The study was principally intended to explore mechanisms and hub drug targets through which modified Lai-Fu decoction (MLFD) acts against chronic heart failure (HF). Using differential gene analysis and network pharmacology, we identified intersecting genes between HF-related genes (HRGs) and targets of active components in MLFD, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Weighted gene coexpression network analysis (WGCNA) was performed to further identify gene modules associated with HF. The final core-gene set was obtained by intersecting these module genes with overlapping genes and lipid metabolism-related genes (LMRGs). Core targets were identified via the protein-protein interaction (PPI) network, Boruta, and Least Absolute Shrinkage and Selection Operator (LASSO). Grounded in seven machine learning algorithms, an ensemble learning model was established to determine hub genes, with their pivotal functions in HF treatment further verified by PPI, KEGG, and molecular docking. 46 active ingredients and 289 corresponding targets were identified from MLFD. Intersection analysis of these targets with HRGs yielded 144 HF-associated drug targets. As functional enrichment analysis revealed, target genes were predominantly enriched in insulin resistance signaling pathways and lipid metabolism biological processes. 144 overlapping genes were further intersected with the HF module genes and LMRGs, yielding 15 pivotal targets. Four core target genes were subsequently identified from 15 pivotal targets by employing machine learning. Concurrently, the hub targets exhibit stable binding affinities with kaempferol, isoliquiritigenin, and other active components in MLFD. MLFD exerts anti-HF effects by modulating lipid metabolism reprogramming.
Glycyrrhizin (GC) is a major bioactive saponin in licorice plants (Glycyrrhiza spp.). A GC-specific single-chain variable fragment (GC-scFv) was constructed from anti-GC monoclonal antibody 2H2. To obtain a soluble recombinant recognition reagent for GC immunoassays, GC-scFv was expressed using a baculovirus–insect cell platform. The variable heavy- and light-chain genes were amplified from 2H2 hybridoma-derived complementary DNA (cDNA) and assembled using a (Gly4Ser)3 linker. The construct was transferred through pET-28a(+) and pCold I into pFastBac1Mel, which contains the honeybee melittin signal sequence for secretion in Sf9 insect cells. GC-scFv was recovered by nickel-chelate affinity chromatography and characterized using indirect competitive enzyme-linked immunosorbent assay (icELISA). The calibration curve was analyzed by semi-logarithmic regression using triplicate wells at each concentration. An anti-T7-tag Western blot detected GC-scFv at approximately 29 kDa in the eluate recovered from culture medium. Free GC produced concentration-dependent inhibition, with a half-maximal inhibitory concentration (IC50) of 0.46 μg/mL and a semi-logarithmic calibration interval of 0.0488–3.125 μg/mL. The apparent limit of detection and apparent limit of quantification, defined as 10
Type 2 diabetes mellitus (T2DM) is frequently complicated by neuropathy, impaired wound healing, and poor glycemic control, creating significant clinical and economic burdens. Adjunctive modalities such as acupuncture and photobiomodulation have gained interest for their potential to support glycemic control and improve diabetes-related complications. This case series examined the therapeutic potential of a synergistic technique combining Class 3B laser photobiomodulation with traditional needle acupuncture. Eleven patients with long-standing T2DM were treated using combined protocols, with outcomes assessed through fasting plasma glucose, HbA1c, neuropathic symptom relief, and wound recovery. Patients demonstrated consistent improvements in glycemic regulation, neuropathic symptoms, sleep quality, and wound healing. Fasting plasma glucose reductions ranged from 36 to 64
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by motor impairment, degeneration of nigrostriatal dopaminergic neurons, and pathological α-synuclein accumulation. Current therapies mainly provide symptomatic relief, while disease-modifying treatments remain limited. This study investigated the neuroprotective effects of a traditional medicine formulation composed of Calculus Bovis, Fel Ursi, and Moschus (BUM) in experimental models of PD. The efficacy of BUM pharmacopuncture solution was evaluated in an MPTP-induced C57BL/6N mouse model and MPP⁺-induced Caenorhabditis elegans models. Motor function in mice was assessed using the rota-rod, pole, and grip strength tests. Nigrostriatal dopaminergic integrity was examined by tyrosine hydroxylase (TH) immunostaining in the substantia nigra pars compacta and striatum. In C. elegans, dopaminergic neurodegeneration and α-synuclein accumulation were assessed using BZ555 and NL5901 transgenic strains, respectively. BUM significantly improved motor performance in MPTP-treated mice, as evidenced by increased rota-rod latency, reduced pole descent time, and enhanced grip strength. BUM also preserved TH-positive dopaminergic neurons in the substantia nigra and dopaminergic fibers in the striatum. The magnitude of these effects was comparable to that of levodopa. In C. elegans, BUM significantly protected dopaminergic neurons against MPP⁺-induced degeneration and reduced α-synuclein-associated fluorescence. BUM alleviates motor dysfunction, mitigates nigrostriatal dopaminergic neurodegeneration, and reduces α-synuclein accumulation across both vertebrate and invertebrate models of PD. These findings suggest that the BUM multicomponent formulation exerts multitargeted protective effects against PD-related pathology, providing a strong rationale for further mechanistic and translational investigations in neurodegenerative disease research.
This letter provides a critical appraisal of the case report titled “Auricular Acupuncture Effect on Facial Contraction via Middle Ear Muscles Reflexes.” The original report attributes the observed facial contractions to middle-ear muscle reflexes triggered by auricular acupuncture. However, several aspects of the report and its supplementary videos warrant further clarification. Review of the provided materials suggests that the observed facial contractions may have been elicited by high-intensity auditory stimuli rather than by acupuncture itself. Visual analysis indicates that the contractions may originate from the masseter muscle. Due to fascial continuity between the masseter and regional mimic muscles, such contractions may mimic true facial muscle activity. Additionally, alternative diagnostic entities—including hemimasticatory spasm and hemifacial spasm—should be considered, as both can present with unilateral involuntary contractions. Differentiation between masseteric and mimic muscle involvement is essential for accurate interpretation. Clinical examination methods such as palpation, along with electrophysiological techniques including electromyography and electroneurography, may provide valuable diagnostic clarification. Furthermore, confounding clinical factors—such as prior esthetic interventions and occlusal or dental abnormalities—should be taken into account, given their potential to influence masseter muscle activity. If the observed contractions originated from the masseter muscle, the hypothesis attributing them to middle-ear muscle reflexes may require reconsideration. This commentary emphasizes the need for clearer differentiation of underlying mechanisms and encourages additional clinical and electrophysiological evaluation to enhance diagnostic accuracy.
