Projection neurons from medial entorhinal cortex to basolateral amygdala are critical for the retrieval of morphine withdrawal memory.

The medial entorhinal cortex (MEC) is crucial for contextual memory, yet its role in context-induced retrieval of morphine withdrawal memory remains unclear. This study investigated the role of the MEC and its projection neurons from MEC layer 5 to the basolateral amygdala (BLA) (MEC-BLA neurons) in context-induced retrieval of morphine withdrawal memory. Results show that context activates the MEC in morphine withdrawal mice, and the inactivation of the MEC inhibits context-induced retrieval of morphine withdrawal memory. At neural circuits, context activates MEC-BLA neurons in morphine withdrawal mice, and the inactivation of MEC-BLA neurons inhibits context-induced retrieval of morphine withdrawal memory. But MEC-BLA neurons are not activated by conditioning of context and morphine withdrawal, and the inhibition of MEC-BLA neurons do not influence the coupling of context and morphine withdrawal memory. These results suggest that MEC-BLA neurons are critical for the retrieval, but not for the formation, of morphine withdrawal memory.

Trends in breast cancer mortality attributable to metabolic risks in Chinese women from 1990 to 2019: an age-period-cohort analysis.

Objective: Metabolic risks (MRs) are the primary determinants of breast cancer (BC) mortality among women. This study aimed to examine the changing trends in BC mortality associated with MRs and explore how they related to age, time period, and birth cohorts in Chinese women aged 25 and above. Methods: Data were sourced from the Global Burden of Disease Study 2019 (GBD2019). The BC mortality trajectories and patterns attributable to MRs were assessed using Joinpoint regression. The age-period-cohort (APC) model was employed to evaluate cohort and time period effects. Results: The age-standardized mortality rate (ASMR) of BC mortality linked to MRs displayed an escalating trend from 1990 to 2019, demonstrating an average annual percentage change (AAPC) of 1.79% (95% CI: 1.69~1.87). AAPCs attributable to high fasting plasma glucose (HFPG) and high body mass index (HBMI) were 0.41% (95% CI: 0.32~0.53) and 2.75% (95% CI: 2.68~2.82), respectively. APC analysis revealed that BC mortality due to HBMI in women aged 50 and above showed a rise with age and mortality associated with HFPG consistently demonstrated a positive correlation with age. The impact of HBMI on BC mortality significantly outweighed that of HFPG. The risk of BC mortality linked to HBMI has steadily increased since 2005, while HFPG demonstrated a trend of initial increase followed by a decrease in the period effect. Regarding the cohort effect, the relative risk of mortality was greater in the birth cohort of women after the 1960s of MRs on BC mortality, whereas those born after 1980 displayed a slight decline in the relative risk (RR) associated with BC mortality due to HBMI. Conclusion: This study suggests that middle-aged and elderly women should be considered as a priority population, and control of HBMI and HFPG should be used as a primary tool to control metabolic risk factors and effectively reduce BC mortality.

Summary of the best evidence for the prevention of nasal injury in preterm infants with nasal noninvasive ventilation.

Background: Due to immaturity, the nose of preterm infants can easily be injured, by even a short application of a nasal device. However, 20% to 60% of preterm infants suffer nasal damage while using nasal continuous positive airway pressure (NCPAP) due to weak skin tissue, prolonged use of nasal device, and improper nursing practices, leading to increased risk of infection and decreased compliance and tolerance. In this study, we retrieved, obtained and integrated the related evidences of prevention of nasal injury in premature infants with nasal noninvasive ventilation to provide reference for clinical practice. Methods: We searched the relevant guidelines, expert consensus, evidence summaries and systematic reviews in the databases and guideline websites of the National Institute for Health and Care Excellence (NICE), Scottish Intercollegiate Guidelines Network (SIGN), the Agency for Health care Research and Quality (AHRQ), Guidelines International Network (GIN), the World Health Organization (WHO) guideline websites, Registered Nurses' Association of Ontario (RANO), Association of Women's Health, Obstetric and Neonatal Nurses (AWHONN), European Pressure Ulcer Advisory Panel (EPUAP), Yi Maitong, British Medical Journal best-practice, Cochrane Library, UpToDate, Embase, PubMed, China National Knowledge Infrastructure (CNKI), Wanfang. The search was limited to the time of library establishment to February 2023. Results: In total, 16 articles were included, including six guidelines, three expert consensuses, two evidence summaries and five systematic reviews. Twenty-eight pieces of evidence were summarized from six aspects: risk assessment, ventilation and connection, skin protection, skin assessment, training and support, and continuous quality improvement. Conclusions: This study summarized the best evidence for the prevention of nasal injury in premature infants through nasal noninvasive ventilation. It is suggested that nurses should consider the actual clinical situation when applying the suggestions from the evidence, formulate corresponding nursing measures, and reduce the occurrence of nasal injury in premature infants.

Different projection neurons of basolateral amygdala participate in the retrieval of morphine withdrawal memory with diverse molecular pathways.

Context-induced retrieval of drug withdrawal memory is one of the important reasons for drug relapses. Previous studies have shown that different projection neurons in different brain regions or in the same brain region such as the basolateral amygdala (BLA) participate in context-induced retrieval of drug withdrawal memory. However, whether these different projection neurons participate in the retrieval of drug withdrawal memory with same or different molecular pathways remains a topic for research. The present results showed that (1) BLA neurons projecting to the prelimbic cortex (BLA-PrL) and BLA neurons projecting to the nucleus accumbens (BLA-NAc) participated in context-induced retrieval of morphine withdrawal memory; (2) there was an increase in the expression of Arc and pERK in BLA-NAc neurons, but not in BLA-PrL neurons during context-induced retrieval of morphine withdrawal memory; (3) pERK was the upstream molecule of Arc, whereas D1 receptor was the upstream molecule of pERK in BLA-NAc neurons during context-induced retrieval of morphine withdrawal memory; (4) D1 receptors also strengthened AMPA receptors, but not NMDA receptors, -mediated glutamatergic input to BLA-NAc neurons via pERK during context-induced retrieval of morphine withdrawal memory. These results suggest that different projection neurons of the BLA participate in the retrieval of morphine withdrawal memory with diverse molecular pathways.

Relationship between gut microbiota dysbiosis and immune indicator in children with sepsis.

Sepsis is a life-threatening multiple-organ injury caused by disordered host immune response to microbial infection. However, the correlation between gut microbiota dysbiosis and immune indicators remains unexplored. To address this gap in knowledge, we carried out 16 S rDNA sequencing, analyzed clinical fecal samples from children with sepsis (n = 30) and control children (n = 25), and obtained immune indicators, including T cell subtypes (CD3+, CD3+CD4+, CD3+CD8+, and CD4/CD8), NK cells, cytokines (IL-2, IL-4, IL-6, IL-10, TNF-α and IFN-γ), and immunoglobulin indices (IgA, IgE, IgM and IgG). In addition, we analyzed the correlation between gut microbiota dysbiosis and immune indicators, and evaluated the clinical discriminatory power of discovered bacterial biomarkers. We found that children with sepsis exhibited gut bacterial dysbiosis and low alpha diversity. The Spearman's rank correlation coefficient suggested that Rhodococcus erythropolis had a significantly positive correlation with IFN-γ and CD3+ T cells. Klebsiella pneumoniae and Streptococcus mitis were significantly correlated with NK cells. Bacteroides uniformis was significantly positively correlated with IgM and erythrocyte sedimentation rate, and Eubacterium eligens was significantly positively correlated with IL-4 and CD3+CD8+ T cells. The biomarkers discovered in this study had strong discriminatory power. These changes in the gut microbiome may be closely related to immunologic dysfunction and to the development or exacerbation of sepsis. However, a large sample size is required for verification.

Leptin Promotes the Proliferation and Neuronal Differentiation of Neural Stem Cells through the Cooperative Action of MAPK/ERK1/2, JAK2/STAT3 and PI3K/AKT Signaling Pathways.

The potential of neural stem cells (NSCs) for neurological disorders the treatment has relied in large part upon identifying the NSCs fate decision. The hormone leptin has been reported to be a crucial regulator of brain development, able to influence the glial and neural development, yet, the underlying mechanism of leptin acting on NSCs' biological characteristics is still poorly understood. This study aims to investigate the role of leptin in the biological properties of NSCs. In this study, we investigate the possibility that leptin may regulate the NSCs' fate decision, which may promote the proliferation and neuronal differentiation of NSCs and thus act positively in neurological disorders. NSCs from the embryonic cerebral cortex were used in this study. We used CCK-8 assay, ki67 immunostaining, and FACS analysis to confirm that 25-100 ng/mL leptin promotes the proliferation of NSCs in a concentration-dependent pattern. This change was accompanied by the upregulation of p-AKT and p-ERK1/2, which are the classical downstream signaling pathways of leptin receptors b (LepRb). Inhibition of PI3K/AKT or MAPK/ERK signaling pathways both abolished the effect of leptin-induced proliferation. Moreover, leptin also enhanced the directed neuronal differentiation of NSCs. A blockade of the PI3K/AKT pathway reversed leptin-stimulated neurogenesis, while a blockade of JAK2/STAT3 had no effect on it. Taken together, our results support a role for leptin in regulating the fate of NSCs differentiation and promoting NSCs proliferation, which could be a promising approach for brain repair via regulating the biological characteristics of NSCs.

Burden of falls attributable to low bone mineral density among people aged 60 years and over in China from 1990 to 2019.

Objective: Falls in older people have become a major public health, economic and societal problem. Osteoporosis predisposes older adults to high risk of falls, which were the most common outcome attributable to low bone mineral density (LBMD). In this study, we analyze the long-term trends in falls burden attributable to LBMD among people aged 60 years and over from 1990 to 2019, using data from the Global Burden of Diseases, Injuries, and Risk Factors Study 2019 (GBD 2019). Methods: Data from GBD 2019 were used to assess the long-term trends in mortality and disability-adjusted life-year (DALY) rates by Joinpoint regression. The age-period-cohort (APC) model was used to evaluate the effects of age, period and cohort on mortality rate of falls attributable to LBMD. Results: The mortality and DALYs rates of falls attributable to LBMD among people aged 60 years and over increased from 1990 to 2019, with average annual percentage changes (AAPCs) of 1.74% (95% CI: -1.47 to 2.01%) and 0.99% (95% CI: 0.80-1.19%), respectively. APC analysis revealed that the mortality rate due to LBMD significantly increased among the older people over the age of 75 years. The risk of falls mortality due to LBMD during the period of 1990-2019 initially declined but later elevated. An overall increasing risk for falls death attributable to LBMD was presented across birth cohorts, but in cohorts born after 1930, the upward trend has slowed down. The overall net drift per year attributable to LBMD was above 0. The corresponding results showed that the negative impact of period and cohort effects among males was more pronounced than those among females. Conclusions: Falls attributable to LBMD remain an ongoing health burden in the older people in China, and the mortality has been on the rise from 1990 to 2019, especially among the older people aged 80+ years group. The prevention and treatment of LBMD should be emphasized, especially among males and oldest-old people. Furthermore, there is an urgent need to strengthen the implementation of system-wide, integrated and effective public health policies and other health interventions in China.

Nucleus accumbens circuit disinhibits lateral hypothalamus glutamatergic neurons contributing to morphine withdrawal memory in male mice.

The lateral hypothalamus (LH) is physiologically critical in brain functions. The LH also plays an important role in drug addiction. However, neural circuits underlying LH involvement of drug addiction remain obscure. In the present study,our results showed that in male mice, during context-induced expression of morphine withdrawal memory, LH glutamatergic neurons played an important role; dopamine D1 receptor-expressing medium spiny neurons (D1-MSNs) projecting from the core of nucleus accumbens (NAcC) to the LH were an important upstream circuit to activate LH glutamatergic neurons; D1-MSNs projecting from the NAcC to the LH activated LH glutamatergic neurons through inhibiting LH local gamma-aminobutyric acid (GABA) neurons. These results suggest that disinhibited LH glutamatergic neurons by neural circuits from the NAcC importantly contribute to context-induced the expression of morphine withdrawal memory.

Identification of a 17ß-estradiol-degrading Microbacterium hominis SJTG1 with high adaptability and characterization of the genes for estrogen degradation.

Environmental estrogen contamination poses severe threat to wildlife and human. Biodegradation is an efficient strategy to remove the wide-spread natural estrogen, while strains suitable for hostile environments and fit for practical application are rare. In this work, Microbacterium hominis SJTG1 was isolated and identified with high degrading efficiency for 17ß-estradiol (E2) and great environment fitness. It could degrade nearly 100% of 10 mg/L E2 in minimal medium in 6 days, and remove 93% of 1 mg/L E2 and 74% of 10 mg/L E2 in the simulated E2-polluted solid soil in 10 days. It maintained stable E2-degrading efficiency in various harsh conditions like non-neutral pH, high salinity, stress of heavy metals and surfactants. Genome mining and comparative genome analysis revealed that there are multiple genes potentially associated with steroid degradation in strain SJTG1. One 3ß/17ß-hydroxysteroid dehydrogenase HSD-G129 induced by E2 catalyzed the 3ß/17ß-dehydrogenation of E2 and other steroids efficiently. The transcription of hsd-G129 gene was negatively regulated by the adjacent LysR-type transcriptional regulator LysR-G128, through specific binding to the conserved site. E2 can release this binding and initiate the degradation process. This work provides an efficient and adaptive E2-degrading strain and promotes the biodegrading mechanism study and actual remediation application.

Two kinds of transcription factors mediate chronic morphine-induced decrease in miR-105 in medial prefrontal cortex of rats.

Chronic morphine administration alters gene expression in different brain regions, an effect which may contribute to plastic changes associated with addictive behavior. This change in gene expression is most possibly mediated by addictive drug-induced epigenetic remodeling of gene expression programs. Our previous studies showed that chronic morphine-induced decrease of miR-105 in the medial prefrontal cortex (mPFC) contributed to context-induced retrieval of morphine withdrawal memory. However, how chronic morphine treatment decreases miR-105 in the mPFC still remains unknown. The present study shows that chronic morphine induces addiction-related change in miR-105 in the mPFC via two kinds of transcription factors: the first transcription factor is CREB activated by mu receptors-ERK-p90RSK signaling pathway and the second transcription factor is glucocorticoid receptor (GR), which as a negative transcription factor, mediates chronic morphine-induced decrease in miR-105 in the mPFC of rats.

Mycoplasma gallisepticum induced exosomal gga-miR-193a to disturb cell proliferation, apoptosis, and cytokine production by targeting the KRAS/ERK signaling pathway.

Mycoplasma gallisepticum (MG) is the main pathogen of chronic respiratory disease (CRD), an infectious disease in chickens with high morbidity. Exosomal miRNAs are emerging as important regulators in host immune response to microbial invasion. Previously, we found that gga-miR-193a was significantly up-regulated in exosomes from MG-infected primary chicken type II pneumocytes (CP-IIs). Therefore, the purpose of this study was to investigate the role of exosomal gga-miR-193a in MG infection. Exosomes were isolated and identified via ultracentrifugation, transmission electron microscopy, and nanoparticle-tracking analysis. Real-time quantitative PCR and Western blot were used to detect the gene expression. Enzyme-linked immunosorbent assay was used to examine the levels of the inflammatory cytokines. CCK-8 and flow cytometry assays were applied to analyze the cell functions. The results showed that MG infection induced high expression of gga-miR-193a in exosomes from CP-IIs. Moreover, exosomes secreted by MG-infected CP-IIs could selectively transport gga-miR-193a into DF-1 cells. Exosomal gga-miR-193a internalized by DF-1 cells inhibited cell proliferation, promoted apoptosis, and increased interleukin-1ß and tumor necrosis factor-α secretions by targeting the RAS/ERK signaling pathway. These results suggest that MG induced the secretion of gga-miR-193a by exosomes to damage the life activities of normal cells, which partially interpreted the mechanism of MG establishing systemic chronic infection in the body.

Frailty and long-term survival of patients with colorectal cancer: a meta-analysis.

BACKGROUND: Frailty has been related with the risk of postoperative complication in patients with colorectal cancer (CRC). However, the association between frailty and long-term survival in patients with CRC has not been comprehensively evaluated. We performed a meta-analysis to systematically evaluate the relationship between frailty and long-term survival of these patients. METHODS: Relevant cohort studies with follow-up duration ≥ 1 year were identified from Medline, Embase, and Web of Science. A random-effect model after incorporation of the between-study heterogeneity was selected to pool the results. RESULTS: Ten cohort studies with 35,546 patients were included, and 4100 (11.5%) of them had frailty. Pooled results showed that patients with frailty had worse overall survival compared to those without frailty at baseline (relative risk [RR]: 2.21, 95% confidence interval [CI] 1.43-3.41, P < 0.001; I2 = 92%). Results were consistent for studies adjusting age (RR: 2.20, P < 0.001) or including older cancer patients only (RR: 2.28, P = 0.002). Subgroup analyses showed that difference in study design, follow-up duration, or study quality scores may not significantly affect the findings (P for subgroup analyses all > 0.05). Further meta-analyses with two datasets showed that frailty was also associated with worse cancer-specific survival (RR: 4.60, 95% CI 2.75-7.67, P < 0.001; I2 = 38%) and recurrence-free survival (RR: 1.72, 95% CI 1.30-2.28, P < 0.001; I2 = 0%). CONCLUSIONS: Frailty at admission is associated with worse survival of patients with colorectal cancer.

Characterization of the Tellurite-Resistance Properties and Identification of the Core Function Genes for Tellurite Resistance in Pseudomonas citronellolis SJTE-3.

Tellurite is highly toxic to bacteria and commonly used in the clinical screening for pathogens; it is speculated that there is a potential relationship between tellurite resistance and bacterial pathogenicity. Until now, the core function genes of tellurite resistance and their characteristics are still obscure. Pseudomonas citronellolis SJTE-3 was found able to resist high concentrations of tellurite (250 µg/mL) and formed vacuole-like tellurium nanostructures. The terZABCDE gene cluster located in the large plasmid pRBL16 endowed strain SJTE-3 with the tellurite resistance of high levels. Although the terC and terD genes were identified as the core function genes for tellurite reduction and resistance, the inhibition of cell growth was observed when they were used solely. Interestingly, co-expression of the terA gene or terZ gene could relieve the burden caused by the expression of the terCD genes and recover normal cell growth. TerC and TerD proteins commonly shared the conserved sequences and are widely distributed in many pathogenic bacteria, highly associated with the pathogenicity factors.

The 3-Oxoacyl-(Acyl-Carrier-Protein) Reductase HSD-X1 of Pseudomonas Citronellolis SJTE-3 Catalyzes the Conversion of 17ß-estradiol to Estrone.

BACKGROUND: Pseudomonas citronellolis SJTE-3 can efficiently degrade 17ß-estradiol (E2) and other estrogenic chemicals. However, the enzyme responsible for E2 metabolism within strain SJTE-3 has remained unidentified. OBJECTIVE: Here, a novel 3-oxoacyl-(acyl-carrier protein) (ACP) reductase, HSD-X1 (WP_ 009617962.1), was identified in SJTE-3 and its enzymatic characteristics for the transformation of E2 were investigated. METHODS: Multiple sequence alignment and homology modelling were used to predict the protein structure of HSD-X1. The concentrations of different steroids in the culture of recombinant strains expressing HSD-X1 were determined by high performance liquid chromatography. Additionally, the transcription of hsd-x1 gene was investigated using reverse transcription and quantitative PCR analysis. Heterologous expression and affinity purification were used to obtain recombinant HSD- X1. RESULTS: The transcription of hsd-x1 gene in P. citronellolis SJTE-3 was induced by E2. Multiple sequence alignment (MSA) indicated that HSD-X1 contained the two consensus regions and conserved residues of short-chain dehydrogenase/reductases (SDRs) and 17ß-hydroxysteroid dehydrogenases (17ß-HSDs). Over-expression of hsd-x1 gene allowed the recombinant strain to degrade E2. Recombinant HSD-X1 was purified with a yield of 22.15 mg/L and used NAD+ as its cofactor to catalyze the oxidization of E2 into estrone (E1) while exhibiting a Km value of 0.025 ± 0.044 mM and a Vmax value of 4.92 ± 0.31 mM/min/mg. HSD-X1 could tolerate a wide range of temperature and pH, while the presence of divalent ions exerted little influence on its activity. Further, the transformation efficiency of E2 into E1 was over 98.03% across 15 min. CONCLUSION: Protein HSD-X1 efficiently catalyzed the oxidization of E2 and participated in estrogen degradation by P. citronellolis SJTE-3.

Metabolism analysis of 17α-ethynylestradiol by Pseudomonas citronellolis SJTE-3 and identification of the functional genes.

Synthetic estrogens are the most hazardous and persistent environmental estrogenic contaminants, with few reports on their biodegradation. Pseudomonas citronellolis SJTE-3 degraded natural steroids efficiently and metabolized 17α-ethynylestradiol (EE2) with the addition of different easily used energy sources (glucose, peptone, ethanol, yeast extract, fulvic acid and ammonia). Over 92% of EE2 (1 mg/L) and 55% of EE2 (10 mg/L) in culture were removed in seven days with the addition of 0.1% ethanol, and the EE2-biotransforming efficiency increased with the increasing ethanol concentrations. Two novel intermediate metabolites of EE2 (C22H22O and C18H34O2) were identified with high-performance liquid chromatography (HPLC) and GC-Orbitrap/MS. Comparative analysis and genome mining revealed strain SJTE-3 contained a unique genetic basis for EE2 metabolism, and the putative EE2-degrading genes exhibited dispersed distribution. The EE2 metabolism of strain SJTE-3 was inducible and the transcription of eight genes were significantly induced by EE2. Three genes (sdr3, yjcH and cyp2) encoding a short-chain dehydrogenase, a membrane transporter and a cytochrome P450 hydroxylase, respectively, were vital for EE2 metabolism in strain SJTE-3; their over-expression accelerated EE2 metabolic processes and advanced the generation of intermediate metabolites. This work could promote the study of bacterial EE2 metabolism mechanisms and facilitate efficient bioremediation for EE2 pollution.

The National Cancer Institute and Cannabis and Cannabinoids Research.

The landscape of both recreational and medicinal cannabis use has changed dramatically over the past decade; however, research examining the risks and benefits of cannabis and cannabinoid use has lagged significantly behind the increased media promotion and their use by the general public and cancer patients. The National Cancer Institute (NCI) has supported cannabis-related research projects and funding opportunity announcements. In addition, NCI organized a virtual symposium on December 15-18, 2020, to discuss recent research findings on the use of cannabis and cannabinoids in relationship to cancer risk, prevention, and care. Specifically, the symposium sought to highlight the state of the science regarding cannabis, including the chemical constituents of cannabis (eg, cannabinoids), and cancer research involving cannabis, including cancer epidemiology, use in cancer patients, cancer biology and prevention, and preclinical and clinical cancer symptom and treatment side effect management with cannabis and cannabinoids as therapeutics. The symposium identified promising areas of future study, current barriers to conducting the research, and strategies to overcome those barriers. The series of papers in this special edition provide a summary of the symposium sessions as well as a synopsis of opportunities and challenges related to conducting research in this area.

'Trend in premature mortality from four major NCDs in Nanjing, China, 2007-2018'.

BACKGROUND: This study aims to analyze the trends of premature mortality caused from four major non-communicable diseases (NCDs), namely cardiovascular disease (CVD), cancer, chronic respiratory diseases, and diabetes in Nanjing between 2007 and 2018 and project the ability to achieve the "Healthy China 2030" reduction target. METHODS: Mortality data of four major NCDs for the period 2007-2018 were extracted from the Death Information Registration and Management System of Chinese Center for Disease Control and Prevention. Population data for Nanjing were provided by the Nanjing Bureau of Public Security. The premature mortality was calculated using the life table method. Joinpoint regression model was used to estimate the average annual percent changes (AAPC) in mortality trends. RESULTS: From 2007 to 2018, the premature mortality from four major NCDs combined in Nanjing decreased from 15.5 to 9.5%, with the AAPC value at - 4.3% (95% CI [- 5.2% to - 3.4%]). Overall, it can potentially achieve the target, with a relative reduction 28.6%. The premature mortality from cancer, CVD, chronic respiratory diseases and diabetes all decreased, with AAPC values at - 4.2, - 5.0%, - 5.9% and - 1.6% respectively. A relative reduction of 40.6 and 41.2% in females and in rural areas, but only 21.0 and 12.8% in males and in urban areas were projected. CONCLUSION: An integrated approach should be taken focusing on the modifiable risk factors across different sectors and disciplines in Nanjing. The prevention and treatment of cancers, diabetes, male and rural areas NCDs should be enhanced.

[Advances in the bioaugmentation-assisted remediation of petroleum contaminated soil].

Bioremediation is considered as a cost-effective, efficient and free-of-secondary-pollution technology for petroleum pollution remediation. Due to the limitation of soil environmental conditions and the nature of petroleum pollutants, the insufficient number and the low growth rate of indigenous petroleum-degrading microorganisms in soil lead to long remediation cycle and poor remediation efficiency. Bioaugmentation can effectively improve the biodegradation efficiency. By supplying functional microbes or microbial consortia, immobilized microbes, surfactants and growth substrates, the remediation effect of indigenous microorganisms on petroleum pollutants in soil can be boosted. This article summarizes the reported petroleum-degrading microbes and the main factors influencing microbial remediation of petroleum contaminated soil. Moreover, this article discusses a variety of effective strategies to enhance the bioremediation efficiency, as well as future directions of bioaugmentation strategies.

Projection from the basolateral amygdala to the anterior cingulate cortex facilitates the consolidation of long-term withdrawal memory.

The process through which early memories are transferred to the cerebral cortex to form long-term memories is referred to as memory consolidation, and the basolateral amygdala (BLA) is an important brain region involved in this process. Although functional connections between the BLA and multiple brain regions are critical for the consolidation of withdrawal memory, whether the projection from the BLA to the anterior cingulate cortex (ACC) is involved in the formation or consolidation of withdrawal memory remains unclear. In this paper, we used a chemical genetic method to specifically label the BLA-ACC projection in a combined morphine withdrawal and conditioned place aversion (CPA) animal model. We found that (1) the inhibition of the BLA-ACC projection during conditioning had no effects on the formation of early withdrawal memory; (2) the inhibition of the BLA-ACC projection had no effects on the retrieval of either early or long-term withdrawal memory; and (3) the persistent inhibition of the BLA-ACC projection after early withdrawal memory formation could inhibit the formation of long-term withdrawal memory and decrease Arc protein expression in the ACC. These results suggested that the persistent activation of the BLA-ACC projection after the formation of early withdrawal memory facilitates the formation of long-term withdrawal memory by increasing the plasticity of ACC neurons.

Puerarin inhibits Mycoplasma gallisepticum (MG-HS)-induced inflammation and apoptosis via suppressing the TLR6/MyD88/NF-κB signal pathway in chicken.

Mycoplasma gallisepticum (MG) is the primary etiological agent of chicken chronic respiratory disease (CRD), which mainly causes inflammatory damage of the host respiratory system. Previous studies suggest that puerarin (PUE) plays a pivotal regulatory role in inflammatory diseases, whereas the impacts of PUE on MG-induced inflammation remain unclear. This study investigated the effects of PUE on MG-HS infection in vitro and in vivo and indicated its potential therapeutic and preventive value. Experimental results showed that PUE significantly suppressed pMGA1.2 expression, promoted MG-infected cell proliferation and cell cycle process by reducing apoptosis. Histopathological examination of lung tissue showed severe histopathological lesions including thickened alveolar walls, narrowed alveolar cavity, and inflammatory cell infiltration in the MG-infected chicken group. However, PUE treatment significantly ameliorated MG-induced pathological damage in lung. Compared to the MG-infected group, PUE effectively inhibited the expression of MG-induced inflammatory genes, including tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), cytokines interleukin-6 (IL-6), toll-like receptor 6 (TLR6), myeloid differentiation primary response gene 88 (MyD88) and nuclear factor κB (NF-κB). Moreover, PUE dose-dependently inhibited MG-induced NF-κB p65 to enter the cell nucleus. In conclusion, our findings indicate that PUE treatment can efficiently inhibit MG-induced inflammatory response and apoptosis, and protect the lung from MG infection-induced damage by inhibiting the TLR6/MyD88/NF-κB signaling pathway activation. The study suggests that PUE may be a potential anti-inflammatory agent defense againstMGinfection in chicken.