The role of universal stress protein Usp1413 in meropenem adaptive resistance and environmental stress responses in .

Although various mechanisms of carbapenem-resistance have been identified in the nosocomial pathogen , the critical process of resistance evolution and the factors involved in are not well understood. Herein, we identified a universal stress protein Usp1413 which played an important role in adaptive resistance of to meropenem (MEM). Based on RNA-Seq and genome sequencing, Usp1413 was not only one of the most downregulated USPs, but also the bare one having mutation of tyrosine and glycine inserted at the site of 229-230 (YG229-230) under the stimulation of MEM.

Impact of miR-29c-3p in the Nucleus Accumbens on Methamphetamine-Induced Behavioral Sensitization and Neuroplasticity-Related Proteins.

Methamphetamine (METH) abuse inflicts both physical and psychological harm. While our previous research has established the regulatory role of miR-29c-3p in behavior sensitization, the underlying mechanisms and target genes remain incompletely understood. In this study, we employed the isobaric tags for relative and absolute quantitation (iTRAQ) technique in conjunction with Ingenuity pathway analysis (IPA) to probe the putative molecular mechanisms of METH sensitization through miR-29c-3p inhibition.

Genomic Features and Comparative Genomic Analysis of Streptococcus sp. v1. nov., Isolated from an Endophthalmitis Patient.

Endophthalmitis is an acute inflammatory intraocular condition that can cause permanent vision loss. The treatment strategy and visual outcome partly depend on the identification of the agents of pathogens. In this study, metagenomic sequencing was conducted to investigate the microbial and antibiotic resistance genes (ARGs) composition in the vitreous (intraocular body fluid) of an endophthalmitis patient, who progressed rapidly and accompanied by severe pain.

The optimized carbapenem inactivation method for objective and accurate detection of carbapenemase-producing .

The modified carbapenem inactivation method (mCIM) recommended by the Clinical and Laboratory Standards Institute is not applicable for detecting carbapenemases in . Four currently reported phenotypic detection methods, namely, the modified Hodge test, the mCIM, the adjusted mCIM, and the simplified carbapenem inactivation method (sCIM), did not perform well in our 90 clinical isolates. Thus, the minimal inhibitory concentrations (MICs) of carbapenems and the existence and expression of carbapenemase-encoding genes were detected to explain the results.

Probiotic Species and Their Biosurfactants Eliminate Acinetobacter baumannii Biofilm in Various Manners.

Acinetobacter baumannii is a critical biofilm-forming pathogen that has presented great challenges in the clinic due to multidrug resistance. Thus, new methods of intervention are needed to control biofilm-associated infections. In this study, among three tested species, Lactobacillus rhamnosus showed significant antimaturation and antiadherence effects against A.

Uncovering the Secretion Systems of : Structures and Functions in Pathogenicity and Antibiotic Resistance.

Infections led by strains are of great concern in healthcare environments due to the strong ability of the bacteria to spread through different apparatuses and develop drug resistance. Severe diseases can be caused by in critically ill patients, but its biological process and mechanism are not well understood. Secretion systems have recently been demonstrated to be involved in the pathogenic process, and five types of secretion systems out of the currently known six from Gram-negative bacteria have been found in .

Progranulin from different gliocytes in the nucleus accumbens exerts distinct roles in FTD- and neuroinflammation-induced depression-like behaviors.

Background: Neuroinflammation in the nucleus accumbens (NAc) is well known to influence the progression of depression. However, the molecular mechanisms triggering NAc neuroinflammation in depression have not been fully elucidated. Progranulin (PGRN) is a multifunctional growth factor that is linked to the innate immune response and inflammation, and PGRN plays a key role in neurodegenerative diseases such as frontotemporal dementia (FTD).

Maternal Methamphetamine Exposure Influences Behavioral Sensitization and Nucleus Accumbens DNA Methylation in Subsequent Generation.

The deleterious effects of methamphetamine (METH) exposure extend beyond abusers, and may potentially impact the vulnerability of their offspring in developing addictive behaviors. Epigenetic signatures have been implicated in addiction, yet the characteristics to identify prenatal METH abuse to offspring addiction risk remains elusive. Here, we used escalating doses of METH-exposed mouse model in F0 female mice before and during pregnancy to simulate the human pattern of drug abuse and generated METH-induced behavioral sensitization to investigate the addictive behavior in offspring mice.

Alterations in gut microbiota affect behavioral and inflammatory responses to methamphetamine in mice.

Rationale And Objectives: Methamphetamine (METH) is a highly addictive and widely abused drug that causes severe neuroinflammation in the human brain. The gut microbiota has a tremendous impact on the core symptoms of neuropsychiatric disorders via the microbiota-gut-brain (MGB) axis. However, it is not clear whether alterations in the gut microbiota are involved in METH exposure.

cGAS modulates cytokine secretion and bacterial burdens by altering the release of mitochondrial DNA in pseudomonas pulmonary infection.

Cyclic GMP-AMP synthase (cGAS) is essential for fighting against viruses and bacteria, but how cGAS is involved in host immune response remains largely elusive. Here, we uncover the crucial role of cGAS in host immunity based on a Pseudomonas aeruginosa pulmonary infection model. cGAS mice showed more heavy bacterial burdens and serious lung injury accompanied with exorbitant proinflammatory cytokines than wild-type mice.

Dopamine D3 receptor signaling alleviates mouse rheumatoid arthritis by promoting Toll-like receptor 4 degradation in mast cells.

Dopamine receptors are involved in several immunological diseases. We previously found that dopamine D3 receptor (D3R) on mast cells showed a high correlation with disease activity in patients with rheumatoid arthritis, but the mechanism remains largely elusive. In this study, a murine collagen-induced arthritis (CIA) model was employed in both DBA/1 mice and D3R knockout mice.

Dopamine D3 receptor in the nucleus accumbens alleviates neuroinflammation in a mouse model of depressive-like behavior.

We recently reported that dopamine D3 receptor (D3R) was involved in inflammation-related depression. Nucleus accumbens (NAc) inflammation is implicated in the development and progression of depression, but its regulatory mechanism remains largely unknown. In a mouse model of NAc neuroinflammation induced by bilateral NAc injection of lipopolysaccharide (LPS), we observed that NAc neuroinflammation triggered depressive-like behaviors, and D3R expression decline and microglial activation in the NAc.

Curcumin alleviates imiquimod-induced psoriasis in progranulin-knockout mice.

Recent advances have revealed that progranulin (PGRN) is related to the aetiology of psoriasis. Moreover, curcumin, a compound derived from turmeric, has been proposed as a potential therapeutic approach in psoriasis-like dermatitis, but it is still unclear whether curcumin affects the development of psoriasis-like skin lesions under PGRN-deficient conditions. Therefore, in this study, we developed a mouse model of psoriatic skin lesions using topical application of imiquimod (IMQ) in both wild type and PGRN-knockout mice to test this possibility.

Phenotypic and genotypic characteristics of Acinetobacter baumannii enrolled in the relationship among antibiotic resistance, biofilm formation and motility.

Acinetobacter baumannii is an important pathogen in clinical. The factors of biofilm formation, antibiotic resistance and motility contribute great to A. baumannii in persisting in stressed environment, and further leads to nosocomial infections.

Serum Progranulin As a Risk Predictor in Patients with Acute Myocardial Infarction.

BACKGROUND Although progranulin was recently proposed as an adipokine that may be involved in glucose metabolic and inflammatory diseases, the role of serum progranulin in cardiovascular disease is elusive and remains disputed. The aim of our research was to determine the concentration of serum progranulin in Chinese patients with cardiovascular disease, notably in acute myocardial infarction (AMI), and its relationship to other cardiometabolic risk factors. MATERIAL AND METHODS This prospective observational study included 342 Chinese AMI patients and 255 healthy control subjects.

Microglial activation contributes to depressive-like behavior in dopamine D3 receptor knockout mice.

We previously demonstrated that the dopamine D3 receptor (D3R) inhibitor, NGB2904, increases susceptibility to depressive-like symptoms, elevates pro-inflammatory cytokine expression, and alters brain-derived neurotrophic factor (BDNF) levels in mesolimbic dopaminergic regions, including the medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and ventral tegmental area (VTA) in mice. The mechanisms by which D3R inhibition affects neuroinflammation and onset of depression remain unclear. Here, using D3R-knockout (D3RKO) and congenic wild-type C56BL/6 (WT) mice, we demonstrated that D3RKO mice displayed depressive-like behaviors, increased tumornecrosisfactor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 levels, and altered BDNF expression in selected mesolimbic dopaminergic regions.

Methamphetamine exacerbates neuroinflammatory response to lipopolysaccharide by activating dopamine D1-like receptors.

Methamphetamine (METH) is a highly addictive and widely abused drug worldwide. Although much research is on the drug's direct effects, METH may also alter host immunity. The mechanism by which METH influences immunity remains elusive.

Dopamine Alters Lipopolysaccharide-Induced Nitric Oxide Production in Microglial Cells via Activation of D1-Like Receptors.

Dopamine (DA) is important in the maintenance of normal nervous system function. DA is the target of multiple drugs, and it induces critical alterations in immune cells. However, these impacts are controversial, and the mechanism remains unclear.

Inhibitory effects of methamphetamine on mast cell activation and cytokine/chemokine production stimulated by lipopolysaccharide in C57BL/6J mice.

Previous studies have demonstrated that methamphetamine (MA) influences host immunity; however, the effect of MA on lipopolysaccharide (LPS)-induced immune responses remains unknown. Mast cells (MCs) are considered to serve an important role in the innate and acquired immune response, but it remains unknown whether MA modulates MC activation and LPS-stimulated cytokine production. The present study aimed to investigate the effect of MA on LPS-induced MC activation and the production of MC-derived cytokines in mice.

Ago2 and Dicer1 are involved in METH-induced locomotor sensitization in mice via biogenesis of miRNA.

microRNA (miRNA) play important roles in drug addiction and act as a post-transcriptional regulator of gene expression. We previously reported extensive downregulation of miRNAs in the nucleus accumbens (NAc) of methamphetamine (METH)-sensitized mice. However, the regulatory mechanism of this METH-induced downregulation of miRNAs has yet to be elucidated.

The inhibitory effect of levo-tetrahydropalmatine on the methamphetamine-induced spatial memory impairment in mice.

Methamphetamine (METH) administration results in addiction and memory impairment. Previous studies have suggested that levo-tetrahydropalmatine (l-THP), an alkaloid purified from the Chinese herb Corydalis, attenuates the behavioral changes induced by METH. Therefore, in this study, we explored whether l-THP could also protect against the METH-induced memory impairment examined using the Morris water maze (MWM).

Methamphetamine modulates the production of interleukin-6 and tumor necrosis factor-alpha via the cAMP/PKA/CREB signaling pathway in lipopolysaccharide-activated microglia.

Methamphetamine (METH) elicits neuroinflammatory effects that may implicate its regulatory role on the microglial immune response. However, the mechanism underlying this remains unclear. In the present study, the effects of METH on lipopolysaccharide (LPS)-induced interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) productions were tested in BV-2 cells and primary microglial cells.