Voacangine protects hippocampal neuronal cells against oxygen-glucose deprivation/reoxygenation-caused oxidative stress and ferroptosis by activating the PI3K-Akt-FoxO signaling.

Voacangine, a naturally occurring alkaloid, has been testified to display beneficial effects on a variety of human diseases, but its role in ischemic stroke is unclear. The impacts of voacangine on oxygen-glucose deprivation/reoxygenation (OGD/R)-tempted hippocampal neuronal cells are investigated. The bioinformatics analysis found that voacangine is a bioactive ingredient that may have good effects on ischemic stroke. KEGG pathways analysis found that voacangine may regulate ischemic stroke through modulating the PI3K-Akt-FoxO signaling pathway. Voacangine could mitigate OGD/R-tempted cytotoxicity in HT22 cells. Voacangine mitigated OGD/R-tempted oxidative stress in HT22 cells by diminishing reactive oxygen species level and enhancing superoxide dismutase level. Voacangine mitigated OGD/R-tempted ferroptosis in HT22 cells. Voacangine promoted activation of the PI3K-Akt-FoxO signaling in OGD/R-induced HT22 cells. Inactivation of the PI3K-Akt-FoxO signaling pathway reversed the protective effects of voacangine against OGD/R-tempted oxidative stress, cytotoxicity, and ferroptosis in HT22 cells. In conclusion, voacangine protects hippocampal neuronal cells against OGD/R-caused oxidative stress and ferroptosis by activating the PI3K-Akt-FoxO signaling.

Mechanism and potential contributing factors to temporomandibular joint osteoarthritis.

OBJECTIVE: To investigate the mechanism of and potential contributing factors to temporomandibular joint osteoarthritis (TMJOA) caused by oestrogen deficiency with a persistent high bite force. MATERIALS AND METHODS: A TMJOA model was generated by subjecting 6-week-old female rats to ovariectomy (OVX) and feeding them a hard feed. The rats (n = 12/group) were divided into sham (control); OVX; OVX+hard feed (HF); OVX+hard feed+local-joint injection of 17ß-oestradiol (an oestrogen) (E2); and OVX+hard feed+local-joint injection of rapamycin (an autophagy activator) (RAPA)groups. Condyles were stained with haematoxylin-eosin and Safranin O Fast Green. The expression of Beclin 1, LC3 and p-mTOR in condylar cartilages was analysed. RESULTS: Tissue staining revealed thinner condylar cartilage, varying numbers or fewer hypertrophic chondrocytes, and lower proteoglycan content in the cartilage matrix of the OVX group. These characteristics were more pronounced in the HF group, but were significantly recovered in the E2 and RAPA groups. Immunohistochemical staining revealed significantly lower autophagic flux in OVX/HF groups and a higher one in E2/RAPA groups. CONCLUSIONS: A persistent high bite force could aggravate TMJOA induced by oestrogen deficiency, and the application of oestrogen or rapamycin could delay its progression. Additionally, autophagy may play a role in the development of TMJOA.

Cognitive dysfunction in a patient with migraine and APT1A2 mutation: a case report.

BACKGROUND: Hemiplegic migraine (HM) is a rare type of migraine with aura. Some reports have described the clinical manifestations in HM patients with the ATP1A2 mutation. But the impact of the ATP1A2 mutation on cognitive profile in HM patients has not been evaluated in detail. Here we report a patient with cognitive dysfunction in specific area. CASE PRESENTATION: A 15-year-old boy with an aura that included disturbances in consciousness, associated with fever, vomiting, hemiplegia, and aphasia. He was diagnosed with HM with the ATP1A2 mutation before. He had trouble in mathematics and depicting three-dimensional things. CONCLUSIONS: The HM with ATP1A2 patient could develop permanent cognitive dysfunction. Therefore, the cognitive quotient should be carefully and comprehensively evaluated.

Characterization of a cytolytic-like gene from the aphid-obligate fungal pathogen Conidiobolus obscurus.

Cytolytic (Cyt)-like genes are known by omics analyses to exist widely in bacterial and fungal pathogens, but their insecticidal activities in fungi remains unknown. A full-length coding sequence of a Cyt-like gene was first amplified from Conidiobolus obscurus (an obligate aphid-pathogenic fungus) through RACE (rapid-amplification of cDNA ends). The deduced protein structure was structurally characterized by a single Cyt-typical α/ß domain. The expression level of the Cyt-like gene in conidia correlated well with the fungal virulence against aphids (r2 = 0.97). The results demonstrate the Cyt-like gene acts as an important virulence factor of C. obscurus against aphids, and has potential for exploitation in aphid control.

Inhibition of WNT signaling in the bone marrow niche prevents the development of MDS in the Apcdel/+ MDS mouse model.

There is accumulating evidence that functional alteration(s) of the bone marrow (BM) microenvironment contribute to the development of some myeloid disorders, such as myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). In addition to a cell-intrinsic role of WNT activation in leukemia stem cells, WNT activation in the BM niche is also thought to contribute to the pathogenesis of MDS and AML. We previously showed that the Apc-haploinsufficient mice (Apcdel/+ ) model MDS induced by an aberrant BM microenvironment. We sought to determine whether Apc, a multifunctional protein and key negative regulator of the canonical ß-catenin (Ctnnb1)/WNT-signaling pathway, mediates this disease through modulating WNT signaling, and whether inhibition of WNT signaling prevents the development of MDS in Apcdel/+ mice. Here, we demonstrate that loss of 1 copy of Ctnnb1 is sufficient to prevent the development of MDS in Apcdel/+ mice and that altered canonical WNT signaling in the microenvironment is responsible for the disease. Furthermore, the US Food and Drug Administration (FDA)-approved drug pyrvinium delays and/or inhibits disease in Apcdel/+ mice, even when it is administered after the presentation of anemia. Other groups have observed increased nuclear CTNNB1 in stromal cells from a high frequency of MDS/AML patients, a finding that together with our results highlights a potential new strategy for treating some myeloid disorders.

A novel mechanism of action for salidroside to alleviate diabetic albuminuria: effects on albumin transcytosis across glomerular endothelial cells.

Salidroside (SAL) is a phenylethanoid glycoside isolated from the medicinal plant Rhodiola rosea. R. rosea has been reported to have beneficial effects on diabetic nephropathy (DN) and high-glucose (HG)-induced mesangial cell proliferation. Given the importance of caveolin-1 (Cav-1) in transcytosis of albumin across the endothelial barrier, the present study was designed to elucidate whether SAL could inhibit Cav-1 phosphorylation and reduce the albumin transcytosis across glomerular endothelial cells (GECs) to alleviate diabetic albuminuria as well as to explore its upstream signaling pathway. To assess the therapeutic potential of SAL and the mechanisms involved in DN albuminuria, we orally administered SAL to db/db mice, and the effect of SAL on the albuminuria was measured. The albumin transcytosis across GECs was explored in a newly established in vitro cellular model. The ratio of albumin to creatinine was significantly reduced upon SAL treatment in db/db mice. SAL decreased the albumin transcytosis across GECs in both normoglycemic and hyperglycemic conditions. SAL reversed the HG-induced downregulation of AMP-activated protein kinase and upregulation of Src kinase and blocked the upregulation Cav-1 phosphorylation. Meanwhile, SAL decreased mitochondrial superoxide anion production and moderately depolarized mitochondrial membrane potential. We conclude that SAL exerts its proteinuria-alleviating effects by downregulation of Cav-1 phosphorylation and inhibition of albumin transcytosis across GECs. These studies provide the first evidence of interference with albumin transcytosis across GECs as a novel approach to the treatment of diabetic albuminuria.

Cell intrinsic and extrinsic factors synergize in mice with haploinsufficiency for Tp53, and two human del(5q) genes, Egr1 and Apc.

Therapy-related myeloid neoplasms (t-MN) are a late complication of the successful use of cytotoxic therapy for patients with cancer. A heterozygous deletions of the long arm of chromosome 5 [del(5q)], observed in 40% of patients, is associated with prior exposure to alkylating agents, and a high frequency of TP53 loss or mutation. In previous studies, we demonstrated that haploinsufficiency of 2 del(5q) genes, Egr1, and Apc, individually play a role in the pathogenesis of hematologic disease in mice. We now show that loss of one copy of Egr1 or Tp53 in an Apc haploinsufficient background (Apc (del/+)) accelerated the development of a macrocytic anemia with monocytosis, early features of t-MN. The development of anemia was significantly accelerated by treatment of mice with the alkylating agent, N-ethyl-N-nitrosourea (ENU), regardless of the levels of expression of Egr1 and Tp53. Transplantation of either wild type; Egr1(+/-); Tp53(+/-); Apc(del/+); or Egr1(+/-), Apc(del/+) bone marrow cells into lethally irradiated Apc(del/+) recipients resulted in rapid development of anemia that was further accelerated by administration of ENU to recipients, demonstrating that the Apc(del/+)-induced anemia was cell extrinsic and potentiated by ENU mutagenesis. These data emphasize the synergistic role of cell intrinsic and cell extrinsic (microenvironment) factors in the pathogenesis of t-MN, and raise awareness of the deleterious effects of cytotoxic therapy on the stromal microenvironment.

Haploinsufficiency of del(5q) genes, Egr1 and Apc, cooperate with Tp53 loss to induce acute myeloid leukemia in mice.

An interstitial deletion of chromosome 5, del(5q), is the most common structural abnormality in primary myelodysplastic syndromes (MDS) and therapy-related myeloid neoplasms (t-MNs) after cytotoxic therapy. Loss of TP53 activity, through mutation or deletion, is highly associated with t-MNs with a del(5q). We previously demonstrated that haploinsufficiency of Egr1 and Apc, 2 genes lost in the 5q deletion, are key players in the progression of MDS with a del(5q). Using genetically engineered mice, we now show that reduction or loss of Tp53 expression, in combination with Egr1 haploinsufficiency, increased the rate of development of hematologic neoplasms and influenced the disease spectrum, but did not lead to overt myeloid leukemia, suggesting that altered function of additional gene(s) on 5q are likely required for myeloid leukemia development. Next, we demonstrated that cell intrinsic loss of Tp53 in hematopoietic stem and progenitor cells haploinsufficient for both Egr1 and Apc led to the development of acute myeloid leukemia (AML) in 17% of mice. The long latency (234-299 days) and clonal chromosomal abnormalities in the AMLs suggest that additional genetic changes may be required for full transformation. Thus, loss of Tp53 activity in cooperation with Egr1 and Apc haploinsufficiency creates an environment that is permissive for malignant transformation and the development of AML.

[Evaluation of therapeutic effect of children's dental treatment under general anesthesia: 111 cases report].

OBJECTIVE: To retrospectively evaluate the efficiency of dental treatment under general anesthesia (GA) in child patients, and analyze the related factors. METHODS: The records of patients treated under GA in the Department of Pediatric Dentistry, Peking University School and Hospital of Stomatology, between Aug 2008 and Jun 2012 were collected and analyzed. Two hundred and twenty eight records were found, of which 111 patients under 18 years old who were recalled more than 3 months after GA were selected randomly. The unplanned treatments including caries, failed restoration, root canal treatment and space maintenance fall-off etc. were recorded and analyzed. The survival rate and median survival time of the teeth were calculated, and a multivariate analysis was performed by Cox proportional hazard model. RESULTS: Totally, there were 1 415 teeth treated under GA. The median survival time was 825 days, 77.0% of the teeth were present during their recall period. The median time of the first unplanned treatment was 215 days, and the failed restoration was the main reason for the unplanned treatment. Other factors such as the age at treatment, gender, total number of decayed teeth, reason for GA, and living place were found unassociated with the survival rate. CONCLUSION: The effect of dental treatment under GA is satisfied. Regular dental visit after GA is very important for children's dental health.

Successful Treatment of Switching EGFR-TKIs for Advanced Lung Adenocarcinoma Due to Interstitial Lung Disease: A Case Report.

INTRODUCTION: Icotinib and almonertinib are efficacious for non-small cell lung cancer (NSCLC) factor patients with epidermal growth receptor (EGFR)-mutation. Patients who previously used EGFR tyrosine kinase inhibitor (EGFR TKI) may switch to another one due to the adverse events. CASE PRESENTATION: Here, we report a case of a 73-year-old male patient with advanced lung adenocarcinoma in which an EGFR (exon 21 L858R substitution) was found. Icotinib (125mg three times daily) was administered initially. He achieved partial response two months later but developed acute interstitial lung disease (grade 2) with dry cough and chest tightness five months later. Icotinib was discontinued, and treatment with methylprednisolone improved the interstitial lung disease. Chemotherapy with pemetrexed, carboplatin, and bevacizumab was initiated as subsequent therapy. Considering the effectiveness of EGFR-TKIs, we decided cautiously to rechallenge the third-generation TKI almonertinib administration. The patient successfully received almonertinib for almost one year without the recurrence of interstitial lung disease and tumor progression. ILD was an infrequent but often life-threatening reaction associated with icotinib. CONCLUSION: This is the first reported case of successful switching from icotinib to another EGFR TKI because of interstitial lung disease associated with icotinib, suggesting that EGFR-TKIs rechallenge because of adverse events rather than progression might provide a significant benefit in patients with EGFR driver positive NSCLC.

Construction and expression of Mycobacterium tuberculosis fusion protein SHR3 and its immunogenicity analysis in combination with various adjuvants.

Tuberculosis (TB) today remains the leading cause of global deaths due to infectious bacterial pathogens. The Bacillus Calmette-Guérin (BCG) vaccine is the only vaccine clinically used to prevent TB. However, its limitations in preventing latent infection and TB reactivation mean that it does not provide comprehensive protection. In this study, we successfully constructed and expressed the multistage fusion protein, SHR3, and used whole blood IFN-γ release assay (WBIA) with flow cytometry to detect antigen specificity, further confirmed by enzyme-linked immunosorbent assay (ELISA). SHR3 and its subfractional proteins stimulated the level of IFN-γ production by lymphocytes from M. tb-infected patients, inducing the production of single-positive and double-positive CD4+ and CD8+ T cells with IFN-γ and IL-2, at levels significantly higher than those of healthy controls. The fusion protein and complex adjuvant group (SHR3/DMT) induced mice to produce significantly higher levels of IgG antibodies and their subclasses, with IgG2a/IgG1 results showing a convergent Th1-type response; mice in the BCG + SHR3/DMT group induced secretion of the highest levels of IL-2, and TNF-α, irrespective of stimulation with purified protein derivative or SHR3. These findings suggest that SHR3/DMT could be a potential subunit vaccine candidate that may serve as an effective booster vaccine after BCG primary immunization.

Construction of direct Z-scheme Co9S8/CdS with tubular heterostructure through the simultaneous immobilization and in-situ reduction strategy for enhanced photocatalytic Cr(VI) reduction under visible light.

Tubular Co9S8/CdS heterostructures have been successfully synthesized by in-situ growing CdS onto Co9S8 nanotubes through a simultaneous immobilization and in-situ reduction strategy. It turned out that the so-obtained heterostructure with Co9S8/CdS molar ratio of 1/10 can display a broad light absorption edge and especially much enhanced capacity for photocatalytic reduction of Cr(VI) under visible light. The characterization analysis and experimental results suggested that an interfacial electrostatic field between Co9S8 and CdS elements in the heterostructure could be constructed due to their different Fermi levels, allowing for more quantities of highly reductive electrons to participate in the photocatalytic reaction. Therefore, the so-obtained Co9S8/CdS (1/10) heterostructures could achieve the photocatalytic reduction efficiency of 100% within 20 min, which was more than two and four times larger than that of pristine CdS and Co9S8, respectively. Moreover, the possible photocatalytic reaction mechanism for reducing Cr(VI) was investigated and found to follow the direct Z-scheme charge transfer pathway. This novel fabrication route for composite photocatalysts with tubular heterostructures could lead to the widespread implementations for the elimination of various harmful pollutants in the process of environmental governance.

Explainable coronary artery disease prediction model based on AutoGluon from AutoML framework.

Objective: This study focuses on the innovative application of Automated Machine Learning (AutoML) technology in cardiovascular medicine to construct an explainable Coronary Artery Disease (CAD) prediction model to support the clinical diagnosis of CAD. Methods: This study utilizes a combined data set of five public data sets related to CAD. An ensemble model is constructed using the AutoML open-source framework AutoGluon to evaluate the feasibility of AutoML in constructing a disease prediction model in cardiovascular medicine. The performance of the ensemble model is compared against individual baseline models. Finally, the disease prediction ensemble model is explained using SHapley Additive exPlanations (SHAP). Results: The experimental results show that the AutoGluon-based ensemble model performs better than the individual baseline models in predicting CAD. It achieved an accuracy of 0.9167 and an AUC of 0.9562 in 4-fold cross-bagging. SHAP measures the importance of each feature to the prediction of the model and explains the prediction results of the model. Conclusion: This study demonstrates the feasibility and efficacy of AutoML technology in cardiovascular medicine and highlights its potential in disease prediction. AutoML reduces the barriers to model building and significantly improves prediction accuracy. Additionally, the integration of SHAP enhances model transparency and explainability, which is critical to ensuring model credibility and widespread adoption in cardiovascular medicine.

Prediction model of malnutrition in hospitalized patients with acute stroke.

OBJECTIVE: The prognosis of stroke patients is greatly threatened by malnutrition. However, there is no model to predict the risk of malnutrition in hospitalized stroke patients. This study developed a predictive model for identifying high-risk malnutrition in stroke patients. METHODS: Stroke patients from two tertiary hospitals were selected as the objects. Binary logistic regression was used to build the model. The model's performance was evaluated using various metrics including the receiver operating characteristic curve, Hosmer-Lemeshow test, sensitivity, specificity, Youden index, clinical decision curve, and risk stratification. RESULTS: A total of 319 stroke patients were included in the study. Among them, 27% experienced malnutrition while in the hospital. The prediction model included all independent variables, including dysphagia, pneumonia, enteral nutrition, Barthel Index, upper arm circumference, and calf circumference (all p < 0.05). The AUC area in the modeling group was 0.885, while in the verification group, it was 0.797. The prediction model produces greater net clinical benefit when the risk threshold probability is between 0% and 80%, as revealed by the clinical decision curve. All p values of the Hosmer test were > 0.05. The optimal cutoff value for the model was 0.269, with a sensitivity of 0.849 and a specificity of 0.804. After risk stratification, the MRS scores and malnutrition incidences increased significantly with escalating risk levels (p < 0.05) in both modeling and validation groups. CONCLUSIONS: This study developed a prediction model for malnutrition in stroke patients. It has been proven that the model has good differentiation and calibration.

Sunvozertinib for patients in China with platinum-pretreated locally advanced or metastatic non-small-cell lung cancer and EGFR exon 20 insertion mutation (WU-KONG6): single-arm, open-label, multicentre, phase 2 trial.

BACKGROUND: Sunvozertinib is an oral, irreversible, and selective tyrosine kinase inhibitor that has a favourable safety profile and encouraging antitumour activity, as shown in phase 1 studies of patients with heavily pretreated non-small cell lung cancer (NSCLC) with EGFR exon 20 insertion mutation (exon20ins). We aimed to assess the antitumour efficacy of sunvozertinib in patients with platinum-pretreated locally advanced or metastatic NSCLC with EGFR exon20ins. METHODS: WU-KONG6 is a single-group, open-label, multicentre phase 2 trial of sunvozertinib monotherapy, conducted across 37 medical centres in China. We enrolled adult patients with pathologically or cytologically confirmed locally advanced or metastatic NSCLC whose tumour tissue carried an EGFR exon20ins mutation. All patients had received at least one line of previous systemic therapy, with at least one line containing platinum-based chemotherapy. The primary endpoint was objective response rate (ORR), as assessed by the independent review committee. The ORR was defined as the percentage of patients who achieved complete or partial response, confirmed by two separate assessments with at least 4-week time interval, until disease progression or initiation of any new anti-cancer therapy. Enrolled patients received sunvozertinib 300 mg once daily until meeting discontinuation criteria per the protocol. Patients who received at least one dose of treatment and were evaluable for efficacy analysis were included in the primary analysis, and all patients who received at least one dose of treatment were included in the safety analysis. This study is registered with ChinaDrugTrials.org, CTR20211009, and ClinicalTrials.gov, NCT05712902, and efficacy and safety follow-up are ongoing. FINDINGS: Between July 19, 2021, and May 6, 2022, 104 patients were enrolled. At data cutoff (Oct 17, 2022), the last enrolled patient had been followed up for about 6 months. Among 97 patients evaluable for efficacy analysis, 59 (61%) patients achieved tumour response, with a confirmed ORR of 61% (95% CI 50-71). All tumour responses were partial responses. Tumour responses were observed irrespective of age, sex, smoking history, EGFR exon20ins subtypes, brain metastasis at baseline, previous lines of therapy, and history of onco-immunotherapy. In total, 19 death events occurred over a median follow-up period of 7·6 months (IQR 6·1-9·4). Sunvozertinib was well tolerated at 300 mg once daily. The most common grade 3 or worse treatment-related adverse events were blood creatine phosphokinase increased (18 [17%] of 104), diarrhoea (eight [8%]), and anaemia (six [6%]). The most common serious treatment-related adverse events were interstitial lung disease (five [5%] of 104), anaemia (three [3%]), vomiting (two [2%]), nausea (two [2%]) and pneumonia (two [2%]). INTERPRETATION: In this phase 2 study, sunvozertinib demonstrated antitumour efficacy in patients with platinum-based chemotherapy pretreated NSCLC with EGFR exon20ins, with a manageable safety profile. A multinational randomised, phase 3 study of sunvozertinib versus platinum-doublet chemotherapy in EGFR exon20ins NSCLC is ongoing (NCT05668988). FUNDING: Dizal Pharmaceutical.

A Comparative Study of Temporomandibular Joints in Adults with Definite Sleep Bruxism on Magnetic Resonance Imaging and Cone-Beam Computer Tomography Images.

OBJECTIVE: The aim was to study the imaging characteristics of the temporomandibular joint (TMJ) of definite sleep bruxers through magnetic resonance imaging (MRI) and cone-beam computer tomography (CBCT). METHODS: Nineteen definite sleep bruxers diagnosed by polysomnography and twenty asymptomatic non-bruxers matched by age, gender, and education level participated in this study. After obtaining MRI and CBCT images of all TMJs of the subjects, evaluation and measurement were conducted, respectively. The analyzed parameters included disc position, disc configuration, joint effusion (JE), joint space or condyle position, and condylar bony changes. RESULTS: Of the 38 joints in the study group, disc deformity and disc displacement of TMJs were both 57.9% when the mouth was closed, and 76.3% showed condylar bony changes, while when the mouth was open, 82% of all TMJs showed physiological biconcave discs. Comparison of joint space revealed that the anterior space was larger in the study group. There was no significant difference between the mild and the moderate to severe sleep bruxism subgroups in the changes of TMJ. CONCLUSION: The results demonstrated that a higher prevalence of disc deformity, disc displacement, JE, and condylar bony changes occurred in temporomandibular joints of sleep bruxers. These changes were not related to the severity of sleep bruxism.

Haploinsufficiency of Apc leads to ineffective hematopoiesis.

Loss of a whole chromosome 5 or a deletion of the long arm of chromosome 5, -5/del(5q), is a recurring abnormality in myeloid neoplasms. The APC gene is located at chromosome band 5q23, and is deleted in more than 95% of patients with a -5/del(5q), raising the question of whether haploinsufficiency of APC contributes to the development of myeloid neoplasms with loss of 5q. We show that conditional inactivation of a single allele of Apc in mice leads to the development of severe anemia with macrocytosis and monocytosis. Further characterization of the erythroid lineage revealed that erythropoiesis is blocked at the early stages of differentiation. The long-term hematopoietic stem cell (LT-HSC) and short-term HSC (ST-HSC) populations are expanded in Apc-heterozygous mice compared with the control littermates; however, the HSCs have a reduced capacity to regenerate hematopoiesis in vivo in the absence of a single allele of Apc. Apc heterozygous myeloid progenitor cells display an increased frequency of apoptosis, and decreased in vitro colony-forming capacity, recapitulating several characteristic features of myeloid neoplasms with a -5/del(5q). Our results indicate that haploinsufficiency of Apc impairs hematopoiesis, and raise the possibility that loss of function of APC contributes to the development of myelodysplasia.

Correlation between Intestinal Flora and Serum Inflammatory Factors in Post-stroke Depression in Ischemic Stroke.

OBJECTIVE: To investigate the correlation between intestinal flora and serum inflammatory factors IL-1, IL-2, IL-6 and hs-CRP in post-stroke depression (PSD) in ischemic stroke patients. STUDY DESIGN: Observational study. Study Place and Duration of Study: Jiulongpo District Hospital of Traditional Chinese Medicine, Chongqing City, China, from October 2018 to May 2020. METHODOLOGY: One hundred and sixty-three patients with ischemic stroke were divided into Group A (PSD) and Group B (no PSD), according to whether they had PSD. Intestinal flora indexes (Enterococcus faecalis, Escherichia coli and Bifidobacterium) and serum IL-1, IL-2, IL-6 and hs-CRP were detected. RESULTS: Among 163 patients with ischemic stroke, 67 (41.10%) had PSD (Group A) and 96 (58.90%) had no PSD (Group B). Contents of Enterococcus faecalis and Escherichia coli in Group A were higher than those in Group B (both p <0.001), and content of Bifidobacterium in Group A was lower than that in Group B (p <0.001). Serum IL-1, IL-2, IL-6 and hs-CRP levels in Group A were higher than those in Group B (all p <0.001). Pearson correlation test showed that contents of Enterococcus faecalis and Escherichia coli in Group A were positively correlated with IL-1, IL-2, IL-6 and hs-CRP, and content of Bifidobacterium was negatively correlated with IL-1, IL-2, IL-6 and hs-CRP. CONCLUSION: There are intestinal flora imbalance and Bifidobacterium undergrowth in patients with PSD, which can lead to overexpression of serum inflammatory factors. Both may be involved in occurrence and progress of PSD in patients with ischemic stroke. Key Words: Ischemic stroke, Post-stroke depression (PSD), Intestinal flora, Inflammatory factors.

Mechanical thrombectomy for acute occlusion of the posterior inferior cerebellar artery: A case report.

BACKGROUND: Mechanical thrombectomy (MT) has been demonstrated to be useful for the treatment of ischemic stroke in patients with large vessel occlusions. However, recanalization by MT is not recommended for distal vessels such as second-order branches of the middle cerebral artery and posterior inferior cerebellar artery (PICA). Because of the small size and tortuosity of these arteries, the risks of using the available endovascular devices outweigh the benefits of treatment. However, MT appears to be effective in patients with primary distal vessel occlusion in eloquent areas, those with a high National Institutes of Health Stroke Scale score, and those ineligible for recombinant tissue plasminogen activator therapy. Here, we report the use of MT for treating acute occlusion of the PICA using a direct-aspiration first-pass technique (ADAPT). CASE SUMMARY: In this case, the patient received acute occlusion of the PICA with ADAPT when right internal carotid artery stenting was performed. CONCLUSION: With the introduction of advanced endovascular devices, MT may now be a feasible treatment for acute occlusion of the PICA.