APTES and CTAB Synergistic Induce a Heterozygous CsPbBr3/Cs4PbBr6 Perovskite Composite and its Application on the Sensitive Fluorescent Detection of Iodide ions.

Recently, all-inorganic halide perovskite quantum dots (IPQD) as a new fluorescent material with excellent fluorescence properties have attracted wide attention. However, their instability in polar solvents is the main factor hindering their application in analysis. Herein, a heterozygous perovskite (CsPbBr3/Cs4PbBr6) was simultaneously prepared and stabilized by a silylanization strategy using (3-aminopropyl)-triethoxysilane (APTES) and cetyltrimethyl ammonium bromide (CTAB) assisted precipitation encapsulation method. The synthesized CsPbBr3/Cs4PbBr6 emitted an independent fluorescence at 520 nm. The obtained CsPbBr3/Cs4PbBr6 exhibited good stability in ethanol/water mixtures. It was used as a fluorescent probe for sensitively detecting iodide ions (I-) by fluorescence quenching mechanism in the concentration range of 1 ~ 70.0 µM with the detection limit (LOD) of 0.83 µM (relative standard deviation (RSD) = 1.33%, n = 20). The simplicity and high selectivity of the proposed fluorescent analysis method were the prominent features. This work could be extended to the other target ion detection by a perovskite fluorescent quenching.

Targeted activation of ferroptosis in colorectal cancer via LGR4 targeting overcomes acquired drug resistance.

Acquired drug resistance is a major challenge for cancer therapy and is the leading cause of cancer mortality; however, the mechanisms of drug resistance are diverse and the strategy to specifically target drug-resistant cancer cells remains an unmet clinical issue. Here, we established a colorectal cancer-derived organoid biobank and induced acquired drug resistance by repeated low-level exposures of chemo-agents. Chemosensitivity profiling and transcriptomic analysis studies revealed that chemoresistant cancer-derived organoids exhibited elevated expression of LGR4 and activation of the Wnt signaling pathway. Further, we generated a monoclonal antibody (LGR4-mAb) that potently inhibited LGR4-Wnt signaling and found that treatment with LGR4-mAb notably sensitized drug-induced ferroptosis. Mechanistically, LGR4-dependent Wnt signaling transcriptionally upregulated SLC7A11, a key inhibitor of ferroptosis, to confer acquired drug resistance. Our findings reveal that targeting of Wnt signaling by LGR4-mAb augments ferroptosis when co-administrated with chemotherapeutic agents, demonstrating a potential opportunity to fight refractory and recurrent cancers.

Do the stent blind insertion into the main portal vein (MPV) and stent diameter influence the surgical outcome of the transjugular intrahepatic portosystemic shunt (TIPS)?

Transjugular intrahepatic portosystemic shunt (TIPS) surgery is a clinical intervention to treat portal hypertension (PH) by deploying a covered stent to establish a shunt path for the portal vein (PV) system, and proper surgical strategy is of great importance to balance the shunt effect and the risk of complications. To understand the clinical strategies of the stent blind insertion and stent selection in clinic, this study investigated the effects of varying stent insertion positions and diameters on the PV hemodynamics and the shunt effect by computational fluid dynamics (CFD) analysis of five post-TIPS subjects. The results showed that the successful TIPS surgeries of the five PH subjects were confirmed by quantifying their pressure drops. The stent insertion positions at the main portal vein (MPV) slightly affected the clinically concerned hemodynamic indexes (i.e., MPV pressure, stent-outlet velocity) and the shunt index (SI). This indicated that the position of the stent going into the MPV may not need to be deliberately selected. Moreover, the covered stents with 6 mm and 8 mm diameters slightly influenced the hemodynamics as well, but the large-diameter stent better improved the shunt effect compared to the small-diameter one. Despite this, the 6 mm stent was suggested thanks to the higher risk of the hepatic encephalopathy (HE) observed in clinic, which indicated the excessive shunt of the 8 mm stent. The current work revealed the effects of different TIPS strategies on the surgical outcome, and could be useful for potential clinical practices.

Robot-assisted sacrohysteropexy vs robot-assisted sacrocolpopexy in women with primary advanced apical prolapse: A retrospective cohort study.

BACKGROUND: This study aimed to evaluate the anatomic and clinical outcomes of robot-assisted sacrohysteropexy (RASH) against robot-assisted sacrocolpopexy (RASC) for the treatment of primary advanced apical prolapse. METHODS: We conducted a retrospective cohort study of all robot-assisted pelvic organ prolapse surgeries for primary advanced apical prolapse (stage ≥II) between January 2011 and May 2021 at an academic tertiary hospital. Surgical outcomes and pelvic organ function were evaluated using the Pelvic Organ Prolapse Quantitative (POP-Q) stage and validated questionnaires (POPDI-6) during preoperative and postoperative 12-month follow-up evaluations. All data were obtained from electronic medical records. RESULTS: A total of 2368 women underwent surgery for apical prolapse repair, and 18 women underwent either RASH (n = 11) or RASC (n = 7). Compared to the RASC group, the RASH group was significantly younger, premenopausal, and less parous. Preoperative prolapse stage, operative time, estimated blood loss, and hospitalization length was comparable between the groups. No intraoperative complications were observed. All women had a median follow-up duration of 24 months (range: 12-108 months). During the 12-month follow-up period, women in the RASH group reported higher satisfaction with the surgery than those in the RASC group (100% vs. 71.4%, p = 0.137). The mesh exposure rate was significantly higher in the RASC group (3/7, 42.9%) than in the RASH group (0/11, 0%) ( p = 0.043), which was found at 12 to 36 months postoperatively and was successfully managed with vaginal estrogen cream. In the RASH group, one woman required reoperation with anterior colporrhaphy for recurrent anterior prolapse at 60 months postoperatively. The apical success rate was 100% at one year postoperatively, without apical recurrence in either group during the follow-up period. CONCLUSION: RASH represents an effective and feasible option for the surgical treatment of advanced primary apical prolapse in women who desire uterine preservation and have a significantly lower risk of mesh erosion than RASC.

O-GlcNAcylation regulates phagocytosis by promoting Ezrin localization at the cell cortex.

O-GlcNAcylation is a post-translational modification that serves as a cellular nutrient sensor and participates in multiple physiological and pathological processes. However, it remains uncertain whether O-GlcNAcylation is involved in the regulation of phagocytosis. Here, we demonstrate a rapid increase in protein O-GlcNAcylation in response to phagocytotic stimuli. Knockout of the O-GlcNAc transferase or pharmacological inhibition of O-GlcNAcylation dramatically blocks phagocytosis, resulting in the disruption of retinal structure and function. Mechanistic studies reveal that the O-GlcNAc transferase interacts with Ezrin, a membrane-cytoskeleton linker protein, to catalyze its O-GlcNAcylation. Our data further show that Ezrin O-GlcNAcylation promotes its localization to the cell cortex, thereby stimulating the membrane-cytoskeleton interaction needed for efficient phagocytosis. These findings identify a previously unrecognized role for protein O-GlcNAcylation in phagocytosis with important implications in both health and diseases.

Loss of Major Histocompatibility Complex Class I, CD8 + Tumor-infiltrating Lymphocytes, and PD-L1 Expression in Ovarian Clear Cell Carcinoma.

Ovarian clear cell carcinoma (OCCC), a chemoresistant ovarian cancer, shows a modest response to anti-programmed death-1/programmed death ligand-1 (PD-1/PD-L1) therapies. The effects of anti-PD-1/PD-L1 therapies rely on cytotoxic T-cell response, which is triggered by antigen presentation mediated by major histocompatibility complex (MHC) class I. The loss of MHC class I with simultaneous PD-L1 expression has been noted in several cancer types; however, these findings and their prognostic value have rarely been evaluated in OCCC. We collected data from 76 patients with OCCC for clinicopathologic analysis. Loss of MHC class I expression was seen in 44.7% of the cases including 39.3% to 47.4% of the PD-L1 + cases and was associated with fewer CD8 + tumor-infiltrating lymphocytes (TILs). PD-L1 positivity was associated with a higher number of CD8 + TILs. Cox proportional hazard models showed that high (≥50/mm 2 ) CD8 + TILs was associated with shorter disease-specific survival (hazard ratio [HR]=3.447, 95% confidence interval [CI]: 1.222-9.720, P =0.019) and overall survival (HR=3.053, 95% CI: 1.105-8.43, P =0.031). PD-L1 positivity using Combined Positive Score was associated with shorter progression-free survival (HR=3.246, 95% CI: 1.435-7.339, P =0.005), disease-specific survival (HR=4.124, 95% CI: 1.403-12.116, P =0.010), and overall survival (HR=4.489, 95% CI: 1.553-12.972, P =0.006). Loss of MHC class I may contribute to immune evasion and resistance to anti-PD-1/PD-L1 therapies in OCCC, and CD8 + TILs and PD-L1 positivity using Combined Positive Score may have a negative prognostic value.

Knockdown of TTC9 inhibits the proliferation, migration and invasion, but induces the apoptosis of lung adenocarcinoma cells.

Lung adenocarcinoma (LUAD) is one of the most commonly diagnosed subtypes of lung cancer, and one of the deadliest cancers. Tetratricopeptide repeat domain 9A (TTC9) is upregulated and has played an oncogenic role in some malignant tumors. However, the expression and role of TTC9 has not yet been elucidated in LUAD. Here, we investigated the expression profiles, biological functions and potential molecular mechanism of the TTC9 gene in LUAD. TTC9 expression was significantly overexpressed in LUAD tissues compared with that in normal lung tissues. TTC9 expression was closely correlated with gender, lymph node metastasis, and survival status in the TCGA-LUAD cohort. Subsequent cellular function assays demonstrated that knockdown of TTC9 promoted PC9 cell apoptosis and inhibited cell proliferation, migration and invasion, leading to cell cycle arrest in G2 phase. Moreover, inhibition of TTC9 suppressed the tumorigenicity of PC9 cells in nude mice. TTC9 might serve as oncogene in LUAD through cancer-related signaling pathways including p38 MAPK pathway. The expression of TTC9 gene might be modulated by DNA copy number variant and DNA methylation. TTC9 was significantly associated with tumor immune infiltration patterns. Accordingly, TTC9 may be a novel therapeutic target for the treatment of LUAD.

Overexpression of ERCC6L correlates with poor prognosis and confers malignant phenotypes of lung adenocarcinoma.

Excision repair cross­complementation group 6 like (ERCC6L) has been reported to be upregulated in a variety of malignant tumors and plays a critical oncogenic role. However, the role and molecular mechanism of ERCC6L in lung adenocarcinoma (LUAD) remain unclear, and were therefore investigated in the present study. Clinical data of patients with LUAD were obtained and bioinformatics analysis was performed to investigate the expression characteristics, prognostic value, and biological function of ERCC6L. In addition, cell function experiments were performed to detect the effect of ERCC6L silencing on the biological behavior of LUAD cells. The results revealed that ERCC6L expression was significantly higher in LUAD tissues vs. normal lung tissues and closely associated with nodal invasion, advanced clinical stage and survival in LUAD. Overexpression of ERCC6L was an independent prognostic biomarker of overall survival, progression­free interval, and disease­specific survival in patients with LUAD. DNA amplification and low methylation levels of ERCC6L suggested regulation at both the genetic and epigenetic levels. The most significant positive genes co­expressed with ERCC6L were mainly enriched in the cell cycle signaling pathway. The major functions of ERCC6L in LUAD cells were positively correlated with the cell cycle, DNA damage, DNA repair, proliferation, invasion and epithelial­mesenchymal transition (EMT). Knockdown of ERCC6L inhibited the proliferative, migratory and invasive abilities of A549 and PC9 cells. It also promoted cell apoptosis, and led to cell cycle arrest in the S phase. ERCC6L may regulate the EMT process through the Wnt/ß­catenin and Wnt/Notch 3 signaling pathways, thus regulating the tumorigenesis and progression of LUAD. The overexpression of ERCC6L may be a biological indicator for the diagnosis and prognosis of LUAD. ERCC6L may be a novel molecular target for the treatment of lung cancer.

A Multifunctional Vanadium-Iron-Oxide Nanoparticle Eradicates Hepatocellular Carcinoma via Targeting Tumor and Endothelial Cells.

Nanoparticles are widely used in biological research and cancer therapy. In hepatocellular carcinoma, several nanoplatforms have been synthesized and studied to improve the drug efficacy; however, these nanoplatforms are still insufficient to eradicate tumors. Herein, we have synthesized a novel vanadium (V)-iron-oxide (ION) nanoparticle (VIO) that combines chemodynamic, photothermal, and diagnostic capacities to enhance the tumor suppression effect in one agent with multiple functions. In the in vitro models, hepatocellular carcinoma cells are significantly inhibited by VIO-based nanoagents. The mechanistic study validates that VIO increases reactive oxygen species (ROS), which led to apoptosis and ferroptosis resulting in cell death. To our surprise, VIO targets not only tumor cells but also endothelial cells. In addition to inducing cell death, VIO also blocks tube formation and cell migration in human umbilical vein endothelial cell (HUVEC) and C166 models, indicating an antiangiogenic potential. In mouse tumor models, VIO retards tumor growth and induces apoptosis in tumor tissues. Furthermore, a significant blood vessel regression is seen in VIO-treated groups accompanied with larger necrotic areas. More interestingly, the activation of photothermal therapy completely eradicates tumor tissues. Taken together, this VIO nanoplatform could be a powerful anticancer candidate for nanodrug development.

Analysis of the expression, function and signaling of glycogen phosphorylase isoforms in hepatocellular carcinoma.

Glycogen phosphorylase (GP) is an essential enzyme for glycolysis via the glycogen degradation pathway. It consists of three isoforms: PYGB (brain form), PYGL (liver form) and PYGM (muscle form). Although the abnormal expression of GP is associated with a variety of tumors, its relationship with hepatocellular carcinoma (HCC) and whether it can be used as a prognostic marker of HCC remains unclear. In the present study, the expression levels of PYGB, PYGL and PYGM were analyzed. It was found that the expression levels of PYGB in tumor tissues were higher than those in normal tissues, particularly in HCC. The high expression of PYGB (hazard ratios=1.801; 95% confidence interval: 1.266-2.562) could predict the poor prognosis of HCC patients but not PYGL and PYGM. Inhibition of PYGB with GP inhibitor CP91149 significantly suppressed the HCC cell proliferation in the HCC cell model. In addition, combination treatment with sorafenib, a standard treatment for HCC, showed a great inhibition on tumor growth and angiogenesis. These findings suggested that PYGB may be used as a therapeutic and prognostic indicator for HCC.

Comparison of the O-RADS and ADNEX models regarding malignancy rate and validity in evaluating adnexal lesions.

OBJECTIVE: This study aimed to compare the ability of the O-RADS and ADNEX models to classify benign or malignant adnexal lesions. METHODS: This retrospective single-center study included women who underwent surgery for adnexal lesions. Two gynecologists independently categorized the adnexal lesions according to the O-RADS and ADNEX models. Four additional readers were included to validate the new quick-access O-RADS flowchart. RESULTS: Among the 322 patients included in this study, 264 (82.0%) had a benign diagnosis, and 58 (18.0%) had a malignant diagnosis. The malignant rates of O-RADS 2, O-RADS 3, O-RADS 4, and O-RADS 5 were 0%, 3.0%, 37.7%, and 78.9%, respectively. The AUC of the O-RADS in the 322 patients was 0.93. On comparing the O-RADS and ADNEX models in the remaining 281 patients, the AUCs of the O-RADS, ADNEX model with CA125, and ADNEX model without CA125 were 0.92, 0.95, and 0.94, respectively. When setting a uniform cutoff of ≥ 10% (≥ O-RADS 4) to predict malignancy, the O-RADS had higher sensitivity than the ADNEX model (96.6% vs. 91.4%), and relatively similar specificity. In addition, the readers with the quick-access flowchart spent less time categorizing O-RADS than the readers with only the original O-RADS table (mean analysis time: 99 min 15 s vs. 111 min 55 s). CONCLUSIONS: The O-RADS classification of the adnexal lesions as benign or malignant was comparable to that of the ADNEX model and had higher sensitivity at the 10% cutoff value. A quick-access O-RADS flowchart was helpful in O-RADS categorization and might shorten the analysis time. KEY POINTS: • Both O-RADS and ADNEX models had good diagnostic performance in distinguishing adnexal malignancy, and O-RADS had higher sensitivity than ADNEX model in uniform 10% cutoff to predict malignancy. • Quick-access O-RADS flowchart was developed to help review O-RADS classification and might help reduce the analysis time.

PgtE Enzyme of Salmonella enterica Shares the Similar Biological Roles to Plasminogen Activator (Pla) in Interacting With DEC-205 (CD205), and Enhancing Host Dissemination and Infectivity by Yersinia pestis.

Yersinia pestis, the cause of plague, is a newly evolved Gram-negative bacterium. Through the acquisition of the plasminogen activator (Pla), Y. pestis gained the means to rapidly disseminate throughout its mammalian hosts. It was suggested that Y. pestis utilizes Pla to interact with the DEC-205 (CD205) receptor on antigen-presenting cells (APCs) to initiate host dissemination and infection. However, the evolutionary origin of Pla has not been fully elucidated. The PgtE enzyme of Salmonella enterica, involved in host dissemination, shows sequence similarity with the Y. pestis Pla. In this study, we demonstrated that both Escherichia coli K-12 and Y. pestis bacteria expressing the PgtE-protein were able to interact with primary alveolar macrophages and DEC-205-transfected CHO cells. The interaction between PgtE-expressing bacteria and DEC-205-expressing transfectants could be inhibited by the application of an anti-DEC-205 antibody. Moreover, PgtE-expressing Y. pestis partially re-gained the ability to promote host dissemination and infection. In conclusion, the DEC-205-PgtE interaction plays a role in promoting the dissemination and infection of Y. pestis, suggesting that Pla and the PgtE of S. enterica might share a common evolutionary origin.

Role of Slit/Robo Signaling pathway in Bone Metabolism.

Slit/Robo signals were initially found to play an essential role in nerve development as axonal guidance molecules. In recent years, with in-depth study, the role of Slit/Robo in other life activities, such as tumor development, angiogenesis, cell migration, and bone homeostasis, has gradually been revealed. Bone is an organ with an active metabolism. Bone resorption and bone formation are closely related through precise spatiotemporal coordination. There is much evidence that slit, as a new bone coupling factor, can regulate bone formation and resorption. For example, Slit3 can promote bone formation and inhibit bone resorption through Robo receptors, which has excellent therapeutic potential in metabolic bone diseases. Although the conclusions of some studies are contradictory, they all affirm the vital role of Slit/Robo signaling in regulating bone metabolism. This paper reviews the research progress of Slit/Robo signaling in bone metabolism, briefly discusses the contradictions in the existing research, and puts forward the research direction of Slit/Robo in the field of bone metabolism in the future.

Maintenance Therapy for Preventing Endometrioma Recurrence after Endometriosis Resection Surgery - A Systematic Review and Network Meta-analysis.

OBJECTIVE: To evaluate the efficacy of different hormone therapies in preventing postoperative endometrioma recurrence. DATA SOURCES: The MEDLINE, COCHRANE, and Embase electronic databases were searched from inception to 30 April 2021. METHODS OF STUDY SELECTION: Randomized controlled trials (RCTs) or cohort studies including reproductive age women with endometriosis undergoing ovarian cystectomy or excision of endometriotic lesions compared the effects of postoperative adjuvant therapy (gonadotropin-releasing hormone agonist [GnRHa]) and postoperative maintenance hormone interventions for more than 1 year (i.e., oral contraceptive pills [OCPs], dienogest [DNG], levonorgestrel-releasing intrauterine system [LNGIUS]) on endometrioma recurrence. TABULATION, INTEGRATION, AND RESULTS: Data collection and analysis of the data were independently performed 2 two reviewers. A total of 11 studies were included, of which 2 were RCTs, and 9 were cohort studies. There were 2394 patients with 6 interventions (cases: 1665, 69.6%) and expectant management (cases: 729, 30.4%). Relative treatment effects were estimated using network meta-analysis and ranked in descending order. The clinical effectiveness of these drugs (vs expectant management) was as follows: GnRHa plus DNG (odds ratio [OR], 0.04; 95% confidence interval [CI], 0.01-0.27), surface under the cumulative ranking (SUCRA) = 94.0; DNG (OR, 0.11; 95% CI, 0.04-0.32), SUCRA = 69.7; GnRHa plus OCP (OR, 0.12; 95% CI, 0.02-0.64), SUCRA = 63.4; GnRHa plus LNGIUS (OR, 0.13; 95% CI, 0.03-0.66), SUCRA = 59.4; and OCP (OR, 0.21; 95% CI, 0.13-0.36), SUCRA = 43.6. The effectiveness of GnRHa (OR, 0.47; 95% CI, 0.12-1.89), SUCRA = 17.3 was not significantly different from that of controls. CONCLUSION: In network meta-analysis, combined postoperative adjuvant therapy and longer maintenance hormone treatment are better than a single agent in preventing postoperative endometrioma recurrence. GnRHa plus DNG maintenance treatment might be the most effective intervention. Large-scale RCTs of these agents are still required.

Synergistic therapeutic effect of low-dose bevacizumab with cisplatin-based chemotherapy for advanced or recurrent cervical cancer.

BACKGROUND: Cisplatin-based chemotherapy (CBC) is highly efficacious for advanced cervical cancer; its efficacy can be enhanced by combining with 15 mg/kg (standard dose) bevacizumab (BEV). However, this standard dose is associated with various adverse events (AEs). Therefore, in this retrospective study, we analyzed the survival outcomes and AEs in patients with advanced or recurrent cervical cancer treated with CBC in combination with BEV 7.5 mg/kg. METHODS: Registered patient data were retrieved between October 2014 and September 2019, and 64 patients with advanced or recurrent cervical cancer treated with CBC + BEV (n = 21) or CBC alone (n = 43) were analyzed. The primary endpoints were progression-free survival (PFS) and overall survival (OS); the secondary endpoints were the frequency and severity of AEs. The Cox proportional-hazards model was applied to explore prognostic factors associated with PFS and OS. RESULTS: The 1-, 2-, and 3-year PFS rates (95% CI) were 36.24% (22.0-50.5), 20.7% (9.8-34.2), and 17.7% (7.7-31.1) for the CBC group; and 71.4% (47.1-86.0), 51.0% (27.9-70.1), and 51.0% (27.9-70.1) for the CBC + BEV group, respectively. The 1-, 2-, and 3-year OS rates were 62.6% (46.4-75.18), 32.4% (18.8-46.9), and 23.2% (11.2-37.6) for the CBC group; and 85.7% (61.9-95.1), 66.6% (42.5-82.5), and 55.5% (27.1-76.7) for the CBC + BEV group, respectively. The CBC + BEV group presented higher PFS and OS rates, p = 0.003 and p = 0.005, respectively. Proteinuria (6 vs 9, p = 0.025) and hypertension (0 vs 10, p < 0.001) were less common, but anemia was more common in the CBC group (35 vs 11, p = 0.021). CONCLUSION: Overall, CBC + BEV significantly improved the PFS and OS compared with CBC alone. CBC + BEV also prevents severe AEs and hence is an efficacious and safe therapeutic option.

Clinical Presentation and Management of Endometriosis-Related Hemorrhagic Ascites: A Case Report and Systematic Review of the Literature.

This study aims to analyze the patient profile and presentation of endometriosis-related hemorrhagic ascites and review its management to raise awareness among gynecologists and improve treatment strategies. We present a case report and engage in a systematic review involving human cases of histologically proven endometriosis with hemorrhagic ascites. Keywords were searched in PubMed/MEDLINE, Cochrane Library, EMBASE, and Ovid Discovery databases from inception until December 2018. Studies that did not include a description of ascites or histopathologic results confirming endometriosis or those that involved patients with other conditions that may contribute to ascites were excluded. The review yielded 73 articles describing 84 premenopausal women with histologically proven endometriosis-related hemorrhagic ascites. Of note, 83% (65/78) of the patients were nulliparous and 69.35% (43/62) were of African descent. The most common chief complaint was abdominal enlargement (58.33%, 49/84) but a host of other symptoms were also reported. Pleural effusion was reported in 32.14% (27/84), and elevated CA-125 was seen in 74.42% (32/43). The majority (64.29%, 54/84) of the patients underwent laparotomy, and an increasing trend of minimally invasive surgical approaches (p<0.001) and fertility-sparing techniques (p<0.001) was observed. The mean ascites volume was 4228.27 mL (SD: 2625.66). Moderate to severe endometriosis was seen in 97.44% (76/78) of cases. The majority of the patients who received medical treatment were given gonadotropin-releasing hormone (GnRH) agonists (63.79%, 37/58). The rate of recurrence after termination or suppression of ovarian function was 8.33% (7/84), and there was a mortality rate of 1.19% (1/84). Diagnosis of endometriosis-related hemorrhagic ascites may be challenging because it mimics several disease entities that cause ascites, thereby warranting a heightened clinical suspicion. Minimally invasive techniques are usually employed to establish a histologic diagnosis. The prevention of recurrence involves the recognition of endometriosis-related hemorrhagic ascites as a manifestation of severe endometriosis, which should prompt therapies directed at suppressing ovarian function. Since affected women are of childbearing age, ovary-preserving surgeries are generally preferred. The rate of recurrence is low after appropriate surgical and medical interventions.

An Insight Into Intestinal Microbiota of Spontaneously Hypertensive Rats After Valsartan Administration.

It has been proven a close relationship between intestinal microbiota and hypertension. Valsartan is a widely used ARB antihypertensive drug; so far, the effect of valsartan on intestinal microbiota remains largely unexplored. Herein, we evaluated the composition, structure and metabolites of intestinal microbiota of spontaneously hypertensive rats (SHRs) after valsartan administration. In the present study, valsartan administration decreased intestinal microbiota diversity, altered gut microbiota composition, leading to 192 unique OTUs deficiency (vs WKY rats) and 10 unique OTUs deficiency (vs SHRs) and did not prove impaired intestinal mucosal barriers. Valsartan decreased the production of isobutyric acid and isovaleric acid in SCFAs. Our findings revealed valsartan administration induced far-reaching and robust changes to the intestinal microbiota of SHRs and provided a better understanding of the relationship between efficacy of valsartan and gastrointestinal tract reaction.

Loss of the virulence plasmid by Shigella sonnei promotes its interactions with CD207 and CD209 receptors.

Introduction. Shigella sonnei, the cause of bacillary dysentery, belongs to Gram-negative enteropathogenic bacteria. S. sonnei contains a 210 kb virulence plasmid that encodes an O-antigen gene cluster of LPSs. However, this virulence plasmid is frequently lost during replication. It is well-documented that after losing the O-antigen and becoming rough strains, the Gram-negative bacteria may express an LPS core on its surface. Previous studies have suggested that by using the LPS core, Gram-negative bacteria can interact with several C-type lectin receptors that are expressed on antigen-presenting cells (APCs).Hypothesis/Gap Statement. S. sonnei by losing the virulence plasmid may hijack APCs via the interactions of LPS-CD209/CD207.Aim. This study aimed to investigate if the S. sonnei rough strain, by losing the virulence plasmid, interacted with APCs that express C-type lectins of human CD207, human CD209a and mouse CD209b.Methodology. SDS-PAGE silver staining was used to examine the O-antigen expression of S. sonnei WT and its rough strain. Invasion assays and inhibition assays were used to examine the ability of S. sonnei WT and its rough strain to invade APCs and investigate whether CD209 and CD207 are receptors for phagocytosis of rough S. sonnei. Animal assays were used to observe the dissemination of S. sonnei.Results. S. sonnei did not express O-antigens after losing the virulence plasmid. The S. sonnei rough strain invades with APCs, including human dendritic cells (DCs) and mouse macrophages. CD209 and CD207 are receptors for phagocytosis of rough S. sonnei. Expression of the O-antigen reduces the ability of the S. sonnei rough strain to be disseminated to mesenteric lymph nodes and spleens.Conclusion. This work demonstrated that S. sonnei rough strains - by losing the virulence plasmid - invaded APCs through interactions with CD209 and CD207 receptors.

Infection-associated Hemophagocytic Syndrome in Critically Ill Patients with COVID-19.

Infection-associated hemophagocytic syndrome (IAHS), a severe complication of various infections, is potentially fatal. This study aims to determine whether IAHS occurs in critically ill patients with coronavirus disease 2019 (COVID-19). We conducted a retrospective observational study on 268 critically ill patients with COVID-19 between February 1st, 2020 and February 26th, 2020. Demographics, clinical characteristics, laboratory results, information on concurrent treatments and outcomes were collected. A diagnosis of secondary hemophagocytic lymphohistiocytosis (sHLH) was made when the patients had an HScore greater than 169. Histopathological examinations were performed to confirm the presence of hemophagocytosis. Of 268 critically ill patients with confirmed SARS-CoV-2 infection, 17 (6.3%) patients had an HScore greater than 169. All the 17 patients with sHLH died. The interval from the onset of symptom of COVID-19 to the time of a diagnosis of sHLH made was 19 days and the interval from the diagnosis of sHLH to death was 4 days. Ten (59%) patients were infected with only SARS-CoV-2. Hemophagocytosis in the spleen and the liver, as well as lymphocyte infiltration in the liver on histopathological examinations, was found in 3 sHLH autopsy patients. Mortality in sHLH patients with COVID-19 is high. And SARS-CoV-2 is a potential trigger for sHLH. Prompt recognition of IAHS in critically ill patients with COVID-19 could be beneficial for improving clinical outcomes.

Expression of eosinophil in peripheral blood of patients with COVID-19 and its clinical significance.

AIMS: To investigate the eosinophil cell (EC) expression in peripheral blood of patients infected with severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) and its clinical significance of diagnosis and prognosis. METHODS: 95 patients, whose nucleic acid test of SARS-CoV-2 was positive to make a definite diagnosis of COVID-19, were selected as the study group. They were admitted at the Chengdu Public Health Clinical Medical Center from January 21 to March 2, 2020. Another 95 healthy subjects and 95 non-infectious fever patients during the same period were selected as the control group. The BC-6900 blood cell analyzer was used to continuously observe and detect ECs in 95 patients with COVID-19 and the control group. The differences in expression levels of ECs in peripheral blood were analyzed. RESULTS: ECs were significantly decreased in 95 (75.8%) COVID-19 patients (P < .01). The absolute EC count IQR was 0.01 × 109/L (0 × 109/L - 0.04 × 109/L), and the EC percentage IQR was 0.3% (0.1% - 0.8%). As the patients' condition improved, the ECs returned to normal, but for those without improvement, ECs continued to decline. CONCLUSIONS: ECs decreased remarkably in patients with COVID-19, and gradually returned to normal after the improvement of the patients' condition, while EC continued to decrease in patients without improvement. It is suggested that ECs have certain clinical significance in the diagnosis and prognosis of COVID-19, and may be a useful index in the early warning of acute infectious diseases.