). Our results suggest: 1) aspirin inhibits the interaction of vWF to GP IbIX. This inhibition appears increased by the association of clopidogrel to aspirin. 2) a new mechanism of inhibition of the platelet function GPIbIX-vWF dependant conjointly to inhibition of cyclooxygenase by aspirin and P2Y12 receptor by clopidogrel.Table I:Biological sensibility according to the five tests (%) in the 4 groups testedGroup (n)ASPItestADPtestCOLtestRISTOtestTRAPtestA (83)84.312.038.373.98.4C (42)38.176.219.227.816.7AC (70)90.074.348.288.222.9LAC (27)100.074.163.0100.029.6 Disclosures: No relevant conflicts of interest to declare.


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