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Hua Jiang

Publications and source records attributed to Hua Jiang.

At least 19 recordsLinked to original sources
PubMed2026

A novel triple-knockout allogeneic BCMA CAR T-cell therapy (CT0590) for multiple myeloma: preclinical and phase 1 study.

Host-versus-graft reaction (HVGR) is a major challenge in allogeneic chimeric antigen receptor (CAR) T-cell therapy. To counter host natural killer (NK) cell attacks, we armored allogeneic, HLA-I-deficient, B-cell maturation antigen (BCMA)-targeting CAR T cells with an NKG2A CAR. In vitro and animal studies demonstrated that allogeneic CAR-NKG2A T cells effectively resisted host NK cell-mediated killing. BCMA and NKG2A dual-targeting allogeneic CAR T cells (CT0590) resisted killing by NK cells and showed robust antitumor activity in preclinical in vivo models. On the basis of these data, a first-in-human study enrolled 5 patients (4 with relapsed and refractory multiple myeloma [RRMM] and 1 with primary plasma cell leukemia [pPCL]). CT0590 was well tolerated and caused no dose-limiting toxicities, treatment-related death, or graft-versus-host disease. Three patients achieved confirmed responses, including 2 with stringent complete response (sCR). Notably, sCR in the patient with RRMM was still ongoing (duration of response >23 months) at the time of data cutoff, and sCR in the patient with pPCL lasted for 20 months. Both patients showed robust expansion of universal CAR T cells (maximum concentration of >280 000 copies per μg genomic DNA) and higher baseline NKG2A expression on NK cells than nonresponders. These results suggest that CAR-NKG2A technology may overcome HVGR, especially in patients with elevated NKG2A expression on NK cells. Further studies of CT0590 in RRMM and pPCL are warranted. This trial was registered at www.clinicaltrials.gov as NCT05066022.

Humans↗
PubMed2026

Human Umbilical Cord Mesenchymal Stem Cells in Metabolic Dysfunction-associated Fatty Liver Disease (MAFLD) Therapy: Mechanisms, Clinical Efficacy, and Future Perspectives.

There is currently no approved drug treatment for metabolic dysfunction-related fatty liver disease (MAFLD). Umbilical cord-derived mesenchymal stem cells (UC-MSCs) show therapeutic potential, but their mechanism of action is remains incompletely understood. Different from previous reviews that focused on a single pathway, this article presents three important contributions: First, it constructs an integrated "multi-target synergy network" model, clarifying how UC-MSCs coordinate and regulate the inflammatory, metabolic and fibrotic processes through the interactions between the AMPK/mTOR, Nrf2/HO-1 and TGF-β/Smad pathways; Second, it systematically assesses recent clinical trials (2022-2025), identifying several unaddressed barriers to transformation, including the lack of histological endpoint indicators, batch-to-batch differences, and the absence of dose exploration studies; Third, we integrate the latest developments from 2024 to 2025, particularly mitochondrial transfer (mediated by tunnel nanotubes and accompanied by quantitative efficacy data) and exosome circular RNA networks [Formula: see text], which have not been covered in previous reviews. Based on the above analysis, we also propose specific suggestions for standardized GMP production, mandatory genomic stability testing, and long-term safety registration. This review provides a comprehensive analysis of elaborates on the treatment of MAFLD with UC-MSCs from a mechanistic and translational perspective, based on the extensive updates of relevant literature.

Humans↗
PubMed2026

KIT and FLT3-ITD mutations do not predict outcomes in pediatric core-binding factor acute myeloid leukemia: findings from the C-HUANAN-AML-15 multicenter cohort study.

Although core-binding factor acute myeloid leukemia (CBF-AML) is generally considered a favorable-risk subtype in children, disease relapse remains a significant concern. The prognostic relevance of co-occurring mutations, particularly KIT and FLT3-ITD, remains debatable, and treatment intensity may modulate their impact. This multicenter analysis included 289 children (<&#x2009;14 years) with newly diagnosed CBF-AML enrolled in the C-HUANAN-AML-15 study (2015-2023). KIT and FLT3-ITD mutations were identified via cytogenetic analysis and targeted sequencing. Measurable residual disease (MRD) was evaluated by multiparameter flow cytometry (MFC) and quantitative polymerase chain reaction (PCR) following induction chemotherapy. Survival analyses were performed using Kaplan-Meier and Cox regression methods. This multicenter analysis included 289 children (<&#x2009;14 years) with newly diagnosed CBF-AML enrolled in the C-HUANAN-AML-15 study (2015-2023). KIT and FLT3-ITD mutations were identified via cytogenetic analysis and targeted sequencing. Measurable residual disease (MRD) was evaluated by multiparameter flow cytometry (MFC) and quantitative polymerase chain reaction (PCR) following induction chemotherapy. Survival analyses were performed using Kaplan-Meier and Cox regression methods. KIT mutations were detected in 103 patients (35.6%), predominantly involving exon 17 (69.9%), and were associated with extramedullary disease, sex chromosome loss, and trisomy 22. No significant differences in 5-year event-free survival (EFS), overall survival (OS), or cumulative incidence of relapse (CIR) were observed between patients with and without KIT mutations. FLT3-ITD mutations (5.5% of patients) did not adversely affect outcomes. Neither mutation independently predicted survival. MRD positivity (MFC-MRD&#x2009;&#x2265;&#x2009;0.1%) after the second induction cycle strongly predicted inferior EFS and OS and higher CIR, with corresponding results observed for molecular MRD and parallel findings for PCR-based MRD. In this large multicenter cohort, KIT and FLT3-ITD mutations did not adversely affect the prognosis of pediatric CBF-AML treated according to the C-HUANAN-AML-15 protocol. MRD after induction was the most powerful predictor of relapse and survival, underscoring its importance for risk stratification in future pediatric AML trials.

Humans↗
PubMed2026

Robotic Needle Insertion for CT-guided Percutaneous Biopsy of Thoracoabdominal Lesions: A Prospective Multicenter Randomized Trial.

Purpose To compare safety and feasibility between a novel CT-guided robotic system and the conventional freehand technique for puncture biopsy of thoracoabdominal lesions. Materials and Methods In this prospective multicenter randomized trial, individuals with suspected lesions were enrolled between July 2023 and April 2024 across three university teaching hospitals and randomized to the robot-assisted group (n = 82) or the freehand group (n = 83). Procedure outcomes included the technical success rate, targeting error, number of CT scans and needle adjustments, puncture time, and complications. Descriptive and inferential statistics were calculated. Results A total of 165 participants (mean age, 60 years &#xb1; 10 [SD]; 83 male) were included. Compared with the freehand group, the robot-assisted group demonstrated a higher technical success rate (97.56% [80 of 82] vs 62.65% [52 of 83], P < .001), lower targeting error (mean Euclidean deviation: 1.7 mm &#xb1; 1.1 vs 4.5 mm &#xb1; 3.9, P < .001), and fewer CT scans (mean, 4.3 &#xb1; 1.9 vs 5.2 &#xb1; 2.3; P = .002) and needle adjustments (mean, 0.7 &#xb1; 0.7 vs 1.6 &#xb1; 1.6; P = .003). Despite differences in geometric precision, both groups achieved 100% (82 of 82 and 83 of 83) diagnostic yield. The median puncture time was comparable between groups (5.5 minutes &#xb1; 4.3 vs 4.8 minutes &#xb1; 7.0, P = .50). During lung biopsies, the robot-assisted approach yielded fewer complications compared with the freehand approach (4.88% [four of 82] vs 16.87% [14 of 83], P = .014). Conclusion Compared with the freehand approach, robot-assisted biopsy yielded greater precision and reduced adjustments and complications while demonstrating noninferior diagnostic efficacy and comparable duration. Keywords: Robotic Needle Insertion, Biopsy, Thoracoabdominal Lesions, Robot-assisted Biopsy, CT-guided Intervention, Percutaneous Needle Biopsy, Randomized Controlled Trial, Algorithm Development, CT, Clinical Testing, Interventional-Body, Biopsy/Needle Aspiration, Percutaneous, Thorax, Abdomen/GI, Liver, Lung, Kidney &#xa9;RSNA, 2026.

Humans↗
PubMed2026

A Comprehensive Review of Radiomics in Pulmonary Nodule Management: Clinical Applications and Standardization Dilemmas.

Lung cancer is the most common and fatal malignant tumour. Early detection and treatment are likely to reduce mortality, but most pulmonary nodules identified during routine health checks are harmless. Consequently, a clear distinction between benign and malignant nodules is vital to improve early detection and reduce unnecessary interventions. Radiomics, a new omics technology, can be used to extract high-dimensional quantitative features from medical images, providing a profound understanding of tumour pathophysiology. Radiomics has attracted the attention of medical researchers since its formal definition by the Dutch researcher Lambin et al. in 2012. The number of research papers on radiomics has grown tremendously over the past few years. At present, it is used to predict pulmonary nodule malignancy, for noninvasive risk stratification, for integration with genomics to identify genetic mutations associated with lung cancer, and for evaluation of therapeutic responses. With this review, we summarise the literature on radiomics of pulmonary nodules, discuss how it could be used in nodule management, and address the current challenges and future directions for improving precision oncology.

Humans↗
PubMed2025

Repeats mimic pathogen-associated patterns across a vast evolutionary landscape.

An emerging hallmark of many human diseases is transcription of typically silenced repetitive DNA containing pathogen-associated molecular patterns (PAMPs). These PAMPs engage the innate immune system via pattern recognition receptors (PRRs)-a phenomenon known as viral mimicry. We propose a statistical physics framework to quantify viral mimicry by measuring "selective forces" that enrich PAMPs compared to a genome-wide reference distribution. We validate our predictions by identifying repeats that bind different PRRs and show potential viral mimics in different repeat families across eukaryotic genomes, suggesting shared mechanisms drive emergence and retention. We propose two non-exclusive evolutionary hypotheses. The first "repeat-centric" hypothesis posits PAMPs are integral to the repeat life cycle and are therefore enriched as they mediate repeat expansion. The second "organism-centric" hypothesis proposes viral mimicry functions as a cell-intrinsic feedback mechanism for sensing and reacting to transcriptional dysregulation, which provides a selective pressure to maintain PAMPs in genomes.

Humans↗
PubMed2007

Application of EGFP-EGF fusions to explore mechanism of endocytosis of epidermal growth factor.

AIM: To develop a simple method for monitoring protein localization of epidermal growth factor (EGF) in living cells. METHODS: Enhanced green fluorescent protein (EGFP) was used as an autofluorescent tag to label EGF ligands. SDS-PAGE and Western blot analysis were used to detect the expression of the EGFP-tagged EGF (EGFP-EGF) protein. The cell-binding and internalization activity of EGFP-EGF were analyzed by fluorescence-activated cell sorting (FACS) and confocal microscopy. RESULTS: EGFP-EGF protein was expressed in Escherichia coli and purified. A cell-binding assay demonstrated that the EGFP-EGF protein could bind efficiently to the cells expressing EGFR. The binding and internalization of EGFP-EGF can be visualized even at a very low concentration under confocal microscopy. The FACS-based assay for internalization activity indicated the accumulation of internalized EGFP-EGF over time. Furthermore, the results of the competition assay indicated its EGFR binding specificity. Using such a method, it does not need to label EGF with chemicals and avoid light in the experimental process. CONCLUSION: The fusion protein EGFP-EGF has several characters including high sensitivity, stability and convenience for manipulation, and is a powerful tool for the study of EGF endocytosis.

Binding, Competitive↗
PubMed2007

Nerve growth factor prevents the apoptosis-associated increase in acetylcholinesterase activity after hydrogen peroxide treatment by activating Akt.

Acetylcholinesterase (AChE) is thought to play an important role during apoptosis. Our results showed that H2O2 induced AChE activity, a functional marker in apoptosis, increases in neuronal-like PC12 cells. Glutathione, which is involved in cellular redox homeostasis, inhibited the increase of AChE activity, suggesting that reactive oxygen species (ROS) play a key role in this process. Further investigation showed that the elevation of AChE was observed after the degradation of Akt, release of cytochrome c from mitochondria into the cytosol, and activation of caspase family members. When nerve growth factor (NGF) was present, with the maintenance of Akt level, the elevation of AChE, the cytochrome c diffusion, as well as apoptosis were markedly attenuated in H2O2-treated PC12 cells. However, wortmannin, an inhibitor of the PI3K/Akt pathway, accelerated the apoptosis and increased the AChE activity. The overexpression of constitutively activated Akt, which is a downstream signalling element of the NGF receptor TrkA, delayed mitochondrial collapse and inhibited elevation of AChE activity. Thus, NGF prevented apoptosis and elevation of AChE activity by activating the Akt pathway and stabilizing the function of mitochondria.

Acetylcholinesterase↗
PubMed2006

Optical imaging of bacterial infection in living mice using a fluorescent near-infrared molecular probe.

An optical imaging probe was synthesized by attaching a near-infrared carbocyanine fluorophore to an affinity group containing two zinc(II) dipicolylamine (Zn-DPA) units. The probe has a strong and selective affinity for the surfaces of bacteria, and it was used to image infections of Gram-positive S. aureus and Gram-negative E. coli bacteria in living nude mice. After intravenous injection, the probe selectively accumulates at the sites of localized bacterial infections in the thigh muscles of the mice.

Animals↗
PubMed2006

4q loss is potentially an important genetic event in MM tumorigenesis: identification of a tumor suppressor gene regulated by promoter methylation at 4q13.3, platelet factor 4.

In this study, we have elucidated the chromosomal imbalances in the multistep pathogenesis and delineated several critical tumor suppressor gene (TSG) loci in multiple myeloma (MM). By using comparative genomic hybridization, allelotyping, and multicolor interphase fluorescence in situ hybridization, 5 MM cell lines and bone marrow CD138+ plasma cells from 88 Chinese patients with monoclonal gammopathy of undetermined significance (MGUS) and early and advanced stages of MM were investigated. In all MGUS and MM samples, chromosome copy number abnormalities were detected. A higher number of chromosomal imbalances and specific genetic alterations are involved in MGUS to MM transition (-6q, +3p, and +1p) and MM progression (+2p and +9q). In addition to -13q, we first found high frequencies (42% to 46%) of -4q involving high percentages (70% to 74%) of clonal plasma cells in both MGUS and MM, suggesting that inactivation of TSG in this region is also a potentially critical genetic event in MM tumorigenesis. By high-resolution allelotyping, we defined a common deletion region on 4q13.3 and found that a candidate TSG, platelet factor 4, was frequently silenced by promoter hypermethylation in MM (15 of 28) and MM cell lines (5 of 5). These data have opened up a new approach in the molecular targeting therapy and provide novel insights into MM tumorigenesis.

Aged↗
PubMed2006

Directed assembly of mesoscopic metallocycles with controllable size, chirality, and functionality based on the robust Pt-alkynyl linkage.

This paper describes expeditious stepwise directed assembly of large homochiral metallocycles with up to 38 6,6'-bis(alkynyl)-1,1'-binaphthalene bridging ligands (L) and 38 trans-Pt(PEt(3))(2) ([Pt]) centers and with cavities as large as 22 nm in diameter. These unprecedented mesoscopic metallocycles are synthesized by cyclization of different lengths of oligomeric building blocks, L(m)()[Pt](m)()(+1)Cl(2) (m = 1, 2, 3, 5, 7, 11, 19, and 31) and [Pt](n)()L(n)()(+1)H(2) (n = 1, 2, 3, 4, 5, 6, 10, 18, and 30), and have been characterized by a variety of techniques, including (1)H{(31)P}, (13)C{(1)H}, and (31)P{(1)H} NMR spectroscopy, MALDI-TOF MS, elemental analysis, FT-IR, UV-vis, CD, size-exclusion chromatography, and diffusion-ordered NMR spectroscopy. The present synthetic methodology was also extended to the synthesis of non-homochiral metallocycles of very different topologies and macrocyclic structures with additional functional groups precisely placed at different positions. This work provides a general strategy for the construction of nanoscopic and mesoscopic functional supramolecular architectures of controllable size, chirality, and functionality that cannot be accessed from the existing synthetic approaches.

Cyclization↗
PubMed2006

Regulation of acetylcholinesterase expression by calcium signaling during calcium ionophore A23187- and thapsigargin-induced apoptosis.

We have recently reported that acetylcholinesterase expression was induced during apoptosis in various cell types. In the current study we provide evidence to suggest that the induction of acetylcholinesterase expression during apoptosis is regulated by the mobilization of intracellular Ca(2+). During apoptosis, treatment of HeLa and MDA-MB-435s cells with the calcium ionophore A23187 resulted in a significant increase in acetylcholinesterase mRNA and protein levels. Chelation of intracellular Ca(2+) by BAPTA-AM (1,2-bis-(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester), an intracellular Ca(2+) chelator, inhibited acetylcholinesterase expression. A23187 also enhanced the stability of acetylcholinesterase mRNA and increased the activity of acetylcholinesterase promoter, effects that were blocked by BAPTA-AM. Perturbations of cellular Ca(2+) homeostasis by thapsigargin resulted in the increase of acetylcholinesterase expression as well as acetylcholinesterase promoter activity during thapsigargin induced apoptosis in HeLa and MDA-MB-435s cells, effects that were also inhibited by BAPTA-AM. We further demonstrated that the transactivation of the human acetylcholinesterase promoter by A23187 and thapsigargin was partially mediated by a CCAAT motif within the -1270 to -1248 fragment of the human acetylcholinesterase promoter. This motif was able to bind to CCAAT binding factor (CBF/NF-Y). These results strongly suggest that cytosolic Ca(2+) plays a key role in acetylcholinesterase regulation during apoptosis induced by A23187 and thapsigargin.

Acetylcholinesterase↗
PubMed2006

[A pilot study on the impact of the drug resistance on the radioresistance in human pancreatic cancer cell lines].

OBJECTIVE: To investigate the impact of the drug resistance on the radioresistance in human pancreatic cancer cell lines. METHODS: Three drug resistant pancreatic cancer cell sublines induced by fluorouracil (5-FU), adriamycin (ADM) and gemcitabine respectively, SW1990/FU, SW1990/ADM and SW1990/Gz, were tested for the cell cycle and radio-sensitivity with flow cytometry and clonogenic assay. RESULTS: Compared with SW1990, the cell cycle assay indicated higher G(0)/G(1) period percentage in SW1990/FU and SW1990/Gz, but the G(2)/M period percentage decreased; SW1990/FU had the same while SW1990/Gz had lower S period percentage. SW1990/ADM almost had a similar cell cycle with SW1990. Clonogenic assay showed both SW1990/FU and SW1990/Gz had greater survival fraction (SF(2)) than SW1990, but SW1990/ADM had seemingly similar SF(2) as SW1990. CONCLUSION: Drug resistant pancreatic cancer cell lines have reduced G(2)/M period percentage and increased radioresistance.

Antineoplastic Agents↗
PubMed2006

Curcumin-attenuated trinitrobenzene sulphonic acid induces chronic colitis by inhibiting expression of cyclooxygenase-2.

AIM: To explore the possible mechanisms of curcumin in rat colitis induced by trinitrobenzene sulfonic (TNBS) acid. METHODS: Rats with TNBS acid-induced colitis were treated with curcumin (30 mg/kg or 60 mg/kg per day ip). Changes of body weight and histological scores as well as survival rate were evaluated. Leukocyte infiltration was detected by myeloperoxidase (MPO) activity assay. The expression of cyclooxygenase-2 (COX-2) was detected by RT-PCR and Western blot. Inflammation cytokines were determined by RT-PCR. Local concentration of prostaglandin E(2) (PGE(2)) in colon mucosa was determined by ELISA. RESULTS: Curcumin improved survival rate and histological image, decreased the macroscopic scores and MPO activity. Also curcumin reduced the expression of COX-2 and inflammation cytokines. In addition, treatment with curcumin increased the PGE(2) level. CONCLUSION: Curcumin has therapeutic effects on TNBS acid-induced colitis, the mechanisms seem to be related to COX-2 inhibition and PGE(2) improvement.

Animals↗
PubMed2006

[The clinical efficacy of glutamine dipeptides on postoperative patients: an updated systematic review of randomized controlled trials from Europe and Asia (1997 - 2005)].

OBJECTIVE: To examine the effects of parenteral supplementation of glutamine dipeptide on the outcomes of surgical patients. METHODS: The relevant data 1997 to March or May 2005 were retrieved from SCI, Medline, EMBASE, Chinese Cochrane Centre databases. The bibliographies of the retrieved papers and the personal file were searched as well. All the patients in the retrieved papers received parenteral nutrition, whether alanyl-glutamine dipeptide (Ala-Gln) was added was the only difference between the intervention and control groups. Methodological quality assessment was based on the Cochrane Reviewers' Handbook and Jadad's Score Scale. Statistical software RevMan4.2 was used for meta-analysis. The data were treated by intention-to-treat method. RESULTS: A total of 1074 relevant papers were screened. Thirteen prospective randomized controlled clinical trials (RCTs) from European & Asian studies met the inclusion criteria. Ten RCTs reported 355 cases of infectious complications showed that Ala-Gln administration significantly reduced the prevalence of infectious complications with a pooled relative risk (RR) of 0.42 (95% CI 0.24 - 0.72; P = 0.002). Eight studies with 273 cases reported the postoperative length of stay (LOS) and showed that Ala-Gln significantly reduced the postoperative LOS by 3.25 days (95% CI = -4.87 to -1.62; P = 0.00009). There was no significant effect of Ala-Gln on cost of hospitalization, though there was a trend to reduction (2 studies, pooled n = 52, P = 0.2). CONCLUSION: Parenteral Ala-Gln significantly reduces the post-operative infectious morbidity and LOS among surgical patients.

Asia↗