METTL14/YTHDC1-Mediated m6A Modification in Hippocampus Improves Pentylenetetrazol-Induced Acute Seizures.

Epilepsy is a common neurological disorder which can cause significant morbidity and mortality. N6-methyladenosine (m6A), the most common chemical epigenetic modification among mRNA post-transcriptional modifications, implicated in various physiological and pathological processes, but its role in epilepsy is still unknown. Here, we provide strong evidences in support of an association of m6A and its regulatory proteins with epilepsy. Our results indicated that the level of m6A was declined significantly in the dentate gyrus (DG) of hippocampus of pentylenetetrazol (PTZ)-induced seizure mice. Both the seizure-like behaviors and the excessive activation of DG area neuron were significantly mitigated after the administration of m6A agonist betaine. Mechanically, we found that both the m6A methyltransferase METTL14 and recognition protein YTHDC1 were decreased by PTZ stimulation, which might contribute to the reduced m6A level. Additionally, DG-specific over-expression of METTL14 or YTHDC1 by lentivirus injection could significantly ameliorate seizure-like behaviors and prevent the excessive activation of neuron in epilepsy mice induced by PTZ injection, which might be due to the normalized m6A level. Together, this study identified that METTL14/YTHDC1-mediated m6A modification could participate in seizure-like behaviors, which might provide m6A regulation as a potential and novel therapeutic strategy for epilepsy.

Betaine eliminates CFA-induced depressive-like behaviour in mice may be through inhibition of microglia and astrocyte activation and polarization.

Chronic pain can induce not only nociceptive but also depressive emotions. A previous study demonstrated that betaine, a commonly used nutrient supplement, has an anti-nociceptive effect, but whether betaine can alleviate chronic pain-induced depressive emotion is elusive. Our current study found that betaine administration significantly eliminated complete Freund's adjuvant (CFA)-induced pain-related depressive-like behaviour. Mechanistically, betaine treatment inhibited microglia and astrocyte activation. Furthermore, betaine significantly promoted the transition of microglia from the M1 to the M2 phenotype, as well as the transition of astrocytes from the A1 to the A2 phenotype. Additionally, the release of pro-inflammatory factors such as IL-18, IL-1ß and IL-6 and anti-inflammatory factors such as IL-10 in the hippocampus induced by CFA were also reversed by betaine administration. Overall, betaine has therapeutic effects on pain-related depressive-like phenotypes caused by CFA, possibly through altering the polarization of microglia and astrocytes to reduce neuroinflammation.

Role of CD23 Activated ERK Signaling Pathway in the Pathogenesis of Eosinophilic Chronic Sinusitis with Nasal Polyps.

Objective: In the context of the rising prevalence of eosinophilic chronic sinusitis accompanied by nasal polyps, this study aims toinvestigate the role of CD23 in the pathogenesis of eosinophilic chronic sinusitis with nasal polyps. Methods: The cross-sectional study was conducted, 75 patients with chronic sinusitis and nasal polyps treated in our hospital from January 2019 to May 2021 were selected, including 40 cases of eosinophilic patients with the average age of 29.92 years and 35 cases of non-eosinophilic patients with the average age of 30.05 years and 30 patients with the average age of 30.14 years who underwent skull base benign tumor resection in our hospital were selected as the control group, the expression of CD23 in polyp tissue was detected by immunohistochemistry, and the expression of CD23, p-ERK and CCL20 in polyp tissue were detected by Western blot. Specifically, tissue samples were processed and subjected to staining using specific antibodies targeting CD23. The stained sections were then visualized under a microscope to determine the expression levels of CD23. CD23, p-ERK, and CCL20 expressions in polyp tissue were evaluated via Western blot. Total protein was extracted, separated on a gel, transferred to a membrane, and probed with specific antibodies. Chemiluminescence allowed visualization and quantification of protein expressions. Results: Immunohistochemistry showed that CD23 expression was high in the eosinophilic group but low in the non-eosinophilic and control groups. The relative expression levels of CD23 protein, p-ERK protein, and CCL20 protein in polyp tissue s of the eosinophilic group were (0.892 ± 0.092), (0.733 ± 0.101) and (0.813 ± 0.106), respectively, which were significantly higher than those in non-eosinophilic group and control group (P < .05). The relative expression levels of CD23 protein, p-ERK protein, and CCL20 protein in the non-eosinophilic group were (0.461 ± 0.087), 0.412 ± 0.096) and (0.424 ± 0.098), which were significantly higher than those in the control group (P < .05). The relative expression level of CD23 protein in the eosinophilic group was positively correlated with the relative expression levels of p-ERK protein and CCL20 protein (P < .05). The Lund-Kennedy score in the eosinophilic group was (6.10 ± 1.01), which was significantly higher than that in the non-eosinophilic group (P < .05). The relative expression level of CD23 protein in the eosinophilic group was positively correlated with Lund-Kennedy score (P < .05). Conclusion: Eosinophilic chronic sinusitis with nasal polyp mucosal tissue CD23 expression is up-regulated, which is positively correlated with the ERK signaling pathway and disease severity. This study provides valuable insights into potential therapeutic targets that could be explored to develop future treatment modalities. The potential clinical significance of the study is to reveal the important role of CD23 in the pathogenesis of chronic sinusitis with nasal polyps. The upward adjustment of CD23 is positively related to the severity of the disease, which provides valuable guidance for future treatment strategies. This discovery may provide new ways for the development of CD23 treatment methods, so as to better control the progress of the disease of eosinophilic chronic sinusitis with nasal polyps. Further research can explore the molecular mechanism of CD23 regulation, further verify the feasibility of CD23 as the treatment target, and evaluate the potential value of CD23 as a prognostic logo.

Intracellular FGF1 promotes invasion and migration in thyroid carcinoma via HMGA1 independent of FGF receptors.

Background: Fibroblast growth factor 1 (FGF1) is extensively amplified in many tumors and accelerates tumor invasion and metastasis. However, the role and precise molecular mechanism by which FGF1 participates in thyroid cancer (TC) are still unclear. Methods: Quantitative real-time polymerase chain reaction- and western blotting were used to detect the mRNA and protein levels of FGF1, high mobility group A (HMGA1), epithelial-to-mesenchymal transition (EMT)-related factors, and FGFs in both TC tissues and cell lines. Immunohistochemistry was conducted to examine the expression of FGF1 and HMGA1. Immunofluorescence staining was used to detect the coexpression of FGF1 and HMGA1. Transwell and wound healing assays were conducted to evaluate the effects of FGF1 on the capacity of invasion and migration in cells. Results: FGF1 was upregulated in papillary thyroid carcinoma (PTC) tissues and cell lines and was relatively higher in PTC tissues with cervical lymph node metastasis. Furthermore, FGF1 promotes invasion and metastasis through the EMT pathway. Mechanistically, FGF1 promotes EMT through intracellular function independent of FGF receptors. Interestingly, we demonstrated that FGF1 could upregulate HMGA1 in TC cells, and the correlation of FGF1 and HMGA1 was positive in PTC tissues. FGF1 and HMGA1 had obvious colocalization in the nucleus. We further revealed that FGF1 promotes the invasion and migration of TC cells through the upregulation of HMGA1. Conclusion: Intracellular FGF1 could promote invasion and migration in TC by mediating the expression of HMGA1 independent of FGF receptors, and FGF1 may be an effective therapeutic target in TC.

JQ1 attenuates neuroinflammation by inhibiting the inflammasome-dependent canonical pyroptosis pathway in SAE.

Sepsis-associated encephalopathy (SAE) manifests clinically in hyperneuroinflammation. Pyroptosis, which can induce an inflammatory cascade response, has been considered to be a causative factor of SAE. Evidence has shown that the bromo- and extraterminal (BET) proteins (including BRD2, BRD3, BRD4 and BRDT) inhibitor JQ1 can inhibit inflammation and suppress pyroptosis in various diseases. Therefore, we examined the effect of JQ1 on inflammasome-induced pyroptosis in the hippocampus in a mouse model of sepsis induced by lipopolysaccharide (LPS) injection. The results showed that JQ1 treatment alleviated sepsis-related symptoms, protected the blood-brain barrier (BBB), as indicated by upregulated expression of the tight junction proteins occludin and ZO-1, and remarkably rescued neuronal damage in SAE mice. Mechanistically, we demonstrated that JQ1 intervention inhibited the expression of BRD proteins and decreased the expression of inflammasomes by blocking phospho-nuclear factor kappa B (p-NF-κB) signalling, attenuating the canonical pyroptosis (mediated by cleaved-Caspase1/11) pathway and the release of proinflammatory factors in the hippocampus of septic mice. Interestingly, we also found that JQ1 selectively suppressed the activation of hippocampal microglia in SAE mice. Thus, JQ1 protected the hippocampal BBB and neuronal damage through the attenuation of neuroinflammation by inhibiting the inflammasome-dependent canonical pyroptosis pathway induced by LPS injection in mice, and JQ1 may be a promising target for the prevention of SAE.

The roles and mechanisms of the m6A reader protein YTHDF1 in tumor biology and human diseases.

YTHDF1 is the most versatile and powerful reader protein of N 6-methyladenosine (m6A)-modified RNA, and it can recognize both G(m6A)C and A(m6A)C RNAs as ligands without sequence selectivity. YTHDF1 regulates target gene expression by different mechanisms, such as promoting translation or regulating the stability of mRNA. Numerous studies have shown that YTHDF1 plays an important role in tumor biology and nontumor lesions by mediating the protein translation of important genes or by affecting the expression of key factors involved in many important cell signaling pathways. Therefore, in this review we focus on some of the roles of YTHDF1 in tumor biology and diseases.

Noncoding RNAs in triple negative breast cancer: Mechanisms for chemoresistance.

Triple-negative breast cancer (TNBC) is the most aggressive subtype among breast cancers with high recurrence and this condition is partly due to chemoresistance. Therefore, fully understanding the mechanism of TNBC-resistance is the key to overcoming chemoresistance, which will be an effective strategy for TNBC therapy. Various potential mechanisms involved in the chemoresistance of TNBC have been investigated and indicated that noncoding RNAs (ncRNAs) especially microRNAs (miRNAs), long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) take part in most TNBC resistance. The ncRNA-induced chemoresistance process is involved in the alteration of many activities. here, we mainly summarize the mechanisms of ncRNAs in the chemoresistance of TNBC and discuss the potential clinical application of ncRNAs in the treatment of TNBC, indicating that targeting ncRNAs might be a promising strategy for resensitization to chemotherapies.

DPANet: Depth Potentiality-Aware Gated Attention Network for RGB-D Salient Object Detection.

There are two main issues in RGB-D salient object detection: (1) how to effectively integrate the complementarity from the cross-modal RGB-D data; (2) how to prevent the contamination effect from the unreliable depth map. In fact, these two problems are linked and intertwined, but the previous methods tend to focus only on the first problem and ignore the consideration of depth map quality, which may yield the model fall into the sub-optimal state. In this paper, we address these two issues in a holistic model synergistically, and propose a novel network named DPANet to explicitly model the potentiality of the depth map and effectively integrate the cross-modal complementarity. By introducing the depth potentiality perception, the network can perceive the potentiality of depth information in a learning-based manner, and guide the fusion process of two modal data to prevent the contamination occurred. The gated multi-modality attention module in the fusion process exploits the attention mechanism with a gate controller to capture long-range dependencies from a cross-modal perspective. Experimental results compared with 16 state-of-the-art methods on 8 datasets demonstrate the validity of the proposed approach both quantitatively and qualitatively. https://github.com/JosephChenHub/DPANet.

Non-coding RNAs: Key regulators of aerobic glycolysis in breast cancer.

Although extensive research progress has been made in breast cancer in recent years, yet the morbidity and mortality rates of breast cancer are rising, making it the major disease that endangers women's health. Energy metabolism reprogramming is featured by a state termed "aerobic glycolysis" or the Warburg effect that glycolysis is preferred even under aerobic conditions in neoplastic diseases. Widely acknowledged as an emerging hallmark in cancers, this metabolic switch shows a sophisticated role in the pathogenesis of breast cancer. The regulating effect of non-coding RNAs (ncRNAs) composed of microRNAs, long non-coding RNAs and circular RNAs is closely related to the glycolysis in breast cancer. Therefore, understand the mechanisms of ncRNAs of aerobic glycolysis in breast cancer may provide new strategy for the disease.

Inflammation and airway remodeling of the lung in guinea pigs with allergic rhinitis.

Allergic rhinitis (AR) and asthma belong to the category of type I allergic diseases, whose pathological features are airway remodeling of the lung and allergic inflammation. The aim of the present study was to evaluate inflammation and remodeling of lung tissue in a guinea pig model of AR in order to confirm consistent pathological changes of upper and lower airways in AR. Male guinea pigs were randomly divided into an experimental and a control group (n=10 in each). The AR model was established by sensitization through intraperitoneal injection of ovalbumin for three weeks and bilateral nasal local excitation for twelve weeks. All tissues of nasal mucosa and lung were subjected to hematoxylin and eosin as well as toluidine blue staining, and characteristics of remodeling of lung tissue, including thickness of bronchial wall, epithelial mucosa and smooth muscle were histologically determined. Collagen deposition in lung tissue was observed by Masson's trichrome stain. Severe paroxysmal nose scratching action, frequent sneezing, visible outflow of secretion from the anterior naris and frequent nose friction were observed in the AR model group within 30 min after local excitation. The total symptom scores were significantly increased in the AR model group compared with those in the control group. Obvious inflammatory cell infiltration was observed in the AR model group. Compared with those in the control group, the numbers of eosinophils and mast cells in nasal mucosa and lung tissue were significantly increased. Obvious airway remodeling of the lung was observed in the AR model group. Compared with those in the control group, bronchial wall thickness, epithelial layer thickness and smooth muscle thickness in the airways were significantly increased in the AR model group. Increased collagen deposition was found in the AR model group compared with that in the control group. The results of the present study revealed that inflammation and airway remodeling of lungs arose in guinea pigs with AR, suggesting that pathological changes of upper and lower airways are consistent in this AR model.

[Role and mechanism of the expression of matrix metalloproteinase 9 and tumor necrosis factor α in upper and lower respiratory tract inflammation in rats].

OBJECTIVE: To investigate the role and mechanism of matrix metalloproteinase 9 (MMP-9) and tumor necrosis factor α (TNF-α) in the pathogenesis of allergic rhinitis (AR) and asthma(AS). METHODS: The rat models of AR and AS were made by injecting ovalbumin. The infiltration of eosinophils and mast cells were detected by hematoxylin-eosin (HE) staining and toluidine blue staining respectively, and the expression of MMP-9 and TNF-α in nasal mucosa and lung tissue were examined by immunohistochemical staining (SP method). The relationship of their expression with upper and lower respiratory tract inflammation was analyzed. SPSS 13.0 software was used to analyze the data. RESULTS: The numbers of MMP-9 positive inflammatory cells in nasal mucosa and lung tissue of AR were (154.8 ± 12.0) and (124.0 ± 8.2), (43.2 ± 7.6) and (34.5 ± 5.0) in the control groups, the difference was significant (t value were 24.260, 29.525 respectively, all P < 0.05). The numbers of MMP-9 positive inflammatory cells in nasal mucosa and lung tissue of AS were (149.9 ± 11.7) and (120.1 ± 7.3), (48.6 ± 7.6) and (39.1 ± 5.2) in control groups, the difference was significant (t value were 22.929 and 28.530 respectively, all P < 0.05). The numbers of TNF-α positive inflammatory cells in nasal mucosa and lung tissue of AR were (188.8 ± 17.0), and (134.8 ± 7.9), (57.6 ± 23.3) and (40.3 ± 8.2) in control groups, the difference was significant (t value were 13.836 and 26.220, all P < 0.05). The numbers of TNF-α positive inflammatory cells in nasal mucosa and lung tissue of AS were (179.2 ± 15.4) and (153.5 ± 10.1), (70.5 ± 33.1) and (33.8 ± 14.0) in control groups, the difference was significant (t value were 9.412 and 21.858, all P < 0.05). There was a correlation between the expression of MMP-9 and TNF-α in nasal mucosa and lung tissue of AR (r values were 0.893 and 0.700 respectively, P values were 0.001 and 0.024, respectively) and AS (r values were 0.692 and 0.644 respectively, P values were 0.027 and 0.044 respectively) groups. CONCLUSIONS: The inflammation is similar between AR and AS. The MMP-9 and TNF-α may play an important role in the pathogenesis of upper and lower respiratory tract inflammation.

[Effect of TNF-alpha and MMP-9 in the infiltration of eosinophil granulocyte in nasal polyps].

OBJECTIVE: To study the expression and significance of TNF-alpha, MMP-9 and their relationship with the infiltration of eosinophil granulocyte in nasal polyps. METHOD: The expression of TNF-alpha and MMP-9 was determined in tissues of nasal polyps from 30 patients(nasal polyps group) and in inferior turbinate mucosa tissues from 10 patients(control group) by in situ hybridization and immunohistochemical technique, and the number of eosinophil granulocyte was counted in the same tissue by HE staining. Their correlations with each other were also analyzed in the tissue of nasal polyps. RESULT: The number of TNF-alpha and MMP-9 positive cells and TNF-alpha positive blood vessels in nasal polyps were more than that in control group (P < 0.05). The number of both TNF-alpha positive cells and blood vessels had positive relationships with the number of eosinophil granulocyte, but there was only positive relationship between the number of MMP-9 positive cells and eosinophil granulocyte (P < 0.05). At the same time there was a positive relationship between the number of TNF-alpha and MMP-9 positive cells (P < 0.05). CONCLUSION: TNF-alpha and MMP-9 may play an important role in the pathological mechanism of nasal polyps. TNF-alpha may induce the expression of MMP-9 and promote the migration of eosinophil granulocyte.

[Expression and significance of COX-2 and S-100 positive dendritic cell in laryngeal carcinoma].

OBJECTIVE: To explore the expression of cyclooxygenase-2 (COX-2) and S-100 positive dendritic cell in laryngeal carcinoma tissue and their clinical significance. METHOD: Sixty-five samples of laryngeal carcinoma and thirty-four biopsies of adjacent noncancerous tissue were obtained. Immunohistochemical technique (SP method) was used to detect the expression of COX-2 and S-100 positive dendritic cell, and the relationship of their expression with clinical pathological parameters and prognosis was analyzed. RESULT: The rates of COX-2 expression were 63.08% (41/65)and 14.70% (5/34) in laryngeal carcinoma and control group, respectively. The difference was significant (P < 0.05). The positive expression of COX-2 was correlated with T and clinical stage in laryngeal carcinoma(all P < 0.05). The rates of S-100 positive dendritic cell expression were 61.54% (40/65)and 0 in laryngeal carcinoma and control group, respectively. The difference was significant (P < 0.05). S-100 positive dendritic cells showed significant differences between early and late clinical stage and lymph node metastasis (all P < 0.05). Kaplan-Meier survival analysis showed that patients with positive expression of COX-2 and S-100 positive dendritic cell had worse disease-free and overall survival (P < 0.05). Cox regression analysis showed that S-100 positive dendritic cell was indicated as an independent prognostic factor for survival(P < 0.05). CONCLUSION: COX-2 and S-100 positive dendritic cell are highly expressed in laryngeal carcinoma tissue. It suggests that the expression of COX-2 and S-100 positive dendritic cell is related to the process of carcinogenesis and may be the important indicators in laryngeal carcinoma for prognosis.

[Expression and clinical significance of Ang-2 and MMP-7 in laryngeal carcinoma].

OBJECTIVE: To investigate the expression and clinical significance of Ang-2 and MMP-7 protein in laryngeal carcinoma tissue. METHOD: Immunohistochemical technique was used to detect the expression of Ang-2 and MMP-7 protein in 65 tissues of laryngeal carcinoma and 34 biopsies of adjacent non- cancerous tissue. The relationship between the expression of Ang-2 and MMP-7 and invasion, metastasis or prognosis in laryngeal carcinoma tissue was analyzed. RESULT: The positive rates of Ang-2 and MMP-7 were significantly higher in laryngeal carcinoma tissue than those in adjacent non-cancerous tissue (P < 0.05). The level of Ang-2 and MMP-7 expression had no significant correlations with the age and course as well as the smoking, drinking, histological differentiation of carcinoma and clinical classification (P > 0.05). While the expression of Ang-2 significantly differed between patients with different T stage and clinical stage (P < 0.05), and the expression of MMP-7 was notably correlated with the T stage, clinical stage and lymph node metastases (P < 0.05). There was a correlation between the expression of Ang-2 and MMP-7 (P < 0.05). The Kaplan-Meier survival analysis showed that patients with positive expression of Ang-2 had worse overall survival (P < 0.05). However, MMP-7 expression was not related to overall survival or disease-free survival (all P > 0.05). Cox regression analysis indicated that Ang-2 and MMP-7 expression were independent prognostic factors of laryngeal carcinoma. CONCLUSION: Overexpression of Ang-2 and MMP-7 was observed in laryngeal carcinoma and they might be served as an objective indicator for biological behaviour and prognosis.

Fabrication of spindle Fe(2)O(3)@polypyrrole core/shell particles by surface-modified hematite templating and conversion to spindle polypyrrole capsules and carbon capsules.

By using a surface-modified templating method, Fe(2)O(3)@polypyrrole (PPy) core/shell spindles have been successfully prepared in this paper. The Fe(2)O(3) particles with spindle morphology were initially fabricated as core materials. After the PVP modification, the Fe(2)O(3) spindles were subsequently coated with a tunable thickness layer of PPy by in situ deposition of the conducting polymer from aqueous solution. Hollow PPy spindles were produced by dissolution of the Fe(2)O(3) core from the core/shell particles. High-temperature treatment under vacuum condition covert the hollow PPy spindles into carbon capsules by carbonization of the PPy shell. Transmission electron microscope (TEM), scanning electron microscopy (SEM), Fourier transform infrared spectroscopy (FTIR), thermal gravimetric analysis (TGA) and X-ray photoelectron spectroscopy (XPS) confirmed the formation of the Fe(2)O(3)@PPy core/shell particles, PPy and carbon capsules with spindle morphology.

Preparation of barium strontium titanate Ba(1-x)Sr(x)TiO(3) (0

An ultrasonic irradiation method was applied to the sol/gel synthesis of the single-crystal cubic barium strontium titanate Ba(1-x)Sr(x)TiO(3) (0

A facile method to fabricate carbon-encapsulated Fe(3)O(4) core/shell composites.

One-step synthesis of carbon-encapsulated Fe(3)O(4) core/shell composites is reported. The Fe(3)O(4) cores were formed via the reduction of Fe(3+) by glucose under alkaline conditions obtained by the decomposition of urea. The amorphous carbon shells were carbonized from glucose. A possible formation mechanism for the Fe(3)O(4)@C composite was discussed. In order to characterize these Fe(3)O(4)@C core-shell composites, high-resolution transmission electron microscopy (HR-TEM), x-ray diffraction (XRD), Fourier transform infrared spectroscopy (FT-IR), x-ray photoelectron spectroscopy (XPS) and a superconducting quantum interference device (SQUID) magnetometer were employed to characterize the sample obtained using the above method.

Sonochemical one-directional growth of montmorillonite-polystyrene nanocomposite.

Montmorillonite-exfoliated polystyrene (MMT-PS) nanocomposite was one-pot synthesized by high-intensity ultrasonic irradiation. Moreover, the MMT-PS exhibited one-directional growth during the sonication.

Preparation of polyacrylamide and gamma-zirconium phosphate nanocomposites by intercalative polymerization.

A new inorganic-organic nanocomposite of polyacrylamide (PAM) and gamma-zirconium phosphate (gamma-ZrP) was prepared by intercalative polymerization. Intercalation of acrylamide (AM) monomer in gamma-ZrP was investigated by sonochemical and refluxing methods. High-intensity ultrasound does not induce the polymerization of AM but enhances greatly the intercalation rate. On the other hand, ultrasound also enhanced hydrolyzation of -CONH2 and shrinkage of PAM gel. The interlayer distance of AM-intercalated gamma-ZrP is 16.4 A. The polymerization and intercalation of AM occurred nearly at the same time by refluxing method. The same gamma-ZrP/PAM nanocomposites were obtained with (NH4)2S2O8 treatment.

trans-Diaquabis(thiosemicarbazido-kappa2N,S)nickel(II) dimaleate dihydrate.

In the title compound, [Ni(CH(5)N(3)S)(2)(H(2)O)(2)](C(4)H(3)O(4))(2).2H(2)O, the Ni atom lies on a center of symmetry and is coordinated by N and S atoms from two thiosemicarbazide ligands and the O atoms of two water molecules in a distorted octahedral geometry. In the asymmetric unit, the three components are linked together by one O-H...O and two N-H...O hydrogen bonds. The packing is built from molecular ribbons parallel to the b direction, stabilized by intramolecular hydrogen bonds, and by one N-H...S and two N-H...O intermolecular hydrogen bonds. The ribbons are further connected into columns by N-H...O interactions and then into a three-dimensional network by three O-H...O hydrogen bonds.