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Several studies have demonstrated great potential implications for the gut–lung axis in lung disease etiology and treatment. The gut environment can be influenced by diet, metabolites, microbiotal composition, primary diseases, and medical interventions. These changes modulate the functions of alveolar macrophages (AMs) to shape the pulmonary immune response, which greatly impacts lung health. The immune modulation of AMs is implicated in the pathogenesis of various lung diseases. However, the mechanism of the gut–lung axis in lung diseases has not yet been determined. This mini-review aimed to shed light on the critical nature of communication between the gut and AMs during the development of pulmonary infection, injury, allergy, and malignancy. A better understanding of their crosstalk may provide new insights into future therapeutic strategies targeting the gut–AM interaction.

Transplantation is an important life-saving therapeutic choice for patients with organ or tissue failure once all other treatment options are exhausted. However, most allografts become damaged over an extended period, and post-transplantation survival is limited. Ischemia reperfusion injury (IRI) tends to be associated with a poor prognosis; resultant severe primary graft dysfunction is the main cause of transplant failure. Targeting the cGAS–STING pathway has recently been shown to be an effective approach for improving transplantation outcomes, when activated or inhibited cGAS–STING pathway, IRI can be alleviated by regulating inflammatory response and programmed cell death. Thus, continuing efforts to develop selective agonists and antagonists may bring great hopes to post-transplant patient. In this mini-review, we reviewed the role of the cGAS–STING pathway in transplantation, and summarized the crosstalk between this pathway and inflammatory response and programmed cell death during IRI, aiming to provide novel insights into the development of therapies to improve patient outcome after transplantation.

Several studies have demonstrated that the pulmonary immune response is primarily facilitated by antigen-presenting cells (APCs), and that both professional and non-professional APCs contribute to overall pulmonary immunity. APCs play unique roles and mechanisms in pathogen elimination and immunomodulation. Mucosal immunity exhibits potential advantages over traditional parenteral immunity in that it stimulates immune defenses in mucosal and systemic tissues, which is important for reducing the burden of lung disease. However, obtaining a comprehensive understanding of the crosstalk between mucosal immunity and APC in the context of various lung diseases remains challenging. This mini-review aimed to elucidate the mechanisms of novel mucosal immunity, targeting APC action during lung infections, allergies, and malignant tumorigenesis. This minreview provides important insights into more effective therapeutic approaches for various lung diseases.

Background Nucleotide-binding and leucine-rich repeat (NLR) genes have attracted wide attention due to their crucial role in protecting plants from pathogens. SMRT-RenSeq, combining PacBio sequencing after resistance gene enrichment sequencing (RenSeq), is a powerful method for selectively capturing and sequencing full-length NLRs. Haynaldia villosa , a wild grass species with a proven potential for wheat improvement, confers resistance to multiple diseases. So, genome-wide identification of the NLR gene family in Haynaldia villosa by SMRT-RenSeq can facilitate disease resistance genes exploration. Results In this study, SMRT-RenSeq was performed to identify the genome-wide NLR complement of H. villosa . In total, 1320 NLRs were annotated in 1169 contigs, including 772 complete NLRs . All the complete NLRs were phylogenetically analyzed and 11 main clades with special characteristics were derived. NLRs could be captured with high efficiency when aligned with cloned R genes, and cluster expansion in some specific gene loci was observed. The physical location of NLRs to individual chromosomes in H. villosa showed a perfect homoeologous relationship with group 1, 2, 3, 5 and 6 of other Triticeae species, however, NLRs physically located on 4VL were largely in silico predicted to be located on the homoeologous group 7. Fifteen types of integrated domains (IDs) were integrated in 52 NLRs, and Kelch and B3 NLR-IDs were found to have expanded in H. villosa , while DUF948, NAM-associated and PRT_C were detected as unique integrated domains implying the new emergence of NLR-IDs after H. villosa diverged from other species. Conclusion SMRT-RenSeq is a powerful tool to identify NLR genes from wild species using the baits of the evolutionary related species with reference sequences. The availability of the NLRs from H. villosa provide a valuable library for R gene mining and transfer of disease resistance into wheat.

Advances in lung cancer research applying machine learning (ML) technology have generated many relevant literature. However, there is absence of bibliometric analysis review that aids a comprehensive understanding of this field and its progress. Present article for the first time performed a bibliometric analysis to clarify research status and focus from 2010 to 2021. In the analysis, a total of 2,312 relevant literature were searched and retrieved from the Web of Science Core Collection database. We conducted a bibliometric analysis and further visualization. During that time, exponentially growing annual publication and our model have shown a flourishing research prospect. Annual citation reached the peak in 2017. Researchers from United States and China have produced most of the relevant literature and strongest partnership between them. and appeared to bring more attention to the public. The computer-aided diagnosis, precision medicine, and survival prediction were the focus of research, reflecting the development trend at that period. ML did make a big difference in lung cancer research in the past decade.

Studies have reported an increased risk of adverse pregnancy outcome associated with pre-pregnancy body mass index (BMI). However, the data on such associations in urban areas of southern Chinese women is limited, which drive us to clarify the associations of pre-pregnancy BMI and the risks of adverse pregnancy outcomes (preterm birth (PTB) and low birth weight (LBW)) and maternal health outcomes (gestational hypertension and cesarean delivery). We performed a hospital-based case-control study including 3,864 Southern Chinese women who gave first birth to a live singleton infant from January 2015 to December 2015. PTB was stratified into three subgroups according to gestational age (extremely PTB, very PTB and moderate PTB). Besides, we combined birth weight and gestational age to dichotomise as being small for gestational age (SGA, less than the tenth percentile of weight for gestation) and non-small for gestational age (NSGA, large than the tenth percentile of weight for gestation), gestational week was also classified into categories of term, 34-36 week and below 34 week.. We then divided newborns into six groups: (1) term and NSGA; (2) 34-36 week gestation and NSGA; (3) below 34 week gestation and NSGA; (4) term and SAG; (5) 34-36 week gestation and SAG; (6) below 34 week gestation and SAG. Adjusted logistic regression models was used to estimate the odds ratios of adverse outcomes. Underweight women were more likely to give LBW (AOR = 1.44, 95% CI [1.11-1.89]), the similar result was seen in term and SAG as compared with term and NSAG (AOR = 1.78, 95% CI [1.45-2.17]), whereas underweight was significantly associated with a lower risk of gestational hypertension (AOR = 0.45, 95% CI [0.25-0.82) and caesarean delivery (AOR = 0.74, 95% CI [0.62-0.90]). The risk of extremely PTB is relatively higher among overweight and obese mothers in a subgroup analysis of PTB (AOR = 8.12, 95% CI [1.11-59.44]; AOR = 15.06, 95% CI [1.32-172.13], respectively). Both maternal overweight and obesity were associated with a greater risk of gestational hypertension (AOR = 1.71, 95% CI [1.06-2.77]; AOR = 5.54, 95% CI [3.02-10.17], respectively) and caesarean delivery (AOR = 1.91, 95% CI [1.53-2.38]; AOR = 1.85, 95% CI [1.21-2.82], respectively). Our study suggested that maternal overweight and obesity were associated with a significantly higher risk of gestational hypertension, caesarean delivery and extremely PTB. Underweight was correlated with an increased risk of LBW and conferred a protective effect regarding the risk for gestational hypertension and caesarean delivery for the first-time mothers among Southern Chinese.

Key message Phenotypical, physiological and genetic characterization was carried out on the hybrid necrosis gene from Haynaldia villosa , and the related gene Ne-V was mapped to chromosome arm 2VL. Introducing genetic variation from wild relatives into common wheat through wide crosses is a vital strategy for enriching genetic diversity and promoting wheat breeding. However, hybrid necrosis, a genetic autoimmunity syndrome, often occurs in the offspring of interspecific or intraspecific crosses, restricting both the selection of hybrid parents and the pyramiding of beneficial genes. To utilize the germplasms of Haynaldia villosa (2 n  = 2 x  = 14, VV), we conducted wide hybridization between durum wheat (2 n  = 4 x  = 28, AABB) and multiple H. villosa accessions to synthesize the amphiploids (2 n  = 6 x  = 42, AABBVV). This study revealed that 61.5% of amphiploids derived from the above crosses exhibited hybrid necrosis, with some amphiploids even dying before reaching maturity. However, the initiation time and severity of necrosis varied dramatically among the progenies, suggesting that there were multiple genetic loci or multiple alleles in the same genetic locus conferring to hybrid necrosis in H. villosa accessions. Genetic analysis was performed on the F 2 and derived F 2:3 populations, which were constructed between amphiploid STH59-1 with normal leaves and amphiploid STH59-2 with necrotic leaves. A semidominant hybrid necrosis-related gene, Ne-V, was mapped to an 11.8-cM genetic interval on the long arm of chromosome 2V, representing a novel genetic locus identified in Triticum- related species. In addition, the hybrid necrosis was correlated with enhanced H 2 O 2 accumulation and cell death, and it was influenced by the temperature and light. Our findings provide a foundation for cloning the Ne-V gene and exploring its molecular mechanism.

Park green spaces (PGSs) are an important component of urban natural carbon sinks, while their spatial morphological patterns can affect the carbon sequestration capacity themselves. This study selected six typical urban parks in the central district of Shanghai and analyzed the correlation between spatial morphological indices and CO2 concentration distribution of the PGSs based on ENVI-met and BRT models. It further explored the interaction mechanisms in the carbon cycling process of urban PGSs under the influence of different spatial morphology. The results shows that urban PGSs play the role of carbon sink in diurnal period, and the difference of CO2 concentration distribution in green space is the largest at 11 a.m. The green biomass (Gb) and arboreal area ratio (Ar) are the most important indices affecting the distribution of carbon concentration. The two indices describing spatial patterns, namely, Cohesion (Co) and canopy density (CanopyD) also significantly impact CO2 concentration. These indices have a positive impact on carbon sinks. The parkway area ratio (Pr) is a disturbing index that also has an obvious negative impact on the distribution of CO2 concentration. The moderate herbs area ratio (Hr) and open land area ratio (Or) are conducive to regulating the microclimate environment and enhancing carbon sink capacity. There is an interactive relationship between spatial indices and microclimate environment indices, as well as physical and physiological indices in the carbon sink process of green areas. The study suggested that in green space management aiming at carbon reduction, combined with the influence threshold of Gb on carbon reduction and paying attention to the importance of green amount on carbon sequestration, the vegetation density and allocation ratio should be rationally distributed to form a park green space landscape with efficient carbon fixation.

Key messageA new functional Pm21 haplotype, Pm21(8#), was cloned from the new wheat-H. villosa translocation line T6VS(8#)·6DL, which confers the same strong resistance to powdery mildew through a different resistance mechanism.Broad-spectrum disease resistance genes are desirable in crop breeding for conferring stable, durable resistance in field production. Pm21(4#) is a gene introduced from wild Haynaldia villosa into wheat that confers broad-spectrum resistance to wheat powdery mildew and has been widely used in wheat production for approximately 30 years. The discovery and transfer of new functional haplotypes of Pm21 into wheat will expand its genetic diversity in production and avoid the breakdown of resistance conferred by a single gene on a large scale. Pm21(4#) previously found from T6VS(4#)·6AL has been cloned. In this study, a new wheat-H. villosa translocation, T6VS(8#)·6DL, was identified. A new functional Pm21 haplotype, designated Pm21(8#), was cloned and characterized. The genomic structures and the splicing patterns of Pm21(4#) and Pm21(8#) were different, and widespread sequence diversity was observed in the gene coding region and the promoter region. In the field, Pm21(8#) conferred resistance to Blumeria graminis f. sp. tritici (Bgt), similar to Pm21(4#), indicating that Pm21(8#) was also a resistance gene. However, Bgt development during the infection stage was obviously different between Pm21(4#)- and Pm21(8#)-containing materials under the microscopic observation. Pm21(4#) inhibited the formation of haustoria and the development of hyphae in the initial infection stage, while Pm21(8#) limited the growth of hyphae and inhibited the formation of conidiophores in the late infection stage. Therefore, Pm21(8#) is a new functional Pm21 haplotype that provides a new gene resource for wheat breeding.

PurposeColorectal cancer (CRC) is a severe health condition characterized by high mortalities. NudC domain containing 1 (NUDCD1) is abnormally upregulated in multiple tumors and is recognized as a cancer antigen. In CRC, NUDCD1 upregulation accelerates tumor progression by activating the IGF1R-ERK1/2 signaling pathway. Its specific regulatory mechanisms, however, remain unclear.MethodsIn the present study, we predicted the regulators of NUDCD1 and analyzed the expression profile of NUDCD1 in CRC tissues using the gene chip dataset. We also determined the regulation between miR-144, NUDCD1 and IGF1R-ERK1/2 signaling in vitro and in vivo. Then, the expression of miR-144 in CRC tissues was detected and its cell functions were verified in vitro.ResultsAs predicted by bioinformatics, we found that NUDCD1 is a predicted target of miR-144 and confirmed that miR-144 directly binds to NUDCD1. In vitro and in vivo, miR-144 was determined to specifically regulate NUDCD1 expression and as such, can reduce the activity of the IGF1R-ERK1/2 signaling pathway. Moreover, miR-144 was significantly downregulated in CRC tissues; its levels were significantly negatively correlated with CRC primary range and lymph node metastasis. Cell function studies verified that miR-144 acts as a tumor suppressor, because it significantly inhibits the proliferation, metastasis, and invasion of CRC cells as well as inducing cell cycle arrest and apoptosis.ConclusionsOur study demonstrates that miR-144 regulates IGF1R-ERK1/2 signaling via NUDCD1 to inhibit CRC cell proliferation and metastasis. The miR-144/NUDCD1/IGF1R-ERK1/2 signaling axis may be crucial in the progression of CRC.