Comparative transcriptome revealed the molecular responses of Aconitum carmichaelii Debx. to downy mildew at different stages of disease development.

BACKGROUND: Aconitum carmichaelii Debx. has been widely used as a traditional medicinal herb for a long history in China. It is highly susceptible to various dangerous diseases during the cultivation process. Downy mildew is the most serious leaf disease of A. carmichaelii, affecting plant growth and ultimately leading to a reduction in yield. To better understand the response mechanism of A. carmichaelii leaves subjected to downy mildew, the contents of endogenous plant hormones as well as transcriptome sequencing were analyzed at five different infected stages. RESULTS: The content of 3-indoleacetic acid, abscisic acid, salicylic acid and jasmonic acid has changed significantly in A. carmichaelii leaves with the development of downy mildew, and related synthetic genes such as 9-cis-epoxycarotenoid dioxygenase and phenylalanine ammonia lyase were also significant for disease responses. The transcriptomic data indicated that the differentially expressed genes were primarily associated with plant hormone signal transduction, plant-pathogen interaction, the mitogen-activated protein kinase signaling pathway in plants, and phenylpropanoid biosynthesis. Many of these genes also showed potential functions for resisting downy mildew. Through weighted gene co-expression network analysis, the hub genes and genes that have high connectivity to them were identified, which could participate in plant immune responses. CONCLUSIONS: In this study, we elucidated the response and potential genes of A. carmichaelii to downy mildew, and observed the changes of endogenous hormones content at different infection stages, so as to contribute to the further screening and identification of genes involved in the defense of downy mildew.

Secondary metabolites isolated from Trichoderma hamatum b-3 and their fungicidal activity.

An undescribed trichodenone derivative (1), two new diketopiperazines (3 and 4) along with a bisabolane analog (2) were isolated from Trichoderma hamatum b-3. The structures of the new findings were established through comprehensive analyses of spectral evidences in HRESIMS, 1D and 2D NMR, Marfey's analysis as well as comparisons of ECD. The absolute configuration of 2 was unambiguously confirmed by NMR, ECD calculation and Mo2(AcO)4 induced circular dichroism. Compounds 1-4 were tested for their fungicidal effects against eight crop pathogenic fungi, among which 1 showed 51% inhibition against Sclerotinia sclerotiorum at a concentration of 50 µg/mL.

Selenium Lessens Osteoarthritis by Protecting Articular Chondrocytes from Oxidative Damage through Nrf2 and NF-κB Pathways.

Osteoarthritis (OA) causes joint pain and disability due to the abnormal production of inflammatory cytokines and reactive oxygen species (ROS) in chondrocytes, leading to cell death and cartilage matrix destruction. Selenium (Se) intake can protect cells against oxidative damage. It is still unknown whether Se supplementation is beneficial for OA. This study investigated the effects of Se on sodium iodoacetate (MIA)-imitated OA progress in human chondrocyte cell line (SW1353 cells) and rats. The results showed that 0.3 µM of Se treatment could protect SW1353 cells from MIA-induced damage by the Nrf2 pathway by promoting the gene expression of glutathione-synthesis-related enzymes such as the glutamate-cysteine ligase catalytic subunit, the glutamate-cysteine ligase modifier subunit, and glutathione synthetase. In addition, glutathione, superoxide dismutase, glutathione peroxidase, and glutathione reductase expressions are also elevated to eliminate excessive ROS production. Moreover, Se could downregulate NF-κB, leading to a decrease in cytokines, matrix proteases, and glycosaminoglycans. In the rats, MIA-induced cartilage loss was lessened after 2 weeks of Se supplementation by oral gavage; meanwhile, glutathione synthesis was increased, and the expressions of pro-inflammatory cytokines were decreased. These results suggest that Se intake is beneficial for OA due to its effects of decreasing cartilage loss by enhancing antioxidant capacity and reducing inflammation.

Uric acid, high density lipoprotein cholesterol levels and their ratio are related to microbial enterotypes and serum metabolites in females with a blood stasis constitution.

BACKGROUND: Blood stasis constitution in traditional Chinese medicine (TCM) is believed to render individuals more susceptible to metabolic diseases. However, the biological underpinnings of this constitutional imbalance remain unclear. METHODS: This study explored the association between blood stasis constitution, serum metabolic markers including uric acid (UA), high-density lipoprotein cholesterol (HDLC), their ratio (UHR), serum metabolites, and gut microbiota. Clinical data, fecal and serum samples were acquired from 24 individuals with a blood stasis constitution and 80 individuals with a balanced constitution among healthy individuals from Guangdong. Gut microbiota composition analysis and serum metabolomics analysis were performed. RESULTS: Females with a blood stasis constitution had higher UA levels, lower HDLC levels, and higher UHR in serum, suggesting a higher risk of metabolic abnormalities. Analysis of the gut microbiome revealed two distinct enterotypes dominated by Bacteroides or Prevotella. Intriguingly, blood stasis subjects were disproportionately clustered within the Bacteroides-rich enterotype. Metabolomic analysis identified subtle differences between the groups, including lower phenylalanine and higher trimethylaminoacetone levels in the blood stasis. Several differential metabolites displayed correlations with HDLC, UA, or UHR, unveiling potential new markers of metabolic dysregulation. CONCLUSIONS: These findings elucidate the intricate interplay between host constitution, gut microbiota, and serum metabolites. The concept of blood stasis offers a unique perspective to identify subtle alterations in microbiome composition and metabolic pathways, potentially signaling underlying metabolic vulnerability, even in the presence of ostensibly healthy profiles. Continued investigation of this TCM principle may reveal critical insights into the early biological processes that foreshadow metabolic deterioration.

The association of hernia-specific and procedural risk factors with early complications in ventral hernia repair: ACHQC analysis.

BACKGROUND: Many surgical risk assessment tools emphasize patient-specific risk factors. Our objective was to use a hernia-specific database to assess risk factors of complications in ventral hernia repair (VHR) focusing on hernia-specific and procedural factors. METHODS: The ACHQC database was queried for elective VHR in adults from 2012 to 2023. Primary outcome was overall 30-day complications. Multivariable logistic regression was used for analysis. RESULTS: 41,526 VHR were included. The rate of 30-day complications was 18%, surgical site infection 3%, surgical site occurrence requiring procedural intervention 4%, readmission 4%, reoperation 2%, and mortality 0.2%. Multivariable analysis demonstrated that BMI, ASA, frailty, COPD, anticoagulants, defect width, incisional and recurrent hernias, presence of stoma or prior mesh, prior abdominal wall infection, non-clean wound, operative time, open approach and myofascial release were associated with 30-day complications (OR â€‹= â€‹1.01-1.66). Preoperative chlorhexidine, bowel preparation and fascial closure were associated with lower complication risk (OR â€‹= â€‹0.70-0.89). CONCLUSION: Hernia and procedural risk factors are associated with early complications following elective VHR. These factors need to be included in surgical risk assessment tools, to supplement patient-specific factors.

Colonic microflora and plasma metabolite-based comparative analysis of unilateral ureteral obstruction-induced chronic kidney disease after treatment with the Chinese medicine FuZhengHuaYuJiangZhuTongLuo and AST-120.

Background: Many researchers have investigated the use of Chinese herbs to delay the progression of chronic kidney disease (CKD) through their effects on colonic microflora and microbiota-derived metabolites. However, whether FuZhengHuaYuJiangZhuTongLuo (FZHY) has effects that are similar to those of AST-120 on CKD needs to be elucidated. Methods: In this study, we compared the effects of FZHY and AST-120 on the colonic microbiota and plasma metabolites in the CKD rat model. We developed a unilateral ureteral obstruction (UUO)-induced CKD rat model and then administered FZHY and AST-120 to these model rats. Non-targeted metabolomic LC-MS analysis, 16S rRNA sequencing, and histopathological staining were performed on plasma, stool, and kidney tissues, respectively, and the joint correlation between biomarkers and metabolites of candidate bacteria was analyzed. Results: Our results showed that administering FZHY and AST-120 effectively ameliorated UUO-induced abnormal renal function and renal fibrosis and regulated the composition of microbiota and metabolites. Compared to the UUO model group, the p_Firmicutes and o_Peptostreptococcales_Tissierellales were increased, while 14 negative ion metabolites were upregulated and 21 were downregulated after FZHY treatment. Additionally, 40 positive ion metabolites were upregulated and 63 were downregulated. On the other hand, AST-120 treatment resulted in an increase in the levels of g_Prevotellaceae_NK3B31_group and f_Prevotellaceae, as well as 12 upregulated and 23 downregulated negative ion metabolites and 56 upregulated and 63 downregulated positive ion metabolites. Besides, FZHY increased the levels of candidate bacterial biomarkers that were found to be negatively correlated with some poisonous metabolites, such as 4-hydroxyretinoic acid, and positively correlated with beneficial metabolites, such as l-arginine. AST-120 increased the levels of candidate bacterial biomarkers that were negatively correlated with some toxic metabolites, such as glycoursodeoxycholic acid, 4-ethylphenol, and indole-3-acetic acid. Conclusion: FZHY and AST-120 effectively reduced kidney damage, in which, the recovery of some dysregulated bacteria and metabolites are probably involved. As their mechanisms of regulation were different, FZHY might play a complementary role to AST-120 in treating CKD.

Effects of allicin on growth performance, antioxidant profile, and microbiota compared to monensin of growing goats.

Allicin is a sulfur-containing compound extracted from raw garlic (Allium sativum L.). We compared the effect of allicin addition on growth performance, serum biochemical parameters, and rumen microbiota of goats compared to monensin. Twenty-four Anhui white goats were assigned randomly to one of three dietary treatments: 1) a basal diet (CON); 2) the basal diet with allicin addition at 750 mg per head per day (AC); 3) the basal diet with monensin addition at 30 mg per kg of diet (MS). Animals were fed for 8 weeks. Results showed the average daily gain, and feed efficiency was increased with allicin and monensin addition. Serum levels of IgG, total superoxide dismutase, and glutathione peroxidase were higher in the AC group than those in the CON and MS groups. The microbiota analysis revealed that monensin addition mainly affected genera related to carbohydrate and protein metabolism, and allicin mainly affected genera related to energy metabolism and intestinal health. In conclusion, allicin could improve growth performance and have advantages over monensin in improving the antioxidant capacity and immune function of goats. Allicin may be a potential alternative to monensin.

[Effect and mechanism of Jiedu Huoxue Decoction in regulating YAP/ACSL4 pathway to inhibit ferroptosis in treatment of acute kidney injury].

Jiedu Huoxue Decoction(JDHX), first recorded in the Correction on Errors in Medical Works by WANG Qing-ren, is an effective formula screened out from ancient formulas by the traditional Chinese medicine(TCM) master ZHANG Qi to treat acute kidney injury(AKI) caused by heat, toxicity, stasis, and stagnation. This paper elucidated the therapeutic effect of JDHX on AKI and probed into the potential mechanism from ferroptosis. Thirty-two male C57BL/6 mice were randomized into four groups(n=8): normal, model, and low-and high-dose JDHX. Since the clinical treatment of AKI depends on supportive or alternative therapies and there is no specific drug, this study did not include a positive drug group. The low dose of JDHX corresponded to half of clinically equivalent dose, while the high dose corresponded to the clinically equivalent dose. Mice were administrated with JDHX by gavage daily for 7 consecutive days, while those in the normal group and the model group were administered with the corresponding volume of distilled water. On day 5 of drug administration, mice in other groups except the normal group were injected intraperitoneally with cisplatin solution at a dose of 20 mg·kg~(-1) to induce AKI, and the normal group was injected with saline. All of the mice were sacrificed 72 h after modeling, blood and kidney samples were collected for subsequent analysis. The levels of serum creatine(Scr) and blood urea nitrogen(BUN) were measured by the commercial kits. The expression level of kidney injury molecule 1(KIM-1) in the serum was measured by enzyme-linked immunosorbent assay. Hematoxylin-eosin(HE) staining, periodic acid-Schiff(PAS) staining, and Prussian blue staining were employed to observe the pathological changes, glycogen deposition, and iron deposition, respectively, in the renal tissue. In addition, the levels of glutathione(GSH), superoxide dismutase(SOD), and catalase(CAT) in the renal tissue were examined by biochemical colorimetry. Western blot was performed to determine the protein levels of acyl-CoA synthetase long chain family member 4(ACSL4), lysophosphatidylcholine acyltransferase 3(LPCAT3), and Yes-associated protein(YAP, a key molecule in the Hippo pathway) in the renal tissue. Immunohistochemistry was then employed to detect the location and expression of YAP in the renal tissue. Real-time fluorescence quantitative polymerase chain reaction(qRT-PCR) was performed to measure the mRNA levels of ACSL4 and glutathione peroxidase 4(GPX4). Compared with the normal group, the model group showed elevated serum levels of Scr, BUN, and KIM-1. In the AKI model group, the tubular epithelial cells underwent atrophy and necrotic detachment, disappearance of brush border, and some tubules became protein tubules or experienced vacuole-like degeneration. In addition, this group presented widening of the interstitium or even edema, increased renal tubule injury score, and obvious glycogen and iron deposition in parts of the renal tissue. Moreover, the model group had lower GSH, SOD, and CAT levels, higher ASCL4 and LPCAT3 levels, and lower GPX4 expression and higher YAP expression than the normal group. Compared with the model group, high dose of JDHX effectively protected renal function, lowered the levels of Scr, BUN and KIM-1, alleviated renal pathological injury, reduced glycogen and iron deposition, and elevated the GSH, SOD, and CAT levels in the renal tissue. Furthermore, JDHX down-regulated the protein levels of ACSL4, LPCAT3, and YAP and up-regulated the level of GPX4, compared with the model group. In conclusion, JDHX can protect mice from cisplatin-induced AKI by inhibiting ferroptosis via regulating the YAP/ACSL4 signaling pathway.

Degradation of Cell Wall Polysaccharides during Traditional and Tank Fermentation of Chinese Liupao Tea.

The increase of polysaccharides in the dark tea pile process is thought to be connected to the cell wall polysaccharides' breakdown. However, the relationship between tea polysaccharides (TPSs) and tea cell wall polysaccharides has not been further explored. In this study, the structural changes in the cell wall polysaccharides [e.g., cellulose, hemicellulose (HC), and pectin] in Liupao tea were characterized before and after traditional fermentation and tank fermentation. Additionally, the degradation mechanism of tea cell wall polysaccharides during fermentation was assessed. The results showed that cellulose crystallinity decreased by 11.9-49.6% after fermentation. The molar ratio of monosaccharides, such as arabinose, rhamnose, and glucose in HC, was significantly reduced, and the molecular weight decreased. The esterification degree and linearity of water-soluble pectin (WSP) were reduced. TPS content increases during pile fermentation, which may be due to HC degradation and the increase in WSP caused by cell wall structure damage. Microorganisms were shown to be closely associated with the degradation of cell wall polysaccharides during fermentation according to correlation analyses. Traditional fermentation had a greater effect on the cellulose structure, while tank fermentation had a more noticeable impact on HC and WSP.

Transcription Factors and Their Regulatory Roles in the Male Gametophyte Development of Flowering Plants.

Male gametophyte development in plants relies on the functions of numerous genes, whose expression is regulated by transcription factors (TFs), non-coding RNAs, hormones, and diverse environmental stresses. Several excellent reviews are available that address the genes and enzymes associated with male gametophyte development, especially pollen wall formation. Growing evidence from genetic studies, transcriptome analysis, and gene-by-gene studies suggests that TFs coordinate with epigenetic machinery to regulate the expression of these genes and enzymes for the sequential male gametophyte development. However, very little summarization has been performed to comprehensively review their intricate regulatory roles and discuss their downstream targets and upstream regulators in this unique process. In the present review, we highlight the research progress on the regulatory roles of TF families in the male gametophyte development of flowering plants. The transcriptional regulation, epigenetic control, and other regulators of TFs involved in male gametophyte development are also addressed.

Herbal medicine and gut microbiota: exploring untapped therapeutic potential in neurodegenerative disease management.

The gut microbiota that exists in the human gastrointestinal tract is incredibly important for the maintenance of general health as it contributes to multiple aspects of host physiology. Recent research has revealed a dynamic connection between the gut microbiota and the central nervous system, that can influence neurodegenerative diseases (NDs). Indeed, imbalances in the gut microbiota, or dysbiosis, play a vital role in the pathogenesis and progression of human diseases, particularly NDs. Herbal medicine has been used for centuries to treat human diseases, including NDs. These compounds help to relieve symptoms and delay the progression of NDs by improving intestinal barrier function, reducing neuroinflammation, and modulating neurotransmitter production. Notably, herbal medicine can mitigate the progression of NDs by regulating the gut microbiota. Therefore, an in-depth understanding of the potential mechanisms by which herbal medicine regulates the gut microbiota in the treatment of NDs can help explain the pathogenesis of NDs from a novel perspective and propose novel therapeutic strategies for NDs. In this review, we investigate the potential neuroprotective effects of herbal medicine, focusing on its ability to regulate the gut microbiota and restore homeostasis. We also highlight the challenges and future research priorities of the integration of herbal medicine and modern medicine. As the global population ages, access to this information is becoming increasingly important for developing effective treatments for these diseases.

Daphnepedunins G and H, anti-HIV macrocyclic 3,4-seco-daphnane orthoesters from Daphne pedunculata.

Daphnepedunins G (1) and H (2) with unusual macrocyclic 3,4-seco-daphnane orthoester structure were isolated from Daphne pedunculata. Their structures were determined by physicochemical and spectroscopic analyses combined with synthetic methods, including methyl esterification, derivatization reaction using a chiral anisotropic agent, and biomimetic conversion. Compounds 1 and 2 along with their methyl esters 1a and 2a were evaluated for anti-HIV activity, among which 1a and 2a exhibited potent activity with IC50 values of 1.08 and 1.17 µM, respectively.

Determining the Association Between Insurance Type and Myofascial Release in Large Ventral Hernias.

INTRODUCTION: Abdominal wall reconstruction (AWR) utilizes advanced myofascial releases to perform complex ventral hernia repair (VHR). The relationship between the performance of AWR and disparities in insurance type is unknown. METHODS: The Abdominal Core Health Quality Collaborative was queried for adults who had undergone an elective VHR between 2013 and 2020 with a hernia size ≥10 cm. Patients with missing insurance data were excluded. Comparison groups were divided by insurance type: favorable (private, Medicare, Veteran's Administration, Tricare) or unfavorable (Medicaid and self-pay). Propensity score matching compared the cumulative incidence of AWR between the favorable and unfavorable insurance comparison groups. RESULTS: In total, 26,447 subjects met inclusion criteria. The majority (89%, n = 23,617) had favorable insurance, while (11%, n = 2830) had unfavorable insurance. After propensity score matching, 2821 patients with unfavorable insurance were matched to 7875 patients with favorable insurance. The rate of AWR with external oblique release or transversus abdominis release was significantly higher (23%, n = 655) among the unfavorable insurance group compared to those with favorable insurance (21%, n = 1651; P = 0.013). CONCLUSIONS: This study provides evidence that patients with unfavorable insurance may undergo AWR with external oblique or transversus abdominis release at a greater rate than similar patients with favorable insurance. Understanding the mechanisms contributing to this difference and evaluating the financial implications of these trends represent important directions for future research in elective VHR.

Integrating network pharmacology and experimental verification to explore the mucosal protective effect of Chimonanthus nitens Oliv. Leaf Granule on ulcerative colitis.

ETHNOPHARMACOLOGICAL RELEVANCE: Chimonanthus nitens Oliv. Leaf Granule (COG) is a commonly used clinical preparation of traditional Chinese medicine for the treatment of cold, but there are folk reports that it can treat diarrhea and other gastrointestinal diseases. Therefore, the mechanism of COG in the treatment of ulcerative colitis with diarrhea as the main symptom needs to be studied. AIM OF THE STUDY: Combined network pharmacology and experimental validation to explore the mechanism of COG in the treatment of ulcerative colitis. MATERIALS AND METHODS: First, the main components of COG were characterized by liquid chromatography-mass spectrometry (LC-MS); subsequently, a network pharmacology approach was used to screen the effective chemical components and action targets of COG to construct a target network of COG for the treatment of ulcerative colitis (UC). The protein-protein interaction network (PPI) and literature reports were combined to identify the potential targets of COG for the treatment of UC. Finally, the predicted results of network pharmacology were validated by animal and cellular experiments. RESULTS: 19 components of COG were characterized by LC-MS, among which 10 bioactive components could act on 377 potential targets of UC. Key therapeutic targets were collected, including SRC, HSP90AA1, PIK3RI, MAPK1 and ESR1. KEGG results are enriched in pathways related to oxidative stress. Molecular docking analysis showed good binding activity of main components and target genes. Animal experiments showed that COG significantly relieved the colitis symptoms in mice, regulated the Treg/Th17 balance, and promoted the secretion of IL-10 and IL-4, along with the inhibition of IL-1ß and TNF-α. Additionally, COG reduced the apoptosis of colon epithelial cells, and significantly improved the levels of SOD, MAO, GSH-px, and inhibited MDA, iNOS, eNOS in colon. Also, it increased the expression of tight junction proteins such as ZO-1, Claudin1, Occludin and E-cadherin. In vitro experiments, COG inhibited the oxidative stress and inflammatory injury of HCT116 cells induced by LPS. CONCLUSIONS: Combining network pharmacology and in vitro and in vivo experiments, COG was verified to have a good protective effect in UC, which may be related to enhancing antioxidation in colon tissues.

LC-MS identification, isolation, and structural elucidation of anti-HIV macrocyclic daphnane orthoesters from Edgeworthia chrysantha.

The occurrence of macrocyclic daphnane orthoesters (MDOs) with a 1-alkyl group originating from a C14 aliphatic chain is extremely limited in the plant kingdom and has only been isolated from Edgeworthia chrysantha. In the present study, LC-ESI-MS/MS analysis was performed on different parts of E. chrysantha, including flower buds, flowers, leaves, and stems, and resulted in the identification of seven MDOs in all the four plant parts, including two previously unreported compounds 1 and 7. Further LC-MS guided isolation was carried out to afford compounds 1 and 7, and their structures were determined by various spectroscopic analyses. These compounds were also evaluated for anti-HIV activity, thus expanding insights into the structure-activity relationships for MDOs.

Naringin alleviates pneumonia caused by Klebsiella pneumoniae infection by suppressing NLRP3 inflammasome.

Klebsiella pneumoniae (Kpn) is an important pathogen of hospital-acquired pneumonia, which can lead to sepsis and death in severe cases. In this study, we simulated pneumonia induced by Kpn infection in mice to investigate the therapeutic effect of naringin (NAR) on bacterial-induced lung inflammation. Mice infected with Kpn exhibited increases in white blood cells (WBC) and neutrophils in the peripheral blood and pathological severe injury of the lungs. This injury was manifested by increased expression of the inflammatory cytokines interleukin (IL)- 18, IL-1ß, tumor necrosis factor-α (TNF-α) and IL-6, and elevated the expression of NLRP3 protein. NAR treatment could decrease the protein expression of NLRP3, alleviate lung inflammation, and reduce lung injury in mice caused by Kpn. Meanwhile, molecular docking results suggest NAR could bind to NLRP3 and Surface Plasmon Resonance (SPR) analyses also confirm this result. In vitro trials, we found that pretreated with NAR not only inhibited nuclear translocation of nuclear factor (NF)-κB protein P65 but also attenuated the protein interaction of NLRP3, caspase-1 and ASC and inhibited the assembly of NLRP3 inflammasome in mice AMs. Additionally, NAR could reduce intracellular potassium (K+) efflux, inhibiting NLRP3 inflammasome activation. These results indicated that NAR could protect against Kpn-induced pneumonia by inhibiting the overactivation of the NLRP3 inflammasome signaling pathway. The results of this study confirm the efficacy of NAR in treating bacterial pneumonia, refine the mechanism of action of NAR, and provide a theoretical basis for the research and development of NAR as an anti-inflammatory adjuvant.

Long-term outcome of children with acute promyelocytic leukemia: a randomized study of oral versus intravenous arsenic by SCCLG-APL group.

Realgar-Indigo naturalis formula (RIF), an oral traditional Chinese medicine mainly containing Realgar (As4S4), is highly effective in treating adult acute promyelocytic leukemia (APL). However, the treatment efficacy and safety of RIF have not been verified in pediatric patients. SCCLG-APL group conducted a multicenter randomized non-inferiority trial to determine whether intravenous arsenic trioxide (ATO) can be substituted by oral RIF in treating pediatric APL. Of 176 eligible patients enrolled, 91 and 85 were randomized to ATO and RIF groups, respectively. Patients were treated with the risk-adapted protocol. Induction, consolidation, and 96-week maintenance treatment contained all-trans-retinoic acid and low-intensity chemotherapy, and either ATO or RIF. The primary endpoint was 5-year event-free survival (EFS). The secondary endpoints were adverse events and hospital days. After a median 6-year follow-up, the 5-year EFS was 97.6% in both groups. However, the RIF group had significantly shorter hospital stays and lower incidence of infection and tended to have less cardiac toxicity. All 4 relapses occurred within 1.5 years after completion of maintenance therapy. No long-term arsenic retentions were observed in either group. Substituting oral RIF for ATO maintains treatment efficacy while reducing hospitalization and adverse events in treating pediatric APL patients, which may be a future treatment strategy for APL.

Isolation and identification of two pathogens causing leaf spot of Fritillaria taipaiensis P. Y. Li. in China.

Fritillaria taipaiensis P. Y. Li is one of the biological sources for Fritillariae Cirrhosae Bulbus. Its bulbs are widely used for treating respiratory diseases such as pneumonia, bronchitis and influenza. Cultivated F. taipaiensis suffers from many diseases during its growing season. Leaf spot is a destructive disease that is increasingly affecting F. taipaiensis and can cause an incidence of up to 30% in severe cases. Leaf spot inhibits the growth of F. taipaiensis by causing disease spots on the surface of leaves. In severe cases, these spots can result in leaf desiccation and blackspot formation at the lesion site, leading to a decrease in photosynthesis. Leaf spot has shown little benefit, and it can even result in a reduced yield of bulbs and the death of plants. According to previous studies, Alternaria alternata has been identified as the pathogen of leaf spot in many medicinal plants, but the main pathogens of the leaf spot of F. taipeiensis remains uncertain. In this paper, five isolates from diseased leaves of F. taipaiensis were isolated and purified and the pathogenicity test showed that isolates B-5 and B-7 induced leaf spot symptoms on healthy F. taipaiensis leaves. Integrating multiple phylogenetic analyses of rDNA using Internal transcribed spacer region (ITS), Beta-tubulin (TUB2), RNA polymerase II second largest subunit (RPB2) and Translation elongation factor 1-alpha (TEF1-a) primers, strain B-5 and strain B-7 were eventually identified as Didymella segeticola and A. alternata. This is also the first report on the pathogens that cause leaf spot in F. taipaiensis in China.

Shoutai Pill Enhances Endometrial Receptivity in Controlled Ovarian Hyperstimulation Mice by Improving the In-Vivo Immune Environment.

BACKGROUND: The Shoutai pill (STP) is a classic formulation in traditional Chinese medicine. Preliminary experimental observations from our study suggest that it is effective in enhancing endometrial receptivity. However, the underlying mechanisms by which STP influences endometrial receptivity remain to be elucidated. PURPOSE: The objective of this study is to investigate the effects and mechanisms of the STP formulation in enhancing endometrial receptivity in controlled ovarian hyperstimulation (COH) model mice. METHODS: The network pharmacology analysis identified target proteins associated with the reduction of endometrial receptivity by STP. The COH mouse model was established using the GnRHa+PMSG+HCG protocol. The levels of MHC-1 and MHC-2 in mouse serum were measured using the ELISA method, while the levels of IL-1B, IL-4, IL-10, IP-10, IL-1a, IL-2, IL-17, TNF-a, and IFN-y were measured using liquid chip technology. RESULTS: STP exhibited a significant improvement in the immune environment of COH model mice. The major active components of STP were identified as beta-sitosterol and quercetin, among others. Furthermore, AKT1, VEGFA, and several immune factors, such as TNF, IFN, IL1B, and IL10, were identified as key targets for regulating endometrial receptivity. STP enhanced the expression of IL-10, IL-4, and IP-10 in the mice while reducing the expression levels of IL-2, IL-17, TNF-α, and IFN-γ in COH mice. These effects led to the modulation of early high expression of IL-1B and an improvement in endometrial receptivity. CONCLUSION: This study demonstrates that STP can modulate in-vivo immune factors throughout the COH process, subsequently restoring the immune equilibrium within the endometrium, thereby enhancing the endometrial receptivity in the COH model mice.