In adult patients with idiopathic inflammatory myopathies (IIM) and a history of cancer, the risk of subsequent cancer is unclear. We describe our centre's experience with recurrent and new primary cancer development after IIM symptom onset.

A retrospective cohort study was conducted at The Johns Hopkins Myositis Center, analysing adult IIM patients enrolled from 2003 to 2024 with a documented cancer history. Patients were categorised into three groups: 1. remained cancer-free, 2. had cancer recurrence, or 3. developed a new primary cancer.

Among 2,476 IIM patients, 280 (11%) had a cancer history, with 39 (14%) diagnosed within the 3 years prior to IIM symptom onset. Of these, 29 (74%) remained cancer-free after symptom onset over a median follow-up period of 5.5 (IQR 6.7) years. Six patients (16%) experienced cancer recurrence, and four (10%) developed a new primary cancer after IIM symptom onset. The median time from index cancer to recurrence was 2.4 (IQR 1.6) years, whereas the time from index cancer to new primary was 1.4 (IQR 1.0) years. Of the ten patients who developed either recurrence or a new primary cancer after IIM symptom onset, all were diagnosed within the first three years after IIM symptom onset.

In our tertiary referral centre, approximately one quarter of adult IIM patients who had a cancer diagnosis in the three years before IIM onset went on to develop an additional malignancy, either a recurrence or a new primary.

Interstitial lung disease (ILD) affects a significant proportion of adults and children with idiopathic inflammatory myopathies (IIM-ILD and JIIM-ILD). Despite its major impact on mortality and therapeutic decision‑making, robust studies and clinical trials to inform evidence‑based practice are strikingly scarce. Heterogeneous clinical manifestations, variable testing practices, and lack of widely accepted nomenclature and standardised endpoint definitions magnify the challenges to design clinical trials for this novel disease subtype.Thus, the Myositis Clinical Trials Consortium (MCTC) developed the IIMILD working group (WG) to bridge the gaps and address the challenges unique to these patients. The IIM-ILD WG will accomplish these objectives by leveraging MCTC's global network of over 960 members, including physicians from multiple specialties, researchers, industry collaborators, and patient-support organisations. Collectively, the paper emphasises the need for structured phenotyping, unified terminology, and validated outcome measures as indispensable prerequisites for designing rigorous, multicentre trials in patients with IIM-ILD and JIIM-ILD. By leveraging the MCTC platform, the IIM-ILD Working Group will accelerate therapeutic development and ultimately improve outcomes for adults and children afflicted with IIM-associated ILD.

To assess the efficacy of point application therapy (PAT) in alleviating the exacerbation of chronic respiratory diseases represented by bronchial asthma.

In this multicenter randomized placebo-controlled trial, eligible bronchial asthma patients received placebo PAT on the dog days of the first summer to establish a baseline, and then patients who continued to participate in the trial and repassed the eligibility review were randomized to receive regular or placebo PAT in the next two consecutive summers. The primary outcome was the change from baseline in the number of asthma exacerbations at 24 months. Secondary outcomes included severity of asthma exacerbation, asthma control test (ACT) score, percentage of forced expiratory volume in 1 s (FEV₁) to the predicated value (FEV₁%pred), peak expiratory flow (PEF), ratio of FEV₁ to forced vital capacity (FEV₁/FVC), and use of palliative drugs during bronchial asthma exacerbations at 12 and 24 months. The adverse events (AEs) were also assessed.

A total of 835 patients with bronchial asthma were randomized in this trial. Compared with the placebo control, the PAT significantly decreased the mean number of asthma exacerbations (1.42; 95% confidence interval, 0.69 to 2.14; P < 0.001), and increased the FEV₁%pred at 24 months (P = 0.039) and FEV₁/FVC at 12 months (P = 0.01) and 24 months (P = 0.01). There were no significant differences between the groups in PEF or ACT score at 12 and 24 months, or in FEV₁%pred at 12 months. Treatment-related AEs were mild and more common in the PAT group than in the placebo PAT group. No serious AEs were reported.

PAT conducted on dog days could reduce asthma exacerbations in patients with bronchial asthma.

To evaluate the effectiveness and safety of multiple acupuncture therapies in the treatment of allergic rhinitis (AR) using a network Meta-analysis.

This network Meta-analysis adhered to the PRISMA-NMA guideline. Eight databases were systematically searched from inception to December 31, 2023, and retrieved references were managed using EndNote 20. The risk of bias in individual studies was assessed with the Cochrane RoB 2.0 tool (ROB 2.0). Data analysis was performed using R 4.2.1 and STATA 15.1.

A total of 56 studies that had enrolled 4859 patients with AR were included. Hand acupuncture (HA) combined with acupoint catgut embedding (AE), hand acupuncture with heat sensitive moxibustion (HA + HSM), and acupoint application were the most effective in attaining the clinical effective rate. HA + AE, hand acupuncture with indirect moxibustion (HA + IM), and electroacupuncture (EA) with AE ranked the highest with respect to the Rhinoconjunctivitis Quality of Life Questionnaire Score. HA + IM, HA, and HA + EA yielded the best Total Nasal Symptom Score, whereas HA + AE, EA + AE, and HA had the best results for the Total Non-Nasal Symptom Score. However, subgroup analyses of clinical efficacy revealed that HA + HSM had the best therapeutic effects in the short term, whereas HA + AE was the most effective in the medium to long term.

Combined acupuncture and moxibustion therapy may be a safe and effective intervention for patients with AR. HA + IM and HA + AE exhibited the most desirable therapeutic effects compared with other acupuncture and moxibustion therapies.

To investigate the key targets and mechanisms of the Wenyang Huayin decoction (WYHYD, ) in treating bronchial asthma with cold fluid retention syndrome using network pharmacology and animal experiments.

On the one hand, we used network pharmacology method to explored the chemical components of the WYHYD and the main targets of bronchial asthma were acquired. Besides, a protein interaction network was built after protein interaction analysis to find potential protein functional modules. Then, we constructed the "WYHYD component-bronchial asthma target-pathway" network. On the other hand, the experimental intervention was as follows: first, we formed a rat model of bronchial asthma. Thereafter, we used the WYHYD to treat the disease while observing autophagy-related indicators as the core target of network pharmacology.

The network pharmacology revealed that there are 122 potential therapeutic targets in treating bronchial asthma with WYHYD. The biological processes mainly involved in the WYHYD included Gene Ontology: 0110032: positive regulation of G2/MI transition of the medical cell cycle etc. and four major signaling pathways were involved. During laboratory investigations, various signs and clinical manifestations of the rat model group were the same. After administering the WYHYD, lung function, pathological sections, inflammatory factors, and other microscopic indicators improved to varying degrees, providing evidence for the study results. Meanwhile, we verified that the core targets of WYHYD in treating asthma through the intervention of autophagy are tumor necrosis factor, caspase 8, interleukin 1 beta, sirtuin 1, phosphatidylinositol 3-kinase catalytic subunit type 3, C-C chemokine receptor type 7, L/YN kinase, and protein tyrosine kinase 2.

This preliminary study revealed the treatment process of bronchial asthma with multi-component, multi-target, and multi-pathway mechanisms of the WYHYD.

Idiopathic inflammatory myopathies (IIM) can affect multiple organs, including the heart, potentially leading to arrhythmia, heart failure, and thereby a poor prognosis. We hypothesised that cardiac and skeletal muscle involvement in patients with IIM share pathological mechanisms, and that severe skeletal muscle involvement may be associated with cardiac involvement. The aim of this study was to identify disease-related parameters that indicate cardiac involvement in newly diagnosed patients with IIM.

In this prospective study, 34 newly diagnosed patients with IIM and 9 age- and gender-matched healthy controls underwent cardiac magnetic resonance imaging, blood analyses for skeletal muscle markers, and assessments of IIM-specific disease features.

Cardiac involvement was detected by cardiac magnetic resonance imaging in 47% of patients with newly diagnosed IIM, presenting as ongoing myocarditis/perimyocarditis (44%), ongoing pericarditis (25%) or previous myocarditis (31%). IIM patients with cardiac involvement had significantly more prevalent myositis (p=0.018) and higher levels of serum markers of muscle inflammation (myoglobin, p=0.039; alanine aminotransferase, p=0.045 and aspartate aminotransferase p=0.005) compared to IIM without cardiac involvement. IIM with ongoing myocarditis/peri-myocarditis displayed significantly elevated cardiac troponin I (cTnI) levels than IIM with ongoing pericarditis (p=0.015) or previous myocarditis (p=0.015). Additionally, cTnI levels were strongly correlated to myositis (as clinical manifestation, p=0.011), creatin kinase (p=0.001), myoglobin (p=0.001), lactate dehydrogenase (p=0.008) and aspartate aminotransferase (p=0.0.001).

Cardiac involvement as detected by cardiac magnetic resonance imaging is common at time of diagnosis in patients with IIM and is closely linked to the severity of skeletal muscle involvement.

Cardiac fibrosis post-myocardial infarction (MI) induces adverse cardiac remodeling, ultimately resulting in heart failure. Exosomes (EXOs) derived from mesenchymal stem cells (MSCs) have emerged as potent modulators of post-infarction remodeling, capable of limiting fibrotic responses. Our previous study showed that growth differentiation factor 15 as pretreatment promoted the protective effects of MSCs against myocardial fibrosis post-MI via paracrine actions. We investigated whether exosomes derived from GDF15-treated iPSC-MSCs (GDF15-iPSC-MSC-EXOs) could alleviate post-MI fibrosis and further explored the mechanistic pathways underlying their effects. In a mouse model of MI, EXOs released from iPSC-MSCs and GDF15-treated iPSC-MSCs were collected from culture supernatants and subsequently administered intramuscularly around the infarct area. Cardiac fibrosis was assessed by Masson's trichrome staining. A collagen synthesis model in mouse cardiac fibroblasts (mCFs) was established by transforming growth factor-β1 (TGF-β1) treatment in vitro. The mitochondrial morphology of mCFs under TGF-β1 stimulation was evaluated by Mitotracker staining. Delivery of EXOs from GDF15-treated iPSC-MSCs resulted in less fibrotic remodeling and better ventricular function after MI than exosomes from untreated cells. In TGF-β1-stimulated fibroblasts, both exosome types reduced fibrosis markers by preventing mitochondrial fission, with GDF15-iPSC-MSC-EXOs affording stronger protection. These effects were partly attenuated in the presence of the mitochondrial fission activator FCCP. Mechanistically, GDF15, which is rich in GDF15-iPSC-MSC-EXOs, inhibited TGF-β1-induced mCF activation via repression of the MFAP4/ERK/Drp1 pathway through a direct physical interaction with MFAP4. GDF15 conditioning strengthened the capacity of iPSC-MSC-derived exosomes to mitigate cardiac fibrosis following MI via inhibition of mitochondrial fragmentation in CFs by repressing the MFAP4/ERK/Drp1 pathway. GDF15 pretreatment is a novel strategy to enhance the cardioprotection of iPSC-MSC-EXOs against cardiac fibrosis post-MI.

Intravascular hemolysis accompanies diverse diseases, yet blood-based markers (eg, plasma-free hemoglobin [PFH], haptoglobin, lactate dehydrogenase [LDH], and bilirubin) are variably sensitive, nonspecific, or impractical for point-of-care use. We evaluated urinary carbonic anhydrase 1 (CA1) as a mechanistically grounded, urine-based marker of hemolysis in a multicenter study spanning the United Kingdom, Bangladesh, and Peru. We enrolled 234 participants: healthy adults and adults with inherited anemias (Oxford), newborns in intensive care (London), children and adults with complicated or uncomplicated malaria (Bangladesh), and adults attending rural clinics for various medical reasons (Peru). Urine CA1 and hemoglobin (Hb) were quantified by enzyme-linked immunosorbent assay and immunoblot, with CA1:Hb stoichiometry used to distinguish intravascular hemolysis from urogenital blood contamination. Relationships with PFH, LDH, bilirubin, Hb, C-reactive protein (CRP), and clinical variables were tested using regression, principal component analysis, and decision tree. Reference urine samples were predominantly CA1-negative/Hb-negative. In inherited anemias, urinary CA1 was highest in sickle cell disease and correlated with serum LDH and inversely with blood Hb. In neonates, longitudinal CA1 trajectories stratified infants into physiological, transient, and sustained hemolysis groups; higher CA1 levels were associated with prematurity, elevated CRP and lower white blood cell count. Urinary CA1 was detected in Bangladeshi patients with elevated PFH and in cases of intravascular hemolysis not identified by PFH. Among Peruvian participants, urinary CA1 correlated with raised CRP level, consistent with inflammation being a prohemolytic trigger. To enable rapid and cost-effective testing, a lateral flow device was developed and verified for excellent sensitivity and specificity. Urinary CA1 provides a sensitive and practical readout of intravascular hemolysis suitable for point-of-care testing globally.

Berberine, an isoquinoline quaternary alkaloid, is a molecule with significant therapeutic adaptability. It has been identified, isolated, and measured in a wide range of plant families and species. Of these, Berberis stands out as a significant natural source of berberine, with Berberis vulgaris (B. vulgaris) bark being one of the most notable. The numerous health benefits associated with berberine include its potential use in the treatment of diseases, such as cancer, cardiovascular diseases, diabetes, and neurological disorders. The principal use of berberine has been for its antidiarrheal properties, which may have several modes of action. Its potent antioxidant and anti-inflammatory effects are responsible for its preventive action against stomach ulcers, and it has been found to kill dangerous gut bacteria while boosting the species and numbers of health-promoting bacteria. It protects the colon by influencing the production of several immune factors in addition to upregulating the Wnt-β creatinine signaling cascade. Berberine has shown its potential in regulating cholesterol metabolism by elevating the levels of low-density lipoprotein receptor in the liver. This review comprehensively examines the pharmacokinetics, multifaceted bioactivities, and gut-protective roles of berberine, providing a detailed analysis of its diverse physiological functions and potential clinical applications to advance the understanding and management of gastrointestinal diseases.

To investigate the effects of Jinlida granules (, JLD) on body weight, glucose tolerance, intestinal inflammation and barrier function in high-fat diet (HFD)-induced obese rats and explore the regulation of the gut microbiota as a potential treatment mechanism.

Sprague-Dawley rats were divided into control, HFD, low-dose JLD (L-JLD), high-dose JLD (H-JLD), and sitagliptin groups. The rats, with the exception of those in the control group, were fed a HFD to establish an obesity model while simultaneously receiving 0.5% carboxymethyl cellulose, L-JLD, H-JLD or sitagliptin for 25 weeks. We assessed body weight, conducted oral glucose tolerance tests, and analysed faecal samples using metagenomic sequencing. Haematoxylin-eosin (HE), Masson and immunohistochemical (IHC) staining were employed to evaluate histological changes in the colon tissue. Immunofluorescence (IF) staining was used to measure the expression levels of Zonula occludens-1 (ZO-1) and Claudin-1 in colon tissue. The colon tissue was also subjected to transcriptomic evaluation.

JLD treatment significantly reduced body weight and enhanced glucose tolerance in obese rats. It alleviated colonic tissue damage, decreased collagen deposition, inhibited macrophage infiltration, and increased the expression of the tight junction proteins ZO-1 and Claudin-1. Metagenomic analysis revealed JLD-induced shifts in the gut microbiota composition (increasing the abundance of Turicibacter, Faecalibaculum, Coriobacteriaceae and Lactobacillus reuteri), enriching beneficial bacteria and metabolic pathways (increasing the biosynthesis of various secondary metabolites, ascorbate and aldarate metabolism, oxidative phosphorylation, C5-branched dibasic acid metabolism and beta-alanine metabolism). Transcriptomic analysis revealed downregulation of inflammatory and immune pathways (inhibition of the tumour necrosis factor signalling pathway, advanced glycation end products-receptor for advanced glycation end products signalling pathway, toll-like receptor signalling pathway, and interleukin-17 signalling pathway), suggesting a comprehensive modulatory effect of JLD on intestinal health and metabolic function.

JLD granules effectively improve glucose tolerance and ameliorate obesity-related intestinal dysfunctions in HFD-induced obese rats. These benefits are likely mediated through the modulation of the gut microbiota, the suppression of intestinal inflammation, the enhancement of barrier function, and the attenuation of proinflammatory pathways. Our findings offer novel insights into the therapeutic potential of JLD, emphasizing its role in integrating gut microbiota management into the treatment of metabolic disorders.