A machine learning approach to predicting vascular calcification risk of type 2 diabetes: A retrospective study.

BACKGROUND: Recently, patients with type 2 diabetes mellitus (T2DM) have experienced a higher incidence and severer degree of vascular calcification (VC), which leads to an increase in the incidence and mortality of vascular complications in patients with T2DM. HYPOTHESIS: To construct and validate prediction models for the risk of VC in patients with T2DM. METHODS: Twenty-three baseline demographic and clinical characteristics were extracted from the electronic medical record system. Ten clinical features were screened with least absolute shrinkage and selection operator method and were used to develop prediction models based on eight machine learning (ML) algorithms (k-nearest neighbor [k-NN], light gradient boosting machine, logistic regression [LR], multilayer perception [(MLP], Naive Bayes [NB], random forest [RF], support vector machine [SVM], XGBoost [XGB]). Model performance was evaluated using the area under the receiver operating characteristic curve (AUC), accuracy, and precision. RESULTS: A total of 1407 and 352 patients were retrospectively collected in the training and test sets, respectively. Among the eight models, the AUC value in the NB model was higher than the other models (NB: 0.753, LGB: 0.719, LR: 0.749, MLP: 0.715, RF: 0.722, SVM: 0.689, XGB:0.707, p < .05 for all). The k-NN model achieved the highest sensitivity of 0.75 (95% confidence interval [CI]: 0.633-0.857), the MLP model achieved the highest accuracy of 0.81 (95% CI: 0.767-0.852) and specificity of 0.875 (95% CI: 0.836-0.912). CONCLUSIONS: This study developed a predictive model of VC based on ML and clinical features in type 2 diabetic patients. The NB model is a tool with potential to facilitate clinicians in identifying VC in high-risk patients.

Pulmonary thromboembolism associated with hereditary antithrombin III deficiency: A case report.

BACKGROUND: Thrombophilia is a coagulation disorder closely associated with venous thromboembolism. Hereditary antithrombin III (AT III) deficiency is a type of genetic thrombophilia. In China, genetic thrombophilia patients mainly suffer from deficiencies in AT III, protein S, and protein C. Multiple mutations in the serpin family C member 1 (SERPINC1) can affect AT III activity, resulting in thrombosis. CASE PRESENTATION: This case presented a 17-year-old adolescent female who developed lower extremity venous thrombosis and subsequently pulmonary embolism (PE) following a right leg injury. A missense mutation in gene SERPINC1 of c.331 T > C, p.S111P was detected on the patient, resulting in a decreased AT III activity and an elevated risk of thrombosis. The patient received anticoagulation treatment for approximately 5 months. During follow-up, the blood clot gradually dissolved, and there have been no recurrent thrombotic events reported thus far. DISCUSSION: Hereditary AT deficiency can be classified into two types based on the plasma levels of the enzymatic activity and antigen. Type I is a quantitative defect, while Type II is a qualitive defect. Until 2021, 486 SERPINC1 gene mutations have been registered, more than 18% of which are point mutations. The SERPINC1 mutation c.331 T > C in was firstly reported in 2017, which was classified into type I AT III deficiency. CONCLUSION: Hereditary thrombophilia is a coagulation disorder with a high omission diagnostic rate. Minor mutations in the SERPINC1 gene can also lead to hereditary AT III deficiency, which in turn can cause PE. We emphasized the importance of etiological screening for hereditary thrombophilia in venous thromboembolism patients without obvious high-risk factors. Long-term anticoagulation treatment and avoidance of potential thrombosis risk factors are critical for such patients.

Localized Administration of Bcar3 siRNA via Nano-Self-Assembly to Treat Idiopathic Pulmonary Fibrosis by Disrupting Macrophage-Fibroblast Crosstalk.

Background: Idiopathic pulmonary fibrosis (IPF) is a severe interstitial lung disease characterized by chronic lung injury leading to macrophage infiltration and fibroblast activation. However, there is no effective therapeutic strategy targeting the crucial crosstalk between macrophages and fibroblasts to halt IPF progression. Methods: Studies were conducted in IPF patients and fibrotic mice models to elucidate the role of Bcar3 in the pathogenesis of pulmonary fibrosis. The effect of Bcar3 on macrophage polarization, fibroblast activation, and related signaling pathways were next investigated to unravel the underlying mechanisms. Results: Our study elucidates a marked increase in Bcar3 expression in lung tissues from IPF patients and fibrotic mice, recording 1.7 and 7.8-fold increases compared to control subjects, respectively. Additionally, Bcar3 was found to significantly enhance macrophage activation and fibroblast differentiation, observable in both in vivo and in vitro settings. Mechanistically, the upregulation of Bcar3 in macrophages was reliant on Stat6, while in fibroblasts, it depended on TGFßR1/Smad3. Furthermore, Bcar3 augmented IL-4/Stat6 pathway in macrophages and TGF-ß/Smad3 pathway in fibroblasts, supporting a synergistic activation loop that expedited lung fibrogenesis. Notably, intratracheal injection of liposomes containing Bcar3 siRNA precisely delivered gene therapeutics to lung macrophages and fibroblasts, effectively reducing Bcar3 expression to 59% of baseline levels. Importantly, this intervention protected mice from lung fibrosis induced by either FITC or bleomycin, as well as human precision-cut lung slices against TGF-ß1 stimulation. Conclusion: Our study underscores the pivotal role of Bcar3 in orchestrating the macrophage-fibroblast crosstalk during pulmonary fibrosis progression. Targeting Bcar3 emerges as a novel therapeutic avenue to halt IPF progression and enhance patient prognosis.

Pulmonary arterial sarcoma: A case report.

RATIONALE: Pulmonary artery sarcoma (PAS) is a rare malignant tumor primarily originating from the pulmonary artery's intima or subintima. Approximately one-third of cases are classified as undifferentiated type. Its clinical manifestations lack specificity, dyspnea is the main symptom but can also present with chest pain, cough, hemoptysis, and other discomforts, making it prone to misdiagnosis as pulmonary embolism (PE). PATIENT CONCERNS: A 50-year-old woman was admitted to the hospital with "dyspnea for more than 3 months, aggravated for 2 days," and computed tomography pulmonary angiography suggesting "bilateral multiple pulmonary embolisms." DIAGNOSES: The patient was initially misdiagnosed as PE, and was later definitively diagnosed as undifferentiated pleomorphic sarcoma of the pulmonary artery by pathologic biopsy. INTERVENTIONS AND OUTCOMES: The patient was initially treated with anticoagulant therapy, but her dyspnea was not relieved. After that, she underwent positron emission computed tomography (PET-CT) and other investigations, which suggested the possibility of PAS, and then she underwent pulmonary endarterectomy to remove the lesion, which relieved her symptoms and was advised to seek further medical attention from the Department of Oncology and Department of Radiotherapy. LESSONS: PAS can be easily misdiagnosed as PE. If a diagnosis of PE is made, but anticoagulation or even thrombolytic therapy proves ineffective, and there is no presence of PE causative factors such as deep vein thrombosis in the lower extremities, or D-dimer levels are not high, one should be cautious and consider the possibility of PAS.

Natural products as pharmacological modulators of mitochondrial dysfunctions for the treatment of diabetes and its complications: An update since 2010.

Diabetes, characterized as a well-known chronic metabolic syndrome, with its associated complications pose a substantial and escalating health and healthcare challenge on a global scale. Current strategies addressing diabetes are mainly symptomatic and there are fewer available curative pharmaceuticals for diabetic complications. Thus, there is an urgent need to identify novel pharmacological targets and agents. The impaired mitochondria have been associated with the etiology of diabetes and its complications, and the intervention of mitochondrial dysfunction represents an attractive breakthrough point for the treatments of diabetes and its complications. Natural products (NPs), with multicenter characteristics, multi-pharmacological activities and lower toxicity, have been caught attentions as the modulators of mitochondrial functions in the therapeutical filed of diabetes and its complications. This review mainly summarizes the recent progresses on the potential of 39 NPs and 2 plant-extracted mixtures to improve mitochondrial dysfunction against diabetes and its complications. It is expected that this work may be useful to accelerate the development of innovative drugs originated from NPs and improve upcoming therapeutics in diabetes and its complications.

Effect and molecular mechanism of Sulforaphane alleviates brain damage caused by acute carbon monoxide poisoning:Network pharmacology analysis, molecular docking, and experimental evidence.

Sulforaphane (SFN) has attracted much attention due to its ability on antioxidant, anti-inflammatory, and anti-apoptotic properties, while its functional targets and underlying mechanism of action on brain injury caused by acute carbon monoxide poisoning (ACOP) have not been fully elucidated. Herein, we used a systematic network pharmacology approach to explore the mechanism of SFN in the treatment of brain damage after ACOP. In this study, the results of network pharmacology demonstrated that there were a total of 81 effective target genes of SFN and 36 drug-disease targets, which were strongly in connection with autophagy-animal signaling pathway, drug metabolism, and transcription disorders in cancer. Upon the further biological function and KEGG signaling pathway enrichment analysis, a large number of them were involved in neuronal death, reactive oxygen metabolic processes and immune functions. Moreover, based on the results of bioinformatics prediction associated with multiple potential targets and pathways, the AMP-activated protein kinase (AMPK) signaling pathway was selected to elucidate the molecular mechanism of SFN in the treatment of brain injury caused by ACOP. The following molecular docking analysis also confirmed that SFN can bind to AMPKα well through chemical bonds. In addition, an animal model of ACOP was established by exposure to carbon monoxide in a hyperbaric oxygen chamber to verify the predicted results of network pharmacology. We found that the mitochondrial ultrastructure of neurons in rats with ACOP was seriously damaged, and apoptotic cells increased significantly. The histopathological changes were obviously alleviated, apoptosis of cortical neurons was inhibited, and the number of Nissl bodies was increased in the SFN group as compared with the ACOP group (p < .05). Besides, the administration of SFN could increase the expressions of phosphorylated P-AMPK and MFN2 proteins and decrease the levels of DRP1, Caspase3, and Casapase9 proteins in the brain tissue of ACOP rats. These findings suggest that network pharmacology is a useful tool for traditional Chinese medicine (TCM) research, SFN can effectively inhibit apoptosis, protect cortical neurons from the toxicity of carbon monoxide through activating the AMPK pathway and may become a potential therapeutic strategy for brain injury after ACOP.

Potentiating humoral and cellular immunity using a novel hybrid polymer-lipid nanoparticle adjuvant for HBsAg-VLP vaccine.

Aluminium adjuvants are commonly used in vaccines to stimulate the immune system, but they have limited ability to promote cellular immunity which is necessary for clearing viral infections like hepatitis B. Current adjuvants that do promote cellular immunity often have undesired side effects due to the immunostimulants they contain. In this study, a hybrid polymer lipid nanoparticle (HPLNP) was developed as an efficient adjuvant for the hepatitis B surface antigen (HBsAg) virus-like particle (VLP) vaccine to potentiate both humoral and cellular immunity. The HPLNP is composed of FDA approved polyethylene glycol-b-poly (L-lactic acid) (PEG-PLLA) polymer and cationic lipid 1, 2-dioleoyl-3-trimethylammonium-propane (DOTAP), and can be easily prepared by a one-step method. The cationic optimised vaccine formulation HBsAg/HPLNP (w/w = 1/600) can maximise the cell uptake of the antigen due to the electrostatic adsorption between the vaccine nanoparticle and the cell membrane of antigen-presenting cells. The HPLNP prolonged the retention of the antigen at the injection site and enhanced the lymph node drainage of antigen, resulting in a higher concentration of serum anti-HBsAg IgG compared to the HBsAg group or the HBsAg/Al group after the boost immunisation in mice. The HPLNP also promoted a strong Th1-driven immune response, as demonstrated by the significantly improved IgG2a/IgG1 ratio, increased production of IFN-γ, and activation of CD4 + and CD8 + T cells in the spleen and lymph nodes. Importantly, the HPLNP demonstrated no systemic toxicity during immunisation. The advantages of the HPLNP, including good biocompatibility, easy preparation, low cost, and its ability to enhance both humoral and cellular immune responses, suggest its suitability as an efficient adjuvant for protein-based vaccines such as HBsAg-VLP. These findings highlight the promising potential of the HPLNP as an HBV vaccine adjuvant, offering an alternative to aluminium adjuvants currently used in vaccines.

Metabolic profiles of type 2 diabetes and their association with renal complications.

CONTEXT: The components of metabolic syndrome (MetS) are interrelated and associated with renal complications in patients with type 2 diabetes (T2D). AIMS: We aimed to reveal prevalent metabolic profiles in patients with T2D and identify which metabolic profiles were risk markers for renal progression. METHODS: A total of 3556 participants with T2D from a hospital (derivation cohort) and 931 participants with T2D from a community survey (external validation cohort) were included. The primary outcome was the onset of diabetic kidney disease (DKD), and secondary outcomes included eGFR decline, macroalbuminuria, and end-stage renal disease (ESRD). In the derivation cohort, clusters were identified using the five components of MetS, and their relationships with the outcomes were assessed. To validate the findings, participants in the validation cohort were assigned to clusters. Multivariate odds ratios (ORs) of the primary outcome were evaluated in both cohorts, adjusted for multiple covariates at baseline. RESULTS: In the derivation cohort, six clusters were identified as metabolic profiles. Compared with cluster 1, cluster 3 (severe hyperglycemia) had increased risks of DKD (HR [95% CI]: 1.72 [1.39-2.12]), macroalbuminuria (2.74 [1.84-4.08]), ESRD (4.31 [1.16-15.99]), and eGFR decline [P < 0.001]; cluster 4 (moderate dyslipidemia) had increased risks of DKD (1.97 [1.53-2.54]) and macroalbuminuria (2.62 [1.61-4.25]). In the validation cohort, clusters 3 and 4 were replicated to have significantly increased risks of DKD (adjusted ORs: 1.24 [1.07-1.44] and 1.39 [1.03-1.87]). CONCLUSIONS: We identified six prevalent metabolic profiles in patients with T2D. Severe hyperglycemia and moderate dyslipidemia were validated as significant risk markers for DKD.

Potentiating the Immune Responses of HBsAg-VLP Vaccine Using a Polyphosphoester-Based Cationic Polymer Adjuvant.

Virus-like particle (VLP)-based vaccines are required to be associated with a suitable adjuvant to potentiate their immune responses. Herein, we report a novel, biodegradable, and biocompatible polyphosphoester-based amphiphilic cationic polymer, poly(ethylene glycol)-b-poly(aminoethyl ethylene phosphate) (PEG-PAEEP), as a Hepatitis B surface antigen (HBsAg)-VLP vaccine adjuvant. The polymer adjuvant effectively bound with HBsAg-VLP through electrostatic interactions to form a stable vaccine nanoformulation with a net positive surface charge. The nanoformulations exhibited enhanced cellular uptake by macrophages. HBsAg-VLP/PEG-PAEEP induced a significantly higher HBsAg-specific IgG titer in mice than HBsAg-VLP alone after second immunization, indicative of the antigen-dose sparing advantage of PEG-PAEEP. Furthermore, the nanoformulations exhibited a favorable biocompatibility and in vivo tolerability. This work presents the PEG-PAEEP copolymer as a promising vaccine adjuvant and as a potentially effective alternative to aluminum adjuvants.

Acute pulmonary embolism with arrhythmia associated with minimal change disease in adults: a case report.

Background: Minimal change disease (MCD) is a common pathological type of nephrotic syndrome (NS), and is one of the most common causes of NS in children, but is not common in adults. MCD is sensitive to corticosteroid therapy and has a good prognosis, but is prone to relapse. Venous thromboembolism (VTE) is less common in MCD. Case presentation: We report a case of acute pulmonary embolism (PE) with arrhythmia associated with MCD in adults. The hypercoagulable state caused by MCD through multiple systems may be one of the important causes of thrombosis in this patient. In addition to the conventional corticosteroid therapy, he was started on anticoagulation for VTE and PE. His hospital course was complicated by atrial tachyarrhythmias initially controlled by amiodarone but he required readmission due to recurrent atrial flutter. His clinical condition became more stable after radiofrequency ablation. Conclusion: VTE associated with MCD in adults is rare. Treatment of MCD with corticosteroids may be associated with a higher risk of developing blood clots. This type of case is relatively rare and should be paid attention to. The mechanism of VTE in MCD is still a direction worthy of further research.

Bioactive fatty acid analog-derived hybrid nanoparticles confer antibody-independent chemo-immunotherapy against carcinoma.

Typical chemo-immunotherapy against malignant carcinoma, is characterized by the combined application of chemotherapeutic agents and monoclonal antibodies for immune checkpoint blockade (ICB). Temporary ICB with antibodies would not depress tumor intrinsic PD-L1 expression and potential PD-L1 adaptive upregulation during chemotherapy, thus exerting limited immunotherapy efficacy. Herein, we developed novel polymer-lipid hybrid nanoparticles (2-BP/CPT-PLNs) for inducing PD-L1 degradation by inhibiting palmitoylation with bioactive palmitic acid analog 2-bromopalmitate (2-BP) to replace PD-L1 antibody (αPD-L1) for ICB therapy, thus achieving highly efficient antitumor immune via immunogenic cell death (ICD) induced by potentiated chemotherapy. GSH-responsive and biodegradable polymer-prodrug CPT-ss-PAEEP10 assisted as a cationic helper polymer could help to stabilize 2-BP/CPT-PLNs co-assembled with 2-BP, and facilitate the tumor site-specific delivery and intracellular release of water-insoluble camptothecin (CPT) in vivo. 2-BP/CPT-PLNs would reinforce cytotoxic CD8+ T cell-mediated antitumor immune response via promoting intratumoral lymphocytes cells infiltration and activation. 2-BP/CPT-PLNs significantly prevented melanoma progression and prolonged life survival of mice beyond the conventional combination of irinotecan hydrochloride (CPT-11) and αPD-L1. Our work first provided valuable instructions for developing bioactive lipid analogs-derived nanoparticles via lipid metabolism intervention for oncotherapy.

Primary pulmonary artery tumors easily misdiagnosed as pulmonary embolism: A review.

Primary pulmonary artery tumors (PPATs), originating from the pulmonary artery intima, are rare tumors characterized by pulmonary artery luminal occlusion and pulmonary hypertension. Diagnosis of this rare entity is a challenging dilemma with the need for a high expertise in the radiological and pathological identification of PPATs. computed tomographic pulmonary angiography of PPATs may show filling defects, which are easily misdiagnosed. The radionuclide scan, along with other imaging examinations, can assist with the diagnosis, but the pathological diagnosis requires a puncture or surgical resection. Most primary pulmonary artery tumors are malignant, with poor prognosis and lack of specificity in clinical manifestations. However, there is no unified understanding and standard for diagnosis and treatment. In this review, we discuss the status, diagnosis, and treatment of primary pulmonary artery tumors, as well as how clinicians can better understand and treat the disease.

DrugEx v3: scaffold-constrained drug design with graph transformer-based reinforcement learning.

Rational drug design often starts from specific scaffolds to which side chains/substituents are added or modified due to the large drug-like chemical space available to search for novel drug-like molecules. With the rapid growth of deep learning in drug discovery, a variety of effective approaches have been developed for de novo drug design. In previous work we proposed a method named DrugEx, which can be applied in polypharmacology based on multi-objective deep reinforcement learning. However, the previous version is trained under fixed objectives and does not allow users to input any prior information (i.e. a desired scaffold). In order to improve the general applicability, we updated DrugEx to design drug molecules based on scaffolds which consist of multiple fragments provided by users. Here, a  Transformer model was employed to generate molecular structures. The Transformer is a multi-head self-attention deep learning model containing an encoder to receive scaffolds as input and a decoder to generate molecules as output. In order to deal with the graph representation of molecules a novel positional encoding for each atom and bond based on an adjacency matrix was proposed, extending the architecture of the Transformer. The graph Transformer model contains growing and connecting procedures for molecule generation starting from  a given scaffold based on fragments. Moreover, the generator was trained under a reinforcement learning framework to increase the number of desired ligands. As a proof of concept, the method was applied to design ligands for the adenosine A2A receptor (A2AAR) and compared with SMILES-based methods. The results show that 100% of the generated molecules are valid and most of them had a high predicted affinity value towards A2AAR with given scaffolds.

Nomogram for Predicting Intraoperative Hemodynamic Instability in Patients With Normotensive Pheochromocytoma.

CONTEXT: Intraoperative hemodynamic instability (HI) deteriorates surgical outcomes of patients with normotensive pheochromocytoma (NP). OBJECTIVE: To characterize the hemodynamics of NP and develop and externally validate a prediction model for intraoperative HI. METHODS: Data on 117 patients with NP (derivation cohort) and 40 patients with normotensive adrenal myelolipoma (NAM) who underwent laparoscopic adrenalectomy from January 2011 to November 2021 were retrospectively collected. Data on 22 patients with NP (independent validation cohort) were collected from another hospital during the same period. The hemodynamic characteristics of patients with NP and NAM were compared. Machine learning models were used to identify risk factors associated with HI. The final model was visualized via a nomogram. RESULTS: Forty-eight (41%) out of 117 patients experienced HI, which was significantly more than that for NAM. A multivariate logistic regression including age, tumor size, fasting plasma glucose, and preoperative systolic blood pressure showed good discrimination measured by area under curve (0.8286; 95% CI 0.6875-0.9696 and 0.7667; 95% CI 0.5386-0.9947) for predicting HI in internal and independent validation cohorts, respectively. The sensitivities and positive predictive values were 0.6667 and 0.7692 for the internal and 0.9167 and 0.6111 for the independent validations, respectively. The final model was visualized via a nomogram and yielded net benefits across a wide range of risk thresholds in decision curve analysis. CONCLUSION: Patients with NP experienced HI during laparoscopic adrenalectomy. The nomogram can be used for individualized prediction of intraoperative HI in patients with NP.

QRS-T angle as a predictor of pulmonary arterial hypertension: A review.

Spatial QRS-T angle is a vector projection of ventricular gradient, reflecting the heterogeneity of ventricular repolarization. The QRS vector is projected into three dimensional (3D) space to obtain the frontal QRSf vector and Tf vector. The frontal QRS-T Angle can be obtained by simple calculation. In several studies of diseases that cause pulmonary hypertension, there has been evidence that changes in the QRS-T Angle can predict disease. Electrocardiogram (ECG) is a cheap and noninvasive test, and its clinical significance in the diagnosis of pulmonary hypertension should be further studied.

Trichoid sensilla on honey bee proboscises as inspiration for micro-viscometers.

Sensing physical properties of liquids, such as viscosity, is of great significance for both biological organisms and industrial applications. For terrestrial organisms feeding on liquids, such as honey bees that forage nectar, sensing viscosity may help to determine the quality of food sources. Previous experiments showed that honey bees exhibit strong preferences for less viscous nectar; however, the physical mechanism underlying how they perceive viscosity remains unexplored. In this study, we propose that the western honey bee (Apis melliferaL.) is capable of distinguishing viscosity using the slender trichoid sensilla emerging from a ball and socket-like joint on the proboscis. Observations of the trichoid sensilla using transmission electron microscopy reveal physical characteristics that are typical of mechanosensory structures. Additionally, we found that bees actively alter the rate at which they feed based on the liquid's viscosity and not its sugar content, hinting at their sensing of viscosity. Through mathematical modeling, we found that the sensitivity of the biological viscometer was determined by its length, and the optimal sensitivity for a western honey bee occurs when the tongue interacts with nectar with a viscosity of 4.2 mPa·s, coinciding with the viscosities typically found in the wild. Our findings broaden insights into how honey bees adapt to varying-viscosity nectar from the perspective of mechanical sensing, and how the bee-flower partnership may be based around the optimal nectar viscosity for feeding. By understanding how bees may sense viscosity at the micrometer scale, we may motivate new technologies for micro-viscometers.

Duchenne muscular dystrophy involves the myocardium and causes arrhythmia: Case report.

Background: Patients with muscular dystrophy have mutations in the gene that can lead to severe muscle wasting, respiratory issues or heart failure between ages 30 and 40. Currently, there is no effective treatment for DMD-induced heart failure. Case presentation: We report a patient with recurrent unexplained fever and muscle soreness was definitely diagnosed with DMD. An analysis of the patient's genetics revealed a nonsense mutation (C.1207G > T). His DMD was treated with hormones. Also, the patient's fever is under control because of hormone therapy. However, as the disease progresses, the heart structure and function gradually change, and eventually malignant arrhythmias occur. Conclusion: We report a rare case of DMD involving the heart causing heart failure and malignant arrhythmia. Currently, no complete treatment is available for these patients, but our treatment regimen may benefit our patient and improve his outcomes.

Acute pulmonary embolism following corticosteroid administration in acute severe ulcerative colitis with gastrointestinal bleeding: A case report.

Background: Ulcerative colitis often leads to gastrointestinal bleeding and venous thromboembolism (VTE). At present, there is no clear conclusion about anticoagulant therapy for these patients. Treatment for ulcerative colitis usually includes 5-aminosalicylic acid, corticosteroid, and biologics. Acute ulcerative colitis, usually caused by infection, is usually severe and can be life-threatening. Case presentation: We report the development of VTE in a patient with severe acute ulcerative colitis who experienced gastrointestinal bleeding following hormonal therapy. The patient's indicators suggested that his blood was hypercoagulable and that his prognosis was poor. Conclusion: Patients with ulcerative colitis are prone to form VTE. The use of corticosteroids during treatment increases the risk of thrombus. Anticoagulation strategy for patients with ulcerative colitis after gastrointestinal bleeding is a problem that needs to be discussed.

Corrigendum: Case report: An unusual case of desmin myopathy associated with heart failure and arrhythmia.

[This corrects the article DOI: 10.3389/fcvm.2022.944459.].

Metabolic reprogramming: A novel metabolic model for pulmonary hypertension.

Pulmonary arterial hypertension, or PAH, is a condition that is characterized by pulmonary artery pressures above 20 mmHg (at rest). In the treatment of PAH, the pulmonary vascular system is regulated to ensure a diastolic and contraction balance; nevertheless, this treatment does not prevent or reverse pulmonary vascular remodeling and still causes pulmonary hypertension to progress. According to Warburg, the link between metabolism and proliferation in PAH is similar to that of cancer, with a common aerobic glycolytic phenotype. By activating HIF, aerobic glycolysis is enhanced and cell proliferation is triggered. Aside from glutamine metabolism, the Randle cycle is also present in PAH. Enhanced glutamine metabolism replenishes carbon intermediates used by glycolysis and provides energy to over-proliferating and anti-apoptotic pulmonary vascular cells. By activating the Randle cycle, aerobic oxidation is enhanced, ATP is increased, and myocardial injury is reduced. PAH is predisposed by epigenetic dysregulation of DNA methylation, histone acetylation, and microRNA. This article discusses the abnormal metabolism of PAH and how metabolic therapy can be used to combat remodeling.