Phylogenetic placement and comparative analysis of the mitochondrial genomes of Idiostoloidea (Hemiptera: Heteroptera).

The classification system and the higher level phylogenetic relationships of Pentatomomorpha, the second largest infraorder of Heteroptera (Insecta: Hemiptera), have been debated and remain controversial over decades. In particular, the placement and phylogenetic relationship of Idiostoloidea are not well resolved, which hampers a better understanding of the evolutionary history of Pentatomomorpha. In this study, for the first time, we reported the complete mitochondrial genome for two narrowly distributed families of Idiostoloidea (including Idiostolidae and Henicocoridae), respectively. The length of the mitochondrial genome of Monteithocoris hirsutus and Henicocoris sp. is 16,632 and 16,013 bp, respectively. The content of AT is ranging from 75.15% to 80.48%. The mitogenomic structure of Idiostoloidea is highly conservative and there are no gene arrangements. By using the Bayesian inference, maximum likelihood, and Bayesian site-heterogeneous mixture model, we inferred the phylogenetic relationships within Pentatomomorpha and estimated their divergence times based on concatenated mitogenomes and nuclear ribosomal genes. Our results support the classification system of six superfamilies within Pentatomomorpha and confirm the monophyletic groups of each superfamily, with the following phylogenetic relationships: (Aradoidea + (Pentatomoidea + (Idiostoloidea + (Coreoidea + (Pyrrhocoroidea + Lygaeoidea))))). Furthermore, estimated divergence times revealed that most pentatomomorphan superfamilies and families diverged during the Late Jurassic to Early Cretaceous, which coincides with the explosive radiation of angiosperms.

Wogonin alleviates sepsis-induced acute lung injury by modulating macrophage polarization through the SIRT1-FOXO1 pathways.

Sepsis-induced acute lung injury is a common and severe complication of sepsis, for which effective treatments are currently lacking. Previous studies have demonstrated the influence of wogonin in treating acute lung injury (ALI). However, its precise mechanism of action remains unclear. To delve deeper into the mechanisms underlying wogonin's impacts in sepsis-induced acute lung injury, we established a mouse sepsis model through cecal ligation and puncture and conducted further cell experiments using lipopolysaccharide-treated MH-S and MLE-12 cells to explore wogonin's potential mechanisms of action in treating ALI. Our results revealed that wogonin significantly increased the survival rate of mice, alleviated pulmonary pathological damage and inflammatory cell infiltration, and activated the SIRT1-FOXO1 pathway. Additionally, wogonin suppressed the release of pro-inflammatory factors by M1 macrophages and induced the activation of M2 anti-inflammatory factors. Further in vitro studies confirmed that wogonin effectively inhibited M1 macrophage polarization through the activation of the SIRT1-FOXO1 pathway, thereby mitigating lung pathological changes caused by ALI. In summary, our study demonstrated that wogonin regulated macrophage M1/M2 polarization through the activation of the SIRT1-FOXO1 pathway, thereby attenuating the inflammatory response and improving pulmonary pathological changes induced by sepsis-induced ALI. This discovery provided a solid mechanistic foundation for the therapeutic use of wogonin in sepsis-induced ALI, shedding new light on potential strategies for the treatment of sepsis-induced ALI.

Mechanism of flavonols on detoxification, migration and transformation of indium in rhizosphere system.

Soil contamination by toxic heavy metal induces serious environmental hazards. In recent years, the use of indium (In) in semiconductor products has increased considerably and the release of In is inevitable, which will pose great risk to the ecosystem. The interaction between metal and plants which are the fundamental components of all ecosystems are an indispensable aspect of indium assessment and remediation. The role of flavonols, which is essential to plant resistance to In stress, remains largely unknown. FLS1 related lines of A. thaliana (Col, fls1-3 and OE) were exposed to In stress in soil and flavonols as root exudates were analyzed in exogenous application test. The accumulation and release of flavonols could be induced by In stress. However, flavonols exhibited different function in vivo and in vitro of plant. The basic function of flavonols was to affect root morphology via regulating auxin, but being intervened by In stress. The synthesis and accumulation of flavonols in vivo could activate the antioxidant system and the metal detoxification system to alleviate the toxic effects of In on plant. In addition, plants could make phone calls to rhizosphere microbes for help when exposed to In. Flavonols in vitro might act as the information transmission. Combination of endogenous and exogenous flavonols could affect the migration and transformation of In in soil-plant system via metal complexation and transportation pathway.

Localization of G1A1a Allergenic Domain Destroyed by Thermal Processing.

Glycinin is an important allergenic protein. A1a is the acidic chain of the G1 subunit in glycinin (G1A1a), and it has strong allergenicity. In this study, we used phage display technology to express the protein of G1A1a and its overlapping fragments and an indirect enzyme-linked immunosorbent assay (iELISA) to determine the antigenicity and allergenicity of the expressed protein. After three rounds of screening, it was determined that fragment A1a-2-B-I (151SLENQLDQMPRRFYLAGNQEQEFLKYQQEQG181) is the allergenic domain of G1A1a destroyed by thermal processing. In addition, three overlapping peptides were synthesized from fragments A1a-2-B-I, and a linear epitope was found in this domain through methods including dot blot and iELISA. Peptide 2 (157DQMPRRFYLANGNQE170) showed allergenicity, and after replacing it with alanine, it was found that amino acids D157, Q158, M159, and Y164 were the key amino acids that affected its antigenicity, while Q158, M159, R162, and N168 affected allergenicity.

Microvascular burden and long-term risk of stroke and dementia in type 2 diabetes mellitus.

OBJECTIVE: To examine the associations between microvascular disease (MVD) and risk of stroke, dementia, and their major subtypes among individuals with type 2 diabetes mellitus (T2DM). METHODS: We included 26,173 participants with T2DM from the UK Biobank who had no known stroke or dementia at baseline. MVD burden was reflected by the presence of retinopathy, peripheral neuropathy, and chronic kidney disease. Cox regression models were used to estimate hazard ratios (HRs) and 95 % confidential intervals (CIs) of stroke and dementia associated with overall MVD burden and individual MVD. RESULTS: During a median follow-up of 11.5 years, 1103 incident stroke (964 ischemic and 269 hemorrhagic stroke) and 813 incident dementia (312 Alzheimer's disease and 304 vascular dementia) cases were identified. The risk of stroke, dementia, and their major subtypes all increased with an increasing number of MVD (all P-trend <0.001). The adjusted HRs (95 % CIs) comparing three with no MVD were 5.03 (3.16, 8.02) for all stroke, 4.57 (2.75, 7.59) for ischemic stroke, and 6.60 (2.65, 16.43) for hemorrhagic stroke. The corresponding estimates were 4.28 (2.33, 7.86) for all-cause dementia, 6.96 (3.02, 16.01) for Alzheimer's disease, and 3.81 (1.40, 10.42) for vascular dementia. Among the three MVD, chronic kidney disease showed the strongest associations with both stroke subtypes, while peripheral neuropathy was most strongly associated with both dementia subtypes. CONCLUSIONS: Risk of stroke, dementia, and their major subtypes increased with an increasing number of MVD. The associations of individual MVD with stroke and dementia varied substantially by types of MVD.

Social vulnerability assessment under different extreme precipitation scenarios: A case study in Henan Province, China.

Extreme precipitation usually cause grievous losses&casualties, which varies greatly under different scenarios. This paper took Henan province as an example, it innovatively constructed three different extreme precipitation scenarios and built indicators system of social vulnerability from exposure, sensitivity and resilience based on MOVE framework. Social Vulnerability Indexs(SoVI) were then calculated by mathematical models under three different reoccurrence intervals. The results show that SoVI was low in the west and high in the north. High SoVI areas expanded to the middle and south as recurrence intervals increased. SoVI in each area of Henan province increased along with the recurrence intervals at different growth rates. The larger the recurrence interval was, the faster the SoVI increased. The results indicate SoVI is greatly affected by disaster levels, which need to be incorporated into social vulnerability. This study provides not only a new thought for social vulnerability assessment, but also a reference for the policymakers to formulate related risk management policies.

Arsenic pollution concerning surface water and sediment of Jie River: A pilot area where gold smelting enterprises are concentrated.

A comprehensive monitoring and risk assessment of arsenic (As) pollution concerning surface water and sediment is performed in the Jie River basin, where gold smelting enterprises are concentrated. The study area is divide into six regions, labeled as A, B, C, D, E, and F, from sewage outlets to downstream. Results shows that with far away from the sewage outlets, the total As concentrations in water and sediment gradually decrease from regions A to F. However, in region F, the concentration of bioavailable As significantly increases in the sediment due to the higher pH, leading to the transformation of As(V) into more mobile As(III). In sediment, Paracladius sp. exhibits strong resistance to As pollution in sediment, which can potentially elevate the risk of disease transmission. In water bodies, diatoms and euglena are the main phytoplankton in the Jie River while toxic cyanobacteria exhibits lower resistance to As pollution. Overall, measures should be taken to ecologically remediate the sediment in downstream while implementing appropriate isolation methods to prevent the spread of highly contaminated sediments from regions near sewage outlets.

Ethnicity-specific blood pressure thresholds based on cardiovascular and renal complications: a prospective study in the UK Biobank.

BACKGROUND: The appropriateness of hypertension thresholds for triggering action to prevent cardiovascular and renal complications among non-White populations in the UK is subject to question. Our objective was to establish ethnicity-specific systolic blood pressure (SBP) cutoffs for ethnic minority populations and assess the efficacy of these ethnicity-specific cutoffs in predicting adverse outcomes. METHODS: We analyzed data from UK Biobank, which included 444,418 participants from White, South Asian, Black Caribbean, and Black African populations with no history of cardiorenal complications. We fitted Poisson regression models with continuous SBP and ethnic groups, using Whites as the referent category, for the composite outcome of atherosclerotic cardiovascular disease, heart failure, and chronic kidney disease. We determined ethnicity-specific thresholds equivalent to the risks observed in Whites at SBP levels of 120, 130, and 140 mm Hg. We adjusted models for clinical characteristics, sociodemographic factors, and behavioral factors. The performance of ethnicity-specific thresholds for predicting adverse outcomes and associated population-attributable fraction (PAF) was assessed in ethnic minority groups. RESULTS: After a median follow-up of 12.5 years (interquartile range, 11.7-13.2), 32,662 (7.4%) participants had incident composite outcomes. At any given SBP, the predicted incidence rate of the composite outcome was the highest for South Asians, followed by White, Black Caribbean, and Black African. For an equivalent risk of outcomes observed in the White population at an SBP level of 140 mm Hg, the SBP threshold was lower for South Asians (123 mm Hg) and higher for Black Caribbean (156 mm Hg) and Black African (165 mm Hg). Furthermore, hypertension defined by ethnicity-specific thresholds was a stronger predictor and resulted in a larger PAF for composite outcomes in South Asians (21.5% [95% CI, 2.4,36.9] vs. 11.3% [95% CI, 2.6,19.1]) and Black Africans (7.1% [95% CI, 0.2,14.0] vs. 5.7 [95% CI, -16.2,23.5]) compared to hypertension defined by guideline-recommended thresholds. CONCLUSIONS: Guideline-recommended blood pressure thresholds may overestimate risks for the Black population and underestimate risks for South Asians. Using ethnicity-specific SBP thresholds may improve risk estimation and optimize hypertension management toward the goal of eliminating ethnic disparities in cardiorenal complications.

Non-classical 11ß-hydroxylase deficiency caused by a novel heterozygous mutation: a case report and review of the literature.

PURPOSE: 11ß-hydroxylase deficiency (11ß-OHD) constitutes a rare form of congenital adrenal hyperplasia (CAH), typically accounting for ~5-8% of CAH cases. Non-classical 11ß-OHD is reported even more rarely and frequently results in misdiagnosis or underdiagnosis due to its mild clinical symptoms. METHODS: A clinical, biochemical, radiological, and genetic study was conducted on a 9-year-old girl presenting with mild breast development, axillary hair growth, and advanced bone age. Additionally, a comprehensive review and synthesis of the literature concerning 11ß-OHD were conducted. RESULTS: The patient presented with breast enlargement, axillary hair development, and accelerated growth over the past year. Laboratory tests revealed levels of cortisol, luteinizing hormone, testosterone, and progesterone that were below normal. A gonadotropin-releasing hormone (GnRH) stimulation test suggested the possibility of central precocious puberty. Radiologic examination revealed a 2-year advance in bone age, while bilateral adrenal ultrasonography showed no abnormalities. Her mother exhibited hirsutism, while her father's physical examination revealed no abnormalities. Whole-exon genetic testing of the child and her parents indicated a heterozygous mutation of c.905_907delinsTT in exon 5 of the 11ß-hydroxylase gene (CYP11B1) in the child and her mother. This mutation resulted in a substitution of aspartic acid with valine at amino acid position 302 of the coding protein. This frameshift resulted in a sequence of 23 amino acids, culminating in a premature stop codon (p.Asp302ValfsTer23). A review of the previous literature revealed that the majority of heterozygous mutations in 11ß-OHD were missense mutations, occurring primarily in exons 2, 6, 7, and 8. The most common mutation among 11ß-OHD patients was the change of Arg-448 to His (R448H) in CYP11B1. Furthermore, bioinformatics analyses revealed that heterozygous mutation of c.905_907delinsTT had deleterious effects on the function of CYP11B1 and affected the stability of the protein, presumably leading to a partial impairment of enzyme activity. The results of the in vitro functional study demonstrated that the missense mutant (p.Asp302ValfsTer23) exhibited partial enzymatic activity. CONCLUSIONS: We report a novel heterozygous mutation of CYP11B1 (c.905_907delinsTT), enriching the spectrum of genetic variants of CYP11B1. This finding provides a valuable case reference for early diagnosis of non-classical patients with 11ß-OHD.

Unveiling the Anticancer Mechanism of Echinops davuricus: Isolation and Evaluation of AKR1B10 Inhibitors.

Five compounds (1-5), one long-chain fatty acid (1), two thiophenes (2 and 3), one alkaloid (4), and one phenyl ester (5), were isolated from the aerial part of Echinops davuricus. The structures of the products were established by performing detailed nuclear magnetic resonance (NMR) analysis, and the structure of compound 1 was determined via high-resolution electrospray ionization mass spectrometry (HRESIMS) and NMR. Compounds 1, 4, and 5 were isolated from Echinops davuricus for the first time. Based on network pharmacology methods, AKR1B10 was selected as a key anticancer target. Compounds 1 and 5 exhibited significant AKR1B10 inhibitory activities, with IC50 values of 156.0±1.00 and 146.2±1.50 nM, respectively, with epalrestat used as the positive control (81.09±0.61 nM). Additionally, the interactions between the active compounds and AKR1B10 were evaluated via molecular docking. Ultimately, the GO and KEGG enrichment analysis indicated that the key signaling pathways associated with the active compounds may be related to the PI3K-Akt, MAPK, apoptotic, cellular senescence, and TNF signaling pathways and the human diseases corresponding to the targets are cancer. Our study reveals for the first time the anticancer properties of Echinops davuricus and provides a comprehensive understanding of its application in traditional medicine.

Surficial engineering of active hydroxyls for ambient formaldehyde oxidation via enhanced Lewis acidity over Zr-doped cryptomelane materials.

Lewis acids of solid catalysts have been featured for a pivotal role in promoting various reactions. Regarding the oxidation protocol to remove formaldehyde, the inherent drawback of the best-studied MnO2 materials in acidic sites has eventually caused deficiency of active hydroxyls to sustain low-temperature activity. Herein, the cryptomelane-type MnO2 was targeted and it was tuned via incorporation of Zr metal, exhibiting great advances in not only the complete HCHO-to-CO2 degradation but also cycling performance. Zr species were existent in doping state in the MnO2 lattice, rendering lower crystallinity and breaking the regular growth of MnO2 crystallites, which thereby tripled surface area and created larger volume of smaller mesopores. Meantime, the local electronic properties of Mn atoms were also changed by Zr doping, i.e., more low-valence Mn species were formed due to the electron transfer from Zr to Mn. The results of infrared studies demonstrate the higher possession of Lewis acid sites on ZrMn, and this high degree of electrophilic agents favored the production of hydroxyl species. Furthermore, the reactivity of surface hydroxyls, as investigated by CO temperature programmed reduction and temperature programmed desorption of adsorbed O2, was obviously improved as well after Zr modification. It is speculated jointly with the characterizations of the post-reaction catalysts that the accelerated production of active hydroxyls helped rapidly convert formaldehyde into key intermediate-formate, which was then degraded into CO2, avoiding the side reaction path with undesired intermediate-hydrocarbonate-over the pristine MnO2, where active sites were blocked and formaldehyde oxidation was inhibited. Additionally, Zr decoration could stabilize Lewis acidity to be more resistant to heat degeneration, and this merit brought about advantageous thermal recyclability for cycled application.

Sarcopenia and treatment failure in inflammatory bowel disease: a systematic review and meta-analysis.

BACKGROUND: The association between sarcopenia and treatment outcomes in inflammatory bowel disease (IBD) is currently a subject of controversy. METHODS: A systematic search was performed of PubMed, Embase, Web of Science, and the Cochrane Library for studies published until April 2023. The quality assessment of each included study was performed using the Newcastle-Ottawa Scale. RESULTS: Seventeen studies were included with 2,895 IBD patients. Sarcopenia exhibited an increased risk of treatment failure (OR=2.00, 95% CI: 1.43-2.79) and notably increased the need for surgery (OR=1.54,95%CI:1.06-2.23) as opposed to a pharmacologic treatment plan change (OR=1.19, 95% CI:0.71-2.01) among IBD patients. However, no significant association was found between sarcopenia and treatment failure in corticosteroid (OR=1.21, 95% CI: 0.55-2.64) or biologic agent (OR=1.65, 95% CI: 0.93-2.92) cohorts. Sarcopenia was also linked to elevated treatment failure risks in patients with Crohn's disease (OR=1.82, 95% CI: 1.15-2.90) and those diagnosed with ulcerative colitis (OR=2.55, 95% CI: 1.05-6.21), spanning both Asian (OR=1.88, 95% CI: 1.29-2.74) and non-Asian regions (OR=2.17, 95% CI: 1.48-3.18). CONCLUSIONS: Sarcopenia was considered a novel marker for use in clinical practice to predict treatment failure, specifically, the need for surgery in IBD patients. This distinct cohort necessitates clinical attention and tailored care strategies.

Efficacy of polysaccharide iron complex in IDA rats: A comparative study with iron protein succinylate and ferrous succinate.

Iron deficiency anemia (IDA) is the most common nutrient-related health problem in the world. There is still a lack of comprehensive comparative study on the efficacies of commonly used iron supplements such as polysaccharide iron complex (PIC), iron protein succinylate (IPS) and ferrous succinate (FS) for IDA. In this study, we compared the PIC, IPS and FS efficacies in IDA rats via intragastric administration. The results showed that the three iron supplements had similar efficacies. PIC/IPS/FS at a dose of 15 mg Fe/kg/d for 10 d increased the hematological and serum biochemical parameters to 2.15/2.12/2.18 (Hb), 1.71/1.67/1.69 (RBC), 2.10/2.11/2.12 (HCT), 1.26/1.22/1.22 (MCV), all 1.34 (MCH), 1.15/1.15/1.14 (MCHC), 1.94/1.82/1.91 (SF), 9.75/9.67/9.53 (SI), and 23.30/22.68/21.64 (TS) times, and reduced TIBC to 0.42/0.43/0.44 times, compared to untreated IDA rats. PIC performed slightly better than IPS and FS in restoring MCV level. Meanwhile, the heart, spleen and kidney coefficients reduced to 67%/74%/65% (heart), all 59% (spleen) and 87%/88%/88% (kidney), and the liver coefficient increased to 116%/115%/116%, compared to untreated IDA rats. The liver iron content was found to be more affected by IDA than the spleen iron content. PIC/IPS/FS at 15 mg Fe/kg/d increased organ iron contents to 4.20/3.97/4.03 times (liver) and 1.36/1.24/1.41 times (spleen) within 10 d compared to untreated IDA rats, and PIC-H and FS were slightly better than IPS in restoring spleen iron content. The results of this study can provide useful data information for the comparison of three iron supplements, PIC, IPS and FS.

Defective kernel 58 encodes an Rrp15p domain-containing protein essential to ribosome biogenesis and seed development in maize.

Ribosome biogenesis is a highly dynamic and orchestrated process facilitated by hundreds of ribosomal biogenesis factors and small nucleolar RNAs. While many of the advances are derived from studies in yeast, ribosome biogenesis remains largely unknown in plants despite its importance to plant growth and development. Through characterizing the maize (Zea mays) defective kernel and embryo-lethal mutant dek58, we show that DEK58 encodes an Rrp15p domain-containing protein with 15.3% identity to yeast Rrp15. Over-expression of DEK58 rescues the mutant phenotype. DEK58 is localized in the nucleolus. Ribosome profiling and RNA gel blot analyses show that the absence of DEK58 reduces ribosome assembly and impedes pre-rRNA processing, accompanied by the accumulation of nearly all the pre-rRNA processing intermediates and the production of an aberrant processing product P-25S*. DEK58 interacts with ZmSSF1, a maize homolog of the yeast Ssf1 in the 60S processome. DEK58 and ZmSSF1 interact with ZmCK2α, a putative component of the yeast UTP-C complex involved in the small ribosomal subunit processome. These results demonstrate that DEK58 is essential to seed development in maize. It functions in the early stage of pre-rRNA processing in ribosome biogenesis, possibly through interacting with ZmSSF1 and ZmCK2α in maize.

Development of AKR1B10 inhibitors from Ajuga nipponensis based on diseases and targets.

Ten compounds (1-10) including one new neoclerodane diterpenoid (1) and nine known compounds were isolated from the whole plants of Ajuga nipponensis. Their structures were established by performing detailed analysis of NMR, the structure of 1 was determined using HRESIMS, 1D and 2D NMR, UV, and IR. Compounds 1 and 4-10 were isolated from Ajuga nipponensis for the first time. And it was the first time to report compounds 9 and 10 as natural products. Based on network pharmacology methods, 45 key targets were selected, which were compounds mapping to diseases. And compounds 2, 3, 7, and a (ajugacumbin B) exhibited excellent AKR1B10 inhibitory activities, with IC50 values of 53.05 ± 0.75, 87.22 ± 0.85, 61.85 ± 0.66, and 85.19±1.02 nM respectively, with Epalrestat used as the positive control (82.09 ± 1.62 nM). Additionally, the interaction between active compounds and AKR1B10 had been discussed according to the molecular docking results. Ultimately, the analysis of GO and KEGG enrichment indicated that the key signaling pathway of the active compounds may be related to prostate cancer. Our study results demonstrate the hypoglycemic and anti-tumor properties of A. nipponensis for the first time, and provide a comprehensive understanding of its application in traditional medicine. Furthermore, this article establishes a reference for further research on the optimized experimental design of novel AKR1B10 inhibitors.

A novel Recjf Exo signal amplification strategy based on bioinformatics-assisted truncated aptamer for efficient fluorescence detection of AFB1.

Aflatoxin B1 (AFB1) is a typical mycotoxin that signifacntly endangers public health and economy. In this study, we systematically studied the interaction of aptamers with AFB1 using circular dichroism, molecular dynamics, molecular docking, and fluorescence analysis. The truncated sequence aptamers were screened using molecular docking. We successfully obtained the AFB1 aptamer with higher affinity and its truncated form was enhanced by 5.2-fold compared to the initial AFB1 aptamer. In addition, for rapid detection of AFB1, we designed a fluorescent nano-adaptor sensing platform using RecJf exonuclease signal amplification strategy based on the optimal aptamer. The aptasensor showed satisfactory sensitivity towards AFB1 with a linear detection range of 1-400 ng/mL and a detection limit of 0.57 ng/mL. The aptasensor was successfully applied to the determination of AFB1 in soybean oil and corn oil with recoveries of 91.02 %-106.59 % and 87.39 %-110.61 %, respectively. The successful application of the AFB1 aptasensor, developed through bioinformatics truncation of the aptamer, provides a novel approach to creating a cost-effective, eco-friendly, and rapid aptamer sensing platform.

Localization of an IgE epitope of glycinin A2 peptide chain.

INTRODUCTION: One of the main allergens in soybeans is glycinin, which seriously impacts the normal lives of allergic people. Previous studies have confirmed that thermal processing and thermal processing combined with ultrahigh-pressure processing could significantly reduce the antigenicity of glycinin. The dominant antigen region of acidic peptide chain A2 of G2 subunit was located by phage display experiment. METHODS: In this paper, overlapping peptides and alanine substitution techniques were used to explore the key amino acids that significantly affect the antigenicity of A2 peptide chain. The purity of peptide 1, peptide 2 and peptide 3 was identified by mass spectrometry and high-performance liquid chromatography, and the results showed that the purity of the synthesized overlapping peptide was more than 90%. SDS-PAGE showed that the peptide was successfully coupled with bovine serum albumin. The antigenicity of the coupling peptide was tested by ELISA and Dot-Blot, and the allergenicity was detected by reacting with the serum of patients with soybean globulin allergy. CONCLUSION: The results showed that peptide 3 has stronger antigenicity and sensitization. Alanine substitution technology allowed one to perform site-directed mutagenesis on peptide 3. Dot-Blot and ELISA tests showed that D259, E260, E261, Q263 and C266 may be the key amino acids that significantly affect the antigenicity of peptide 3. The research presented is of great significance for correctly guiding the production of safe food and preventing the occurrence of food allergic diseases. © 2023 Society of Chemical Industry.

Sarcopenia and treatment failure in inflammatory bowel disease: a systematic review and meta-analysis

Background: The association between sarcopenia and treatment outcomes in inflammatory bowel disease (IBD) is currently a subject of controversy. Methods: A systematic search was performed of PubMed, Embase, Web of Science, and the Cochrane Library for studies published until April 2023. The quality assessment of each included study was performed using the Newcastle-Ottawa Scale. Results: Seventeen studies were included with 2,895 IBD patients. Sarcopenia exhibited an increased risk of treatment failure (OR=2.00, 95% CI: 1.43-2.79) and notably increased the need for surgery (OR=1.54,95%CI:1.06-2.23) as opposed to a pharmacologic treatment plan change (OR=1.19, 95% CI:0.71-2.01) among IBD patients. However, no significant association was found between sarcopenia and treatment failure in corticosteroid (OR=1.21, 95% CI: 0.55-2.64) or biologic agent (OR=1.65, 95% CI: 0.93-2.92) cohorts. Sarcopenia was also linked to elevated treatment failure risks in patients with Crohn's disease (OR=1.82, 95% CI: 1.15-2.90) and those diagnosed with ulcerative colitis (OR=2.55, 95% CI: 1.05-6.21), spanning both Asian (OR=1.88, 95% CI: 1.29-2.74) and non-Asian regions (OR=2.17, 95% CI: 1.48-3.18). Conclusions: Sarcopenia was considered a novel marker for use in clinical practice to predict treatment failure, specifically, the need for surgery in IBD patients. This distinct cohort necessitates clinical attention and tailored care strategies (AU)

Identification of monocyte-associated pathways participated in the pathogenesis of pulmonary arterial hypertension based on omics-data.

Pulmonary arterial hypertension (PAH) is one kind of chronic and uncurable diseases that can cause heart failure. Immune microenvironment plays a significant role in PAH. The aim of this study was to assess the role of immune cell infiltration in the pathogenesis of PAH. Differentially expressed genes based on microarray data were enriched in several immune-related pathways. To evaluate the immune cell infiltration, based on the microarray data sets in the GEO database, we used both ssGSEA and the CIBERSORT algorithm. Additionally, single-cell RNA sequencing (scRNA-seq) data was used to further explicit the specific role and intercellular communications. Then receiver operating characteristic curves and least absolute shrinkage and selection operator were used to discover and test the potential diagnostic biomarkers for PAH. Both the immune cell infiltration analyses based on the microarray data sets and the cell proportion in scRNA-seq data exhibited a significant downregulation in the infiltration of monocytes in PAH. Then, the intercellular communications showed that the interaction weighs of most immune cells, including monocytes changed between the control and PAH groups, and the ITGAL-ITGB2 and ICAM signaling pathways played critical roles in this process. In addition, ITGAM and ICAM2 displayed good diagnosis values in PAH. This study implicated that the change of monocyte was one of the key immunologic features of PAH. Monocyte-associated ICAM-1 and ITGAL-ITGB2 signaling pathways might be involved in the pathogenesis of PAH.

Deletion in 1p36.33-p36.32 is associated with pancytopenia: a case report.

BACKGROUND: 1P36 deletion syndrome is recognized as the most common terminal microdeletion syndrome in humans, characterized by early developmental delay and consequent intellectual disability, seizure disorder, and distinctive facial features. Variable deletion locations may attributed to phenotypic variability. However, the abnormal phenotypes of hematology are rarely reported in 1P36 deletion syndrome patients. CASE PRESENTATION: We present a case of postnatal intellectual disability accompanied by pancytopenia. Copy number variation analysis revealed a pathogenic deletion in 1p36.331p36.32 with a deletion size of 2.21 Mb. Following successful treatment with glucocorticoids, the patient was diagnosed with immuno-related hemocytopenia (IRH). DISCUSSION: The patient experienced IRH, an uncommon characteristic of 1p36 deletion syndrome. The deletion fragment of 1p36.33-p36.32, particularly the loss of GNB1 gene, has been associated with the development of pancytopenia. Genotype-phenotype correlations are valuable in identifying the genes responsible for various clinical characteristics of the syndrome by associating phenotypic variation with specific genes located within the chromosome deletion region. Genome sequencing is recommended in cases where clinical manifestations indicate the presence of a genetic disorder but pose diagnostic challenges.