Carboxymethyl chitosan-methacrylic acid gelatin hydrogel for wound healing and vascular regeneration.

At present, wound dressings in clinical applications are primarily used for superficial skin wounds.However these dressings have significant limitations, including poor biocompatibility and limited ability to promote wound healing. To address this issue, t this study used aldehyde polyethylene glycol as the cross-linking agent to design a carboxymethyl chitosan-methacrylic acid gelatin hydrogel with enhanced biocompatibility, which can promote wound healing and angiogenesis.The CSDG hydrogel exhibites acid sensitivity, with a swelling ratio of up to 300%. Additionally, it exhibited excellent resistance to external stress, withstanding pressures of up to 160 kPa and self-deformation of 80%. Compared to commercially available chitosan wound gels, the CSDG hydrogel demonstrates excellent biocompatibility, antibacterial properties, and hemostatic ability. Both in vitro and in vivo results showed that the CSDG hydrogel accelerated blood vessel regeneration by upregulating the expression of CD31, IL-6, FGF, and VEGF, thereby promoting rapid healing of wounds. In conclusion, this study successfully prepared the CSDG hydrogel wound dressings, providing a new approach and method for the development of hydrogel dressings based on natural macromolecules. .

Iron promotes ovarian cancer malignancy and advances platinum resistance by enhancing DNA repair via FTH1/FTL/POLQ/RAD51 axis.

Iron is crucial for cell DNA synthesis and repair, but an excess of free iron can lead to oxidative stress and subsequent cell death. Although several studies suggest that cancer cells display characteristics of 'Iron addiction', an ongoing debate surrounds the question of whether iron can influence the malignant properties of ovarian cancer. In the current study, we initially found iron levels increase during spheroid formation. Furthermore, iron supplementation can promote cancer cell survival, cancer spheroid growth, and migration; vice versa, iron chelators inhibit this process. Notably, iron reduces the sensitivity of ovarian cancer cells to platinum as well. Mechanistically, iron downregulates DNA homologous recombination (HR) inhibitor polymerase theta (POLQ) and relieves its antagonism against the HR repair enzyme RAD51, thereby promoting DNA damage repair to resist chemotherapy-induced damage. Additionally, iron tightly regulated by ferritin (FTH1/FTL) which is indispensable for iron-triggered DNA repair. Finally, we discovered that iron chelators combined with platinum exhibit a synergistic inhibitory effect on ovarian cancer in vitro and in vivo. Our findings affirm the pro-cancer role of iron in ovarian cancer and reveal that iron advances platinum resistance by promoting DNA damage repair through FTH1/FTL/POLQ/RAD51 pathway. Our findings highlight the significance of iron depletion therapy, revealing a promising avenue for advancing ovarian cancer treatment.

Acute ischemia induces spatially and transcriptionally distinct microglial subclusters.

BACKGROUND: Damage in the ischemic core and penumbra after stroke affects patient prognosis. Microglia immediately respond to ischemic insult and initiate immune inflammation, playing an important role in the cellular injury after stroke. However, the microglial heterogeneity and the mechanisms involved remain unclear. METHODS: We first performed single-cell RNA-sequencing (scRNA-seq) and spatial transcriptomics (ST) on middle cerebral artery occlusion (MCAO) mice from three time points to determine stroke-associated microglial subclusters and their spatial distributions. Furthermore, the expression of microglial subcluster-specific marker genes and the localization of different microglial subclusters were verified on MCAO mice through RNAscope and immunofluorescence. Gene set variation analysis (GSVA) was performed to reveal functional characteristics of microglia sub-clusters. Additionally, ingenuity pathway analysis (IPA) was used to explore upstream regulators of microglial subclusters, which was confirmed by immunofluorescence, RT-qPCR, shRNA-mediated knockdown, and targeted metabolomics. Finally, the infarct size, neurological deficits, and neuronal apoptosis were evaluated in MCAO mice after manipulation of specific microglial subcluster. RESULTS: We discovered stroke-associated microglial subclusters in the brains of MCAO mice. We also identified novel marker genes of these microglial subclusters and defined these cells as ischemic core-associated (ICAM) and ischemic penumbra-associated (IPAM) microglia, according to their spatial distribution. ICAM, induced by damage-associated molecular patterns, are probably fueled by glycolysis, and exhibit increased pro-inflammatory cytokines and chemokines production. BACH1 is a key transcription factor driving ICAM generation. In contrast, glucocorticoids, which are enriched in the penumbra, likely trigger IPAM formation, which are presumably powered by the citrate cycle and oxidative phosphorylation and are characterized by moderate pro-inflammatory responses, inflammation-alleviating metabolic features, and myelinotrophic properties. CONCLUSIONS: ICAM could induce excessive neuroinflammation, aggravating brain injury, whereas IPAM probably exhibit neuroprotective features, which could be essential for the homeostasis and survival of cells in the penumbra. Our findings provide a biological basis for targeting specific microglial subclusters as a potential therapeutic strategy for ischemic stroke.

Wwl70-induced ABHD6 inhibition attenuates memory deficits and pathological phenotypes in APPswe/PS1dE9 mice.

Synaptic dysfunction plays a crucial role in the pathogenesis of Alzheimer's disease (AD). α/ß-hydrolase domain-containing 6 (ABHD6) contributes to synaptic dysfunctions, and ABHD6 inhibition has shown potential therapeutic value in neurological disorders. However, the role of ABHD6 in AD has not been fully defined. In this study, we demonstrated that adeno-associated virus (AAV) mediated shRNA targeting ABHD6 in hippocampal neurons attenuated synaptic dysfunction and memory impairment of APPswe/PS1dE9 (APP/PS1) mice, while it didn't affect the amyloid-beta (Aß) levels and neuroinflammation in the brains. In addition, intraperitoneal injection of wwl70, a specific inhibitor of ABHD6, improved synaptic plasticity and memory function in APP/PS1 mice, which might attribute to the activation of endogenous cannabinoid signaling. Furthermore, wwl70 significantly decreased the Aß levels and neuroinflammation in the hippocampus of AD mice, and enhanced Aß phagocytized by microglia. In conclusion, for the first time our data have shown that ABHD6 inhibition might be a promising strategy for AD treatment, and wwl70 is a potential candidate for AD drug development pipeline.

Data quantity governance for machine learning in materials science.

Data-driven machine learning (ML) is widely employed in the analysis of materials structure-activity relationships, performance optimization and materials design due to its superior ability to reveal latent data patterns and make accurate prediction. However, because of the laborious process of materials data acquisition, ML models encounter the issue of the mismatch between a high dimension of feature space and a small sample size (for traditional ML models) or the mismatch between model parameters and sample size (for deep-learning models), usually resulting in terrible performance. Here, we review the efforts for tackling this issue via feature reduction, sample augmentation and specific ML approaches, and show that the balance between the number of samples and features or model parameters should attract great attention during data quantity governance. Following this, we propose a synergistic data quantity governance flow with the incorporation of materials domain knowledge. After summarizing the approaches to incorporating materials domain knowledge into the process of ML, we provide examples of incorporating domain knowledge into governance schemes to demonstrate the advantages of the approach and applications. The work paves the way for obtaining the required high-quality data to accelerate materials design and discovery based on ML.

Primary malignant melanoma of the cervix: A comprehensive analysis of case reports in the Chinese population.

PURPOSE: Malignant melanoma is a tumor generated from the basal melanocytes of human epidermis. Primary malignant melanoma of the cervix (PMMC) is derived from cervical melanocytes. It is an uncommon disease, mostly occurring in perimenopausal women. PMMC has a bad prognosis and lacks a defined protocol or treatment standards. The aim of this study was to analyze the impact of different surgical procedures and different adjuvant treatment modalities on their prognosis and to find risk factors for their prognosis by integrating published case report data based on the Chinese population. METHODS AND RESULTS: This study included 165 patients with PMMC in the Chinese population. We used the Kaplan-Meier method to build the survival curve, and the log-rank test to examine the variations among the subgroups. Prognostic factors were examined utilizing the Cox proportional hazards regression model. We found that patients who underwent radical hysterectomy-based surgery, those who underwent lymphadenectomy, and those who underwent other treatments in addition to surgery had significantly better survival rates. The overall analysis, showed that age, and FIGO Stage II, III, and IV, increased the risk of death. Moreover, radical hysterectomy (RH), total hysterectomy (TAH), lymphadenectomy, and adjuvant therapy were correlated with a decreased mortality risk. CONCLUSION: After summarizing the current data, we recommend radical hysterectomy, and lymphadenectomy treatment for patients with PMMC. For patients who had already undergone surgery, other treatment options had a positive effect on prognosis. For patients who had already undergone surgery, other treatment options had a positive effect on prognosis; therefore patient-specific treatment options need to be further discussed.

Determination of the role of hippocampal astrocytes in the bilateral common carotid artery stenosis mouse model by RNA sequencing.

INTRODUCTION: Bilateral common carotid artery stenosis (BCAS) is used experimentally to model vascular dementia (VaD). Previous studies have primarily focused on the degradation of brain white matter after BCAS. However, hippocampal abnormalities are equally important, and hippocampal astrocytes are specifically involved in neural circuits that regulate learning and memory. Whether hippocampal astrocytes participate in the pathogenesis of BCAS-induced VaD has not been well studied. Therefore, in the present study, we attempted to explore the role of hippocampal astrocytes in BCAS. METHODS: Two months after BCAS, behavioral experiments were conducted to investigate changes in neurological function in sham and BCAS mice. A ribosome-tagging approach (RiboTag) profiling strategy was used to isolate mRNAs enriched in hippocampal astrocytes, and the RNA was sequenced and analyzed using transcriptomic methods. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was utilized to validate the results of RNA sequencing. Immunofluorescence analyses were conducted to evaluate the number and morphology of hippocampal astrocytes. RESULTS: We observed significant short-term working memory impairment in BCAS mice. Moreover, the RNA obtained through RiboTag technology was specific to astrocytes. Transcriptomics approaches and subsequent validation studies revealed that the genes that showed expression changes in hippocampal astrocytes after BCAS were mainly involved in immune system processes, glial cell proliferation, substance transport and metabolism. Furthermore, the number and distribution of astrocytes in the CA1 region of the hippocampus tended to decrease after modeling. CONCLUSION: In this study, comparisons between sham and BCAS mice showed that the functions of hippocampal astrocytes were impaired in BCAS-induced chronic cerebral hypoperfusion-related VaD.

A monoamine oxidase B inhibitor ethyl ferulate suppresses microglia-mediated neuroinflammation and alleviates ischemic brain injury.

Microglia are the resident macrophages in the brain, which play a critical role in post-stroke neuroinflammation. Accordingly, targeting neuroinflammation could be a promising strategy to improve ischemic stroke outcomes. Ethyl ferulate (EF) has been confirmed to possess anti-inflammatory properties in several disease models, including acute lung injury, retinal damage and diabetes-associated renal injury. However, the effects of EF on microglial activation and the resolution of post-stroke neuroinflammation remains unknown. Here, we found that EF suppressed pro-inflammatory response triggered by lipopolysaccharide (LPS) stimulation in primary microglia and BV2 cell lines, as well as post-stroke neuroinflammation in an in vivo transient middle cerebral artery occlusion (tMCAO) stroke model in C57BL/6 mice, consequently ameliorating ischemic brain injury. Furthermore, EF could directly bind and inhibit the activity of monoamine oxidase B (MAO-B) to reduce pro-inflammatory response. Taken together, our study identified a MAO-B inhibitor, Ethyl ferulate, as an active compound with promising potentials for suppressing post-stroke neuroinflammation.

Preliminary Analysis of Cervical Cancer Immunotherapy.

Cervical cancer is one of the most common gynecologically malignancies worldwide. Although vaccine and cervical cancer screening including human papillomavirus testing, cytology testing, and colposcopy have developed rapidly in recent years, effectively reducing cervical cancer mortality, cervical cancer remains a malignancy with higher female fatality rates worldwide and has a high risk for socioeconomically disadvantaged groups. The combination of platinum-paclitaxel and chemotherapy, possibly with the addition of bevacizumab, is currently the treatment of choice for advanced cervical cancer, but it only has remission purposes. Therefore, new therapeutic strategies are needed for both locally advanced and metastatic cervical cancer. Here, we make a preliminary analysis of cervical cancer immunotherapy.

Bergapten attenuates microglia-mediated neuroinflammation and ischemic brain injury by targeting Kv1.3 and Carbonyl reductase 1.

Microglia-mediated neuroinflammation plays a vital role in the pathogenesis of ischemic stroke, which serves as a prime target for developing novel therapeutic agent. However, feasible and effective agents for controlling neuroinflammation are scarce. Bergapten were acknowledged to hold therapeutic potential in restricting inflammation in multiple diseases, including peripheral neuropathy, migraine headaches and osteoarthritis. Here, we aimed to investigate the impact of bergapten on microglia-mediated neuroinflammation and its therapeutic potential in ischemic stroke. Our study demonstrated that bergapten significantly reduced the expression of pro-inflammatory cytokines and the activation of NF-κB signaling pathway in LPS-stimulated primary microglia. Mechanistically, bergapten suppressed cellular potassium ion efflux by inhibiting Kv1.3 channel and inhibits the degradation of Carbonyl reductase 1 induced by LPS, which might contribute to the anti-inflammatory effect of bergapten. Furthermore, bergapten suppressed microglial activation and post-stroke neuroinflammation in an experimental stroke model, leading to reduced infarct size and improved functional recovery. Thus, our study identified that bergapten might be a potential therapeutic compound for the treatment of ischemic stroke.

Fraxetin alleviates microglia-mediated neuroinflammation after ischemic stroke.

Background: Neuroinflammation, which is mainly mediated by excessive microglia activation, plays a major role in ischemic stroke. Overactivated microglia secrete numerous inflammatory cytokines, causing excessive inflammatory responses and ultimately exacerbating ischemic brain injury. Hence, compounds that attenuate neuroinflammation could become promising drug candidates for ischemic stroke. Fraxetin has an anti-inflammatory effect in many inflammatory diseases. However, whether it possesses an anti-inflammatory capacity in microglia-mediated neuroinflammation after ischemic brain injury is unknown. Our study aimed to investigate the suppression effect of fraxetin on neuroinflammation in lipopolysaccharide (LPS)-activated microglia and establish whether fraxetin could alleviate ischemic brain injury in a rodent model of ischemic stroke. Methods: For the in vitro experiment, primary microglia were obtained from 1-day-old C57/BL6J mice. The cells were activated with LPS and treated with fraxetin at a non-cytotoxic concentration. Real-time PCR, enzyme-linked immunosorbent assays, and immunofluorescence staining were used to evaluate the anti-inflammatory effects of fraxetin. The potential molecular mechanisms were explored and verified through RNA-sequencing analysis, western blotting and real-time PCR. For the in vivo experiment, focal ischemia was induced by middle cerebral artery occlusion (MCAO) in 8-week-old male C57/BL6J mice. Fraxetin (5 mg/kg) or an equal volume of saline was injected into mice intraperitoneally after MCAO, and 2% 2,3,5-triphenyltetrazolium chloride staining was applied to measure infarct volume. Behavioral tests were conducted to measure neurological deficits in the mice. Real-time PCR, western blotting, and immunofluorescence staining were used to examine the expression of inflammatory cytokines and microglia activation in the ischemic penumbra. Results: Fraxetin effectively inhibited the expression of proinflammatory cytokines including inducible nitric oxide synthase, tumor necrosis factor-α, interleukin-1 beta, and interleukin-6 in LPS-activated microglia. Fraxetin also suppressed the PI3K/Akt/NF-κB signaling pathway in activated microglia, which contributed to its anti-inflammatory effects. Furthermore, the administration of fraxetin attenuated ischemic brain injury and behavioral deficits after stroke. Finally, fraxetin was found to attenuate the activation of microglia both in vitro and in vivo. Conclusions: Our results suggest that fraxetin has a suppression effect on microglia-mediated neuroinflammation, and this effect is associated with the PI3K/Akt/NF-κB signaling pathway. Fraxetin may therefore have potential neuroprotective properties for ischemic stroke.

Feibi decoction-medicated serum inhibits lipopolysaccharide-induced inflammation in RAW264.7 cells and BMDMs.

Feibi decoction (FBD) is a traditional Chinese herbal medicine and has been clinically used in the treatment of pulmonary fibrosis (PF), which is characterized by diffuse interstitial inflammation and exaggerated collagen accumulation. However, the potential mechanisms remain to be elucidated. The present study aimed to investigate the effect of FBD-medicated serum (FBDS) on lipopolysaccharide (LPS)-induced inflammation in macrophages. In RAW264.7 macrophages and bone marrow-derived macrophages (BMDMs), FBDS treatment significantly inhibited the production of pro-inflammatory cytokines induced by LPS. In addition, it was indicated that FBDS treatment suppressed the activation of NF-κB and Smad2/Smad3 following LPS treatment. Furthermore, FBDS treatment decreased the expression of transforming growth factor-ß1 and chitinase-3-like protein 1. In conclusion, the results demonstrated that treatment with FBDS inhibited LPS-induced inflammation in RAW264.7 and BMDM cells. These data may improve understanding of the effect of FBD on anti-inflammation and help determine the mechanisms underlying the alleviation of PF via FBD.

Mucinous Ovarian Tumors With Anaplastic Mural Nodules: Case Report.

Ovarian mucinous cystic tumors may be associated with various types of mural nodules, which can be classified as benign or malignant (anaplastic carcinoma, sarcoma, carcinosarcoma). However, anaplastic malignant nodules have rarely been reported. Here, we present a case of a 35-year-old woman who presented with abdominal discomfort. Ultrasonography showed a large cystic mass in the pelvic and abdominal cavities measuring 337 × 242 mm. Abdominal computed tomography revealed upper anterior and posterior uterine pelvic cystic lesions based on multiple nodule partition walls and classes. During hospitalization, the patient underwent exploratory laparotomy, which revealed a poorly differentiated ovarian malignant tumor, and subsequent surgical excision was performed. The pathological analysis of the surgical samples of the right ovary revealed a mucinous ovarian tumor, while the mural nodules were classified as anaplastic carcinoma. After surgery, the patient started receiving chemotherapy. Unfortunately, the patient died 6 months later. Mucinous tumor occurring with an anaplastic carcinoma is rare, and the current diagnostic methods are not sufficient in providing an early and accurate diagnosis. Most patients are already in the advanced stage upon diagnosis and combined with poorly differentiated pathological features, the prognosis is extremely poor. Clinicians need to improve the clinical evaluation before surgery and conduct preoperative preparation and communication to improve the prognosis of patients as much as possible.

Bisphenol A induces ovarian cancer cell proliferation and metastasis through estrogen receptor-α pathways.

Bisphenol A (BPA) is a widely used raw material that can be detected both in the environment and in the human body. Due to its estrogen-like effects, wide concerns have been raised about the potential role of BPA in the initiation and development of hormone-dependent cancers. Ovarian cancer is the most common reproductive system cancer and has a high mortality rate in women. Despite recent investigations into BPA's carcinogenic effects, studies on its role in ovarian cancer development remain limited. In this study, we aimed to assess the effect of BPA at various environmentally relevant concentrations on proliferation and metastasis of ovarian cancer cells. We discovered that BPA can stimulate proliferation of OVCAR-3 ovarian cancer cells after exposure for up to 5 days. Strikingly, BPA enhanced ovarian cancer cell migration, invasion, and adhesion (to vascular endothelial cells) through upregulation of matrix metalloproteinase-2 (MMP-2), MMP-9, and intercellular cell adhesion molecule-1 (IMAC-1). The stimulatory effects of BPA on cancer cell proliferation and metastasis were reversed by treatment with an ERα inhibitor, but not by treatment with an ERß inhibitor. Together, these results suggest that BPA induces proliferation and metastasis of ovarian cancer cells through ERα signaling pathways. This study provides new insights into the carcinogenic effects of BPA with regard to ovarian cancer.

Tuning wall thickness of TiO2 microtubes for an enhanced photocatalytic activity with thickness-dependent charge separation efficiency.

TiO2 microtubes with tunable wall thickness have been synthesized by a one-step electrospinning method linked with a calcination process. The wall thickness of TiO2 microtubes can be easily tuned by altering the dosage of liquid paraffin. The influence of the thickness on the light-harvesting ability and separation efficiency of the photogenerated carriers was studied using ultraviolet-visible (UV-vis) diffuse reflectance spectroscopy, photoluminescence emission spectroscopy, and photocurrent density measurements. Results show that TiO2 microtubes with an appropriate thickness exhibit enhanced light scattering effect, UV-vis light-harvesting ability, charge separation efficiency, and photocatalytic performance. The degradation rates of rhodamine B and 2,4-dinitrophenol by using TiO2 microtubes synthesized at a dosage of 0.14 g/mL liquid paraffin are 99.9% within 60 min and 97.8% within 40 min, respectively, which are higher than most of the reported values. All these results suggest that our work provides an ideal strategy for adjusting the wall thickness of TiO2 microtubes and new approach to enhance the photocatalytic performance of TiO2.

Flexible Carbon-Fiber/Semimetal Bi Nanosheet Arrays as Separable and Recyclable Plasmonic Photocatalysts and Photoelectrocatalysts.

In this work, we prepared flexible carbon-fiber/semimetal Bi nanosheet arrays from solvothermal-synthesized carbon-fiber/Bi2O2CO3 nanosheet arrays via a reductive calcination process. The flexible carbon-fiber/semimetal Bi nanosheet arrays can function as photocatalysts and photoelectrocatalysts for 2,4-dinitorphenol oxidation. Compared with carbon-fiber/Bi2O2CO3 nanosheet arrays, the newly designed flexible carbon-fiber/semimetal Bi nanosheet arrays show enhanced ultraviolet-visible (UV-vis) light absorption efficiency and photocurrent, photocatalytic, and photoelectrocatalytic activities. Photocatalytic analyses indicate that the surface plasmon resonance (SPR) of semimetal Bi occurs under solar-simulated light irradiation during the photocatalytic process. The carbon-fiber traps the hot electrons exerted from the SPR of semimetal Bi and creates holes in the semimetal Bi nanosheets, which boosts the photocatalytic activity of the carbon fiber through plasmonic sensitization. Both photocatalytic experiments and density functional theory (DFT) calculations indicate that the electrons transferred to the carbon fiber and the holes created in semimetal Bi contribute to the formation of •O2- and •OH, respectively. The synergistic effect between electrocatalysis and photocatalysis under the solar-simulated light results in almost complete degradation of 2,4-dinitorphenol during the photoelectrocatalytic process. This work realizes a non-noble-metal plasmonic catalyst and provides a new avenue for the commercialization of photocatalysis and photoelectrocatalysis using the separable and recyclable carbon-fiber/semimetal Bi nanosheet arrays in the environment-related field.

CAVD, towards better characterization of void space for ionic transport analysis.

Geometric crystal structure analysis using three-dimensional Voronoi tessellation provides intuitive insights into the ionic transport behavior of metal-ion electrode materials or solid electrolytes by mapping the void space in a framework onto a network. The existing tools typically consider only the local voids by mapping them with Voronoi polyhedra vertices and then define the mobile ions pathways using the Voronoi edges connecting these vertices. We show that in some structures mobile ions are located on Voronoi polyhedra faces and thus cannot be located by a standard approach. To address this deficiency, we extend the method to include Voronoi faces in the constructed network. This method has been implemented in the CAVD python package. Its effectiveness is demonstrated by 99% recovery rate for the lattice sites of mobile ions in 6,955 Li-, Na-, Mg- and Al-containing ionic compounds extracted from the Inorganic Crystal Structure Database. In addition, various quantitative descriptors of the network can be used to identify and rank the materials and further used in materials databases for machine learning.

Number 2 Feibi Recipe Reduces PM2.5-Induced Lung Injury in Rats.

Air pollution is the main cause of respiratory diseases. Fine particulates with the diameter below 2.5 µm can get into the alveoli and then enter the blood circulation through the lung tissue ventilation function and cause multiple systemic diseases especially the respiratory diseases. This study investigated the pathological mechanism of the lungs injury in rats induced by PM2.5 and the effect and mechanism of the Chinese herbal medicine number 2 Feibi Recipe (number 2 FBR) on lungs injury. In this experiment, Wistar rats were used. Lungs injury was induced by PM2.5. Number 2 FBR was used to treat the rats. The result showed that number 2 FBR could improve the lung injury in the rats. Meanwhile, it significantly reduced pathological response and inflammatory mediators including interleukin-6 (IL-6), interleukin-13 (IL-13), interleukin-17 (IL17), monocyte chemotactic protein-1 (MCP-1), and transforming growth factor-α (TNF-α) and upregulated glutathione peroxidase (GSH-Px) in the PM2.5 induced lung injury in the rats. Collectively, number 2 FBR appears to attenuate the lungs injury in rats induced by PM2.5.

m-Cresol purple functionalized surface enhanced Raman scattering paper chips for highly sensitive detection of pH in the neutral pH range.

Herein, a pH sensitive paper SERS chip was prepared by selecting m-cresol purple, a molecule with halochromic properties in the neutral pH range as a Raman reporter. The adsorbed m-cresol purple underwent a reversible change in its electronic configuration from a non-resonant species to a resonant species, which resulted in a significant Raman signal intensity variation due to the transformation of the sensing mode from SERS to surface-enhanced resonance Raman scattering (SERRS). The chips have a sensitive pH range of 6.0 to 8.0 and exhibited good performance for the detection of natural water samples with detection precision of approximately 0.03 pH units, suggesting great potential for environmental pH monitoring applications.