Application of the "3-2-1" body surface localization method in intertrochanteric femoral fractures: a technical note.

In femoral intertrochanteric fractures, poor incision positioning may result in inaccurate intramedullary nail placement direction, which increases the difficulty of reduction and thus the size and number of incisions. Repeated intraoperative fluoroscopy not only increases the radiation exposure of the surgeon but also affects the operative outcomes. This technical note proposes a method of identifying incision positioning preoperatively using the "3-2-1" body surface localization method. This auxiliary positioning technique uses a body surface locator and the lower limb force axis. It can predict the incisions for the needle insertion point, spiral blade, and locking nails, create minimally invasive incisions, avoid incorrect incision position, facilitate accurate intraoperative intramedullary nail placement, reduce the incision size, intraoperative bleeding, and radiation exposure, and improve surgical efficiency and reduction quality.

Annexin A1 binds PDZ and LIM domain 7 to inhibit adipogenesis and prevent obesity.

Obesity is a global issue that warrants the identification of more effective therapeutic targets and a better understanding of the pivotal molecular pathogenesis. Annexin A1 (ANXA1) is known to inhibit phospholipase A2, exhibiting anti-inflammatory activity. However, the specific effects of ANXA1 in obesity and the underlying mechanisms of action remain unclear. Our study reveals that ANXA1 levels are elevated in the adipose tissue of individuals with obesity. Whole-body or adipocyte-specific ANXA1 deletion aggravates obesity and metabolic disorders. ANXA1 levels are higher in stromal vascular fractions (SVFs) than in mature adipocytes. Further investigation into the role of ANXA1 in SVFs reveals that ANXA1 overexpression induces lower numbers of mature adipocytes, while ANXA1-knockout SVFs exhibit the opposite effect. This suggests that ANXA1 plays an important role in adipogenesis. Mechanistically, ANXA1 competes with MYC binding protein 2 (MYCBP2) for interaction with PDZ and LIM domain 7 (PDLIM7). This exposes the MYCBP2-binding site, allowing it to bind more readily to the SMAD family member 4 (SMAD4) and promoting its ubiquitination and degradation. SMAD4 degradation downregulates peroxisome proliferator-activated receptor gamma (PPARγ) transcription and reduces adipogenesis. Treatment with Ac2-26, an active peptide derived from ANXA1, inhibits both adipogenesis and obesity through the mechanism. In conclusion, the molecular mechanism of ANXA1 inhibiting adipogenesis was first uncovered in our study, which is a potential target for obesity prevention and treatment.

Repeated misdiagnosis of small intestine bronchogenic cyst: a case report.

Bronchogenic cysts are uncommon congenital malformations of the respiratory system. These cysts can be categorized as intrapulmonary, mediastinal, or ectopic. Ectopic bronchogenic cysts, which lack distinctive clinical and imaging features, are particularly challenging to diagnose. This study presents a 48-year-old woman having a small intestinal bronchogenic cyst. She was repeatedly misdiagnosed as having an ovarian chocolate cyst or a cystic mass of bladder origin three years ago. However, no cyst was found during the operation. Half a year prior to presenting at our hospital, the patient developed frequent urination, prompting her to seek further treatment. We eventually discovered a cyst in the small intestine. The histological evaluation of the specimen showed a bronchogenic cyst. Small intestine bronchogenic cysts are extremely rare and easily misdiagnosed. It should be considered as one of the differential diagnoses of pelvic cysts. Particularly, when intraoperative exploration of the pelvic cavity fails to detect any cysts, consideration should be given to the possibility of small intestine bronchogenic cysts.

Clinical experience of bench surgery combined with autotransplantation after three-dimensional laparoscopic nephrectomy for the treatment of highly complex renal tumor.

OBJECTIVE: To assess the feasibility and safety of three-dimensional (3D) laparoscopic nephrectomy in combination with bench surgery and autotransplantation for treating highly complex renal tumors. MATERIALS AND METHODS: The clinical data of six patients with highly complex renal cell carcinoma were collected. All patients underwent 3D laparoscopic nephrectomy in combination with bench surgery and autotransplantation by the same surgeons, two of them had previously undergone laparoscopic partial nephrectomy for contralateral renal cancer. RESULTS: The total operative time was 366 ± 65 min, the warm ischemia time (WIT) was 1.3 ± 0.4 min, and the cold ischemia time was 121 ± 26 min. While one patient received a diluted autologous blood transfusion, the intraoperative blood loss was 217 ± 194 ml. No increase in the serum creatinine (SCr) level was observed at postoperative day 30 compared with the preoperative time, and none of the patients received dialysis either during the hospital stay or to date. Although one patient underwent nephrectomy due to tumor recurrence in the transplanted kidney, the others reported no tumor recurrence or distant metastases on imaging to date. CONCLUSION: 3D laparoscopic nephrectomy, when combined with bench surgery and autotransplantation, can become a feasible option for treating highly complex renal cell carcinoma cases when expecting to preserve renal function maximally.

NAD+ rescues aging-induced blood-brain barrier damage via the CX43-PARP1 axis.

Blood-brain barrier (BBB) function deteriorates during aging, contributing to cognitive impairment and neurodegeneration. It is unclear what drives BBB leakage in aging and how it can be prevented. Using single-nucleus transcriptomics, we identified decreased connexin 43 (CX43) expression in cadherin-5+ (Cdh5+) cerebral vascular cells in naturally aging mice and confirmed it in human brain samples. Global or Cdh5+ cell-specific CX43 deletion in mice exacerbated BBB dysfunction during aging. The CX43-dependent effect was not due to its canonical gap junction function but was associated with reduced NAD+ levels and mitochondrial dysfunction through NAD+-dependent sirtuin 3 (SIRT3). CX43 interacts with and negatively regulates poly(ADP-ribose) polymerase 1 (PARP1). Pharmacologic inhibition of PARP1 by olaparib or nicotinamide mononucleotide (NMN) supplementation rescued NAD+ levels and alleviated aging-associated BBB leakage. These findings establish the endothelial CX43-PARP1-NAD+ pathway's role in vascular aging and identify a potential therapeutic strategy to combat aging-associated BBB leakage with neuroprotective implications.

Metabolic profiling reveals altered tryptophan metabolism in patients with kawasaki disease.

Kawasaki disease (KD) is a childhood vasculitis disease that is difficult to diagnose, and there is an urgent need for the identification of accurate and specific biomarkers. Here, we aimed to investigate metabolic alterations in patients with KD to determine novel diagnostic and prognostic biomarkers for KD. To this end, we performed untargeted metabolomics and found that several metabolic pathways were significantly enriched, including amino acid, lipid, and tryptophan metabolism, the latter of which we focused on particularly. Tryptophan-targeted metabolomics was conducted to explore the role of tryptophan metabolism in KD. The results showed that Trp and indole acetic acid (IAA) levels markedly decreased, and that l-kynurenine (Kyn) and kynurenic acid (Kyna) levels were considerably higher in patients with KD than in healthy controls. Changes in Trp, IAA, Kyn, and Kyna levels in a KD coronary arteritis mouse model were consistent with those in patients with KD. We further analyzed public single-cell RNA sequencing data of patients with KD and revealed that their peripheral blood mononuclear cells showed Aryl hydrocarbon receptor expression that was remarkably higher than that of healthy children. These results suggest that the Trp metabolic pathway is significantly altered in KD and that metabolic indicators may serve as novel diagnostic and therapeutic biomarkers for KD.

The mechanism and therapy of aortic aneurysms.

Aortic aneurysm is a chronic aortic disease affected by many factors. Although it is generally asymptomatic, it poses a significant threat to human life due to a high risk of rupture. Because of its strong concealment, it is difficult to diagnose the disease in the early stage. At present, there are no effective drugs for the treatment of aneurysms. Surgical intervention and endovascular treatment are the only therapies. Although current studies have discovered that inflammatory responses as well as the production and activation of various proteases promote aortic aneurysm, the specific mechanisms remain unclear. Researchers are further exploring the pathogenesis of aneurysms to find new targets for diagnosis and treatment. To better understand aortic aneurysm, this review elaborates on the discovery history of aortic aneurysm, main classification and clinical manifestations, related molecular mechanisms, clinical cohort studies and animal models, with the ultimate goal of providing insights into the treatment of this devastating disease. The underlying problem with aneurysm disease is weakening of the aortic wall, leading to progressive dilation. If not treated in time, the aortic aneurysm eventually ruptures. An aortic aneurysm is a local enlargement of an artery caused by a weakening of the aortic wall. The disease is usually asymptomatic but leads to high mortality due to the risk of artery rupture.

Gasdermin D Deficiency in Vascular Smooth Muscle Cells Ameliorates Abdominal Aortic Aneurysm Through Reducing Putrescine Synthesis.

Abdominal aortic aneurysm (AAA) is a common vascular disease associated with significant phenotypic alterations in vascular smooth muscle cells (VSMCs). Gasdermin D (GSDMD) is a pore-forming effector of pyroptosis. In this study, the role of VSMC-specific GSDMD in the phenotypic alteration of VSMCs and AAA formation is determined. Single-cell transcriptome analyses reveal Gsdmd upregulation in aortic VSMCs in angiotensin (Ang) II-induced AAA. VSMC-specific Gsdmd deletion ameliorates Ang II-induced AAA in apolipoprotein E (ApoE)-/- mice. Using untargeted metabolomic analysis, it is found that putrescine is significantly reduced in the plasma and aortic tissues of VSMC-specific GSDMD deficient mice. High putrescine levels trigger a pro-inflammatory phenotype in VSMCs and increase susceptibility to Ang II-induced AAA formation in mice. In a population-based study, a high level of putrescine in plasma is associated with the risk of AAA (p < 2.2 × 10-16 ), consistent with the animal data. Mechanistically, GSDMD enhances endoplasmic reticulum stress-C/EBP homologous protein (CHOP) signaling, which in turn promotes the expression of ornithine decarboxylase 1 (ODC1), the enzyme responsible for increased putrescine levels. Treatment with the ODC1 inhibitor, difluoromethylornithine, reduces AAA formation in Ang II-infused ApoE-/- mice. The findings suggest that putrescine is a potential biomarker and target for AAA treatment.

[Vacuum sealing drainage as an adjuvant treatment of severe scrotal infectious disease: Clinical analysis of 9 cases].

OBJECTIVE: To evaluate the clinical effectiveness of vacuum sealing drainage (VSD) in the treatment of severe scrotal infectious diseases and to summarize the practical experience obtained during its implementation. METHODS: Clinical data from 9 patients with severe scrotal infectious diseases were compiled. All patients underwent debridement assisted by a VSD device in addition to conventional treatment measures. RESULTS: Following debridement with VSD device, combined with systemic anti-infection treatment and nutritional support, all patients exhibited favorable therapeutic outcomes, with no fatalities. The average duration of debridement was 81±27 minutes. One patient necessitated secondary debridement and skin grafting, while another was transferred to the ICU due to septic shock. CONCLUSIONS: The application of VSD device can streamline the treatment process for severe scrotal infectious diseases, alleviate patient discomfort, and promote patient recovery.

HDL Structure.

HDL has various protein components, including enzymes, complement components, apolipoproteins, protease inhibitors, etc. In addition to proteins, lipids are also a significant component of HDL. These components and their structure determine the function of HDL. HDL is heavily involved in the acute response phase, complement regulation phase, hemostasis phase, immune response phase, and protease inhibition phase. Among the apolipoproteins, the predominant component is Apo A-I, which confers various atherogenic activities to HDL. Apo A-II, Apo-C, Apo-D, Apo-F, Apo-H, Apo-J, and Apo-O, which can bind free fatty acids, regulate the activity of many proteins involved in HDL metabolism, inhibit lipid transfer, and control the endogenous coagulation cascade. A major functional component is the enzyme LCAT, which helps catalyze the conversion of cholesterol to plasma-based lipoproteins and then to cholesteryl esters. Another enzyme associated with HDL is human paraoxonase, calcium-, PON1-, PON2-, and PON3-dependent lactone enzyme with catalytic activity, including reversible binding to substrates. PAF-AH is a phospholipase with lipoprotein properties, and HDL and LDL particles are commonly bound to plasma PAF-AH for circulation. As for lipid components, PC is an essential phospholipid subclass and may be a biomarker for constitutive inflammation. Sphingolipids, such as sphingomyelin and ceramide, also play an indispensable role in HDL function. In different physiological and pathological stages and plasma environments, HDL can exhibit different structural features, such as discoid HDL and spherical rHDL.

HDL and Endothelial Function.

Plasmid high-density lipoprotein (HDL) is a critical biomarker in predicting cardiovascular diseases. Endothelial cells are physically located in the intima of blood vessels, which directly contact with circulating substances. Numerous previous studies have demonstrated that HDL exert protective effects on maintaining endothelial integrity and enhance anti-inflammatory functions, etc. In this chapter, we introduced how HDL benefit endothelial functions. We summarized the function of HDL on endothelial cell, such as endothelial permeability, proliferation, migration, apoptosis, etc. In addition, we discussed the effects of HDL on classical endothelial functions, such as coagulation and vasodilation. Although HDL have huge effects on endothelial functions, lots of cardiovascular diseases such as atherosclerosis could not be fully prevented and treated. Thus, a further understanding of the relationship between HDL and endothelial cell is needed, which would create a potential therapeutic approach to cardiovascular diseases.

Conversion of failed proximal femoral nail antirotation to uncemented or cemented femoral component fixation: a multicentre retrospective study with a median 10-year follow-up.

BACKGROUND: Conversion of a failed proximal femoral nail antirotation (PFNA) to a total hip arthroplasty (THA) is becoming increasingly universal. However, consensus has not been reached regarding which device (uncemented or hybrid THA) to use. The aim of this retrospective study was to compare the clinical outcomes of the conversion of failed PFNAs to uncemented versus hybrid THAs in the elderly population. METHODS: Consecutive elderly patients with prior failed PFNAs treated with uncemented or hybrid THA from January 2008 to December 2019 were retrospectively identified from two medical centres. The primary outcome was implant survival after THA revision; secondary outcomes were the functional outcomes assessed using the Harris Hip Score (HHS) and the incidence of key THA-related complications. RESULTS: A total of 236 patients (uncemented THA, n = 116; hybrid THA, n = 120) were eligible for this study. Kaplan-Meier survival curves demonstrated that the 10-year cumulative survival rates were 0.801 (95% confidence interval [CI], 0.783-0.852) in the uncemented THA group versus 0.925 (95% CI, 0.861-0.964) in the hybrid THA group (hazard ratio [HR] 0.36 [95% CI 0.24-0.56], p = 0.004). From the 72nd month after the revision to the last follow-up, functional outcomes differed considerably between cohorts (each p < 0.05), and the rate of key THA-related complications was comparable between cohorts (p = 0.004). CONCLUSION: For elderly patients with prior failed PFNAs who experienced uncemented or hybrid THA, hybrid THA revision may provide a clinically significant improvement over uncemented THA revision with regard to implant survival, functional outcomes, and THA-related complications compared to uncemented THA revision.

Prognostic Value of Elevated Levels of Plasma N-Acetylneuraminic Acid in Patients With Heart Failure.

BACKGROUND: Cardiac sialylation is involved in a variety of physiological processes in the heart. Altered sialylation has been implicated in heart failure (HF) mice. However, its role in patients with HF is unclear, and the potential effect of modulation of cardiac sialylation is worth exploring. METHODS: We first assessed the association between plasma N-acetylneuraminic acid levels and the incidence of adverse cardiovascular events in patients with HF over a median follow-up period of 2 years. Next, immunoblot analysis and lectin histochemistry were performed in cardiac tissue to determine the expression levels of neuraminidases and the extent of cardiac desialylation. Finally, the therapeutic impact of a neuraminidase inhibitor was evaluated in animal models of HF. RESULTS: Among 1699 patients with HF, 464 (27%) died of cardiovascular-related deaths or underwent heart transplantation. We found that the elevated plasma N-acetylneuraminic acid level was independently associated with a higher risk of incident cardiovascular death and heart transplantation (third tertile adjusted hazard ratio, 2.11 [95% CI, 1.67-2.66], P<0.001). In addition, in cardiac tissues from patients with HF, neuraminidase expression was upregulated, accompanied by desialylation. Treatment with oseltamivir, a neuraminidase inhibitor, in HF mice infused with isoproterenol and angiotensin II significantly inhibited desialylation and ameliorated cardiac dysfunction. CONCLUSIONS: This study uncovered a significant association between elevated plasma N-acetylneuraminic acid level and an increased risk of a poor clinical outcome in patients with HF. Our data support the notion that desialylation represents an important contributor to the progression of HF, and neuraminidase inhibition may be a potential therapeutic strategy for HF.

Untargeted metabolomics identifies succinate as a biomarker and therapeutic target in aortic aneurysm and dissection.

AIMS: Aortic aneurysm and dissection (AAD) are high-risk cardiovascular diseases with no effective cure. Macrophages play an important role in the development of AAD. As succinate triggers inflammatory changes in macrophages, we investigated the significance of succinate in the pathogenesis of AAD and its clinical relevance. METHODS AND RESULTS: We used untargeted metabolomics and mass spectrometry to determine plasma succinate concentrations in 40 and 1665 individuals of the discovery and validation cohorts, respectively. Three different murine AAD models were used to determine the role of succinate in AAD development. We further examined the role of oxoglutarate dehydrogenase (OGDH) and its transcription factor cyclic adenosine monophosphate-responsive element-binding protein 1 (CREB) in the context of macrophage-mediated inflammation and established p38αMKOApoe-/- mice. Succinate was the most upregulated metabolite in the discovery cohort; this was confirmed in the validation cohort. Plasma succinate concentrations were higher in patients with AAD compared with those in healthy controls, patients with acute myocardial infarction (AMI), and patients with pulmonary embolism (PE). Moreover, succinate administration aggravated angiotensin II-induced AAD and vascular inflammation in mice. In contrast, knockdown of OGDH reduced the expression of inflammatory factors in macrophages. The conditional deletion of p38α decreased CREB phosphorylation, OGDH expression, and succinate concentrations. Conditional deletion of p38α in macrophages reduced angiotensin II-induced AAD. CONCLUSION: Plasma succinate concentrations allow to distinguish patients with AAD from both healthy controls and patients with AMI or PE. Succinate concentrations are regulated by the p38α-CREB-OGDH axis in macrophages.

Alternol Sensitizes Renal Carcinoma Cells to TRAIL-Induced Apoptosis.

Purpose: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a member of the TNF family, can selectively induce cancer cell death while sparing normal cells. However, the application of TRAIL-based antitumor therapies has been hindered due to drug resistance. Alternol is a new compound isolated from microbial fermentation that possesses antitumor activity in different tumors. In our research, we discovered that alternol can sensitize TRAIL-induced apoptosis in renal carcinoma cells (RCCs). Materials and Methods: Cytotoxic activity was measured by MTT assay. Apoptosis was probed using the PI/annexin V method. Real-time PCR and western blot were used to test the levels of mRNA and protein, respectively. Luciferase assay was used to investigate whether CHOP regulated the expression of death receptor (DR) 5 through transcription. A xenogeneic tumor transplantation model was used to evaluate the anticancer effects of alternol/TRAIL in vivo. Results: When the mechanisms were investigated, we discovered that alternol increased DR5 expression. DR5 knockdown by siRNA eliminated the enhanced effect of alternol on TRAIL-mediated apoptosis. Alternol reduced the expression of antiapoptotic proteins and increased the levels of proapoptotic proteins. Moreover, alternol increased the level of CHOP, which is necessary for the enhancing effect of alternol on TRAIL-induced apoptosis, given that downregulation of CHOP abrogated the synergistic effect. DR5 upregulation induced by alternol required the production of reactive oxygen species (ROS). Removing ROS inhibited the induction of DR5 and blocked the antiapoptotic proteins induced by alternol. Conclusion: Taken together, our research suggested that alternol increased TRAIL-mediated apoptosis via inhibiting antiapoptotic proteins and upregulating DR5 levels via ROS generation and the CHOP pathway.

ICAM-1 Activates Platelets and Promotes Endothelial Permeability through VE-Cadherin after Insufficient Radiofrequency Ablation.

Radiofrequency ablation (RFA) for hepatocellular carcinoma (HCC) often leads to aggressive local recurrence and increased metastasis, and vascular integrity and platelets are implicated in tumor metastasis. However, whether interactions between endothelial cells and platelets induce endothelial permeability in HCC after insufficient RFA remains unclear. Here, significantly increased CD62P-positive platelets and sP-selectin in plasma are observed in HCC patients after RFA, and tumor-associated endothelial cells (TAECs) activate platelets and are susceptible to permeability after heat treatment in the presence of platelets in vitro. In addition, tumors exhibit enhanced vascular permeability after insufficient RFA in mice; heat treatment promotes platelets-induced endothelial permeability through vascular endothelial (VE)-cadherin, and ICAM-1 upregulation in TAECs after heat treatment results in platelet activation and increased endothelial permeability in vitro. Moreover, the binding interaction between upregulated ICAM-1 and Ezrin downregulates VE-cadherin expression. Furthermore, platelet depletion or ICAM-1 inhibition suppresses tumor growth and metastasis after insufficient RFA in an orthotopic tumor mouse model, and vascular permeability decreases in ICAM-1-/- mouse tumor after insufficient RFA. The findings suggest that ICAM-1 activates platelets and promotes endothelial permeability in TAECs through VE-cadherin after insufficient RFA, and anti-platelet and anti-ICAM-1 therapy can be used to prevent progression of HCC after insufficient RFA.

Eva1a ameliorates atherosclerosis by promoting re-endothelialization of injured arteries via Rac1/Cdc42/Arpc1b.

AIMS: Eva-1 homologue 1 (Eva1a) is a novel protein involved in the regulation of cardiac remodelling and plaque stability, but little is known about its role in re-endothelialization and the development of atherosclerosis (AS). Thus, in the present study, we aimed to elucidate the function of Eva1a in re-endothelialization and AS. METHODS AND RESULTS: Wire injuries of carotid and femoral arteries were established in Eva1a-/- mice. Eva1a-deficient mice were crossed with apolipoprotein E-/- (ApoE-/-) mice to evaluate AS development and re-endothelialization of carotid artery injuries. Denudation of the carotid artery at 3, 5, and 7 days was significantly aggravated in Eva1a-/- mice. The neointima of the femoral artery at 14 and 28 days was consequently exacerbated in Eva1a-/- mice. The area of atherosclerotic lesions was increased in Eva1a-/-ApoE-/- mice. To explore the underlying mechanisms, we performed transwell, scratch migration, cell counting kit-8, and bromodeoxyuridine assays using cultured human aorta endothelial cells (HAECs), which demonstrated that EVA1A promoted HAEC migration and proliferation. Proteomics revealed that the level of actin-related protein 2/3 complex subunit 1B (Arpc1b) was decreased, while Eva1a expression was absent. Arpc1b was found to be a downstream molecule of EVA1A by small interfering RNA transfection assay. Activation of Rac1 and Cdc42 GTPases was also regulated by EVA1A. CONCLUSION: This study provides insights into anti-atherogenesis effects of Eva1a by promoting endothelium repair. Thus, Eva1a is a promising therapeutic target for AS.

Functional, Magnetic Resonance Imaging, and Second-Look Arthroscopic Outcomes After Pullout Repair for Avulsion Tears of the Posterior Lateral Meniscus Root.

BACKGROUND: Little data exist in the literature regarding second-look arthroscopic outcomes after pullout repair for avulsion tears of the posterior lateral meniscus root. PURPOSE: To (1) assess the functional, magnetic resonance imaging (MRI), and second-look arthroscopic outcomes after pullout repair for avulsion tears of the posterior lateral meniscus root; (2) determine which demographic and clinical factors influenced healing of the repaired posterior lateral meniscus root; and (3) compare outcomes between different meniscal healing status groups. STUDY DESIGN: Case series; Level of evidence, 4. METHODS: A total of 31 patients underwent pullout repair for avulsion tears of the posterior lateral meniscus root and had a minimum 2-year follow-up. Functional outcomes were assessed using patient-reported scores (Lysholm, Tegner, and International Knee Documentation Committee [IKDC] scores). Lateral meniscal extrusion, cartilage degeneration of the lateral compartment, and healing of the repaired posterior lateral meniscus root were assessed via MRI. The healing status was also assessed using second-look arthroscopic surgery, and the patients were divided into different healing status groups. RESULTS: The postoperative patient-reported scores improved significantly compared with the preoperative values (P = .001). Lateral meniscal extrusion was reduced significantly from 3.37 ± 0.82 mm preoperatively to 0.63 ± 0.80 mm at final follow-up (P = .001). The grade of cartilage degeneration of the lateral compartment progressed from 0.69 ± 0.67 preoperatively to 0.95 ± 0.83 at final follow-up (P = .213). MRI scans showed complete healing in 28 patients (90.3%) and partial healing in 3 patients (9.7%). Second-look arthroscopic surgery showed stable healing in 18 of 23 patients (78.3%) and lax healing in 5 of 23 patients (21.7%). Patients with stable healing had significantly higher Lysholm and IKDC scores, more reduction of meniscal extrusion, and less progression of cartilage degeneration than did patients with lax healing (P < .05). Concomitant anterior cruciate ligament reconstruction was found to significantly positively influence healing of the repaired posterior lateral meniscus root (P = .047). CONCLUSION: Pullout repair for avulsion tears of the posterior lateral meniscus root yielded significantly improved patient-reported scores, reduced meniscal extrusion, and a satisfactory healing rate at final follow-up. Patients with stable healing had significantly better functional and MRI outcomes than did patients with lax healing.

A Non-Invasive Nanoprobe for In Vivo Photoacoustic Imaging of Vulnerable Atherosclerotic Plaque.

Vulnerable atherosclerotic (AS) plaque is the major cause of cardiovascular death. However, clinical methods cannot directly identify the vulnerable AS plaque at molecule level. Herein, osteopontin antibody (OPN Ab) and NIR fluorescence molecules of ICG co-assembled Ti3 C2 nanosheets are reported as an advanced nanoprobe (OPN Ab/Ti3 C2 /ICG) with enhanced photoacoustic (PA) performance for direct and non-invasive in vivo visual imaging of vulnerable AS plaque. The designed OPN Ab/Ti3 C2 /ICG nanoprobes successfully realize obvious NIR fluorescence imaging toward foam cells as well as the vulnerable AS plaque slices. After intravenous injection of OPN Ab/Ti3 C2 /ICG nanoprobes into AS model mice, in vivo imaging results show a significantly enhanced PA signal in the aortic arch accumulated with vulnerable plaque, well indicating the remarkable feasibility of OPN Ab/Ti3 C2 /ICG nanoprobes to distinguish the vulnerable AS plaque. The proposed OPN Ab/Ti3 C2 /ICG nanoprobes not only overcome the clinical difficulty to differentiate vulnerable plaque, but also achieve the non-invasively specific in vivo imaging of vulnerable AS plaque at molecule level, greatly promoting the innovation of cardiovascular diagnosis technology.