BACKGROUND: The characteristics of patients with intracerebral hemorrhage (ICH) complicated by alcohol use disorders (AUD) are not well understood. Investigating the clinical characteristics and prognosis of this subgroup (AUD-ICH) is necessary.
METHODS: This study involved young males with ICH who were admitted to our hospital between January 2013 and March 2022. Based on drinking patterns, the included cases were divided into three groups: AUD, occasional drinking, and non-drinking. We compared the clinical characteristics and prognosis of patients in the three groups. The effect of AUD on hematoma expansion and long-term dysfunction was explored by developing regression models. The potential mediating role of hematoma density heterogeneity within the relationship between AUD and hematoma expansion was examined through mediation analysis.
RESULTS: This study included 222 cases of male patients with ICH, with a mean age of 54.16. AUD patients had a higher risk of hematoma expansion and dysfunction compared to occasional drinkers (odds ratio [OR] 2.966, p=0.028 for hematoma expansion; hazard ratio [HR] 2.620, p=0.006 for dysfunction) and non-drinkers (OR 3.505, p=0.011 for hematoma expansion; HR 2.795, P=0.003 for dysfunction). The mediation analysis showed that the indirect effect through hematoma density heterogeneity on the relationship between AUD and hematoma expansion was significant, with a mediated proportion of 19.3%.
CONCLUSIONS: AUD was an independent risk factor for hematoma expansion and long-term dysfunction in young male patients with ICH. Hematoma density heterogeneity partially mediated the relationship between AUD and hematoma expansion.

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BACKGROUND: Patients requiring extraction of infected or dysfunctional cardiac implantable electronic devices (CIED) have high morbidity and mortality. The Micra™ leadless cardiac pacemaker (LCP) may be beneficial for patients requiring permanent pacemaker therapy after CIED extraction.
METHODS: This study aimed to assess the feasibility, timing and outcomes of LCP implantation in patients who underwent CIED extraction due to infection or dysfunction. The local Micra™ LCP registry was reviewed for LCP implantations and CIED extractions.
RESULTS: Micra™ LCP implantation was scheduled for 48 consecutive patients (21 women, 44%) undergoing CIED extraction for infection (n = 38, 79%) or dysfunction (n = 10, 21%), and feasible in 47 (98%). Complete CIED removal was feasible in 44 patients (92%) and in 37/38 patients with infected CIED (97%). Overall, 32 LCP (67%) were implanted in a single procedure: 3 (6%) before and 13 (27%) after CIED extraction. LCP were implanted in a single procedure in 24/38 patients (63%) with infected CIED and in 8/10 patients (80%) with dysfunctional CIED. The in-hospital mortality rate was 6% (n = 3), and the survival rates at 30 days, 90 days and 1 year were 94% (n = 45/48), 90% (n = 43/48), and 85% (n = 41/48), respectively. No recurrent LCP-related mortality or infections occurred during a median follow-up of 15 (interquartile range, 12-41) months.
CONCLUSIONS: Two-thirds of LCPs could be implanted in a single procedure with CIED extraction; no recurrent infections were detected. Overall, Micra™ LCP implantation in patients requiring CIED extraction was feasible.

This report emphasizes the need for interdisciplinary collaboration in diagnosing and treating pediatric obstructive sleep apnea (OSA). OSA, affecting 1% to 4% of children, often results from adenotonsillar hypertrophy, craniofacial disorders, or obesity. While adenotonsillectomy is the primary treatment, about 75% of children, especially those with craniofacial disorders or obesity, continue to experience OSA symptoms post-surgery. To address these cases, several medical fields emphasize the necessity and demand for interdisciplinary collaboration in managing pediatric OSA. Therefore, the authors aimed to develop the Pediatric Obstructive Sleep Apnea Diagnostic Examination Form (POSADEF). This form, based on clinical experience and the literature, captures craniofacial and functional characteristics linked to pediatric OSA. A case study of an eight-year-old girl with OSA, who was unsuccessfully treated with adenotonsillectomy, underlines the importance of the diagnostic examination form. The orthodontic assessment revealed craniofacial disorders and subsequent treatment with maxillary expansion and functional appliance therapy resolved her OSA symptoms. This case demonstrates the value of POSADEF in enabling comprehensive evaluation and treatment across medical disciplines. POSADEF is designed to assist health care professionals in diagnosing craniofacial and orofacial anomalies contributing to pediatric OSA.

Nasal valve dysfunction can substantially impact nasal airflow and overall quality of life. This review provides a comprehensive examination of nasal valve dysfunction, including its mechanisms, classification, and surgical management. The nasal valves include internal and external valves, each of which plays a crucial role in regulating nasal airflow. Subclassification of the external nasal valve into alar and rim valves helps specify the site of obstruction when present and informs the choice of surgical intervention. Dynamic nasal valve obstruction, often characterized by inspiratory collapse of the nasal valve, must be distinguished from static obstruction, which refers to nasal valve stenosis. Accurate identification of the location and mechanism of nasal valve dysfunction is essential for effective management. Various surgical procedures target specific components of the nasal valve and can produce favorable functional outcomes. The selection of surgical procedures, whether individually or in combination, should be tailored to the characteristics of nasal valve dysfunction and the external nasal characteristics of the patient. Strict adherence to proper surgical techniques is imperative for achieving optimal treatment outcomes.

Arrhythmia and cardiac hypertrophy are two very common cardiovascular diseases that can lead to heart failure and even sudden death, thus presenting a serious threat to human life and health. According to global statistics, nearly one million people per year die from arrhythmia, cardiac hypertrophy and other associated cardiovascular diseases. Hence, there is an urgent need to find new treatment targets and to develop new intervention measures. Recently, mitochondrial dysfunction has been examined in relation to heart disease with a view to lowering the incidence of arrhythmia and cardiac hypertrophy. The heart is the body\'s largest energy consuming organ, turning over about 20 kg of adenosine triphosphate (ATP) per day in the mitochondria. Mitochondrial oxidative phosphorylation (OXPHOS) produces up to 90% of the ATP needed by cardiac muscle cells for contraction and relaxation. Dysfunction of heart mitochondria can therefore induce arrhythmia, cardiac hypertrophy and other cardiovascular diseases. Mitochondrial DNA (mtDNA) mutations cause disorders in OXPHOS and defects in the synthesis of muscle contraction proteins. These lead to insufficient production of secondary ATP, increased metabolic requirements for ATP by the myocardium, and the accumulation of reactive oxygen species (ROS). The resulting damage to myocardial cells eventually induces arrhythmia and cardiac hypertrophy. Mitochondrial damage decreases the efficiency of energy production, which further increases the production of ROS. The accumulation of ROS causes mitochondrial damage and eventually leads to a vicious cycle of mitochondrial damage and low efficiency of mitochondrial energy production. In this review, the mechanism underlying the development of arrhythmia and cardiac hypertrophy is described in relation to mitochondrial energy supply, oxidative stress, mtDNA mutation and Mitochondrial dynamics. Targeted therapy for arrhythmia and cardiac hypertrophy induced by mitochondrial dysfunction is also discussed in terms of its potential clinical value. These strategies should improve our understanding of mitochondrial biology and the pathogenesis of arrhythmia and cardiac hypertrophy. They may also identify novel strategies for targeting mitochondria in the treatment of these diseases.

Despite recent advances in cancer therapy, anthracycline-based combination therapy remains the standardized first-line strategy and has been found to have effective antitumor actions. Anthracyclines are extremely cardiotoxic, which limits the use of these powerful chemotherapeutic agents. Although numerous studies have been conducted on the cardiotoxicity of anthracyclines, the precise mechanisms by which doxorubicin causes cardiomyocyte death and myocardial dysfunction remain incompletely understood. This review highlights recent updates in mechanisms and therapies involved in doxorubicin-induced cardiomyocyte death, including autophagy, ferroptosis, necroptosis, pyroptosis, and apoptosis, as well as mechanisms of cardiovascular dysfunction resulting in myocardial atrophy, defects in calcium handling, thrombosis, and cell senescence. We sought to uncover potential therapeutic approaches to manage anthracycline cardiotoxicity via manipulation of crucial targets involved in doxorubicin-induced cardiomyocyte death and dysfunction.

UNASSIGNED: There is limited knowledge on cognitive performance in Behçet\'s disease (BD), the majority of which come from patients with neuro-Behçet\'s disease. However, the influence of BD on cognitive function in patients without neurological involvement is still not well understood.The aim of the study was to determine the frequency of cognitive involvement in BD patients without evident neuropsychiatric symptoms and to identify associated clinical variables in those patients.
UNASSIGNED: Forty BD patients who fulfilled the diagnostic International Criteria for Behçet \'s Disease (ICBD) without obvious neuropsychiatric manifestations were studied and compared with forty healthy controls matched for age, sex, and education. A comprehensive medical history, rheumatological, neurological, psychiatric, and psychometric assessment were applied for all patients. Behçet\'s disease Current Activity Form (BDCAF) was used to assess disease activity. For patients as well as controls, validated Arabic versions of the Wechsler Adult Intelligence Scale-Revised and Wechsler Memory Scale-Revised were used for assessment of cognitive function. Anxiety and depression were additionally assessed for both groups using the anxiety and depression subdivisions of the Arabic Version of Symptom Checklist 90 Revised.
UNASSIGNED: Cognitive impairment was identified in 37.5% of BD patients compared to none of the controls. Memory represents the cognitive domain most frequently affected. Cognitive involvement was significantly associated with current corticosteroid use and depression as measured by SCL-90-R. On the other hand, neither the activity of the disease nor the level of anxiety was associated with cognitive involvement.
UNASSIGNED: Cognitive dysfunction is reported in BD patients distinctly and independently of clinically overt neurologic involvement. Prevalence of cognitive impairment in patients with BD is strikingly high at 37.5%, whereas the control group exhibited no such signs. Psychological assessment should be performed for every BD patient to reveal any cognitive involvement. It is highly recommended to encourage psychological intervention to prevent any further deterioration, especially in patients who are experiencing depression or currently using corticosteroids.

We conducted a retrospective review of patients who underwent valved homograft conduits (VHC) for right ventricular outflow tract (RVOT) reconstruction at our center. Long-term outcomes were analyzed, and risk factors affecting the long-term durability of VHC were explored. Kaplan-Meier survival curves were used to evaluate survival, freedom from VHC reintervention, and freedom from VHC dysfunction. Multivariate Cox proportional hazards regression model was used to analyze the risk factors for late VHC dysfunction. A total of 290 patients who underwent VHC for RVOT reconstruction in our center were enrolled. Seven patients occurred early death, all of which were in the non-Ross group. Two hundred and sixty-five patients were followed up for 85 (0.3-176.0) months. Six patients occurred late death, all in the non-Ross group. Six patients underwent VHC reintervention. During the follow-up period, 52 patients developed VHC dysfunction. Freedom from VHC dysfunction was higher in the Ross group than in the non-Ross group in the whole cohort. Multivariate Cox regression analysis showed that age < 6 years and non-Ross operation were independent risk factors for VHC dysfunction. Freedom from VHC dysfunction was higher in the Ross group than in the non-Ross group in patients younger than 6 years of age at surgery. However, there was no significant difference in freedom from VHC dysfunction between the two groups in patients older than 6 years. Long-term outcomes of VHC for RVOT reconstruction are satisfactory. Age < 6 years and non-Ross operation are independent risk factors for VHC dysfunction. The long-term survival rate and durability of VHC in Ross group were better than those in non-Ross group. The advantage of long-term durability of VHC in the Ross group was mainly reflected in patients aged < 6 years at operation.

OBJECTIVE: NK cells play a vital role in tumor immune resistance. Various factors affect NK cell activity. While NK cell dysfunction has been observed in numerous malignancies, the underlying mechanisms in gastric cancer remain unclear.
METHODS: Flow cytometry was used to identify the phenotypic distribution and expression of activated receptors on NK cells. ELISA was used to determine the expression of cytokines. We examined the expression of NK cell-related genes and explored their association with survival and prognosis. Additionally, we conducted PCR detection of miR-552-5p expression levels in plasma exosomes of patients and investigated its correlation with phenotypic distribution and activated receptors. We used flow cytometry and ELISA to verify the role of miR-552-5p in NK cell dysfunction. Furthermore, we investigated the potential role of PD-1/PD-L1 in regulating NK cell dysfunction in patients\' cells.
RESULTS: We observed a significant decrease in the percentage of NKG2D and NKp30 and IFN-γ and TNF-α in patients than in healthy volunteers. Patients with low levels of CD56, CD16, NKG2D, and NKP46 exhibited poorer survival prognoses. Moreover, increased expression levels of plasma exosomal miR-552-5p in patients were negatively associated with NK cell phenotypic distribution and activated receptor expression. MiR-552-5p downregulated the secretion of perforin, granzyme, and IFN-γ as well as the expression of NKp30, NKp46, and NKG2D. Additionally, it suppressed the cytotoxicity of NK cells. The inhibitory effect of miR-552-5p, on NK cell function was reversed when anti-PD-L1 antibodies were used.
CONCLUSIONS: Exosomal miR-552-5p targets the PD-1/PD-L1 axis, leading to impaired NK cell function.