Different Degrees Of Inflammation Research Articles

Pathogenicity of Citrobacter freundii Causing Mass Mortalities of Macrobrachium rosenbergii and Its Induced Host Immune Response.

Citrobacter freundii is an opportunistic pathogen of freshwater aquatic animals, which severely restricts the sustainable development of the aquaculture industry. In this study, a dominant strain, named FSNM-1, was isolated from the hepatopancreas of diseased Macrobrachium rosenbergii. This strain was identified as C. freundii based on a comprehensive analysis of its morphological, physiological, and biochemical features and molecular identification. Challenge experiments were conducted to assess the pathogenicity of C. freundii to M. rosenbergii. The results showed that the FSNM-1 strain had high virulence to M. rosenbergii with a median lethal dose (LD50) of 1.1 × 106 CFU/mL. Histopathological analysis revealed that C. freundii infection caused different degrees of inflammation in the hepatopancreas, gills, and intestines of M. rosenbergii. The detection of virulence-related genes revealed that the FSNM-1 strain carried colonization factor antigen (cfa1, cfa2), ureases (ureG, ureF, ureD, ureE), and outer membrane protein (ompX), and virulence factor detection showed that the FSNM-1 strain had lecithinase, amylase, lipase, gelatinase, and hemolysin activities but did not produce protease and DNase activities. To investigate the immune response of M. rosenbergii to C. freundii, the expression levels of ALF3, MyD88, SOD, proPO, TRAF6, and TNF immune-related genes were monitored at different points of time in the hepatopancreas, gills, intestines, and hemocytes of M. rosenbergii after infection. The results demonstrated a significant upregulation in the expression levels of the ALF3, MyD88, SOD, proPO, TRAF6, and TNF genes in M. rosenbergii at the early stage of C. freundii infection. This study highlights C. freundii as a major pathogen causing mass mortality in M. rosenbergii and provides valuable insights into its virulence mechanisms and the host's immune response.

Trending Screen Addiction: Emerging Risk Of Increased Virtual Autism Among Toddlers.

only in Pakistan but worldwide. In Pakistan alone, approximately 33 million people suffer from Type 2 diabetes mellitus, with an additional 11 million adults with impaired glucose tolerance, while approximately nine million people with diabetes remain undiagnosed.1 Diabetes causes many fatal complications including hypertension, myocardial infarction, stroke, chronic kidney disease, neuropathy, etc. To lower the morbidity and mortality rates, prompt screening and treatment of complications of diabetes should be done, especially the lesser-known complications. In the past, a strong association between idiopathic pulmonary fibrosis and diabetes was noted by some physicians. This association was established by Stefan Kopf et al.2 More recently a study funded by Diabetes UK (a British-based patient, healthcare professional, and research charity) at the Imperial College of London claimed that there is a strong association between lung disorders and Type 2 diabetes mellitus.3 This study examined data from approximately 500,000 individuals in 17 large-scale investigations. According to the investigation, type 2 diabetics' elevated blood sugar levels directly affect lung function. For instance an increase in typical blood sugar levels from 4 mmol/L to 12 mmol/L. might cause a 20% decline in lung function and capacity. Dr. Ben Jones, Dr. Marika Kaakinen and Dr. Elizabeth Robertson were in pivotal positions in this research and they all quoted lung disorders occurring in Type 2 diabetic patients as a direct complication of diabetes.3 Rajasurya V et al defined diabetic lung or diabetic pneumopathy as a condition characterized by progressive lung disease caused by the microvascular complications associated with diabetes mellitus.4 The direct complications of diabetes mellitus in the lungs include interstitial lung disease and idiopathic pulmonary fibrosis. Interstitial lung disease involves different degrees of inflammation and fibrosis in the pulmonary parenchyma and Idiopathic pulmonary fibrosis involves chronic progressive fibrosis leading to progressive pulmonary failure.4 Knowing the extent of diabetic patients present in Pakistan and how quickly this number can escalate,5 a clinical trial should be replicated on a larger population. There is a need to establish protocols for screening of diabetes related pneumopathy. People should be educated about these lesser-known complications of diabetes, and diabetic patients should be trained to perform pulmonary function tests at home. Overall these measures will surely help to improve the quality of life of a diabetic patient and to reduce gross morbidity and mortality rates.

Diabetic Pneumopathy: A Latest Finding.

Madam, Diabetes is one of the major causes of death not only in Pakistan but worldwide. In Pakistan alone, approximately 33 million people suffer from Type 2 diabetes mellitus, with an additional 11 million adults with impaired glucose tolerance, while approximately nine million people with diabetes remain undiagnosed1. Diabetes causes many fatal complications including hypertension, myocardial infarction, stroke, chronic kidney disease, neuropathy, etc. To lower the morbidity and mortality rates, prompt screening and treatment of complications of diabetes should be done, especially the lesser-known complications. In the past, a strong association between idiopathic pulmonary fibrosis and diabetes was noted by some physicians. This association was established by Stefan Kopf et al2. More recently a study funded by Diabetes UK (a British-based patient, healthcare professional, and research charity) at the Imperial College of London claimed that there is a strong association between lung disorders and Type 2 diabetes mellitus3. This study examined data from approximately 500,000 individuals in 17 large-scale investigations. According to the investigation, type 2 diabetics' elevated blood sugar levels directly affect lung function. For instance an increase in typical blood sugar levels from 4 mmol/L to 12 mmol/L. might cause a 20% decline in lung function and capacity. Dr. Ben Jones, Dr. Marika Kaakinen and Dr. Elizabeth Robertson were in pivotal positions in this research and they all quoted lung disorders occurring in Type 2 diabetic patients as a direct complication of diabetes3. Rajasurya V et al defined diabetic lung or diabetic pneumopathy as a condition characterized by progressive lung disease caused by the microvascular complications associated with diabetes mellitus4. The direct complications of diabetes mellitus in the lungs include interstitial lung disease and idiopathic pulmonary fibrosis. Interstitial lung disease involves different degrees of inflammation and fibrosis in the pulmonary parenchyma and Idiopathic pulmonary fibrosis involves chronic progressive fibrosis leading to progressive pulmonary failure4. Knowing the extent of diabetic patients present in Pakistan and how quickly this number can escalate5,a clinical trial should be replicated on a larger population. There is a need to establish protocols for screening of diabetes related pneumopathy. People should be educated about these lesser-known complications of diabetes, and diabetic patients should be trained to perform pulmonary function tests at home. Overall these measures will surely help to improve the quality of life of a diabetic patient and to reduce gross morbidity and mortality rates.

Non-Alcoholic Fatty Liver Disease-Associated Hepatocellular Carcinoma: Effect of Hepatic Steatosis on Major Hepatocellular Carcinoma Features at MRI

Background Non-alcoholic fatty liver disease has become the leading chronic liver disease in the developed world, with a prevalence of 6%-35%. Its pathological spectrum ranges from simple steatosis (non-alcoholic fatty liver) to different degrees of inflammation and liver cell damage [nonalcoholic steatohepatitis (NAFLD)]. NAFLD has gained attention in recent years because of its association with hepatocellular carcinoma (HCC). Objective To see how hepatic fat fraction affects LIRADS major hepatocellular carcinoma features on magnetic resonance imaging. Patients and Methods Our study included 60 patients who had had a liver MR scan and exhibited MRI features in keeping with HCC. We categorize the patients into two groups: hepatic steatosis and non- hepatic steatosis groups based on MRI hepatic fat signal fraction. LI-RADS major and ancillary features were evaluated in all HCCs. Between October 2021 and April 2022, a retrospective search was conducted to find all patients with HCC who underwent an MRI of the liver at the radiology department of Ain Shams University's Faculty of medicine. Results In the current study, a higher proportion of HCCs show non- enhancing capsule in patients with hepatic steatosis; 5 HCC (5/30; 16.7%), while in the non-hepatic steatosis group no HCCs 0 (0%) showed non-enhancing capsule. The effect of ancillary features on diagnostic accuracy is still being researched. As regards the impact of the degree of fatty liver on the major and ancillary HCC features, the “enhancing capsule”, “mild-moderate T2 hyperintensity” and “restricted DWI” features are less commonly seen in cases of moderate to severe hepatic steatosis than in those of mild hepatic steatosis. Our study also showed that HCCs tends to be of a smaller size as the hepatic steatosis degree increased. Conclusion The findings of our retreopective study are coincide with a recent retrospective studies demonstrated that “enhancing capsule” feature of HCC was less frequently observed in patients with hepatic steatosis compared to non-hepatic steatosis patients. We compared the MRI features of HCC in patients with hepatic steatosis to those in patients without hepatic steatosis. Our findings imply that existing imaging criteria for the noninvasive characterization of HCC in individuals with hepatic steatosis should be utilised with care.

Comparison of the different monosodium urate crystals in the preparation process and pro-inflammation

ObjectivesThe deposition of monosodium urate (MSU) crystals within synovial joints and tissues is the initiating factor for gout arthritis. Thus, MSU crystals are a vital tool for studying gout’s molecular mechanism in animal and cellular models. This study mainly compared the excellence and worseness of MSU crystals prepared by different processes and the degree of inflammation induced by MSU crystals.MethodsMSU crystals were prepared using neutralization, alkali titration, and acid titration methods. The crystals’ shape, length, quality, and uniformity were observed by polarized light microscopy and calculated by the software Image J. The foot pad and air pouch models were used to assess the different degrees of inflammation induced by the MSU crystals prepared by the three different methods at different time points. Paw swelling was evaluated by caliper. In air pouch lavage fluid, inflammatory cell recruitment was measured by hemocytometer, and the level of IL-1β, TNF-α, and IL-18 by ELISA. Inflammatory cell infiltration was assayed by immunohistochemistry of air pouch synovial slices.ResultsFor the preparation of MSU crystals with the same uric acid, the quantity acquired by the alkalization method was highest, followed by neutralization, with the acid titration method being the lowest. The crystals prepared by neutralization were the longest. The swelling index of the foot pad induced by MSU crystals prepared by acid titration was significantly lower than that of the other methods at 24 h. The inflammatory cell recruitment and level of IL-1β, TNF-α, and IL-18 in air pouch lavage fluid were lowest in animals with crystals prepared by acid titration. IL-1β secretion induced by MSU crystals prepared by acid titration was significantly lower than that of the other two groups, but there was no significant difference in IL-18 secretion between the three groups in THP-1 macrophages and BMDMs.ConclusionsAll three methods can successfully prepare MSU crystals, but the levels of inflammation induced by the crystals prepared by the three methods were not identical. The degree of inflammation induced by MSU crystals prepared by neutralization and alkalization is greater than by acid titration, but the quantity of MSU crystals obtained by the alkalization method is higher and less time-consuming. Apparently, the window of inflammation triggered by acid titration preparation is shorter compared to other forms of crystal preparation. Overall, MSU crystals prepared by the alkaline method should be recommended for studying the molecular mechanisms of gout in animal and cellular models.

NF-κB signaling pathway mechanism in cow intertoe skin inflammation caused by Fusobacterium necrophorum.

Fusobacterium necrophorum is the main pathogen inducing bovine foot rot. The infected site is often accompanied by a strong inflammatory response, but the specific inflammatory regulatory mechanism remains unclear. A cow skin explants model was established to elucidate the mechanism of F. necrophorum bacillus causing foot rot in cows, and to provide reference for future clinical practice. Cow intertoe skin explants were cultured in vitro, and F. necrophorum bacteria solution and nuclear factor-κB (NF-κB) inhibitor BAY 1-7082 were added to establish an in vitro infection model. Hematoxylin and eosin staining, terminal - deoxynucleotidyl transferase mediated nick end labeling, and immunohistochemistry were used to detect the pathological changes of the skin explants infected with F. necrophorum, the degree of tissue cell apoptosis, and the expression of the apoptosis-related protein Caspase-3, respectively. RT-qPCR, Western blot, and ELISA were used to detect the activation of the NF-κB pathway and inflammatory cytokines by F. necrophorum. The intertoe skin structure of cows infected with F. necrophorum changed with different degrees of inflammation, and the degree of tissue cell apoptosis was significantly increased (P < 0.01). In addition, infection with F. necrophorum significantly increased the phosphorylation level of IκBα protein and up-regulated the expression level of NF-κB p65. The high expression and transcriptional activity of NF-κB p65 significantly increased the expression and concentration of the inflammatory cytokines TNF-α, IL-1β, and IL-8, thus inducing the occurrence of an inflammatory response. However, inhibition of NF-κB p65 activity significantly decreased the expression of inflammatory factors in the intertoe skin of cows infected with F. necrophorum. F. necrophorum activates NF-κB signaling pathway by increasing the expression of TNF-α, IL-1β, IL-8 and other inflammatory factors, leading to foot rot in dairy cows.

Microstructural alterations in different types of lesions and their perilesional white matter in relapsing-remitting multiple sclerosis based on diffusion kurtosis imaging.

In multiple sclerosis (MS), contrast enhancement lesions and chronic active lesions have been demonstrated to have different degrees of inflammation. Accordingly, they exist different degrees of tissue damage, one is short and acute, and another is slow and longstanding. This study aimed to explore whether diffusion parameters can differentiate different types of lesions, and investigate the microstructural damage between different types of MS lesions by using diffusion magnetic resonance imaging (dMRI) and its correlation with clinical biomarkers of disability and cognitive states. We retrospectively identified 77 contrast enhancement lesions (CELs), 384 iron rim lesions (IRLs), 393 non-iron rim lesions (NIRLs), their corresponding perilesional white matter (PLWM), and 68 normal-appearing white matter (NAWM) from 68 relapsing-remitting MS (RRMS). Additionally, 44 white matter in healthy controls (WM in HCs) were also enrolled in this study. The DTI and DKI parameters were measured in the above white matter, including kurtosis fractional anisotropy (KFA), fractional anisotropy (FA), mean kurtosis (MK), and mean diffusivity (MD). All the patients were assessed with the Digital Span Test (DST), the Symbol Digit Modalities Test (SDMT), the Mini-Mental State Examination (MMSE), the Montreal Cognitive Assessment (MoCA), and the Expanded Disability Status Scale (EDSS). The lowest KFA, FA, MK values and the highest MD values were found in CELs, followed by IRLs, NIRLs, NAWM, and WM in HCs. In KFA and FA values, there were significant differences between each type of lesion, as well as each type of PLWM (P < 0.05). The MK values of CELs and IRLs were significantly lower than NIRLs, but inversely for MD (P < 0.05). There were no differences between CELs and IRLs for MK (P=1) and MD (P=0.261). The results of MK and MD values in CELs-PLWM and IRLs-PLWM were similar to the CELs and IRLs. There were no significant differences between NAWM and WM in HCs in all the enrolled diffusion parameters (P >0.05) and the FA values between NIRLs-PLWM and NAWM or between NIRLs-PLWM and WM in HCs were no significant differences (P >0.05). The KFA and MD values in IRLs-PLWM (r =0.443, P =0.021; r =-0.518, P =0.006) were correlated with the DST scores and the KFA of CELs-PLWM (r =0.396, P =0.041) was correlated with SDMT scores. Our findings demonstrate that the KFA values have the potential to distinguish different types of MS white matter tissues. Furthermore, the diffusion parameters can reflect the microstructure abnormalities in different MS lesions and might help us better understand the pathological mechanism and lesion evolution.

Association between morphological manifestations of inflammatory bowel disease and biochemical markers of inflammation

Aim. To determine morphological and morphometric changes in the structure of the mucous membrane of the large intestine and their relationship with the content of short-chain volatile fatty acids and fecal calprotectin in patients with inflammatory bowel disease. Materials and methods. We examined 68 patients with inflammatory bowel disease, including 30 women and 38 men aged 20–66 years, 55 patients were with ulcerative colitis and 13 patients – with Crohn’s disease. Histological examination focused on changes in the mucous membrane of the large intestine. Determination of short-chain volatile fatty acids in feces was performed using gas chromatography. Calprotectin content was measured in fecal samples by enzyme-linked immunosorbent assay. Results. Significant correlations were found between epithelial disruption and changes in crypt architecture, infiltration density, and histological activity. The higher degree of inflammation in patients with severe course was combined with a lower level of tissue nonspecific protection, which was detected by the number of goblet cells, eosinophilic and neutrophilic leukocytes. There was a decrease in the fecal concentration of butyric acid in patients with nonspecific ulcerative colitis and Crohn’s disease compared with controls, but a more significant decrease was observed in patients with severe nonspecific ulcerative colitis. The data have confirmed the association between inflammatory bowel disease and the content of short-chain volatile fatty acids, fecal calprotectin in coprofiltrate, which was evidenced by the presence of correlations between low content of short-chain volatile fatty acids and eosinophilic infiltration (r = -0.412; fecal calprotectin levels and disease severity (r = 0.589; P = 0.001), atrophy (r = 0.458; Р &lt; 0.05), infiltration density (r = 0.434; Р &lt; 0.05). Conclusions. All patients with inflammatory bowel disease are characterized by a specific histological picture, which reflected the different degrees of inflammation. Morphometric parameters more accurately show significant atrophic changes in the mucous membrane of the large intestine. The data have confirmed the association between inflammatory bowel disease and the content of short-chain volatile fatty acids and calprotectin in coprofiltrate.

Correlation between serum cytokines and clinicopathological features in patients with drug-induced liver injury.

Objectives: Changes in serum levels of cytokines have been proposed as possible biological markers of tissue damage, including drug-induced liver injury (DILI). Here, we aimed to screen cytokine markers that have guiding significance for the degree of inflammation of DILI. Patients and methods: 54 patients with DILI were retrospectively analyzed as the experimental group, and 14 healthy subjects were randomly selected as the control group. A total of 20 cytokines were detected by using a cytokine protein antibody chip, and differentially expressed proteins were screened. Results: There were significant differences in serum cytokines between DILI patients and healthy controls. Compared with the control group, the DILI group expressed 11 differential proteins. IL-8, TNF RII, TNFα, TNF RI, MIP-1β, MIP-1α, and IL-1β were differentially expressed in DILI patients with different degrees of inflammation from G1 to G4. MIG, IL-12p40, and IL-10 were differentially expressed in the higher degree of inflammation groups (G2, G3, and G4 groups). Tissue inhibitor of metalloproteinases-1 (TIMP-1) was differentially expressed in the group with the highest inflammation degree (G4 group). Chemokine C-C motif ligand 1 (I-309) was only differentially expressed in the lowest inflammation group (G1 group). Conclusion: The changes and differential expression of specific cytokine levels were helpful for evaluating different degrees of inflammation of DILI.

Association between interleukin-6 and lower urinary tract symptoms of benign prostatic hyperplasia

ObjectiveTo evaluate the association between IL-6 in prostatic tissue/blood sample and BPH-LUTS, so as to preliminarily discover an indicator of inflammation that could show the severity of LUTS. Patients and methodsThe prostatic tissues and blood samples were collected from 56 patients who underwent transurethral plasmakinetic resection of the prostate (TUPKRP). The association between IL-6 detected on prostatic tissues/blood sample and LUTS parameters, including international prostate symptom score (IPSS), peak flow rate (Qmax) and urodynamic parameters were analyzed with SPSS version 18.0, and p-value <0.05 was chosen as the criterion for statistical significance. ResultsThe TPSA and prostate volume (PV) were found to be higher in the inflammation group (p=0.021, 0.036). There was a positive association between prostate tissue inflammation and LUTS ([IPSS, storage symptoms score (SSS), voiding symptoms score (VSS), p<0.05], [Qmax, p=0.025], [obstruction, p=0.027] and [AUR, p=0.018]). The level of serum IL-6 was significantly higher in inflammatory group (p=0.008). However, no differences were observed in different degrees of inflammation (p=0.393). The level of IL-6 in prostatic tissue significantly increased with the degree of inflammation (p<0.001), and the intensity of IL-6 expression was statistically correlative with the degree of inflammation (p<0.001). The IL-6 expression in prostatic tissue was statistically relevant with IPSS (p=0.018) and SSS (p=0.012). ConclusionIL-6 expression in prostatic tissue is associated with storage IPSS, suggesting chronic inflammation might contribute to storage LUTS.

SPECT/CT imaging of inflammation and calcification in human carotid atherosclerosis to identify the plaque at risk of rupture

BackgroundCalcification and inflammation are atherosclerotic plaque compositional biomarkers that have both been linked to stroke risk. The aim of this study was to evaluate their co-existing prevalence in human carotid plaques with respect to plaque phenotype to determine the value of hybrid imaging for the detection of these biomarkers. MethodsHuman carotid plaque segments, obtained from endarterectomy, were incubated in [111In]In-DOTA-butylamino-NorBIRT ([111In]In-Danbirt), targeting Leukocyte Function-associated Antigen-1 (LFA-1) on leukocytes. By performing SPECT/CT, both inflammation from DANBIRT uptake and calcification from CT imaging were assessed. Plaque phenotype was classified using histology. ResultsOn a total plaque level, comparable levels of calcification volume existed with different degrees of inflammation and vice versa. On a segment level, an inverse relationship between calcification volume and inflammation was evident in highly calcified segments, which classify as fibrocalcific, stable plaque segments. In contrast, segments with little or no calcification presented with a moderate to high degree of inflammation, often coinciding with the more dangerous fibrous cap atheroma phenotype. ConclusionCalcification imaging alone can only accurately identify highly calcified, stable, fibrocalcific plaques. To identify high-risk plaques, with little or no calcification, hybrid imaging of calcification and inflammation could provide diagnostic benefit.

Assessment of Pulpal Status in Primary Teeth Following Direct Pulp Capping in an Experimental Canine Model.

(1) Background: This study aimed to assess the pulpal response of primary teeth by pulse-oximetry (PO) in a canine model, following direct pulp capping (DPC). (2) Methods: Forty-eight primary teeth from eight canine subjects were divided into three treatment groups, based on the DPC material—calcium hydroxide (CH), MTA, BiodentineTM)—and three corresponding control groups. Data from PO pulp testing were correlated with laser Doppler flowmetry (LDF) testing, computer tomographic (CT) densitometry and histological analysis; the experiment lasted 14 days. (3) Results: SpO₂ recordings revealed statistically significant differences (p = 0.002, <0.05) between the treatment and control groups, and no significant differences (p = 0.257, >0.05) were observed between treatment groups. LDF recordings showed significant differences (p = 0.002, <0.05) between the treatment and control groups and identified significant differences between materials (p = 0.001, <0.05). CT densitometry indicated vital pulps in all teeth, with pulpal inflammation detected in 6/8 CH-capped teeth and 2/8 MTA-capped teeth. Histologic evaluation confirmed vital pulp in all specimens, with different degrees of inflammation. (4) Conclusions: Within its limitations, the present study confirms the diagnostic value of PO evaluation of pulpal status in primary teeth with histologic means after pulp-capping procedures in a canine model. However, various degrees of pulpal inflammation elicited by different pulp-capping materials seem not to correlate with the obtained PO values.

Specific alterations in mucosa-associated bacterial composition in ulcerative colitis (UC) patients with different degrees of inflammation

The aim of this study is to evaluate the specific bacterial communities and alterations and to explore the method predicting the microbiological evolution tendency of ulcerative colitis (UC) patients. A total of 29 UC patients and 18 healthy subjects (HS) were enrolled. UC patients were grouped into mild, moderate and severe UC based on the Mayo Score. The bacterial types of the groups were distinctly different with each other on different classification levels. Interestingly, the bacterial composition of severe UC was distinctly different from others. The Chao and Ace indices of bacterial microbiota were significantly higher in the severe UC group. The main phyla in UC and HS were Firmicutes, Bacteroidetes and Proteobacteria. The percentage of the 3 main phyla in severe UC was lower than that in non-severe UC. Similar to the other groups, the main genera in severe UC were Bacteroides and Escherichia-Shigella. However, Parabacteroides and a type of Prevotella disappeared in the severe UC group. Some types, such as Faecalibacterium and Fusobacterium, decreased. On the contrary, the other types increased. The abundance of the putative pathogenic bacteria in mild UC, moderate UC and severe UC showed an increasing trend (9:11:115). Moreover, Bacillus, Lactococcus and Alloprevotella disappeared in UC. Parabacteroides and a type of Prevotella disappeared in severe UC. Serious dysbacteriosis and abundant putative pathogenic bacteriа are the two important features of severe UC. The percentage phyla and the abundance of putative pathogenic bacteria could be used to predict the evolution tendency.

Efficacy and safety of the combination of modern medicine and traditional Chinese medicine in pulmonary fibrosis caused by novel coronavirus disease: A protocol for Bayesian network meta-analysis.

Background:Novel coronavirus disease (COVID-19) is a kind of pulmonary inflammation induced by New Coronavirus. It seriously threatens people's health and safety. Clinical studies have found that some patients have different degrees of inflammation after discharge from hospital, especially in patients with severe inflammatory lung fibrosis. Early combination of Chinese medicine and modern medicine has important clinical significance. There are still many deficiencies in the current research. We studied the effectiveness of the combination of traditional Chinese medicine and modern medicine in the treatment of pulmonary fibrosis caused by COVID-19, and proposed a network meta-analysis (NMA) scheme.Methods:According to the search strategy, we will search Chinese and English databases to collect all randomized controlled trials of traditional Chinese medicine combined with modern drugs or only using traditional Chinese medicine for new coronavirus-19-induced pulmonary fibrosis between December 1, 2019 and November 15, 2021. First, the literature was screened according to the eligibility criteria, endnotex9 was used to manage the literature, and the Cochrane Collaboration's tool was used to assess the quality of the included literature. Revman 5.3, Stata 14.2, and gemtc14.3 meta-analysis software was then used for data processing and analysis, and the grading of recommendations assessment will be used to develop and evaluate a hierarchy for classifying the quality of evidence for NMA.Results:Through the analysis, the ranking of efficacy and safety of various treatments for pulmonary fibrosis caused by COVID-19 will be drawn, thus providing stronger evidence support for the choice of clinical treatment methods.Conclusion:Traditional Chinese medicine (TCM) combined with modern drugs has played a positive role in the treatment of pulmonary fibrosis caused by COVID-19, and this study may provide more references for the clinical medication of pulmonary fibrosis caused by COVID-19.INPLASY registration number:INPLASY2021110061.

Edwardsiella piscicida, a pathogenic bacterium newly detected in spotted sea bass Lateolabrax maculatus in China

In this study, Edwardsiella piscicida strain 18BJ136 was isolated from diseased spotted sea bass Lateolabrax maculatus, in China, and its pathogenicity in this newly recognized host was investigated. Physiological and biochemical tests showed that 18BJ136 did not produce H2S but utilized d-maltose, and was positive for succinate alkalinization, coumarate, and the ellman reaction. Its growth characteristic showed that it proliferated in a wide range of salinities, but was sensitive to acidity and alkalinity. A PCR analysis showed that 18BJ136 carried at least nine virulence genes: gadB, katB, citC, usp13, esrB, sodB, luxS, fimA, and mukF. A spot test showed that the strain had a variety of extracellular enzyme activities, including hemolysin and protease. Artificial infection experiments indicated that 18BJ136 was strongly virulent in the spotted sea bass, with a median lethal dose (LD50) of 1.23 × 103 cfu/g. Similar to the naturally infected fish, the main clinical symptoms of the artificially infected fish were festering scores of skin, scale shedding, and the swelling of multiple internal organs. The 18BJ136 caused the following histopathological lesions in the spotted sea bass: different degrees of inflammation in each tissue; multiple necrotic foci in the liver, spleen, and head kidney; and severe hemorrhage in the spleen and head kidney. The expression of IL-8, TNF-α, TLR-23, and HSP70 was significantly upregulated after infection (P < 0.05), indicating that the pathogen activated the host’s innate immune response. These results extended our understanding of E. piscicida infection in the spotted sea bass.

Sickle cell anemia: hierarchical cluster analysis and clinical profile in a cohort in Brazil

IntroductionSickle cell anemia is a monogenic disorder caused by a mutation in the β-hemoglobin gene, resulting in sickle hemoglobin that can polymerize. Presentation and clinical course have significant inter-individual variability and classifying these patients for severity is a challenge. MethodsWe applied hierarchical clusters with 10 routine laboratory tests to understand if this grouping could be associated with clinical manifestations. We included 145 adult homozygous patients (SS) at an outpatient clinic in a retrospective study. ResultsWe found five clusters by counting those that had been differentiated by unconjugated bilirubin, reticulocytes, LDH, leukocytes, lymphocytes and monocytes. When comparing groups to clinical findings, the clusters were different only for liver abnormality. Cluster 3 had the lower median of reticulocytes, LDH, leukocytes, lymphocytes and monocytes and a higher percentage of patients under treatment. Clusters 4 and 5 had higher frequencies of liver impairment and higher medians of reticulocytes, LDH, leukocytes, lymphocytes and monocytes. Hemolysis and inflammation seemed to influence the grouping. ConclusionIn our study, cluster analysis showed five groups that exhibited different degrees of inflammation and hemolysis. When comparing clinical data, the result was different only for the criteria of liver abnormality.

Differential Effects of Albumin Infusion between ICU and Non-ICU Hypoalbuminemia Patients

Background: Hypoalbuminemia is frequent among hospitalized patients and is associated with poor outcomes. ICU patients are widely associated with more severe condition making albumin correction seems to be less effective. This study was aimed to compare the results of albumin correction in ICU and non-ICU patients at Sulianti Saroso Hospital, Jakarta. Methods: A cross sectional study was conducted on adult patients in ICU and non-ICU wards who received intravenous albumin infusion at Sulianti Saroso hospital, between January 2013 to March 2018. Paired t-test was used to analyze the changes of albumin level before and after albumin infusion. Results: 123 ICU patients (41 sepsis, 82 non-sepsis) and 206 non-ICU patients (34 sepsis, 172 non-sepsis) who received 20% or 25% albumin infusions were included. Significant increase in albumin levels were observed in sepsis patients both in ICU and non-ICU, while in non-sepsis patients, the significant increase only observed in non-sepsis patients. Overall, mean increase in albumin levels in ICU-and non-ICU patients were 0.13 (0.63) g/dL vs 0.35(0.54) g/dL, respectively (P= &lt; 0,001). Conclusion: Non-ICU patients show better response to albumin infusion compared to ICU patients. This difference is presumably due to different degree of inflammation. It is suggested that the quantity needed for albumin infusion is calculated differently according to clinical condition of the patients

Long-Term Androgen-Induced Nonalcoholic Fatty Liver Disease in a Polycystic Ovary Syndrome Mouse Model is Related to Mitochondrial Dysfunction

Abstract Objective: Metabolic disorders are markedly common in women with polycystic ovary syndrome (PCOS), and nonalcoholic fatty liver disease (NAFLD) is observed in 30%-55% of all PCOS patients. Many studies have reported that autophagy and apoptosis, which are closely related to mitochondrial function, play important roles in the development of NAFLD. Therefore, in this study, we aimed to explore the role of mitochondrial dysfunction caused by liver apoptosis and autophagy imbalance in the development of NAFLD in a PCOS mouse model. Methods: We used a dihydrotestosterone (DHT)-induced PCOS model to mimic the pathological process of hyperandrogenism. Hematoxylin and eosin and Oil Red O staining assays were used to observe the pathological changes in the liver. Western blotting and quantitative real-time polymerase chain reaction were used to perform mitochondrion-related assays. Results: Hepatic steatosis and different degrees of inflammation were observed in the DHT-treated mice. The expression of molecules involved in the respiratory chain and aerobic respiration process was altered. The levels of the key molecules associated with apoptosis and autophagy were abnormal. Conclusions: Androgens may play a role in the process of hepatic steatosis development by affecting mitochondrial function and subsequently inducing apoptosis and autophagy. Such phenomena might be involved in the pathogenesis of NAFLD in women with PCOS.

Long-term androgen excess induces insulin resistance and non-alcoholic fatty liver disease in PCOS-like rats

ObjectiveWomen with polycystic ovary syndrome (PCOS) are at higher risk for metabolic disorders compared to healthy women, and about 51 % of women with PCOS suffer from non-alcoholic fatty liver disease (NAFLD). Investigation into the pathological mechanism behind this association will provide insights for the prevention and treatment of this complication. MethodsDihydrotestosterone (DHT), a nonaromatic androgen, was used to mimic the pathological conditions of hyperandrogenism and insulin resistance. Hematoxylin and eosin staining, Oil Red O staining, immunofluorescent staining, Western blots, and qRT-PCR were used to verify the hepatic steatosis and inflammation, and the latter two methods were also used for energy and mitochondrion-related assays. ELISA was used to measure the level of reactive oxygen species. ResultsTwelve weeks of DHT exposure led to obesity and insulin resistance as well as hepatic steatosis, lipid deposition, and different degrees of inflammation. The expression of molecules involved in respiratory chain and aerobic respiration processes, such as electron transfer complex II, pyruvate dehydrogenase, and succinate dehydrogenase complex subunit A, was inhibited. In addition, molecules associated with apoptosis and autophagy were also abnormally expressed, such as increased Bak mRNA, an increased activated caspase-3 to caspase-3 ratio, and increased Atg12 protein expression. All of these changes are associated with the mitochondria and lead to lipid deposition and inflammation in the liver. ConclusionsLong-term androgen excess contributes to insulin resistance and hepatic steatosis by affecting mitochondrial function and causing an imbalance in apoptosis and autophagy, thus suggesting the pathogenesis of NAFLD in women with PCOS.

Effectiveness of specific stabilization exercise compared with traditional trunk exercise in women with non-specific low back pain: a pilot randomized controlled trial.

BackgroundNon-specific low back pain (LBP) is the leading cause of disability worldwide. The primary physiotherapeutic treatment for LBP is physical exercise, but evidence suggesting a specific exercise as most appropriate for any given case is limited.ObjectiveTo determine if specific stabilization exercise (SSE) is more effective than traditional trunk exercise (TTE) in reducing levels of pain, disability and inflammation in women with non-specific low back pain (LBP).DesignA pilot randomized controlled trial was conducted in Rovira i Virgili University, Catalonia.MethodsThirty-nine females experiencing non-specific LBP were included in two groups: the TTE program and SSE program, both were conducted by a physiotherapist during twenty sessions. The primary outcome was pain intensity (10-cm Visual Analogue Scale). Secondary outcomes were disability (Roland Morris Disability Questionnaire), and inflammation (IL-6 and TNF-α plasma levels). Measurements were taken at baseline, at half intervention, at post-intervention, and a month later.ResultsMean group differences in change from baseline to post-intervention for TTE were: −4.5 points (CI 3.3 to 5.6) for pain, −5.1 points (CI 3.0 to 7.3) for disability, 0.19 pg/mL (95% CI [−1.6–1.2]) for IL-6 levels, and 46.2 pg/mL (CI 13.0 to 85.3) for TNF-α levels. For SSE, differences were: −4.3 points (CI 3.1 to 5.6) for pain, −6.1 points (CI 3.7 to 8.6) for disability, 1.1 pg/mL (CI 0.0 to 2.1) for IL-6 levels , and 12.8 pg/mL (95% CI [−42.3–16.7]) for TNF-α levels. There were an insignificant effect size and no statistically significant overall mean differences between both groups.ConclusionThis study suggests that both interventions (traditional trunk and specific stabilization exercises) are effective in reducing pain and disability in non-specific LBP patients, but the two programs produce different degrees of inflammation change.Clinical trial registration numberNCT02103036.