Primate Model Carrying LMNA Mutation Develops Dilated Cardiomyopathy.

To solve the clinical transformation dilemma of lamin A/C (LMNA)-mutated dilated cardiomyopathy (LMD), we developed an LMNA-mutated primate model based on the similarity between the phenotype of primates and humans. We screened out patients with LMD and compared the clinical data of LMD with TTN-mutated and mutation-free dilated cardiomyopathy to obtain the unique phenotype. After establishment of the LMNA c.357-2A>G primate model, primates were continuously observed for 48 months, and echocardiographic, electrophysiological, histologic, and transcriptional data were recorded. The LMD primate model was found to highly simulate the phenotype of clinical LMD. In addition, the LMD primate model shared a similar natural history with humans.

The role of T-lymphocytes in central nervous system diseases.

The central nervous system (CNS) has been considered an immunologically privileged site. In the past few decades, research on inflammation in CNS diseases has mostly focused on microglia, innate immune cells that respond rapidly to injury and infection to maintain CNS homeostasis. Discoveries of lymphatic vessels within the dura mater and peripheral immune cells in the meningeal layer indicate that the peripheral immune system can monitor and intervene in the CNS. This review summarizes recent advances in the involvement of T lymphocytes in multiple CNS diseases, including brain injury, neurodegenerative diseases, and psychiatric disorders. It emphasizes that a deep understanding of the pathogenesis of CNS diseases requires intimate knowledge of T lymphocytes. Aiming to promote a better understanding of the relationship between the immune system and CNS and facilitate the development of therapeutic strategies targeting T lymphocytes in neurological diseases.

Adaptive Point-Line Fusion: A Targetless LiDAR-Camera Calibration Method with Scheme Selection for Autonomous Driving.

Accurate calibration between LiDAR and camera sensors is crucial for autonomous driving systems to perceive and understand the environment effectively. Typically, LiDAR-camera extrinsic calibration requires feature alignment and overlapping fields of view. Aligning features from different modalities can be challenging due to noise influence. Therefore, this paper proposes a targetless extrinsic calibration method for monocular cameras and LiDAR sensors that have a non-overlapping field of view. The proposed solution uses pose transformation to establish data association across different modalities. This conversion turns the calibration problem into an optimization problem within a visual SLAM system without requiring overlapping views. To improve performance, line features serve as constraints in visual SLAM. Accurate positions of line segments are obtained by utilizing an extended photometric error optimization method. Moreover, a strategy is proposed for selecting appropriate calibration methods from among several alternative optimization schemes. This adaptive calibration method selection strategy ensures robust calibration performance in urban autonomous driving scenarios with varying lighting and environmental textures while avoiding failures and excessive bias that may result from relying on a single approach.

Effects of ACEI/ARB or CCB use on atrial fibrillation in hypertensive patients following permanent pacemaker implantation.

Aims: Permanent pacemaker implantation (PPI) combined with hypertension leads to a higher risk of new-onset atrial fibrillation (NOAF) for patients. Hence, it is essential to study how to reduce this risk. Currently, the effects of the two common anti-hypertensive drugs, angiotensin-converting enzyme inhibitors (ACEI)/angiotensin receptor blockers (ARB) and calcium channel blockers (CCB), on the risk of NOAF for such patients remain unknown. This study aimed to investigate this association. Methods: This single-center retrospective study included hypertensive patients with PPI and without prior history of AF/atrial flutter, heart valve disease, hyperthyroidism, etc. Patients were classified into ACEI/ARB group and CCB group based on their exposure drug information. The primary outcome was NOAF events that occurred within 12 months after PPI. The secondary efficacy assessments were the changes from baseline to follow-up in blood pressure and transthoracic echocardiography (TTE) parameters. A multivariate logistic regression model was used to verify our aim. Results: A total of 69 patients were finally included (51 on ACEI/ARB and 18 on CCB). Both univariate analysis [odds ratio (OR) 0.241, 95% confidence interval (CI) 0.078-0.745] and multivariate analysis (OR: 0.246, 95% CI: 0.077-0.792) demonstrated that ACEI/ARB were associated with a lower risk of NOAF compared to CCB. The mean reduction in left atrial diameter (LAD) from baseline was greater in ACEI/ARB group than in CCB group (P = 0.034). There was no statistical difference between groups in blood pressure and other TTE parameters after treatment. Conclusion: For patients with PPI combined with hypertension, ACEI/ARB may be superior to CCB in selecting anti-hypertensive drugs, as ACEI/ARB further reduces the risk of NOAF. One reason for this may be that ACEI/ARB improves left atrial remodelling such as LAD better.

C9orf72 poly(PR) aggregation in nucleus induces ALS/FTD-related neurodegeneration in cynomolgus monkeys.

Poly(PR) is a dipeptide repeat protein comprising proline and arginine residues. It is one of the translational product of expanded G4C2 repeats in the C9orf72 gene, and its accumulation is contributing to the neuropathogenesis of C9orf72-associated amyotrophic lateral sclerosis and/or frontotemporal dementia (C9-ALS/FTD). In this study, we demonstrate that poly(PR) protein alone is sufficient to induce neurodegeneration related to ALS/FTD in cynomolgus monkeys. By delivering poly(PR) via AAV, we observed that the PR proteins were located within the nucleus of infected cells. The expression of (PR)50 protein, consisting of 50 PR repeats, led to increased loss of cortical neurons, cytoplasmic lipofuscin, and gliosis in the brain, as well as demyelination and loss of ChAT positive neurons in the spinal cord of monkeys. While, these pathologies were not observed in monkeys expressing (PR)5, a protein comprising only 5 PR repeats. Furthermore, the (PR)50-expressing monkeys exhibited progressive motor deficits, cognitive impairment, muscle atrophy, and abnormal electromyography (EMG) potentials, which closely resemble clinical symptoms seen in C9-ALS/FTD patients. By longitudinally tracking these monkeys, we found that changes in cystatin C and chitinase-1 (CHIT1) levels in the cerebrospinal fluid (CSF) corresponded to the phenotypic progression of (PR)50-induced disease. Proteomic analysis revealed that the major clusters of dysregulated proteins were nuclear-localized, and downregulation of the MECP2 protein was implicated in the toxic process of poly(PR). This research indicates that poly(PR) expression alone induces neurodegeneration and core phenotypes associated with C9-ALS/FTD in monkeys, which may provide insights into the mechanisms of disease pathogenesis.

Correlation between COVID-19 vaccination and diabetes mellitus: A systematic review.

BACKGROUND: Coronavirus disease 2019 (COVID-19) is one of the current global public health threats and vaccination is the most effective tool to reduce the spread and decrease the severity of COVID-19. Diabetes is one of the important chronic diseases threatening human health and is a common comorbidity of COVID-19. What is the impact of diabetes on the immunization effect of COVID-19 vaccination? Conversely, does vaccination against COVID-19 exacerbate the severity of pre-existing diseases in patients with diabetes? There are limited and conflicting data on the interrelationship between diabetes and COVID-19 vaccination. AIM: To explore the clinical factors and possible mechanisms underlying the interaction between COVID-19 vaccination and diabetes. METHODS: We conducted a comprehensive search of PubMed, MEDLINE, EMBASE, and Reference Citation Analysis (https://www.referencecitationanalysis.com) online databases, and medRxiv and bioRxiv gray literature using the keywords "SARS-CoV-2", "COVID-19", "vaccine", "vaccination", "antibody", and "diabetes" individually or in combination, with a cut-off date of December 2, 2022. We followed inclusion and exclusion criteria and after excluding duplicate publications, studies with quantifiable evidence were included in the full-text review, plus three manually searched publications, resulting in 54 studies being included in this review. RESULTS: A total of 54 studies were included, from 17 countries. There were no randomized controlled studies. The largest sample size was 350963. The youngest of the included samples was 5 years old and the oldest was 98 years old. The included population included the general population and also some special populations with pediatric diabetes, hemodialysis, solid organ transplantation, and autoimmune diseases. The earliest study began in November 2020. Thirty studies discussed the effect of diabetes on vaccination, with the majority indicating that diabetes reduces the response to COVID-19 vaccination. The other 24 studies were on the effect of vaccination on diabetes, which included 18 case reports/series. Most of the studies concluded that COVID-19 vaccination had a risk of causing elevated blood glucose. A total of 12 of the 54 included studies indicated a "no effect" relationship between diabetes and vaccination. CONCLUSION: There is a complex relationship between vaccination and diabetes with a bidirectional effect. Vaccination may contribute to the risk of worsening blood glucose in diabetic patients and diabetic patients may have a lower antibody response after vaccination than the general population.

Correlation between COVID-19 and hepatitis B: A systematic review.

BACKGROUND: There is growing evidence that patients with coronavirus disease 2019 (COVID-19) frequently present with liver impairment. Hepatitis B virus (HBV) remains a major public health threat in current society. Both severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and HBV can cause liver damage, and current findings on whether HBV infection increases disease severity in COVID-19 patients are inconsistent, and whether SARS-CoV-2 infection accelerates hepatitis B progression or leads to a worse prognosis in hepatitis B patients has not been adequately elucidated. AIM: To explore the complex relationship between COVID-19 and hepatitis B in order to inform the research and management of patients co-infected with SARS-CoV-2 and HBV. METHODS: An experienced information specialist searched the literature in the following online databases: PubMed, China National Knowledge Infrastructure, Google Scholar, Scopus, Wiley, Web of Science, Cochrane, and ScienceDirect. The literature published from December 2019 to September 1, 2022 was included in the search. We also searched medRxiv and bioRxiv for gray literature and manually scanned references of included articles. Articles reporting studies conducted in humans discussing hepatitis B and COVID-19 were included. We excluded duplicate publications. News reports, reports, and other gray literature were included if they contained quantifiable evidence (case reports, findings, and qualitative analysis). Some topics that included HBV or COVID-19 samples but did not have quantitative evidence were excluded from the review. RESULTS: A total of 57 studies were eligible and included in this review. They were from 11 countries, of which 33 (57.9%) were from China. Forty-two of the 57 studies reported abnormalities in liver enzymes, three mainly reported abnormalities in blood parameters, four indicated no significant liver function alterations, and another eight studies did not provide data on changes in liver function. Fifty-seven studies were retrospective and the total number of co-infections was 1932, the largest sample size was 7723, and the largest number of co-infections was 353. Most of the studies suggested an interaction between hepatitis B and COVID-19, while 12 studies clearly indicated no interaction between hepatitis B and COVID-19. Six of the 57 studies clearly reported HBV activation. Six studies were related to liver transplant patients. CONCLUSION: There is some association between COVID-19 and hepatitis B. Future high-quality randomized trials are needed to further elucidate the interaction between COVID-19 and hepatitis B.

A meta-analysis evaluating indirectly GLP-1 receptor agonists and arrhythmias in patients with type 2 diabetes and myocardial infarction.

Aims: At present, the effects of Glucagon-Like Peptide 1 Receptor agonists (GLP-1RAs) on arrhythmia in patients with type 2 diabetes mellitus (T2DM) and myocardial infarction (MI) are still unclear. Hence, this systematic review and meta-analysis aimed to investigate this association. Methods and results: PubMed, Embase, Cochrane Library, and Web of Science were searched from inception to 30 April 2022. Randomized controlled trials (RCTs) that compared GLP-1RAs with placebo and met the critical criterion of a proportion of patients with T2DM and MI > 30% were included to verify our purpose indirectly. The outcomes of interest included atrial arrhythmias, ventricular arrhythmias, atrioventricular block (AVB), sinus arrhythmia, and cardiac arrest. Relative risk (RR) and 95% confidence intervals (CI) were pooled using a random-effects model. We included five RCTs with altogether 31,314 patients. In these trials, the highest proportion of patients with T2DM and MI was 82.6%, while the lowest was 30.7%. Compared to placebo, GLP-1RAs were associated with a lower risk of atrial arrhythmias (RR 0.81, 95% CI 0.70-0.95). There was no significant difference in the risk of ventricular arrhythmias (RR 1.26, 95% CI 0.87-1.80), AVB (RR 0.95, 95% CI 0.63-1.42), sinus arrhythmia (RR 0.62, 95% CI 0.26-1.49), and cardiac arrest (RR 0.97, 95% CI 0.52-1.83) between groups. Conclusion: GLP-1RAs may be associated with reduced risk for atrial arrhythmias, which seems more significant for patients with T2DM combined with MI. More studies are needed to clarify the definitive anti-arrhythmic role of this drug.

Fulminant myocarditis caused by immune checkpoint inhibitor: a case report and possible treatment inspiration.

Immune checkpoint inhibitors (ICIs) have become a new hope for many patients with advanced cancer by blocking tumour immune evasion. However, with the widespread use of ICIs, immune-related adverse events (irAEs) have also been discovered and reported increasingly. Immune-related myocarditis, the most dangerous one of irAEs, still has high mortality in the context of the current treatment. We report the case of a 60-year-old female with fulminant myocarditis induced by ICIs, which caused her to experience frequent ventricular arrhythmias such as ventricular fibrillation and heart failure. She was successfully treated with current mainstream therapies for immune-related myocarditis and additional treatment of sacubitril-valsartan and dapagliflozin. The intriguing observation that the patient condition recovered relatively rapidly in this case shows a possible treatment inspiration, which may be helpful for treating ICIs-associated myocarditis and improving cancer patients' clinical prognosis.

Impact of estimated glomerular filtration rate on long-term clinical outcomes among Chinese patients with atrial fibrillation.

BACKGROUND: Estimated glomerular filtration rate (eGFR) is a widely accepted indicator of renal function. The aim of this study was to evaluate the relationship between eGFR and 3-year clinical outcomes among Chinese patients with atrial fibrillation (AF). METHODS: We retrospectively studied 433 consecutive Chinese patients with AF (51.0% males, mean age 65.6 ± 13.2 years) between February 2013 and December 2017. Baseline clinical data were collected according to medical records. eGFR was calculated by MDRD equation for Chinese patients according to baseline age, sex and serum creatinine. The primary clinical outcome of interest was all-cause mortality. RESULTS: During a median follow-up period of 3.1 (0.5-4.5) years, 73 deaths (16.9%) were recorded. Multivariate Cox regression analyses indicated that eGFR was independently associated with all-cause death in total population [hazard ratio (HR) 0.984; 95% confidence interval (CI) 0.972-0.995, P = 0.006] and patients free of valvular heart diseases (VHDs) (HR 0.975; 95% CI 0.959-0.992, P = 0.003), but not with VHDs. A receiver operating characteristic (ROC) analysis revealed that reduced eGFR predicted all-cause mortality with areas under the ROC curve of 0.637 (95% CI 0.539-0.735, P = 0.004) in AF patients free of VHDs. CONCLUSIONS: eGFR is an independent predictor of 3-year all-cause mortality among Chinese patients with AF, especially among those patients free of VHDs.

S-1 combined with paclitaxel may benefit advanced gastric cancer: Evidence from a systematic review and meta-analysis.

BACKGROUND: Gastric cancer, as one of the increasingly common malignancies, has experienced high morbidity throughout many countries at present. Currently, chemotherapy regimen with more efficacy and safety for advanced gastric cancer (AGC) is needed. We aimed to assess the clinical efficacy and safety of S-1 combined with paclitaxel (PTX) for AGC by performing a systematic review and meta-analysis of the published studies. METHOD: All published randomized controlled trials (RCTs) of S-1 combined with PTX for AGC were searched. Studies that included patients with locally advanced or metastases' gastric cancers were included. We searched the databases included Cochrane Library of Clinical Comparative Trials, MEDLINE, Embase, American Society of Clinical Oncology meeting abstracts and China National Knowledge Internet (CNKI) from 2000 to 2018. We searched the database up to January 2018. The first endpoint was overall survival (OS). Other endpoints were progression-free survival (PFS), objective response rate (ORR) and disease control rate (DCR). Safety analyses were also performed. RESULTS: A total of 7 trials (including 1407 patients, 711 patients in intervention group and 696 patients in control group) were included in the present analysis. S-1 combined with PTX significantly improved the OS [HR = 0.78, 95% CI: 0.60-0.97, P = 0.000],PFS [HR = 0.70, 95% CI: 0.55-0.85, P = 0.000], ORR [RR = 1.30, 95%CI: 1.05-1.60, P = 0.017] and DCR [RR = 1.15, 95%CI: 1.04-1.27, P = 0.008] of patients with AGC. The grade 3 or 4 haematological and non-hematologic toxicities were anemia [RR = 1.71, 95% CI: 1.04-2.79, P = 0.03], neutropenia [RR = 1.65, 95% CI: 1.32-2.06, P < 0.0001] and anorexia [RR = 1.66, 95% CI: 1.05-2.64, P = 0.03] respectively. CONCLUSION: S-1 combined with PTX may be a good choice for patients with AGC. S-1 plus PTX experienced more efficacy and safety when compared with S-1 alone or S-1 plus other drugs.

In vitro study on human umbilical cord mesenchymal stem cells transfected with lentivirus-mediated hNIS-EGFP dual reporter gene and co-labeled with superparamagnetic iron oxide.

The aim of the present study was to establish a stem cell line for multi-mode imaging (in vivo fluorescence imaging, magnetic resonance imaging and 99mTc single-photon emission computed tomography) and to study the biological activity, stemness, proliferative activity and differentiation ability of superparamagnetic iron oxide (SPIO), human sodium/iodide symporter (hNIS) and enhanced green fluorescent protein (EGFP) co-labeled human umbilical cord mesenchymal stem cells (hUCMSCs). The EGFP reporter gene was selected to indirectly reflect the expression of target gene hNIS, and hUCMSCs were re-transfected with the successfully constructed recombinant plasmid pCMV-NIS-EF1-GFP-PGK-puro. When a stem cell line stably expressing hNIS and EGFP was obtained, the cells were incubated with 30 µg/ml SPIO to obtain hNIS, EGFP and SPIO co-labeled stem cells. The protein expressions of hNIS and EGFP were identified using western blot analysis, and the protein function of hNIS was identified by 125I influx and 125I efflux experiments. hNIS-EGFP-hUCMSCs were labeled with SPIO under the mediation of poly-L-lysine, and SPIO, hNIS and EGFP co-labeled hUCMSCs were established successfully. Staining with Prussian blue confirmed that 98% of cells were successfully labeled with SPIO. Western blotting results demonstrated positive hNIS and EGFP protein expression levels, and 125I influx and 125I efflux experiments confirmed that the protein function of hUCMSCs after expressing hNIS was normal. The uptake of 125I was higher in cell lines hNIS-EGFP-hUCMSCs than in control hUCMSCs (fold change: 16.43±2.30 times; P<0.05). The stemness of hNIS-EGFP-hUCMSCs was found to be slightly decreased but not statistically significant; the overall characteristics of stem cells remained unchanged. The assessments of adipogenic and osteogenic differentiation suggest that hNIS-EGFP-hUCMSCs have no significantly different characteristics compared with primary hUCMSCs.

Laser-guided transtibial technique improved single-bundle reconstruction of anterior cruciate ligament.

BACKGROUND: The transtibial tunnel technique achieves equal length reconstruction of the anterior cruciate ligament (ACL). This study aimed to investigate whether transtibial tunnel technique can achieve anatomical reconstruction of ACL. METHODS: For 25 corpses, the anterior soft tissue of the knee joint was detached so that the ligamentous surface was fully exposed, then the knee joint was fixed at 90° with an external fixator and the anterior cruciate ligament was removed. Double-sided laser technology was used to establish spatial conformation of ACL. RESULTS: The male to female ratio of the subjects was 19:6, with an average age of 59.52 ± 11.13 years. Patellar tendon length was 35.23 ± 5.10 mm, tibial eminence length and width was 15.75 ± 2.44 and 7.80 ± 1.28 mm, respectively, and femoral attachment length and width was 15.40 ± 2.17 and 8.97 ± 1.61 mm, respectively. When the flexion turned 90°, the tibial tunnel length was 31.83 ± 4.09 mm and the distance to the tibial plateau, patellar tendon, and medial collateral ligament was 16.33 ± 4.56, 10.79 ± 5.85, and 23.12 ± 5.99 mm, respectively. CONCLUSIONS: With the aid of double-sided laser technology, transtibial tunnel technique can safely achieve single-bundle reconstruction of ACL.

Pituitary adenylate cyclase-activating polypeptide attenuates tumor necrosis factor-α-induced apoptosis in endothelial colony-forming cells.

Endothelial colony-forming cells (ECFCs) are important in angiogenesis and vascular proliferation. Tumor necrosis factor (TNF)-α is a significant risk factor for the development of atherosclerosis and a key proinflammatory cytokine known to induce apoptosis in endothelial cells. Pituitary adenylate cyclase-activating polypeptide (PACAP) is one of the members of the vasoactive intestinal peptide/secretin/growth hormone-releasing hormone/glucagon superfamily and exists in two biological active forms, PACAP 38 and PACAP 27. PACAP has been reported to help prevent endothelial apoptosis via an anti-inflammatory mechanism. However, to the best of our knowledge, the anti-apoptotic potential of PACAP has not been investigated in ECFCs. The aim of the present study was to demonstrate the efficacy of PACAP for decreasing TNF-α-induced apoptosis in ECFCs. The results indicated that PACAP exerts a cytoprotective effect on ECFCs exposed to TNF-α. Furthermore, PACAP partially rescues the proliferation potential of ECFCs inhibited by prolonged TNF-α exposure. These findings support an anti-inflammatory role for PACAP in circulation diseases.

Simvastatin attenuates TNF­α­induced apoptosis in endothelial progenitor cells via the upregulation of SIRT1.

Endothelial progenitor cells (EPCs) originate from the bone marrow and can be classified as either early or late EPCs. The focus of this study was on late EPCs, as they play an important role in angiogenesis and vascular proliferation. Evidence suggests that inflammatory and oxidative changes can increase EPC apoptosis. Of note, tumor necrosis factor-α (TNF-α) is a contributing risk factor to the development of atherosclerosis and plays a key role as both an inflammatory mediator and an inducer of apoptosis in endothelial cells. Additionally, a member of the sirtuin family, silent information regulator type-1 (SIRT1), promotes cell survival by repressing p53- and non-p53-dependent apoptosis in response to DNA damage and oxidative stress. Statins have also been shown to play a key role in the prevention of endothelial apoptosis and senescence via their lipid-lowering and anti-inflammatory actions. However, there is little evidence that statins themselves attenuate EPC apoptosis induced by TNF-α. The aim of this study was to demonstrate the effectiveness of one of the most commonly used statins, simvastatin, on decreasing TNF-α-induced apoptosis in EPCs. The results indicated that SIRT1 protein expression was decreased by TNF-α in a time- and dose-dependent manner and that while TNF-α caused a marked increase in the percentage of apoptotic EPCs, application of simvastatin decreased this percentage. A high concentration of simvastatin promoted the expression of SIRT1 and increased the proliferation of EPCs. In conclusion, findings of this study showed that simvastatin is crucial in counteracting the TNF-α-induced apoptosis of EPCs and that this protection may involve the actions of SIRT1.

Effects of low-level autonomic stimulation on prevention of atrial fibrillation induced by acute electrical remodeling.

BACKGROUND: Rapid atrial pacing (RAP) can induce electrical and autonomic remodeling and facilitate atrial fibrillation (AF). Recent reports showed that low-level vagosympathetic nerve stimulation (LLVNS) can suppress AF, as an antiarrhythmic effect. We hypothesized that LLVNS can reverse substrate heterogeneity induced by RAP. METHODS AND RESULTS: Mongrel dogs were divided into (LLVNS+RAP) and RAP groups. Electrode catheters were sutured to multiple atrial sites, and LLVNS was applied to cervical vagosympathetic trunks with voltage 50% below the threshold slowing sinus rate by ≤ 30 msec. RAP induced a significant decrease in effective refractory period (ERP) and increase in the window of vulnerability at all sites, characterized by descending and elevated gradient differences towards the ganglionic plexi (GP) sites, respectively. The ERP dispersion was obviously enlarged by RAP and more significant when the ERP of GP-related sites was considered. Recovery time from AF was also prolonged significantly as a result of RAP. LLVNS could reverse all these changes induced by RAP and recover the heterogeneous substrate to baseline. Conclusions. LLVNS can reverse the electrical and autonomic remodeling and abolish the GP-central gradient differences induced by RAP, and thus it can recover the homogeneous substrate, which may be the underlying mechanism of its antiarrhythmic effect.

Sugar-bearing tetraphenylethylene: novel fluorescent probe for studies of carbohydrate-protein interaction based on aggregation-induced emission.

Neutral sugar-bearing tetraphenylethenes (TPE) are designed and prepared as "turn-on" luminescent sensors for lectins and glycosidases based on aggregation-induced emission. Through aggregation derived from carbohydrate-lectin binding, multivalent mannosyl-bearing TPE shows a good selectivity and sensitivity to Con A by switching on the fluorescence of water-soluble tetraphenylethylene-based glyco-conjugates in aqueous solution. Meanwhile, cellobiosyl-bearing TPE can be used to investigate enzymatic hydrolysis based on emission enhancing by glycosidase-induced aggregation.

Glucosamine hydrochloride functionalized tetraphenylethylene: a novel fluorescent probe for alkaline phosphatase based on the aggregation-induced emission.

Grafting of glucosamine hydrochloride moieties to tetraphenylethylene (TPE) motif furnished a novel cationic water-soluble tetraphenylethylene derivative (GH-TPE). With aggregation-induced emission properties, GH-TPE was used for fluorometric detection to alkaline phosphatase through enzyme-triggered de-aggregation of the ensemble of GH-TPE and substrate.