PlaqueNet: deep learning enabled coronary artery plaque segmentation from coronary computed tomography angiography.

Cardiovascular disease, primarily caused by atherosclerotic plaque formation, is a significant health concern. The early detection of these plaques is crucial for targeted therapies and reducing the risk of cardiovascular diseases. This study presents PlaqueNet, a solution for segmenting coronary artery plaques from coronary computed tomography angiography (CCTA) images. For feature extraction, the advanced residual net module was utilized, which integrates a deepwise residual optimization module into network branches, enhances feature extraction capabilities, avoiding information loss, and addresses gradient issues during training. To improve segmentation accuracy, a depthwise atrous spatial pyramid pooling based on bicubic efficient channel attention (DASPP-BICECA) module is introduced. The BICECA component amplifies the local feature sensitivity, whereas the DASPP component expands the network's information-gathering scope, resulting in elevated segmentation accuracy. Additionally, BINet, a module for joint network loss evaluation, is proposed. It optimizes the segmentation model without affecting the segmentation results. When combined with the DASPP-BICECA module, BINet enhances overall efficiency. The CCTA segmentation algorithm proposed in this study outperformed the other three comparative algorithms, achieving an intersection over Union of 87.37%, Dice of 93.26%, accuracy of 93.12%, mean intersection over Union of 93.68%, mean Dice of 96.63%, and mean pixel accuracy value of 96.55%.

Mechanisms by Which Electroacupuncture Alleviates Neurovascular Unit Injury after Ischemic Stroke: A Potential Therapeutic Strategy for Ischemic Brain Injury after Stroke.

Stroke is the most common cerebrovascular disease and one of the leading causes of death and disability worldwide. The current conventional treatment for stroke involves increasing cerebral blood flow and reducing neuronal damage; however, there are no particularly effective therapeutic strategies for rehabilitation after neuronal damage. Therefore, there is an urgent need to identify a novel alternative therapy for stroke. Acupuncture has been applied in China for 3000 years and has been widely utilized in the treatment of cerebrovascular diseases. Accumulating evidence has revealed that acupuncture holds promise as a potential therapeutic strategy for stroke. In our present review, we focused on elucidating the possible mechanisms of acupuncture in the treatment of ischemic stroke, including nerve regeneration after brain injury, inhibition of inflammation, increased cerebral blood flow, and subsequent rehabilitation.

Downregulation of LILRB4 Promotes Human Aortic Smooth Muscle Cell Contractile Phenotypic Switch and Apoptosis in Aortic Dissection.

Aortic dissection (AD) is a severe vascular disease with high rates of mortality and morbidity. However, the underlying molecular mechanisms of AD remain unclear. Differentially expressed genes (DEGs) were screened by bioinformatics methods. Alterations of histopathology and inflammatory factor levels in ß-aminopropionitrile (BAPN)-induced AD mouse model were evaluated through Hematoxylin-Eosin (HE) staining and Enzyme-linked immunosorbent assay (ELISA), respectively. Reverse transcription quantitative real-time polymerase chain reaction was performed to detect DEGs expression. Furthermore, the role of LILRB4 in AD was investigated through Cell Counting Kit-8 (CCK-8), wound healing, and flow cytometry. Western blotting was employed to assess the phenotypic switch and extracellular matrix (ECM)-associated protein expressions in platelet-derived growth factor-BB (PDGF-BB)-stimulated in vitro model of AD. In the AD mouse model, distinct dissection formation was observed. TNF-α, IL-1ß, IL-8, and IL-6 levels were higher in the AD mouse model than in the controls. Six hub genes were identified, including LILRB4, TIMP1, CCR5, CCL7, MSR1, and CLEC4D, all of which were highly expressed. Further exploration revealed that LILRB4 knockdown inhibited the cell vitality and migration of PDGF-BB-induced HASMCs while promoting apoptosis and G0/G1 phase ratio. More importantly, LILRB4 knockdown promoted the protein expression of α-SMA and SM22α, while decreasing the expression of Co1, MMP2, and CTGF, which suggested that LILRB4 silencing promoted contractile phenotypic transition and ECM stability. LILRB4 knockdown inhibits the progression of AD. Our study provides a new potential target for the clinical treatment of AD.

PCSK9 inhibitors suppress oxidative stress and inflammation in atherosclerotic development by promoting macrophage autophagy.

OBJECTIVES: Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, a novel class of cholesterol-lowering drugs, can reduce atherosclerosis independent of systemic lipid changes. However, the mechanism by which PCSK9 inhibition protects against arteriosclerosis has not been fully elucidated. Recent evidence has demonstrated a correlation between PCSK9 inhibitors and oxidative stress, which accelerates atherosclerotic development. Moreover, an increasing number of studies have shown that autophagy protects the vasculature against atherosclerosis. Therefore, the aims of this study were to investigate the effect of PCSK9 inhibition on oxidative stress and autophagy in atherosclerosis and determine whether autophagy regulates PCSK9 inhibition-mediated oxidative stress and inflammation in macrophages. METHODS: Male apolipoprotein E (ApoE)-/- mice were fed a high-fat diet (HFD) for 8 weeks and then received the PCSK9 inhibitor (evolocumab), vehicle, or evolocumab plus chloroquine (CQ) for another 8 weeks. ApoE-/- mice in the control group were fed a regular (i.e., non-high-fat) diet for 16 weeks. Additional in vitro experiments were performed in oxidized low-density lipoprotein (ox-LDL)-treated human acute monocytic leukemia cell line THP-1-derived macrophages to mimic the pathophysiologic process of atherosclerosis. RESULTS: PCSK9 inhibitor treatment reduced oxidative stress, lipid deposition, and plaque lesion area and induced autophagy in HFD-fed ApoE-/- mice. Most importantly, the administration of chloroquine (CQ), an autophagy inhibitor, significantly reduced the beneficial effects of PCSK9-inhibitor treatment on oxidative stress, lipid accumulation, inflammation, and atherosclerotic lesions in HFD-fed ApoE-/- mice. The in vitro experiments further showed that the PCSK9 inhibitor enhanced autophagic flux in ox-LDL-treated THP-1-derived macrophages, as indicated by increases in the numbers of autophagosomes and autolysosomes. Moreover, the autophagy inhibitor CQ also reduced PCSK9 inhibition-mediated protection against oxidative stress, generation of reactive oxygen species (ROS) and inflammation in ox-LDL-treated THP-1-derived macrophages. CONCLUSIONS: This study reveals a novel protective mechanism by which PCSK9 inhibition enhances autophagy and thereby reduces oxidative stress and inflammation in atherosclerosis.

Micropodarke fujianensis n. sp. (Annelida: Hesionidae) from Fujian, China.

We describe M. fujianensis n. sp. (Annelida: Hesionidae), collected from the coast of Fujian Province, China, based on morphological and molecular analyses. Micropodarke fujianensis n. sp. is characterized by having two pairs of minute eyes, and neurochaetae of middle segments without basal long teeth. The K2P distances of COI, 16S rRNA, 18S rRNA, 28S rRNA, and histone H3 fragments diverged from the corresponding sequences of the closest related species of Micropodarke in GenBank and BOLD Systems by 22.3%, 10.7%, 0, 1.15%, and 1.1%, respectively. Among the Micropodarke species with such DNA sequences for comparison, M. fujianensis n. sp. is most closely related to M. cf. dubia-a species collected from Daya Bay, China. An updated key to Micropodarke species is provided.

Enhancing the depth perception of DSA images with 2D-3D registration.

Objective: Today, cerebrovascular disease has become an important health hazard. Therefore, it is necessary to perform a more accurate and less time-consuming registration of preoperative three-dimensional (3D) images and intraoperative two-dimensional (2D) projection images which is very important for conducting cerebrovascular disease interventions. The 2D-3D registration method proposed in this study is designed to solve the problems of long registration time and large registration errors in 3D computed tomography angiography (CTA) images and 2D digital subtraction angiography (DSA) images. Methods: To make a more comprehensive and active diagnosis, treatment and surgery plan for patients with cerebrovascular diseases, we propose a weighted similarity measure function, the normalized mutual information-gradient difference (NMG), which can evaluate the 2D-3D registration results. Then, using a multi-resolution fusion optimization strategy, the multi-resolution fused regular step gradient descent optimization (MR-RSGD) method is presented to attain the optimal value of the registration results in the process of the optimization algorithm. Result: In this study, we adopt two datasets of the brain vessels to validate and obtain similarity metric values which are 0.0037 and 0.0003, respectively. Using the registration method proposed in this study, the time taken for the experiment was calculated to be 56.55s and 50.8070s, respectively, for the two sets of data. The results show that the registration methods proposed in this study are both better than the Normalized Mutual (NM) and Normalized Mutual Information (NMI). Conclusion: The experimental results in this study show that in the 2D-3D registration process, to evaluate the registration results more accurately, we can use the similarity metric function containing the image gray information and spatial information. To improve the efficiency of the registration process, we can choose the algorithm with gradient optimization strategy. Our method has great potential to be applied in practical interventional treatment for intuitive 3D navigation.

Large animal models in the study of gynecological diseases.

Gynecological diseases are a series of diseases caused by abnormalities in the female reproductive organs or breast, which endanger women's fertility and even their lives. Therefore, it is important to investigate the mechanism of occurrence and treatment of gynecological diseases. Animal models are the main objects for people to study the development of diseases and explore treatment options. Large animals, compared to small rodents, have reproductive organs with structural and physiological characteristics closer to those of humans, and are also better suited for long-term serial examinations for gynecological disease studies. This review gives examples of large animal models in gynecological diseases and provides a reference for the selection of animal models for gynecological diseases.

Five-year follow-up on two revascularization methods used on patients with left main artery disease and/or multivessel coronary artery disease.

BACKGROUND: Coronary artery bypass graft (CABG) and percutaneous coronary intervention (PCI) are the main treatment methods for left main artery disease (LMAD) and triple-vessel coronary artery disease (TVCAD). OBJECTIVE: This study aimed to evaluate the five-year post-treatment effects of CABG and PCI in patients with severe coronary vasculopathy. METHODS: A total of 430 patients with LMAD and/or triple-vessel coronary artery disease from November 2014 to July 2015 were enrolled retrospectively in the affiliated cardiovascular hospital of Shanxi Medical University and divided into the CABG group and PCI group. The living conditions of the patients were obtained through medical records and telephonic follow-ups five years after the surgery date. The independent risk factors for major adverse cardiovascular and cerebrovascular events (MACCE) were analyzed using logistic regression analysis. The effects of the two treatment methods were followed up and evaluated to measure the predictive ability of the Global Risk Classification (GRC) scoring system for MACCE after five years. RESULTS: There were 212 cases in the CABG group and 218 cases in the PCI group. Smoking (P= 0.047), diabetes (P= 0.031), LVEF (P= 0.020), LMAD (P= 0.008), and anterior descending branch lesions (P= 0.038) were significantly correlated with MACCE. The prevalence of MACCE in the CABG group and PCI group had no significant difference (P= 0.549). The GRC scoring system received an AUC of 0.701 for predicting MACCE. CONCLUSION: For patients with severe coronary artery disease, there was no significant difference in the prevalence of MACCE between the CABG and the PCI groups. Several independent risk factors for MACCE were found. The GRC scoring system showed a strong predictive ability for MACCE after five years of revascularization.

Study on the blood flow characteristics of venous needle retention with different super-hydrophobic surface structures.

A venous retention needle, as an implanted device, is very likely to cause thrombosis. In view of the thrombosis phenomenon caused by retention needles, this paper compares the influence of different superhydrophobic surface retentions on blood flow. Compared with other superhydrophobic bulges, the fluid velocity of the four-prism bulge is the highest (0.08 m/s), and the vorticity and shear force of the hemispherical bulge are higher. A large number of vortices can inhibit thrombosis better. The tire vortices generated in the superhydrophobic convex grooves are important vortices to inhibit thrombosis. The enhancement and development of the tire vortex weakens the resistance near the wall of the needle and reduces the probability of platelet aggregation. The superhydrophobic surface structure studied in this paper can not only provide guidance for the design of venous retention needles with better performance but also provide corresponding technical support for the development of human implantation devices.

Advances of hydrogel combined with stem cells in promoting chronic wound healing.

Wounds can be divided into two categories, acute and chronic. Acute wounds heal through the normal wound healing process. However, chronic wounds take longer to heal, leading to inflammation, pain, serious complications, and an economic burden of treatment costs. In addition, diabetes and burns are common causes of chronic wounds that are difficult to treat. The rapid and thorough treatment of chronic wounds, including diabetes wounds and burns, represents a significant unmet medical need. Wound dressings play an essential role in chronic wound treatment. Various biomaterials for wound healing have been developed. Among these, hydrogels are widely used as wound care materials due to their good biocompatibility, moisturizing effect, adhesion, and ductility. Wound healing is a complex process influenced by multiple factors and regulatory mechanisms in which stem cells play an important role. With the deepening of stem cell and regenerative medicine research, chronic wound treatment using stem cells has become an important field in medical research. More importantly, the combination of stem cells and stem cell derivatives with hydrogel is an attractive research topic in hydrogel preparation that offers great potential in chronic wound treatment. This review will illustrate the development and application of advanced stem cell therapy-based hydrogels in chronic wound healing, especially in diabetic wounds and burns.

Research progress on anti-ovarian cancer mechanism of miRNA regulating tumor microenvironment.

Ovarian cancer is the most deadly malignancy among women, but its complex pathogenesis is unknown. Most patients with ovarian cancer have a poor prognosis due to high recurrence rates and chemotherapy resistance as well as the lack of effective early diagnostic methods. The tumor microenvironment mainly includes extracellular matrix, CAFs, tumor angiogenesis and immune-associated cells. The interaction between tumor cells and TME plays a key role in tumorigenesis, progression, metastasis and treatment, affecting tumor progression. Therefore, it is significant to find new tumor biomarkers and therapeutic targets. MicroRNAs are non-coding RNAs that post-transcriptionally regulate the expression of target genes and affect a variety of biological processes. Studies have shown that miRNAs regulate tumor development by affecting TME. In this review, we summarize the mechanisms by which miRNAs affect ovarian cancer by regulating TME and highlight the key role of miRNAs in TME, which provides new targets and theoretical basis for ovarian cancer treatment.

Omentin inhibits the resistin-induced hypertrophy of H9c2 cardiomyoblasts by inhibiting the TLR4/MyD88/NF-κB signaling pathway.

The recently identified adipocytokine omentin was previously found to be expressed mainly in human omental and visceral adipose tissues. As such, reduced plasma concentrations of omentin were revealed to be associated with increased risks of cardiovascular diseases. Omentin has also been previously demonstrated to exert anti-inflammatory effects. By contrast, resistin is a protein that has been associated with obesity and type-2 diabetes mellitus, and the serum concentration of resistin is increased significantly in these populations. Resistin is involved in mediating inflammation development, where they can promote cardiac hypertrophy in humans through toll-like receptor 4 (TLR4)-related signaling. In the present study, the potential effects of omentin on resistin-induced hypertrophy in H9c2 cardiomyoblasts were investigated. In the absence/presence of omentin, H9c2 cardiomyoblasts were treated with resistin. Omentin was found to significantly inhibit resistin-induced increases in the surface area of H9c2 cardiomyoblasts as determined by immunofluorescence. In addition, omentin significantly inhibited resistin-induced increases in the mRNA expression of atrial natriuretic factor, brain natriuretic peptide, ß-myosin heavy chain (which is a characteristic feature of cardiac hypertrophy) and TLR4, which was determined using reverse-transcription-quantitative PCR. According to western blotting results, omentin significantly inhibited resistin-induced ERK phosphorylation, which is an important mediator of cardiomyoblast hypertrophy. Furthermore, omentin significantly inhibited resistin-induced protein expression of TLR4, myeloid differentiation factor 88 (MyD88) and NF-κB phosphorylation, both of which are important members of inflammatory signaling. To conclude, data from the present study suggest that omentin can inhibit resistin-induced H9c2 cardiomyoblast hypertrophy through inhibition of the TLR4/MyD88/NF-κB signaling pathway. Therefore, omentin serve as an attractive therapeutic target against resistin-induced cardiac hypertrophy.

Gut microbiota: The key to the treatment of metabolic syndrome in traditional Chinese medicine - a case study of diabetes and nonalcoholic fatty liver disease.

Metabolic syndrome mainly includes obesity, type 2 diabetes (T2DM), alcoholic fatty liver (NAFLD) and cardiovascular diseases. According to the ancient experience philosophy of Yin-Yang, monarch-minister compatibility of traditional Chinese medicine, prescription is given to treat diseases, which has the advantages of small toxic and side effects and quick effect. However, due to the diversity of traditional Chinese medicine ingredients and doubts about the treatment theory of traditional Chinese medicine, the mechanism of traditional Chinese medicine is still in doubt. Gastrointestinal tract is an important part of human environment, and participates in the occurrence and development of diseases. In recent years, more and more TCM researches have made intestinal microbiome a new frontier for understanding and treating diseases. Clinically, nonalcoholic fatty liver disease (NAFLD) and diabetes mellitus (DM) often co-occur. Our aim is to explain the mechanism of interaction between gastrointestinal microbiome and traditional Chinese medicine (TCM) or traditional Chinese medicine formula to treat DM and NAFLD. Traditional Chinese medicine may treat these two diseases by influencing the composition of intestinal microorganisms, regulating the metabolism of intestinal microorganisms and transforming Chinese medicinal compounds.

Ginseng glycoprotein and ginsenoside facilitate anti UV damage effects in diabetic rats.

Diabetes mellitus combined with ultraviolet (UV) radiation damage not only brings great mental stress to patients, but also seriously impairs their quality of life. A UV-irradiated diabetic rat trauma skin model was established by us to investigate the effects and possible mechanisms of ginsenoside and glycoprotein on skin trauma repair in UV-irradiated diabetic rats. In the study, ginsenosides and ginseng glycoproteins were extracted from different parts of ginseng roots. It found that it's easier to prepare saponins in ginseng bark and proteins in ginseng core in large quantities. Since glycoprotein-like metabolites are relatively novel ginseng extracts, specifically characterized its structures. It was verified that the ginseng glycoproteins are not toxic to HaCaT cells and can significantly increase the survival of HaCaT cells after UV damage at the in vitro cellular level. Experiments in vivo were conducted to evaluate the therapeutic effects of ginsenoside and ginseng glycoprotein in a rat model of diabetes mellitus combined with UV irradiation injury. Histopathological changes on rat skin after treatment with ginsenoside and ginseng glycoprotein were evaluated by hematoxylin and eosin (H&E) staining and aldehyde fuchsine staining. The expression levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), matrix metalloproteinases (MMPs), hydroxyproline (HYP), interleukin-6 (IL-6), interleukin-1ß (IL-1ß), and tumor necrosis factor-α (TNF-α) were measured. The results indicate that both ginsenoside and ginseng glycoprotein could improve skin damage and ulcers caused by diabetes combined with UV irradiation and could alleviate a range of skin damage caused by the combination of diabetes and UV irradiation, including peroxidation and collagen fiber loss. Ginsenoside and ginseng glycoproteins can be considered as natural product candidates for the development of new drugs to treat diabetes combined with UV irradiation-induced skin damage.

A novel miRNA-762/NFIX pathway modulates LPS-induced acute lung injury.

Severe acute lung injury (ALI) cause significant morbidity and mortality worldwide. MicroRNAs (miRNAs) are possible biomarkers and therapeutic targets for ALI. We aimed to explore the role of miR-762, a known oncogenic factor, in the pathogenesis of ALI. Levels of miR-762 in lung tissues of LPS-treated ALI mice and blood cells of patients with lung injury were measured. Injury of human lung epithelial cell line A549 was induced by LPS stimulation. A downstream target of miR-762, NFIX, was predicted using online tools. Their interactions were validated by luciferase reporter assay. Effects of targeted regulation of the miR-762/NFIX axis on cell proliferation, apoptosis, and inflammatory responses were tested in vitro in A549 cells in vivo with an ALI mouse model. We found that upregulation of miR-762 expression and downregulation of NFIX expression were associated with lung injury. Either miR-762 inhibition or NFIX overexpression in A549 lung cells significantly attenuated LPS-mediated impairment of cell proliferation and viability. Notably, increasing expressions of miR-762 inhibitor or NFIX in vivo via airway lentivirus infection alleviated the LPS-induced ALI in mice. Further, targeted downregulation of miR-762 expression or upregulation of NFIX expression in A549 cells markedly down-regulates NF-κB/IRF3 activation, and substantially reduces the production of inflammatory factors, including TNF-α, IL-6, and IL-8. This study reveals a novel role for the miR-762/NFIX pathway in ALI pathogenesis and sheds new light on targeting this pathway for diagnosis, prevention, and therapy.

In vivo effects of nitrosyl hydrogen on cardiac function and sarcoplasmic reticulum calcium pump (SERCA2a) in rats with heart failure after myocardial infarction.

BACKGROUND: Abnormal Ca2+ circulation in cardiomyocytes is an important cause of decreased myocardial contractility in failing hearts. Nitroxyl hydrogen (HNO) can oxidize Ca2+ cycle-related proteins, alter their biological functions, promote Ca2+ recovery as well as release, and enhance myocardial contractility. In this study, we aim to observe the effect of nitrosyl hydrogen (HNO) on the cardiac function of rats with heart failure and elucidate the underlying mechanism. METHODS: Twenty six male Wistar rats were randomly divided into heart failure group (HF group), Angeli's salt treatment group (HF + AS group) and sham operation group (Sham group). The HF + AS group rats were treated with HNO donor Angeli's salt by intraperitoneal injection of 1 mg/kg/d, and the rats in the HF group and the Sham group were given the same amount of normal saline. Cardiac function was measured by echocardiography before and after treatment. NT-proBNP was measured by enzyme immunoassay (ELISA) kit after treatment. Western blot were used to measure the expression of sarcoplasmic reticulum Ca2+-ATPase (SERCA) in protein levels in rats. The activities of SERCA2a were detected by the biochemical kit finally. RESULTS: We found that Nitrosyl hydrogen could significantly increase LVEF, +dp/dt, -dp/dt (P<0.05), significantly decrease NT-ProBNP and LVEDP (P<0.01), and significantly enhance the activities of SERCA2a protein (P<0.05). CONCLUSIONS: These findings suggest that Nitrosyl hydrogen could improve the cardiac function possibly by increasing protein activities of SERCA2a in rats.

COVID-19 with Cardiovascular Disease: Can It Help Predict Prognosis?

Two recent articles both found that cardiovascular disease was the major comorbidity in patients with COVID-19. Inflammation of the cardiovascular system and hypoxemia in patients with COVID-19 are the important causes of cardiovascular system dysfunction. Through detailed analyses of the cardiovascular system, clinicians may identify specific patterns of cardiovascular abnormalities. If such a model can been established, the prognosis of COVID-19 patients with cardiovascular disease may be predicted.

Surgical management of Boerhaave's syndrome with early and delayed diagnosis in adults: a retrospective study of 88 patients

BACKGROUND: spontaneous esophageal rupture (Boerhaave's syndrome) is a rare and challenging clinical condition. OBJECTIVE: to evaluate the outcome of different surgical treatments for patients with Boerhaave's syndrome with an early diagnosis (< 24 h) and delayed diagnosis (> 24 h), using a retrospective cohort study in a tertiary referral center. PATIENTS AND METHODS: eighty-eight patients with Boerhaave's syndrome who underwent surgical treatment were identified from March 1994 to March 2019 in the First Hospital of Shanxi Medical University. Subsequently, they were retrospectively divided into two groups according to time from symptom onset to diagnosis (group 1, < 24 h, n = 16; group 2, > 24 h, n = 72). Primary suture repair was used in group 1 and reinforcement with a vascular muscle flap was used in group 2, in order to reduce the incidence of fistula. Patients in group 2 were further divided into two subgroups according to reinforcement using diaphragmatic flaps (subgroup 1) or intercostal muscle flaps (subgroup 2). RESULTS: the duration of hospitalization and stay in Intensive Care Unit (ICU) was significantly shorter in group 1 (p = 0.027 and p = 0.001). Group 1 had fewer postoperative esophageal leaks (p = 0.037) compared to group 2. Various aspects were compared in the two subgroups and the differences were not statistically significant (p > 0.05). CONCLUSIONS: it is very important to establish an early diagnosis for patients with Boerhaave's syndrome. Early (< 24 h) and primary suture repair is superior to delayed (> 24 h) primary repair, even for those reinforced with vascular muscle flaps. Furthermore, repair reinforcement with different muscle flaps appears to render similar results for patients with delayed diagnosis

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Surgical management of Boerhaave's syndrome with early and delayed diagnosis in adults: a retrospective study of 88 patients.

BACKGROUND: spontaneous esophageal rupture (Boerhaave's syndrome) is a rare and challenging clinical condition. OBJECTIVE: to evaluate the outcome of different surgical treatments for patients with Boerhaave's syndrome with an early diagnosis (< 24 h) and delayed diagnosis (> 24 h), using a retrospective cohort study in a tertiary referral center. PATIENTS AND METHODS: eighty-eight patients with Boerhaave's syndrome who underwent surgical treatment were identified from March 1994 to March 2019 in the First Hospital of Shanxi Medical University. Subsequently, they were retrospectively divided into two groups according to time from symptom onset to diagnosis (group 1, < 24 h, n = 16; group 2, > 24 h, n = 72). Primary suture repair was used in group 1 and reinforcement with a vascular muscle flap was used in group 2, in order to reduce the incidence of fistula. Patients in group 2 were further divided into two subgroups according to reinforcement using diaphragmatic flaps (subgroup 1) or intercostal muscle flaps (subgroup 2). RESULTS: the duration of hospitalization and stay in Intensive Care Unit (ICU) was significantly shorter in group 1 (p = 0.027 and p = 0.001). Group 1 had fewer postoperative esophageal leaks (p = 0.037) compared to group 2. Various aspects were compared in the two subgroups and the differences were not statistically significant (p > 0.05). CONCLUSIONS: it is very important to establish an early diagnosis for patients with Boerhaave's syndrome. Early (< 24 h) and primary suture repair is superior to delayed (> 24 h) primary repair, even for those reinforced with vascular muscle flaps. Furthermore, repair reinforcement with different muscle flaps appears to render similar results for patients with delayed diagnosis.

MALAT1 affects hypoxia-induced vascular endothelial cell injury and autophagy by regulating miR-19b-3p/HIF-1α axis.

Cardiovascular disease has become the leading cause of death in the world. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays an important role in cardiovascular disease, such as stroke. However, the role of MALAT1 in hypoxia (HYP)-induced vascular endothelial cells (VECs) remains unclear. In the present study, HYP-treated human umbilical vein endothelial cells (HUVECs) were utilized to simulate HYP-induced VEC injury. It was found that after HYP treatment, the levels of MALAT1 and hypoxia-induced factor-1 (HIF-1α) in HUVECs were upregulated, while the level of miR-19b-3p was downregulated. Knockdown of MALAT1 with siRNA significantly reduced the HIF-1α level induced by HYP. In addition, MALAT1 knockdown inhibited HYP-induced HUVECs apoptosis, autophagy and inflammation. The overexpression of HIF-1α overcame the effect of MALAT1 knockdown. Mechanism analysis showed that MALAT1-targeted miR-19b-3p and then regulated downstream HIF-1α. MALAT1 knockdown increased the level of miR-19b-3p in cells, and increased miR-19b-3p further inhibited the expression of HIF-1α, thereby reducing the HYP-induced HUVECs apoptosis, autophagy and inflammation. Taken together, these results suggest that MALAT1 may be a potential target for mitigating HYP-induced endothelial cell injury.