Protectin D1 protects against lipopolysaccharide-induced acute lung injury through inhibition of neutrophil infiltration and the formation of neutrophil extracellular traps in lung tissue

xlomafota13 shared this article with you from Inoreader Protectin D1 protects against lipopolysaccharide-induced acute lung injury through inhibition of neutrophil infiltration and the formation of neutrophil extracellular traps in lung tissue Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1074. doi: 10.3892/etm.2021.10508. Epub 2021 Jul 28. ABSTRACT Protectin D1 (PD1), a DHA-derived lipid mediator, has recently been shown to possess anti-inflammatory and pro-resolving properties. To date, little is known about the effect of PD1 on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. The aim of the present study was to investigate the therapeutic effects of PD1 on LPS-induced ALI and its potential mechanisms of action. ALI was induced via an intraperitoneal injection of LPS, where PD1 (2 ng/mouse) was administered intravenously 30 min after LPS challenge. Mice were sacrificed 24 h after modeling. Lung histopathological changes were assessed using hematoxylin and eosin staining and myeloperoxidase (MPO) activity was tested using immunohistochemistry. Tumor necrosis-α and interleukin-6 levels in the bronchoalveolar lavage fluid (BALF) and serum were measured using ELISA. To detect neutrophil extracellular traps produced by infiltrated neutrophils in the lung tissue, immunofluorescence staining was performed using anti-MPO and anti-histone H3 antibodies. The results indicated that PD1 significantly attenuated histological damage and neutrophil infiltration in lung tissue, reduced the lung wet/dry weight ratio, protein concentration and proinflammatory cytokine levels in BALF and decreased proinflammatory cytokine levels in serum. Moreover, neutrophil citrullinated histone H3 (CitH3) expression was also reduced after PD1 administration. In conclusion, PD1 attenuated LPS-induced ALI in mice via inhibition of neutrophil extracellular trap formation in lung tissue. Therefore, PD1 administration may serve to be a new strategy for treating ALI. PMID:34447467 | PMC:PMC8355679 | DOI:10.3892/etm.2021.10508 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Factors influencing the articular eminence of the temporomandibular joint (Review)

xlomafota13 shared this article with you from Inoreader Factors influencing the articular eminence of the temporomandibular joint (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1084. doi: 10.3892/etm.2021.10518. Epub 2021 Jul 30. ABSTRACT The temporomandibular joint (TMJ), the most complex and evolved joint in humans, presents two articular surfaces: the condyle of the mandible and the articular eminence (AE) of the temporal bone. AE is the anterior root of the zygomatic process of the temporal bone and has an anterior and a posterior slope, the latter being also known as the articular surface. AE is utterly important in the biomechanics of the TMJ, as the mandibular condyle slides along the posterior slope of the AE while the mandible moves. The aim of this review was to assess significant factors influencing the inclination of the AE, especially modifications caused by aging, biological sex or edentulism. Studies have reported variations in the angles of the slopes of the AE between medieval and recent human dry skulls, as well as between subjects of different racial origin. Rec ent articles have emphasized the significant role that tooth loss has on the flattening of the AE. Although some papers have described biological sex or age as factors which could be associated with differences in AE angulations, edentulism seems to be a significant factor impacting on the inclination of the AE. PMID:34447477 | PMC:PMC8355702 | DOI:10.3892/etm.2021.1 0518 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Risk of sudden coronary death based on genetic background in Chinese Han population

xlomafota13 shared this article with you from Inoreader Risk of sudden coronary death based on genetic background in Chinese Han population Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1068. doi: 10.3892/etm.2021.10502. Epub 2021 Jul 28. ABSTRACT Associations between gene variations and sudden cardiac arrest or coronary artery disease have been reported by genome-wide association studies. However, the implication of the genetic status in cases of sudden coronary death (SCD) from the Chinese Han population has remained to be investigated. The present study established a mini-sequencing system to examine putative death-causing single nucleotide polymorphisms (SNPs) using multiplex PCR, single base extension reaction and capillary electrophoresis techniques. A total of 198 samples from the Chinese Han population (age range, 34-71 years; mean age, 53.86 years) were examined using this method. Samples were classified into three groups: Coronary heart disease (CHD, n=70), SCD (n=53) and control (n=75) group. Significant associations were identified for 10, 4 and 6 SNPs in CHD, SCD and sudden de ath from CHD, respectively, using the χ2 test. The SNPs obtained by binary logistic regression may be used to assess and predict the risk of disease. The predictive accuracy of the SNPs in each prediction model and their area under the receiver operating characteristic curve (AUC) values were determined. The AUC of the four SNPs (rs12429889, rs10829156, rs16942421 and rs12155623) to predict CHD was 0.928, the AUC of the six SNPs (rs2389202, rs2982694, rs10183640, rs597503, rs16942421 and rs12155623) to predict SCD was 0.922 and the AUC of the four SNPs (rs16866933, rs4621553, rs10829156 and rs12155623) to predict sudden death from CHD was 0.912. The multifactor dimensionality reduction values were as follows: 0.8690 (prediction model of CHD), 0.7601 (prediction model of SCD) and 0.7628 (prediction model of sudden death from CHD). Taken together, the results of the present study suggested that these SNPs have considerable potential for application in genetic tests to pred ict CHD or SCD. However, further studies are required to investigate the putative functions of these SNPs. PMID:34447461 | PMC:PMC8355668 | DOI:10.3892/etm.2021.10502 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Insights into multidrug-resistant K. pneumoniae urinary tract infections: From susceptibility to mortality

xlomafota13 shared this article with you from Inoreader Insights into multidrug-resistant <em>K. pneumoniae</em> urinary tract infections: From susceptibility to mortality Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1086. doi: 10.3892/etm.2021.10520. Epub 2021 Jul 30. ABSTRACT The incidence of urinary tract infections (UTIs) caused by Klebsiella pneumoniae has exhibited an increasing trend and has become a high burden for many public health systems, especially in hospital settings. Multidrug resistance associated with the production of extended-spectrum β-lactamases (ESBL) among K. pneumoniae isolates is endemic in Southeastern Europe. We retrospectively analyzed 75 cases admitted to 'St. Parascheva' Clinical Hospital of Infectious Diseases in Iasi, Romania, during the first 6 months of 2019 (January 1 to June 30), who had a confirmed diagnosis of K. pneumoniae UTI at discharge. From a total of 75 patients, 34 (45.3%) presented ESBL+ K. pneumoniae. The mean age was 66 years (70.1 for the ESBL+ patients vs. 62.6 for the ESBL- patients, P=0.0365). There was a symmetrical sex distribution (37 men vs. 38 women). Of these, 22 men had ESBL+ K. pneumoniae UTIs, compared to only 15 with an ESBL- strain, P=0.0087. Another risk factor for ESBL+ K. pneumoniae UTIs was the presence of hospitalization in the past 6 months; 20 (58.82%) patients with ESBL+ infections were previously hospitalized, compared to only 5 (12.19%) patients with ESBL- strains, P<0.0001. The urinary catheter carriers presented an increased prevalence of ESBL+ infections (15/34 vs. 5/41, P=0.0012). Regarding mortality, ESBL+ infections caused 6 fatalities, compared to only 1 death in the ESBL- group, P=0.0166. ESBL+ K. pneumoniae strains represent an important cause of healthcare-related UTIs, with a significantly higher mortality rate compared to ESBL- strains. Early identification and adequate management of the risk factors incriminated in ESBL+ UTIs should be a priority for physicians in order to limit the dissemination of the ESBL-producing strains and thus to improve the outcome of these patients. PMID:34447478 | PMC:PMC8355719 | DOI:10.3892/etm.2021.10520 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Astragaloside IV alleviates heart failure by regulating SUMO-specific protease 1

xlomafota13 shared this article with you from Inoreader Astragaloside IV alleviates heart failure by regulating SUMO-specific protease 1 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1076. doi: 10.3892/etm.2021.10510. Epub 2021 Jul 28. ABSTRACT The present study investigated whether the protective effect and mechanism of astragaloside IV (AS-IV) on heart failure (HF) involves small ubiquitin-like modifier (SUMO)-specific protease 1 (Senp1). Mouse HF was established by aortic constriction, inducing pressure overload. The model was confirmed by echocardiography 6 weeks after surgery. Mice were randomly divided into control, HF, HF+AS-IV, and AS-IV groups. Ventricular function was examined by echocardiography. Morphological changes of myocardial tissues were examined by H&E staining. The protein levels of the apoptosis-related proteins, cleaved caspase-3, caspase-3, Bcl2, Bax, and SUMO-Senp1 were determined by Western blotting. H2O2 in isolated mitochondria and cells was determined by Amplex Red. A reactive oxygen species (ROS) detection kit determined ROS levels in isolated mitochondria and HL-1 cells. JC-1 reagent measured mitochondrial membrane potential (ΔΨm). Apoptosis of HL-1 cells was examined by terminal deoxynucleotidyl transferase dUTP nick end labeling. Compared with the control group, the heart weight and heart mass/body weight ratio increased in the HF group (P<0.05). Furthermore, the ejection fraction and left ventricular shortening fraction decreased (P<0.05), while the left ventricular end-diastolic diameter (LVID;d) and end-systolic diameter (LVID;s) increased (P<0.05). Finally, mitochondrial ROS and H2O2 increased (P<0.05), while the ΔΨm decreased (P<0.05). However, AS-IV improved the cardiac function of HF mice, decreased the level of ROS and H2O2 in the myocardium, suppressed the decrease in ΔΨm, and decreased the apoptosis of myocardial cells (P<0.05). AS-IV also decreased the Senp1-overexpression. Furthermore, in HL-1 cells, Senp1-overexpression signifi cantly inhibited the protective effects of AS-IV. AS-IV decreased oxidative stress in cardiomyocytes, decreased mitochondrial damage, inhibited ventricular remodeling, and ultimately improved cardiac function by inhibiting HF-induced Senp1-overexpression. This mechanism provides a novel theoretical basis and clinical treatment for HF. PMID:34447469 | PMC:PMC8355636 | DOI:10.3892/etm.2021.10510 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Giant chondroid lipoma of the breast: A case report and literature review

xlomafota13 shared this article with you from Inoreader Giant chondroid lipoma of the breast: A case report and literature review Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1087. doi: 10.3892/etm.2021.10521. Epub 2021 Jul 30. ABSTRACT Chondroid lipoma is a rare benign lesion affecting the breast, in which the diagnosis of malignancy is difficult to be excluded during preoperative studies. In this respect, a correct histopathological diagnosis is mandatory in order to avoid overdiagnosis and subsequently overtreatment. In the present study, the case of a 61-year-old patient who self-referred for the development of a large tumor at the level of the left breast is reported. Biopsy raised the suspicion of a chondroid lipoma; thus, the patient was submitted to conservative surgery. The lesion was completely excised by performing a total mastectomy. The histopathological studies confirmed the presence of chondroid lipoma, with no signs of malignant transformation. At the 24-month follow-up interval no signs of recurrence were detected. In conclusion, although it may reach significan t dimensions, giant chondroid lipoma of the breast is a benign lesion that may benefit from conservative treatment and does not recur. PMID:34447479 | PMC:PMC8355713 | DOI:10.3892/etm.2021.10521 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Fumaric acid and succinic acid treat gestational hypertension by downregulating the expression of KCNMB1 and TET1

xlomafota13 shared this article with you from Inoreader Fumaric acid and succinic acid treat gestational hypertension by downregulating the expression of KCNMB1 and TET1 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1072. doi: 10.3892/etm.2021.10506. Epub 2021 Jul 28. ABSTRACT The present study hypothesized that fumaric acid and succinic acid may exhibit therapeutic effects on gestational hypertension. During pregnancy, estrogen upregulates ten-eleven translocation 1 (TET1) expression, which subsequently increases calcium-activated potassium channel subunit β1 (KCNMB1) expression. KCNMB1 is associated with hypertension. Fumaric acid and succinic acid are understood to inhibit TET. Therefore, the present study investigated whether fumaric acid and succinic acid exhibit therapeutic effects on gestational hypertension and whether these effects are mediated by TET1 and KCNMB1. Nω-Nitro-L-arginine methyl ester hydrochloride was injected into rats to establish a gestational hypertension model. Dimethyl fumarate (DMF) and succinic acid were administrated into rats to treat gestational hypertension. Rats were divided into fi ve groups: i) Control; ii) model; iii) DMF; iv) succinic acid; and v) DMF + succinic acid. Blood pressure was monitored by a noninvasive meter and urinary protein was determined using a urinary protein kit. Placenta pathology was examined by hematoxylin-eosin staining. Compared with the control group, urinary protein and blood pressure in the model group increased significantly. The placental cells in the control group were arranged orderly. However, in the model group, decidual cellular edema of placenta and vacuolar degeneration were observed, and the intervascular membrane was markedly thicker with plenty of fibrin deposition. These results indicate successful establishment of a gestational hypertension model. However, compared with the model group, urinary protein, blood pressure, edema, vacuoles and fibrin deposition were markedly reduced in the DMF, succinic acid and DMF + succinic acid groups. mRNA and protein levels of TET1 and KCNMB1 in placenta were evaluated by immunohist ochemical analysis, reverse transcription-quantitative polymerase chain reaction and western blotting. The TET1 and KCNMB1 levels in the model group were markedly increased compared with those in the control group. However, compared with the model group, the expression levels were markedly downregulated in the DMF, succinic acid and DMF + succinic acid groups. In conclusion, fumaric acid and succinic acid may treat gestational hypertension by downregulating the expression of KCNMB1 and TET1. PMID:34447465 | PMC:PMC8355717 | DOI:10.3892/etm.2021.10506 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.