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#38625603   2024/04/16 To Up

Flock level socio-economic and other associated risk factors for Peste des petits ruminants (PPR) exposure in sheep and goats in Madhya Pradesh state, India.

To effectively control and eradicate PPR, the comprehensive understanding of risk factors associated with PPR exposure is vital. Hence, this study investigated socioeconomic and other associated risk determinants for PPR exposure at flock level in sheep and goats in a non-vaccination programme implemented Madhya Pradesh state India. A total of 410 sheep and goat flocks, comprised mostly of goats but also some mixed flocks, were surveyed during 2016 using a multistage random sampling procedure. Further, 230 blood samples were also collected from the farmers-reported PPR affected flocks and sera were tested using c-ELISA to confirm PPR exposure. The primary data on socioeconomic factors, farm management factors, health status, vaccination details and other epidemiological risk factors were collected from flock owners and descriptive statistics, chi-square analysis and logistic regression models were fitted to identify the significant risk factors for PPR incidence. The farmer's education, flock size, rearing pattern, and awareness of PPR vaccination were found to be significant pre-disposing risk factors for PPR exposure in the flocks. Hence, the control and eradication strategy need to be designed comprehensively considering the key social factors like education and vaccination awareness along with other flock level risk factors to eradicate PPR by 2030 in consonance with the global plan.
Gurrappa Naidu Govindaraj, Vinayagamurthy Balamurugan, Barada Shankar Mohanty, Sowjanya Kumari, Jayant Tapase, G S Naveenkumar, Parimal Roy, B R Shome

1540 related Products with: Flock level socio-economic and other associated risk factors for Peste des petits ruminants (PPR) exposure in sheep and goats in Madhya Pradesh state, India.

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#38625592   2024/04/16 To Up

miR-29b-3p Affects the Hypertrophy of Ligamentum Flavum in Lumbar Spinal Stenosis and its Mechanism.

To explore the effect of miR-29b-3p on fibrosis and hypertrophy of ligamentum flavum (LF) in lumbar spinal stenosis (LSS) and its underlying mechanism. Patients with LSS and lumbar disc herniation (LDH) (control) undergoing posterior lumbar laminectomy were included in this study. Human LF samples were obtained for LF cell isolation, RNA, and protein extraction. Histomorphological analysis of LF was performed using hematoxylin-eosin (HE) staining. After isolation, culture, and transfection of primary LF cells, different transfection groups were constructed: NC-mimic, miR-29b-3p-mimic, NC-inhibitor, and miR-29b-3p-inhibitor. Quantitative real time polymerase chain reaction (qRT-PCR) was performed to detect the expression of miR-29b-3p in LF and LF cells. Western blot analysis detected the protein expressions of P16 and CyclinD1. ELISA detected the protein expressions of TGF-β1, Smad2, Smad3, TLR4, Type I collagen, and Type III collagen. Finally, LF cell viability was detected using the Cell Counting Kit-8 (CCK8) assay. The thickness of LF was significantly thicker in the LSS group compared to the LDH group (p < 0.05), accompanied by a higher calcification degree, more fibroblasts, and a larger area of collagen fiber proliferation. miR-29b-3p expression was significantly lower in LSS-derived LF tissues and cells than in LDH-derived tissues and cells (both p < 0.05). Compared to the NC-mimic group, the miR-29b-3p-mimic group exhibited significantly higher miR-29b-3p expression, decreased protein expressions of Type I collagen, Type III collagen, TGF-β1, Smad2, Smad3, TLR4, P16, and CyclinD1, and inhibited LF cell proliferation (all p < 0.05). As expected, the miR-29b-3p-inhibitor group displayed contrasting expression patterns (all p < 0.05). Compared to the phosphate buffer saline (PBS) group, the Trimethylamine-N-Oxide (TMAO) group showed significantly increased expressions of TGF-β1, Smad2, Smad3, TLR4, Type I collagen, Type III collagen, P16, and CyclinD1, as well as enhanced LF cell proliferation (all p < 0.05). However, there was no significant difference between the TMAO group and the Ang II group (all p > 0.05). Upregulation of miR-29b-3p expression may play a role in improving LF fibrosis and hypertrophy in LSS by inhibiting P16 expression and suppressing the activation of the TGF-β/Smad signaling pathway. This finding offers new insights into future gene modification therapy for this patient population.
Hongjie Zhang, Zhixiong Hong, Zehua Jiang, Wei Hu, Jiashao Hu, Rusen Zhu

2104 related Products with: miR-29b-3p Affects the Hypertrophy of Ligamentum Flavum in Lumbar Spinal Stenosis and its Mechanism.

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#38625585   2024/04/16 To Up

Differential changes in expression of inflammatory mRNA and protein after oleic acid-induced acute lung injury.

Acute Respiratory Distress syndrome (ARDS) is a clinical syndrome of noncardiac pulmonary edema and inflammation leading to acute respiratory failure. We used the oleic acid infusion pig model of ARDS resembling human disease to explore cytokine changes in white blood cells (WBC) and plasma proteins, comparing baseline to ARDS values. Nineteen juvenile female swine were included in the study. ARDS defined by a PaO/FiO2 ratio < 300 was induced by continuous oleic acid infusion. Arterial blood was drawn before and during oleic acid infusion, and when ARDS was established. Cytokine expression in WBC was analyzed by RT-qPCR and plasma protein expression by ELISA. The median concentration of IFN-γ mRNA was estimated to be 59% ( = 0.006) and of IL-6 to be 44.4% ( = 0.003) of the baseline amount. No significant changes were detected for TNF-α, IL-17, and IL-10 mRNA expression. In contrast, the concentrations of plasma IFN-γ and IL-6 were significantly higher ( = 0.004 and  = 0.048 resp.), and TNF-α was significantly lower ( = 0.006) at ARDS compared to baseline. The change of proinflammatory cytokines IFN-γ and IL-6 expression is different comparing mRNA and plasma proteins at oleic acid-induced ARDS compared to baseline. The migration of cells to the lung may be the cause for this discrepancy.
Regina Golding, Rudolf K Braun, Lorenzo Miller, Michael Lasarev, Timothy A Hacker, Allison C Rodgers, Ava Staehler, Marlowe W Eldridge, Awni Al-Subu

1995 related Products with: Differential changes in expression of inflammatory mRNA and protein after oleic acid-induced acute lung injury.

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#38625487   2024/04/16 To Up

JAML inhibits colorectal carcinogenesis by modulating the tumor immune microenvironment.

It is necessary to explore new targets for the treatment of colon adenocarcinoma (COAD) according to the tumor microenvironment. The expression levels of JAML and CXADR were analyzed by bioinformatics analysis and validation of clinical samples. JAML over-expression CD8 T cell line was constructed, and the proliferation activity was detected by MTT. The production of inflammatory factors was detected by ELISA. The expression of immune checkpoint PD-1 and TIM-3 was detected by Western blot. The apoptosis level was detected by flow cytometry and apoptosis markers. The AOM/DSS mouse model of colorectal cancer was constructed. The expression levels of JAML, CXADR and PD-1 were detected by PCR and Western blot, and the proportion of CD8 T cells and exhausted T cells were detected by flow cytometry. The expression levels of JAML and CXADR were significantly decreased in colon cancer tissues. Overexpression of JAML can promote the proliferation of T cells, secrete a variety of inflammatory factors. Overexpression of CXADR can reduce the proliferation of colorectal cancer cells, promote apoptosis, and down-regulate the migration and invasion ability of tumor cells. Both JAML agonists and PD-L1 inhibitors can effectively treat colorectal cancer, and the combined use of JAML agonists and PD-L1 inhibitors can enhance the effect. JAML can promote the proliferation and toxicity of CD8 T cells and down-regulate the expression of immune checkpoints in colon cancer. CXADR can inhibit the proliferation of cancer cells and promote the apoptosis. JAML agonist can effectively treat colorectal cancer by regulating CD8 T cells.
Shiliang Cheng, Meng Li, Chunguang Li, Yonggang Dai, Jinhua Zhuo, Jue Wang, Jingrong Qian, Zhihao Hao

1080 related Products with: JAML inhibits colorectal carcinogenesis by modulating the tumor immune microenvironment.

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#38625414   2024/04/16 To Up

TIMP-3 Alleviates White Matter Injury After Subarachnoid Hemorrhage in Mice by Promoting Oligodendrocyte Precursor Cell Maturation.

Subarachnoid hemorrhage (SAH) is associated with high mortality and disability rates, and secondary white matter injury is an important cause of poor prognosis. However, whether brain capillary pericytes can directly affect the differentiation and maturation of oligodendrocyte precursor cells (OPCs) and subsequently affect white matter injury repair has still been revealed. This study was designed to investigate the effect of tissue inhibitor of metalloproteinase-3 (TIMP-3) for OPC differentiation and maturation. PDGFRβ and wild-type C57B6J male mice were used to construct a mouse model of SAH via endovascular perforation in this study. Mice were also treated with vehicle, TIMP-3 RNAi or TIMP-3 RNAi + TIMP-3 after SAH. The effect of TIMP-3 on the differentiation and maturation of OPCs was determined using behavioral score, ELISA, transmission electron microscopy, immunofluorescence staining and cell culture. We found that TIMP-3 was secreted mainly by pericytes and that SAH and TIMP-3 RNAi caused a significant decrease in the TIMP-3 content, reaching a nadir at 24 h, followed by gradual recovery. In vitro, the myelin basic protein content of oligodendrocytes after oxyhemoglobin treatment was increased by TIMP-3 overexpression. The data indicates TIMP-3 could promote the differentiation and maturation of OPCs and subsequently improve neurological outcomes after SAH. Therefore, TIMP-3 could be beneficial for repair after white matter injury and could be a potential therapeutic target in SAH.
Peiwen Guo, Xufang Ru, Jiru Zhou, Mao Chen, Yanling Li, Mingxu Duan, Yuanshu Li, Wenyan Li, Yujie Chen, Shilun Zuo, Hua Feng

1890 related Products with: TIMP-3 Alleviates White Matter Injury After Subarachnoid Hemorrhage in Mice by Promoting Oligodendrocyte Precursor Cell Maturation.

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#38625005   2024/04/16 To Up

Ultrasensitive CCL2 Detection in Urine for Diabetic Nephropathy Diagnosis Using a WS-Based Plasmonic Biosensor.

The accurate diagnosis of diabetic nephropathy relies on achieving ultrasensitive biosensing for biomarker detection. However, existing biosensors face challenges such as poor sensitivity, complexity, time-consuming procedures, and high assay costs. To address these limitations, we report a WS-based plasmonic biosensor for the ultrasensitive detection of biomarker candidates in clinical human urine samples associated with diabetic nephropathy. Leveraging plasmonic-based electrochemical impedance microscopy (P-EIM) imaging, we observed a remarkable charge sensitivity in monolayer WS single crystals. Our biosensor exhibits an exceptionally low detection limit (0.201 ag/mL) and remarkable selectivity in detecting CC chemokine ligand 2 (CCL2) protein biomarkers, outperforming conventional techniques such as ELISA. This work represents a breakthrough in traditional protein sensors, providing a direction and materials foundation for developing ultrasensitive sensors tailored to clinical applications for biomarker sensing.
Shuangshuang Gao, Huili Li, Lixuan Liu, Yiming Tian, Rui Wang, Xuanlin Pan, Fusheng Wen, Jianyong Xiang, Anmin Nie, Kun Zhai, Bochong Wang, Congpu Mu, Tianyu Xue, Zhongyuan Liu

2548 related Products with: Ultrasensitive CCL2 Detection in Urine for Diabetic Nephropathy Diagnosis Using a WS-Based Plasmonic Biosensor.

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#38624391   2020/06/10 To Up

Blood Plasma Microfluidic Device: Aiming for the Detection of COVID-19 Antibodies Using an On-Chip ELISA Platform.

COVID-19 is a public health emergency of international concern. Detection of SARS-CoV-2 virus is an important step towards containing the virus spread. Although viral detection using molecular diagnostic methods is quite common and efficient, these methods are prone to errors, laborious and time consuming. There is an urgent need for blood-based tests which are simple to use, accurate, less time consuming, portable and cost-effective. Human blood plasma contains water, proteins, organic and in-organic substances including bacteria and viruses. Blood plasma can be effectively used to detect COVID-19 antibodies. The immune system generates antibodies (IgM/IgG proteins) in response to the virus and identification of these antibodies is related to the presence of the infection in the patient in the past. Therefore, detecting and testing the presence of these antibodies will be extremely useful for monitoring and surveillance of the population (Petherick, Lancet 395:1101-1102, 2020). Herein, we describe and propose a microfluidic ELISA (enzyme-linked immunosorbent assay) system to detect COVID-19 antibodies on a lab-on-chip platform. We propose to first separate plasma from whole human blood using a microfluidic device and subsequently perform the detection of antibodies in the separated plasma using a semi-automated on-chip ELISA.
Siddhartha Tripathi, Amit Agrawal

1572 related Products with: Blood Plasma Microfluidic Device: Aiming for the Detection of COVID-19 Antibodies Using an On-Chip ELISA Platform.

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#38623994   2024/04/16 To Up

MiR-2284b regulation of α-s1 casein synthesis in mammary epithelial cells of dairy goats.

The lactation character of dairy goats is the most important characteristic, and milk protein is an important index to evaluate milk quality. Casein accounts for more than 80% of the total milk protein in goat milk and is the main component of milk protein. Using GMECs (goat mammary epithelial cells) as the research object, the CHECK2 vector of the CSN1S1 gene and the overexpression vector of pcDNA 3.1 were constructed, and the mimics of miR-2284b and the interfering RNA of CSN1S1 were synthesized. Using PCR, RT-qPCR, a dual luciferase activity detection system, EdU, CCK8, cell apoptosis detection and ELISA detection, we explored the regulatory mechanism and molecular mechanism of miR-2284b regulation of αs1-casein synthesis in GMECs. miR-2284b negatively regulates proliferation and apoptosis of GMECs and αs1-casein synthesis. Two new gene sequences of CSN1S1 were discovered. CSN1S1-1/-2 promoted the proliferation of GMECs and inhibited cell apoptosis. However, it had no effect on αs1-casein synthesis. MiR-2284b negatively regulates αs1-casein synthesis in GMECs by inhibiting the CSN1S1 gene. These results all indicated that miR-2284b could regulate αs1-casein synthesis, thus playing a theoretical guiding role in the future breeding process of dairy goats and accelerating the development of dairy goat breeding.
Jinxing Hou, Wenfei Li, Xiaolong Xu, Ao Sun, Ganggang Xu, Zefang Cheng, Haoyuan Zhang, Xiaopeng An

1642 related Products with: MiR-2284b regulation of α-s1 casein synthesis in mammary epithelial cells of dairy goats.

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#38623925   2024/04/16 To Up

Changes in serum inflammatory factors in group B streptococcal infection and their predictive value for premature rupture of membranes complicated by chorioamnionitis.

The aim of this study as to unveil changes in serum inflammatory factors in pregnant women with genital tract group B (GBS) infection and their predictive value for premature rupture of membranes (PROM) complicated by chorioamnionitis (CS) and adverse pregnancy outcomes. The value of serum inflammatory factor levels in predicting PROM complicating CS and adverse pregnancy outcomes in GBS-infected pregnant women was evaluated by ELISA. Serum IL-6, TNF-α, PCT and hs-CRP levels were higher in pregnant women with GBS infection. The combined diagnosis of these factors had excellent diagnostic value in PROM complicating CS and adverse pregnancy outcomes. Joint prediction of IL-6, TNF-α, PCT and hs-CRP has the best predictive value for PROM complicating CS and adverse pregnancy outcomes.
Xiaorui Dong, Xixi Chen, Mengling Xue, Yina Zhang

1476 related Products with: Changes in serum inflammatory factors in group B streptococcal infection and their predictive value for premature rupture of membranes complicated by chorioamnionitis.

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#38623766   2024/04/16 To Up

Granulocyte-Macrophage Colony-Stimulating Factor Reverses Immunosuppression Acutely Following a Traumatic Brain Injury and Hemorrhage Polytrauma in a Juvenile Male Rat Model.

Traumatic brain injury (TBI) is a common cause of morbidity and mortality in children. We have previously shown that TBI with a concurrent extra-cranial injury reliably leads to post-injury suppression of the innate and adaptive immune systems. In patients with post-injury immune suppression, if immune function could be preserved, this might represent a therapeutic opportunity. As such, we examined, in an animal injury model, whether systemic administration of GM-CSF could reverse post-injury immune suppression and whether treatment was associated with neuroinflammation or functional deficit. Prepubescent male rats were injured using a controlled cortical impact model and then removal of 25% blood volume (TBI/H). Sham animals underwent surgery without injury induction, and the treatment groups were: sham and injured animals treated with either saline vehicle or 50 μg/kg GM-CSF. GM-CSF was given following injury and then daily until sacrifice at post-injury day 7. Immune function was measured by assessing TNF-α levels in whole blood and spleen following ex-vivo stimulation with poke weed mitogen (PWM). Brain samples were assessed by multiplex ELISA for cytokine levels and by immunohistochemistry for microglia and astrocyte proliferation. Neuronal cell count was examined using cresyl violet staining. Motor coordination was evaluated using the Rotarod performance test. Treatment with GM-CSF was associated with a significantly increased response to PWM in both whole blood and spleen. GM-CSF in injured animals did not lead to increases in levels of pro-inflammatory cytokines in brain samples but was associated with significant increases in counted astrocytes. Finally, while injured animals treated with saline showed a significant impairment on behavioral testing, injured animals treated with GM-CSF performed similar to uninjured animals. GM-CSF treatment in animals with combined injury led to increased systemic immune cell response in whole blood and spleen in the acute phase following injury. Improved immune response was not associated with elevated pro-inflammatory cytokine levels in brain or functional impairment.
Eric Anthony Sribnick, Timothy Warner, Mark Hall

1028 related Products with: Granulocyte-Macrophage Colony-Stimulating Factor Reverses Immunosuppression Acutely Following a Traumatic Brain Injury and Hemorrhage Polytrauma in a Juvenile Male Rat Model.

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