Research & Bioactivity
Selank is a synthetic heptapeptide analog of the endogenous immunomodulatory peptide tuftsin, and researchers have studied it primarily in the context of anxiety-related behavior, cognitive function, and stress response using animal models. Studies conducted in rodents have examined its potential influence on the GABAergic system, as well as its interactions with enkephalins and other neuropeptides involved in emotional regulation. Research has also investigated Selank's effects on cytokine expression and immune modulation, with in vitro and in vivo studies exploring how it may influence the balance of pro- and anti-inflammatory signaling molecules. Additionally, researchers have examined its role in models of memory and learning, with particular interest in how it interacts with neurotrophic factors such as BDNF in the central nervous system. Some studies have explored its stability and bioavailability characteristics relative to its parent compound, tuftsin, as part of broader efforts to understand its pharmacokinetic profile in preclinical settings.
Published Research
Using nutrient limitation experiments to inform nutrient management thresholds in wadeable streams.
Shupryt M, Chenevert J — 2026
Nitrogen (N) and phosphorus (P) are widely recognized as primary drivers of eutrophication, yet translating ambient nutrient concentrations into predictive assessments of benthic algal limitation remains challenging. In particular, statewide analyses that couple in‑stream chemistry to nutrient limitation outcomes and inform management thresholds are lacking. This gap constrains the ability to design nutrient‑management strategies tailored to specific regions or watersheds. To address this need, we evaluated nutrient limitation using nutrient‑diffusing substrate (NDS) bioassays in 56 wadeable streams across Wisconsin, located within the Midwestern United States, a region characterized by mixed agricultural, urban, and forested land uses. Sites encompassed a broad range of ambient total nitrogen (TN) and total phosphorus (TP) concentrations (TN: 0.22-15.17 mg/L; TP: 7-919 µg/L) with only weak correlation between TN and TP. Limitation responses varied: 41% of sites showed no limitation, 23% were N-limited, 20% co-limited by N and P, and 9% were P-limited. Mixed-effects models indicated that N and combined N × P treatments significantly stimulated algal accrual, whereas P alone had weak effects. Logistic regression identified ambient total N thresholds for a 50% probability of N limitation at 1.37-1.93 mg/L across total P gradients, while P limitation thresholds (14-29 µg/L) were well below Wisconsin's TP standard. These findings suggest that N often exerts stronger control on algal growth and provides a plausible range of TN thresholds needed to constrain excess benthic algal growth in wadeable streams. These results underscore the need for dual-nutrient management strategies in Midwestern streams.
[Pathophysiological aspects of primary Sjögren's disease : From epithelial activation to systemic autoimmunity].
Ritter J, Dörner T — 2026
BACKGROUND: Primary Sjögren's disease (SjD) is a chronic autoimmune disease that predominantly affects exocrine glands but can also show numerous systemic organ manifestations. OBJECTIVE: Presentation of the current understanding of the pathogenesis of the disease, focusing on genetic predisposition, epithelial activation, interferon signature and the resulting B‑T cell interaction, which form the basis for innovative treatment approaches. METHODS: Selective literature review of current original articles, reviews and clinical studies. RESULTS: Current research postulates that SjD triggers epithelial dysregulation through a combination of genetic and epigenetic predispositions, hormonal influences and possible viral triggers. This leads to the release of dsDNA, dsRNA or ssRNA, which in turn activate the innate immune system. Salivary gland epithelial cells (SGECs), plasmacytoid dendritic cells (pDCs), and monocytes produce proinflammatory cytokines and additional immune cells are recruited. The pDCs produce massive amounts of type I interferon. This results in the formation of an inflammatory microenvironment, which causes SGECs to undergo apoptosis, the release of further antigens and the recruitment of T cells. In this context, myeloid cells and SGECs produce large amounts of the cytokine B‑cell activating factor (BAFF). This promotes the further recruitment of B cells. Through Th1 cells and Tfh cells a T-B cell interaction is formed, leading to the development of ectopic germinal centers, including the induction of autoreactive B cells. DISCUSSION: The pathophysiology of SjD is a multistage process in which the early activation of the salivary epithelium and subsequent activation of the innate immune system with IFN play a crucial role in its initiation. This is followed by activation of the adaptive immune system with a focus on T‑B cell interaction and pathological B cell activation. The chronic inflammation in SjD can be understood as positive feedback from the activation of the innate and adaptive immune systems, which innovative therapeutic approaches aim to interrupt. These comprise TLR and IFN blockade, inhibition of T‑B cell interaction via CD154/CD40 blockade (e.g., dazodalibep, iscalimab) or B cell depletion strategies including. anti-BAFF‑R and anti-CD19 CAR-T cells.
Short-term nitrogen addition mediates nutrient allocation and resorption trade-offs in Populus koreana: insights for vegetation restoration on volcanic lava platform.
Yin H, Xu M, Xie L, Yang F, Zhang C, et al. — 2026
BACKGROUND: Ecological stoichiometry serves as a foundational framework for understanding plant nutrient acquisition, allocation, and conservation strategies in extreme environments. The Wudalianchi volcanic lava platform represents a naturally oligotrophic habitat where functions as a keystone pioneer species during early ecological succession. However, the physiological and stoichiometric responses of to nitrogen (N) enrichment remain poorly understood. This knowledge gap constrains both theoretical development of ecological stoichiometry in geologically extreme systems and the formulation of evidence-based ecological restoration strategies for volcanic substrates. To address this, we conducted a controlled short-term N addition experiment across 12 randomized plots (10 m × 10 m each), applying four N treatments: 0 (control), 4, 8, and 16 g N·m⁻²·yr⁻¹. RESULTS: N addition increased soil total organic carbon (TOC) (23.04–142.68%) and total N (TN) (2.94–95.59%), reduced total phosphorus (TP) (7.55–15.09%) and available N: P ratio. N and P concentrations in mature leaves increased significantly (by 28.76–49.87% and 11.13–24.75%, respectively), whereas P concentrations decreased in fine branches and fine roots. Senescent leaf N and P concentrations rose by 6.57–17.60% and 14.10–38.06%, respectively, with a greater increase in P leading to a lower senescent leaf N: P ratio. N resorption efficiency (NRE) increased significantly (by 23.34–33.26%), while P resorption efficiency (PRE) decreased (by 5.67–11.43%). Mature leaf N and P concentrations were positively correlated with soil TN and available P (AP), respectively. In contrast, P concentrations and N: P ratios in fine branches and fine roots correlated negatively with soil AP and the available N: AP ratio, but positively with soil TP and the TN: TP ratio. NRE correlated positively with leaf N concentration, while PRE correlated negatively with both mature leaves P concentration and soil AP. CONCLUSION: Short-term N addition reshapes soil nutrient availability, driving to adopt a “photosynthetic organ-prioritized” nutrient allocation strategy and an N–P resorption trade-off. While N addition partially alleviates N limitation, it concurrently exacerbates P demand, thereby accelerating the transition from N limitation toward N–P co-limitation. These findings refine ecological stoichiometric theory in nutrient-impoverished volcanic ecosystems and offer mechanistically grounded, quantitative guidance for targeted vegetation restoration on lava platforms. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12870-026-08386-0.
Cinnamophilin ameliorates testosterone-induced prostatic hyperplasia and fibrosis by regulating 5α-reductase and TGF-β/Smad signaling pathway.
Han D, Chen CY, Huang X, Liu Y, Sun H, et al. — 2026
OBJECTIVES: Androgen and TGF-β1/Smad signaling pathways play important roles in epithelial-mesenchymal transition (EMT), fibrosis, and the development of benign prostatic hyperplasia (BPH). Cinnamophilin is extracted from . The anti-proliferative and anti-fibrosis effects of cinnamophilin on the prostate remain unclear. This study aimed to investigate the therapeutic effects and molecular mechanism of action of cinnamophilin on prostate growth in testosterone propionate (TP)-treated mice. MATERIALS AND METHODS: The study was conducted both and . TP was injected subcutaneously to induce prostate enlargement and growth. Cinnamophilin (40 mg/kg) was orally administered once a day in TP (7.5 mg/ kg)-treated mice for 28 days. The morphological characteristics and fibrosis of the prostate were examined by H&E (Hematoxylin and Eosin) and Masson's trichrome stain. Protein expression was determined by Western blot. BPH-1 and WPMY-1 cells were treated with different concentrations of cinnamophilin (1-100 μM). RESULTS: Cinnamophilin (40 mg/kg) significantly reduced prostate weight and prostate index in animal models. Cinnamophilin inhibited the protein expression of 5α-reductase type II and prostate-specific antigen (PSA) in TP-treated mice. Cinnamophilin reversed morphological changes, EMT, and fibrosis in TP-treated mice. Cinnamophilin increased E-cadherin but decreased N-cadherin, vimentin, fibronectin, α-SMA, TGFBR2, TGF-β1, p-Smad2/3, collagen I, collagen III, and collagen IV protein expressions. The expression of Smad2/3 was not significantly different among these groups. Cinnamophilin (100 μM) inhibited proliferation at 48 hr in BPH-1 and WPMY-1 cells. CONCLUSION: These findings suggest that cinnamophilin inhibits prostate growth and mitigates EMT and fibrosis by regulating TGFβ/Smad signaling pathways.
Therapeutic Peptides in Orthopaedics: Applications, Challenges, and Future Directions.
Rahman OF, Lee SJ, Seeds WA — 2026
Therapeutic peptides are emerging as promising adjuncts in the management of orthopaedic injuries, grounded in their ability to modulate molecular signaling networks central to cellular medicine. By acting on key pathways such as PI3K/Akt, mTOR, MAPK, TGF-β, and AMPK, peptides exert influence over tissue regeneration, inflammation resolution, and neuromuscular recovery. Wound-healing peptides such as BPC-157, TB-500, and GHK-Cu promote angiogenesis, integrin-mediated extracellular matrix remodeling, and fibroblast activation, whereas growth hormone secretagogues like ipamorelin, CJC-1295, tesamorelin, sermorelin, and AOD-9604 activate IGF-1 signaling and satellite cell repair. Recovery-enhancing agents such as epithalon, delta sleep-inducing peptide, and pinealon target circadian and mitochondrial regulators, and neuroactive peptides like selank, semax, and dihexa enhance brain-derived neurotrophic factor and HGF/c-Met pathways critical to neuroplasticity. Although preclinical studies are promising, there is a current lack of clinical trials. This review integrates current mechanistic insights with orthopaedic relevance, emphasizing safety, efficacy, and future directions for responsible integration into musculoskeletal care.