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Prediction of Inflammatory Response and Hypotensive Syndrome After Cardiac Surgery by Preoperative Copeptin Level

ClinicalTrials.gov study NCT03288610. IPD Sharing: NO. Countries: 1. Publications: 2.

Protective Effect of EECP Against Negative Inflammatory Response and Organ Dysfunction After Cardiovascular Surgery

ClinicalTrials.gov study NCT06728605. IPD Sharing: UNDECIDED. Countries: 1. Publications: 3.

Consequences of Hypoglycaemia on Cardiovascular and Inflammatory Responses

ClinicalTrials.gov study NCT03976271. IPD Sharing: NO. Countries: 2. Publications: 3.

Effect of Docosahexaenoic Acid on the Inflammatory Response and Clinical Outcomes From Surgical Patients

ClinicalTrials.gov study NCT01049529. IPD Sharing: NO. Countries: 1. Publications: 4.

controlledIPD-YESFeb 2026View details →

An Artificial Intelligence-based Approach in Total Knee Arthroplasty: From Inflammatory Responses to Personalized Medicine

ClinicalTrials.gov study NCT06634654. IPD Sharing: YES. Countries: 1. Publications: 1.

Comparison of the Effects of Dexmedetomidine and Ketamine Infusion on the Inflammatory Response in Liver Resection

ClinicalTrials.gov study NCT06219928. IPD Sharing: NO. Countries: 1. Publications: 4.

Influence of of a Lipid Emulsion on Inflammatory Response and Hepatic Function

ClinicalTrials.gov study NCT00600912. IPD Sharing: Not stated. Countries: 1. Publications: 3.

Effect of Transversus Abdominis Plane Block on Anti-inflammatory Response

ClinicalTrials.gov study NCT04232904. IPD Sharing: NO. Countries: 1. Publications: 2.

High Cut-Off Continuous Veno-venous Hemodialysis (CVVHD) in Patients Treated for Acute Renal Failure After Systemic Inflammatory Response Syndrome (SIRS)/Septic Shock

ClinicalTrials.gov study NCT00875888. IPD Sharing: Not stated. Countries: 2. Publications: 5.

Inflammatory Response to Anti Inflammatory Therapy in Children With Sleep Disordered Breathing

ClinicalTrials.gov study NCT00299910. IPD Sharing: Not stated. Countries: 1. Publications: 1.

publicJul 2021View details →

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Data from: Pro-inflammatory immune response is linked to wintering habitat in a migratory shorebird

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opencc-zeroJul 2020View details →

Data from: Alkaline phosphatase, lactic dehidrogenase, inflammatory variables and apparent diffusion coefficients from MRI for prediction of chemotherapy response in osteosarcoma

Background. This present study aimed to assess if clinical, laboratory and MRI were an accurate benchmark in assessing the effectiveness of neoadjuvant chemotherapy in osteosarcoma patients. Methods. This was an observational analytic study with a cross-sectional design. Research subjects were selected using the total sampling method from osteosarcoma patients who underwent neoadjuvant chemotherapy during the period between January 2017– July 2019. Results.Of the 58 patients included in this study, 38 were male and 20 were female aged 5 - 67 years (mean,16-year-old. 37(63.8%) patients underwent neoadjuvant chemotherapy with CAI regimens and 13 (36.2%) with CA. The tumors were classified as stage IIB in 43 (74.1%) patients and stage III in15 (25.9%) patients. After undergoing neoadjuvant chemotherapy, 4 patients had poor MSTS, 30 patients had fair MSTS, 17 and 7 patients had good and excellent MSTS score, respectively. Spearman's test revealed no correlation between tumor necrosis after neoadjuvant chemotherapy with a reduction in tumor size and MSTS score. Wilcoxon test showed significant differences between ALP, ESR, and NLR before and after neoadjuvant chemotherapy in the poor-response group. We found no significant difference between LDH and LMR before and after neoadjuvant chemotherapy in the good-response group. We had 9 patients for ADC value only. No significant statistical differences were found in tumor volumes after chemotherapy in both groups. Conclusion. We demonstrated that ALP level after neoadjuvant chemotherapy was markedly decreased, and was statistically significant in the poor-response group. We also demonstrated that LDH value before neoadjuvant chemotherapy had a strong correlation with degree of necrosis and could be used as a predictive indicator. NLR and LMR cannot be independent prognostic factors. MRI plays an important role in evaluating tumor volumes and preoperative radiological changes, using DWI and water diffusion to predict histological necrosis.

opencc-zeroSep 2020View details →

Revealing the roles of DnaA on the biological characteristics of Brucella and the inflammatory response to Brucella

The Brucella cell cycle, including chromosomal replication and cell division, is coordinated with the virulence of the bacteria. DnaA, a chromosomal replication initiator protein, is an essential regulator of cell cycle progression and is tightly regulated both temporally and spatially because it is activated only once per cell cycle in bacteria. Although DnaA exists in many bacteria, the role of DnaA during Brucella infection, with the exception of its induction of the initiation of chromosome replication, remains unclear. Here, we generated a Brucella strain in which the expression of DnaA was conditionally controlled via anhydrotetracycline (ATc)-induced complementation of a deletion of the dnaA gene encoding the DnaA protein. We found that DnaA is required for Brucella division and activity to response various environmental stresses. As demonstrated by RNA-seq, DnaA was found to be involved in physiological processes, including the regulation of the cell cycle. Moreover, the inactivation of DnaA can inhibit Brucella intracellular trafficking through impaired replicative Brucella-containing vacuole (rBCV) biogenesis. In RAW 264.7 cells, the mutant strain promoted secretion of the proinflammatory cytokines interleukin 1β (IL-1β) and interleukin 6 (IL-6) and reduced survival. In addition, the inhibition of DnaA expression also attenuated the virulence of Brucella, but the resultant strain exhibited excellent immunogenicity to activate host immune responses in a mouse model. Altogether, these findings show that DnaA is involved in Brucella virulence in vitro and in vivo and could become a new target for the development of a safer and more efficient live attenuated Brucella vaccine.

opencc-zeroJan 2021View details →

Nerve ultrasound improves detection of treatment-responsive chronic inflammatory neuropathies

Objective To examine the diagnostic accuracy of nerve ultrasound in a prospective cohort of consecutive patients with a clinical suspicion of chronic inflammatory neuropathies, including chronic inflammatory demyelinating polyneuropathy, Lewis Sumner syndrome and multifocal motor neuropathy, and to determine the added value in the detection of treatment-responsive patients. Methods Between February 2015 and July 2018, we included 100 consecutive incident patients with a clinical suspicion of chronic inflammatory neuropathy. All patients underwent nerve ultrasound, extensive standardized nerve conduction studies (NCS) and other relevant diagnostic investigations. We evaluated treatment response using predefined criteria. A diagnosis of chronic inflammatory neuropathy was established when NCS were abnormal (fulfilling criteria of demyelination of the EFNS/PNS) or when the degree of nerve enlargement detected by sonography was compatible with chronic inflammatory neuropathy and there was response to treatment. Results A diagnosis of chronic inflammatory neuropathy was established in 38 patients. Sensitivity and specificity of nerve ultrasound and NCS were 97.4% and 69.4%, and 78.9% and 93.5%, respectively. The added value of nerve ultrasound in detection of treatment-responsive chronic inflammatory neuropathy patients was 21.1% compared to NCS alone. Conclusions Nerve ultrasound and NCS are complementary techniques with superior sensitivity in the former and specificity in the latter. Addition of nerve ultrasound significantly improves the detection of chronic inflammatory neuropathies. Therefore, it deserves a prominent place in the diagnostic workup of chronic inflammatory neuropathies. Classification of Evidence This study provides Class I evidence that nerve ultrasound is an accurate diagnostic tool to detect chronic inflammatory neuropathies.

opencc-zeroDec 2017View details →

Data from: Microglia responses to pro-inflammatory stimuli (LPS, IFNγ+TNFα) and reprogramming by resolving cytokines (IL-4, IL-10)

Microglia respond to CNS injuries and diseases with complex reactions, often called "activation." A pro-inflammatory phenotype (also called classical or M1 activation) lies at one extreme of the reactivity spectrum. There were several motivations for this study. First, bacterial endotoxin (lipopolysaccharide, LPS) is the most commonly used pro-inflammatory stimulus for microglia, both in vitro and in vivo; however, pro-inflammatory cytokines (e.g., IFNγ, TNFα) rather than LPS will be encountered with sterile CNS damage and disease. We lack direct comparisons of responses between LPS and such cytokines. Second, while transcriptional profiling is providing substantial data on microglial responses to LPS, these studies mainly use mouse cells and models, and there is increasing evidence that responses of rat microglia can differ. Third, the cytokine milieu is dynamic after acute CNS damage, and an important question in microglial biology is: How malleable are their responses? There are very few studies of effects of resolving cytokines, particularly for rat microglia, and much of the work has focused on pro-inflammatory outcomes. Here, we first exposed primary rat microglia to LPS or to IFNγ+TNFα (I+T) and compared hallmark functional (nitric oxide production, migration) and molecular responses (almost 100 genes), including surface receptors that can be considered part of the sensome. Protein changes for exemplary molecules were also quantified: ARG1, CD206/MRC1, COX-2, iNOS, and PYK2. Despite some similarities, there were notable differences in responses to LPS and I+T. For instance, LPS often evoked higher pro-inflammatory gene expression and also increased several anti-inflammatory genes. Second, we compared the ability of two anti-inflammatory, resolving cytokines (IL-4, IL-10), to counteract responses to LPS and I+T. IL-4 was more effective after I+T than after LPS, and IL-10 was surprisingly ineffective after either stimulus. These results should prove useful in modeling microglial reactivity in vitro; and comparing transcriptional responses to sterile CNS inflammation in vivo.

opencc-zeroAug 2019View details →

Data from: Humoral immune responses against gut bacteria In dogs with inflammatory bowel disease

Inflammatory bowel disease (IBD) in dogs is associated with clinical signs of intestinal dysfunction, as well as abnormal lymphocytic and myeloid cell infiltrates in the small and/or large intestine. Thus, in many respects IBD in dogs resembles IBD in humans. However, the factors that trigger intestinal inflammation in dogs with IBD are not well understood and have been variously attributed to immune responses against dietary antigens or intestinal antigens. Previous studies in humans with IBD have documented increased production of IgG and IgA antibodies specific to intestinal bacteria, and this abnormal immune response has been linked to disease pathogenesis. Therefore, we investigated the humoral immune response against gut bacteria in dogs with IBD, using flow cytometry to quantitate IgG and IgA binding. Studies were also done to investigate the source of these antibodies (locally produced versus systemic production) and whether greater antibody binding to bacteria is associated with increased inflammatory responses. We found that dogs with IBD had significantly higher percentages and overall amounts of IgG bound to their intestinal bacteria compared to healthy dogs. Similarly, significantly higher percentages of bacteria were IgA+ bacteria were also found in dogs with IBD. Serum antibody recognition of gut bacteria was not different between healthy dogs and dogs with IBD, suggesting that anti-bacterial antibodies were primarily produced locally in the gut rather than systemically. Importantly, bacteria in the Actinobacteria phylum and in particular the genus Collinsella had significantly greater levels of antibody binding in dogs with IBD. Based on these findings, we concluded that antibody binding to commensal gut bacteria was significantly increased in dogs with IBD, that particular phyla were preferential targets for gut antibodies, and that anti-bacterial antibody responses may play an important role in regulating gut inflammation.

opencc-by-4.0Dec 2023View details →

Silicone induces pro-inflammatory response in 3D skin equivalent

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opencc-by-4.0Jan 2024View details →

Figure 3 from: Nafisah W, Dalilati AZ, Christina YI, Atho'illah MF, Rifa'ia M, Noor TNETA, Nugraha AP (2024) Amstirdam coffee ameliorates Lp-PLA2 and the inflammatory response in an atherosclerosis rats. Pharmacia 71: 1-8. https://doi.org/10.3897/pharmacia.71.e106817

Figure 3 ACE administration increased the level of regulatory T cells in mice fed a high-fat, high-fructose diet for 5 months. The level of regulatory T cell A. CD4+CD25+CD62L+ subsets, B. CD4+CD25+IL-10+ subsets, and C. CD4+CD25+TGF-+subsets of mice fed with HFFD and administration of ACE from flow cytometry analysis. The percentage of regulatory T cell D. CD4+CD25+CD62L+ subsets, E. CD4+CD25+IL-10+ subsets, and F. CD4+CD25+TGF-+ subsets of mice fed with HFFD and administered ACE The data are mean SD (n = 5). N: normal-fed mice (non-high-fat-fructose diet); HFFD: high-fat-fructose diet mice (w/o administration of ACE); D1: HFFD mice receiving ACE 104 mg/kg body weight; D2: HFFD mice receiving ACE 520 mg/kg body weight; D3: HFFD mice receiving ACE 5200 mg/kg body weight. The different notation on the chart was considered significantly different for each group at p<0.05 and vice versa on the DMRT post hoc test.

opencc-by-4.0Jan 2024View details →

Figure 5 from: Nafisah W, Dalilati AZ, Christina YI, Atho'illah MF, Rifa'ia M, Noor TNETA, Nugraha AP (2024) Amstirdam coffee ameliorates Lp-PLA2 and the inflammatory response in an atherosclerosis rats. Pharmacia 71: 1-8. https://doi.org/10.3897/pharmacia.71.e106817

Figure 5 The effect of ACE increased TGF-β production (CD4+TGF-β+) in mice fed with a high fat-fructose diet for 5 months. The expression of TGF-β (CD4+TGF-β+) of mice fed with HFFD and administration of ACE from flow cytometry analysis (Fig. 5G). The percentage of regulatory (CD4+IL-10+) of mice fed with HFFD and administration of ACE (Fig. 5H). Data are mean ± SD (n=5). N: normal fed mice (non-high fat-fructose diet), HFFD: high fat-fructose diet mice (w/o administration of ACE), D1: HFFD mice receiving ACE 104 mg/kg body weight, D2: HFFD mice receiving ACE 520 mg/kg BW, D3: HFFD mice receiving ACE 5200 mg/kg BW. The different notation on the chart was considered significantly different for each group at p < 0.05 and vice versa on DMRT post hoc test.