Utilizing excited-state proton transfer fluorescence quenching mechanism, layered rare earth hydroxides enable ultra-sensitive detection of nitroaromatic.

Convenient, rapid, and accurate detection of nitroaromatic organic toxins and harmful substances is of great significance in research. In the present study, two-dimensional layered rare-earth hydroxides (LYH) were used as ion-exchange matrix materials, and the anionic fluorescent dye molecules (HPTS) were successfully introduced into the LYH structures in situ via a simple and effective "plug-and-play" strategy, which gave the compounds ultra-sensitive fluorescence sensing detection of nitrobenzene, p-nitrotoluene and p-nitrophenol (Fluorescence response time < 1 sec, and the LOD for nitrobenzene, p-nitrophenol and p-nitrotoluene reached an impressive 349 ppb, 22 ppb and 98 ppb, respectively). Combined with theoretical calculations, we elucidated in detail the fluorescence quenching response mechanism of the LYH-HPTS towards nitroaromatic. Additionally, we also constructed fluorescent paper sensor, which effectively transformed the LYH-HPTS from theoretical detection to device application. The LYH-HPTS material is not only simple to synthesize, cost-effective and stable, but also has the features of fast response, excellent sensitivity and selectivity, and good reproducibility, which provides a new approach for the rapid and accurate detection of nitroaromatic.

Inhibition of aquaporin-9 ameliorates severe acute pancreatitis and associated lung injury by NLRP3 and Nrf2/HO-1 pathways.

Inflammation, apoptosis and oxidative stress play crucial roles in the deterioration of severe acute pancreatitis-associated acute respiratory distress syndrome (SAP-ARDS). Unfortunately, despite a high mortality rate of 45 %[1], there are limited treatment options available for ARDS outside of last resort options such as mechanical ventilation and extracorporeal support strategies[2]. This study investigated the potential therapeutic role and mechanisms of AQP9 inhibitor RG100204 in two animal models of severe acute pancreatitis, inducing acute respiratory distress syndrome: 1) a sodium-taurocholate induced rat model, and 2) and Cerulein and lipopolysaccharide induced mouse model. RG100204 treatment led to a profound reduction in inflammatory cytokine expression in pancreatic, and lung tissue, in both models. In addition, infiltration of CD68 + and CD11b + cells into these tissues were reduced in RG100204 treated SAP animals, and edema and SAP associated tissue damage were improved. Moreover, we demonstrate that RG100204 reduced apoptosis in the lungs of rat SAP animals, and reduces NF-κB signaling, NLRP3, expression, while profoundly increasing the Nrf2-dependent anti oxidative stress response. We conclude that AQP9 inhibition is a promising strategy for the treatment of pancreatitis and its systemic complications, such as ARDS.

Sildenafil Enhances the Therapeutic Effect of Islet Transplantation for Diabetic Peripheral Neuropathy via mTOR/S6K1 Pathway.

Purpose: This study aimed to investigate the potential mechanism underlying the therapeutic effect of sildenafil in combination with islet transplantation for diabetic peripheral neuropathy. Methods: A streptozotocin-induced diabetic mouse model was established to evaluate the effects of islet transplantation and sildenafil intervention. The mice were subjected to different interventions for 6 weeks, and histopathological staining and immunohistochemistry techniques were employed to examine the pathological changes and protein expressions of BDNF, MBP, and cleaved caspase-3 in the sciatic nerve tissue. Moreover, RSC96 cells were cocultured with islet cells and sildenafil under high glucose conditions to investigate the potential involvement of the mTOR/S6K1 pathway, BDNF, and MBP proteins. Western blotting was used to detect protein expression in each group. Results: The results showed that islet transplantation can restore sciatic nerve injury in diabetic mice, and sildenafil can enhance the therapeutic effect of islet transplantation. In addition, the combination of sildenafil and islet cells significantly upregulated the expression levels of mTOR/S6K1, BDNF, and MBP in RSC96 cells under high glucose conditions. Conclusions: Islet transplantation can reverse sciatic nerve injury in diabetic mice, and islet cells exhibit a protective effect on RSC96 cells under high glucose conditions via the activation of the mTOR/S6K1 pathway. Sildenafil enhances the therapeutic effect of islet transplantation, which may represent a potential treatment strategy for diabetic peripheral neuropathy.

Ion-Exchange Reaction-Mediated Hierarchical Dual Z-Scheme Heterojunction for Split-Type Photoelectrochemical Immunoassays.

Photoelectrochemical (PEC) immunoassays with ultrasensitive detection abilities are highly desirable for in vitro PEC diagnosis and biological detection. In this paper, dual Z-scheme PEC immunoassays with hierarchical nanostructures (TiO2@NH2-MIL-125@CdS) are synthesized through epitaxial growth of MOF-on-MOF and further in situ derivatization. The dual Z-scheme configuration not only extends the light absorption range but also increases the redox ability due to the interface structure nanoengineering, which synergistically suppresses bulk carrier recombination and promotes the charge transfer efficiency at the electron level. Furthermore, a smart MOF-derived labeling probe (CuO@ZnO nanocube) is designed to develop a split-type PEC biosensor by using prostate-specific antigen (PSA) as a target biomarker. In the presence of PSA, the Ab2-labeled CuO@ZnO would specifically bond to the dual Z-scheme electrode. Then, the MOF-derived CuO@ZnO is dissolved by hydrochloric acid to release Cu2+, which could replace Cd2+ via an ion-exchange reaction, thus leading to the decrease of the photocurrent due to the destruction of the dual Z-scheme configuration. In typical applications, the split-type PEC immunoassay exhibits an excellent detection performance for PSA with a LOD as low as 0.025 pg·mL-1.

Overexpression of Dermokine-α enhances the proliferation and epithelial-mesenchymal transition of pancreatic tumor cells.

Pancreatic cancer is a prevalent malignancy of the digestive system and a major cause of cancer-associated deaths. Previous studies have shown that mutation in the dermokine-ß (DMKN-ß) gene causes pancreatic and colorectal cancer. The role of the carboxy-terminal domain of DMKN-ß and dermokine-α (DMKN-α) genes in cancer tumorigenesis. Herein, the role of DMKN-α in pancreatic cancer (PC) tumorigenesis and the mechanisms underlying this process were investigated. Differentially expressed genes between PC and matched normal cells were identified through RNA-seq analysis, and the corresponding protein expression levels were verified using Western blot analysis. In vivo tumor formation experiment was also performed in nude mice. We found that the DMKN-α gene was overexpressed in cancerous pancreatic cell lines compared to normal pancreatic cell lines. CCK-8, colony formation, RTCA test, wound healing, as well as transwell test showed that the overexpression of DMKN-α enhanced the proliferation, migration, invasion, and EMT of PC cells. In vivo assays confirmed that DMKN-α promotes tumorigenesis. The findings of this study show that DMKN-α is a potential oncogene for pancreatic cancer.

Acadesine alleviates acute pancreatitis-related lung injury by mediating the barrier protective function of pulmonary microvascular endothelial cells.

Severe acute pancreatitis (SAP) is a condition characterized by highly fatal acute inflammation and is usually associated with multiple organ dysfunction syndrome. Acute lung injury (ALI) is the most common complications of SAP, which is the accelerator of other organ dysfunction caused by SAP and the primary cause of early death due to SAP. Acadesine, an adenosine analog and an AMPK activator, has been discovered to modulate glucose and lipid metabolism, and inhibit the production of pro-inflammatory cytokines and iNOS. However, its role in SAP-ALI and its mechanism remains unclear and need to be explored. Herein, we discovered that acadesine mitigated the generation of reactive oxygen species (ROS) in human pulmonary microvascular endothelial cells (HPMECs), alleviated apoptosis and recovered barrier integrity, thereby contributing to anti-inflammatory effects in vitro and in vivo. Moreover, Nrf2 deficiency partially eliminated the effects of acadesine-induced antioxidant effects and thus weakened the protective effects on cells and Nrf2-knockout (Nrf2-/-) mice. This study demonstrates that acadesine attenuated SAP-ALI associated inflammation and tissue damage by modulating the Nrf2-dependent antioxidant pathway by triggering AMPK. These findings are of great significance for the treatment of SAP-related lung injury.

GDF11 ameliorates severe acute pancreatitis through modulating macrophage M1 and M2 polarization by targeting the TGFßR1/SMAD-2 pathway.

Severe acute pancreatitis (SAP), as a typical acute inflammatory injury disease, is one of the acute gastrointestinal diseases with a remarkable mortality rate. Macrophages, typical inflammatory cells involved in SAP, play an important role in the pathogenesis of SAP, which are separated into proinflammation M1 and antiinflammation M2. Growth and differentiation factor 11 (GDF11), as a member of the TGF-ß family also called BMP-11, has been discovered to suppress inflammation. However, the mechanism by which GDF11 inhibits inflammation and whether it can ameliorate SAP are still elusive. The present research aimed to investigate the roles of GDF11 in SAP and the potential immunomodulatory effect of macrophage polarization. The mouse and rat SAP model were constructed by caerulein and retrograde injection of sodium taurocholate respectively. The effects of GDF11 on SAP were observed by serology, histopathology and tissue inflammation, and the effects of GDF11 on the polarization of macrophages in vivo were observed. Raw264.7 and THP1 crells were used to study the effect of GDF11 on macrophage polarization in vitro. To further investigate the causal link underneath, our team first completed RNA and proteome sequencing, and utilized specific suppressor to determine the implicated signal paths. Herein, we discovered that GDF11 alleviated the damage of pancreatic tissues in cerulein induced SAP mice and SAP rats induced by retrograde injection of sodium taurocholate, and further found that GDF11 facilitated M2 macrophage polarization and diminished M1 macrophage polarization in vivo and in vitro. Subsequently, we further found that the regulation of GDF11 on macrophage polarization through TGFßR1/smad2 pathway. Our results revealed that GDF11 ameliorated SAP and diminished M1 macrophage polarization and facilitated M2 macrophage polarization. The Role of GDF11 in modulating macrophage polarization might be one of the mechanisms by which GDF11 played a protective role in pancreatic tissues during SAP.

Recent Progress of Research Regarding the Applications of Stem Cells for Treating Diabetes Mellitus.

At present, the number of diabetes patients has exceeded 537 million worldwide and this number continues to increase. Stem cell therapy represents a new direction for the treatment of diabetes; the use of stem cells overcomes some shortcomings associated with traditional therapies. Functional ß cells play an important role in the pathogenesis of diabetes. As therapeutic targets, functional ß cells are restored by a variety of stem cells, including pluripotent stem cells, mesenchymal cells, and urine-derived stem cells. Although all types of stem cells have their own characteristics, they mainly promote the repair and regeneration of ß cells through directional differentiation, immunomodulation, and paracrine signaling after homing to the injured site. However, stem cell therapy still faces many obstacles, such as low long-term cell survival rate after transplantation, low maintenance time of blood glucose homeostasis, immune rejection, and tumorigenesis. Recently, genetically edited pluripotent stem cells and the cotransplantation of mesenchymal stem cells and islet cells have made significant progress in improving the efficacy of stem cell transplantation processes, also providing powerful tools for the study of the mechanisms underlying diabetes and disease modeling. In this review, we first focused on: (1) stem cells as a pool for the differentiation of insulin-producing cells; (2) stem cells as a source for regenerative repair of damaged islets and as a potential cotransplanted population with islets; (3) the potential of combining gene editing with stem cell therapy; and (4) selection of the stem cell transplantation approach. Based on these topics, we discuss the challenges within the field of adapting stem cell-supported and stem cell-derived transplantations and the promising routes for overcoming these problems.

Agrimoniin sensitizes pancreatic cancer to apoptosis through ROS-mediated energy metabolism dysfunction.

BACKGROUND: Pancreatic cancer is a fatal tumor, which is one of the most common malignant tumors at present. Patients with pancreatic cancer also respond poorly to chemotherapy or radiation therapy and may be accompanied by serious adverse reactions. Therefore, to find an effective way to inhibit the initiation and progression of pancreatic cancer is important to improve the survival and development of patients. Agrimoniin, a polyphenol compounds isolated from Agrimonia pilosa ledeb, has antiviral, antimicrobial, and anticancer activities in vivo and in vitro. However, its molecular mechanism in pancreatic cancer remains to be determined. PURPOSE: We aimed to investigate the effect of agrimoniin in pancreatic cancer and its underlying mechanism in vivo and in vitro. METHODS: The proliferation was detected by colony formation, cell proliferation and toxicity, and real-time cell analysis techniques. The apoptosis was detected by flow cytometry and Western blot. Flow cytometry was used to measure the level of reactive oxygen species (ROS) and apoptosis. The level of intracellular ROS or mitochondrial membrane potential was measured with a DCFH-DA or JC-1 probe. Cell metabolism assays were analyzed and evaluated by using Agilent Seahorse Bioscience XF96 Extracellular Flux Analyzer. The target proteins were analyzed by Western blot. Subcutaneous cancer models in nude mice were established to evaluate the anticancer effects in vivo. RESULTS: Agrimoniin inhibited cell growth and promoted cell apoptosis by regulating cell metabolism in pancreatic cancer cells. Agrimoniin increased the ROS level in pancreatic cancer cells by suppressing Nrf2-dependent ROS scavenging system and disrupting normal mitochondrial membrane potential. We also found that agrimoniin significantly disrupted mitochondrial function and reduced the protein expression of mTOR/HIF-1α pathway and subsequently decreased oxygen consumption rate and extracellular acidification rate. Eventually, agrimoniin affected intracellular energy metabolism and induced apoptosis of pancreatic cancer cells. CONCLUSIONS: These findings reveal the novel function of agrimoniin in promoting apoptosis of pancreatic cancer cells through mediating energy metabolism dysfunction. Altogether, the potential new targets and their synergies discovered in this research are of great significance for cancer treatment and drug development.

Bioinspired Two-Dimensional Structure with Asymmetric Wettability Barriers for Unidirectional and Long-Distance Gas Bubble Delivery Underwater.

Gas bubble manipulations in liquid have long been a concern because of their vital roles in various gas-related fields. To deal with the weakness in long-distance gas transportation of previous works, we took inspiration from the ridgelike structure on Nepenthes pitcher's peristome and successfully prepared a two-dimensional superaerophilic surface decorated with asymmetric aerophobic barriers capable of unidirectional and long-distance gas bubble delivery. For the first time, this process was investigated by in situ bubble-releasing experiments recorded by a high-speed camera and finite element modeling, which demonstrates a kinetic process regulated by the anisotropic motion resistance arising from the patterns. Furthermore, the Nepenthes alata-inspired two-dimensional surface (NATS) was integrated into a water electrolysis system for H2 directional transportation and efficient collection. As a result, the NATS design was proved to be a potential solution for facile manipulation of gas bubbles and provides a simple, adaptive, and reliable strategy for long-range gas transport underwater.

Novel Fe4-based metal-organic cluster-derived iron oxides/S,N dual-doped carbon hybrids for high-performance lithium storage.

Metal-organic frameworks (MOFs) have been extensively used in the fabrication of new advanced electrode materials for lithium ion batteries (LIBs). However, low-productivity and high-cost are some of the main challenges of MOF-derived electrodes. Herein, we report a simple solvothermal procedure to fabricate novel Fe4-based metal-organic clusters (Fe-MOCs) with their subsequent conversion to an S,N dual-doped carbon framework incorporating iron oxides under a N2 atmosphere (namely Fe2O3@Fe3O4-SNC). The as-prepared Fe2O3@Fe3O4-SNC composite, owing to the strong interaction between the dual-doped carbon and iron oxides, shows excellent lithium storage performance as an anode with high pseudocapacitance. Furthermore, DFT computational analyses confirm that the hybrid shows excellent adsorption ability with a low energy barrier due to strong electronic interactions between the iron oxides and S,N-doped carbon matrix. In addition, Fe2O3@Fe3O4-SNC-based LIB shows high energy and power densities at the full-cell level, confirming this synthesis strategy to be a promising approach towards MOC-derived electrode materials for their application in LIBs and beyond-lithium batteries.

Anionic metal-organic framework as a unique turn-on fluorescent chemical sensor for ultra-sensitive detection of antibiotics.

Herein, an anionic metal-organic framework, formulated as {[Zn3(OH)(bmipia)(H2O)3]4·[Zn(H2O)6.5]2}n (FCS-3), was prepared from zinc ions and semi-rigid carboxylate ligands of 5-[N,N-bis(5-methylisophthalic acid)amion] isophthalic acid (H6bmipia) and was employed as a unique fluorescence turn-on chemical sensor for the ultra-sensitive detection of various antibiotics in the aqueous phase.

Characterization and clinical validation of patient-specific three-dimensional printed tissue-equivalent bolus for radiotherapy of head and neck malignancies involving skin.

PURPOSE: Megavoltage radiotherapy to irregular superficial targets is challenging due to the skin sparing effect. We developed a three-dimensional bolus (3DB) program to assess the clinical impact on dosimetric and patient outcomes. MATERIALS AND METHODS: Planar commercial bolus (PCB) and 3DB density, clarity, and net bolus effect were rigorously evaluated prior to clinical implementation. After IRB approval, patients with cutaneous or locally advanced malignancies deemed to require bolus for radiotherapy treatment were treated with custom 3DB. RESULTS: The mean density of 3DB and PCB was of 1.07 g/cm 3 and 1.12 g/cm3, respectively. 3DB optic clarity was superior versus PCB at any material thickness. Phantom measurements of superficial dose with 3DB and PCB showed excellent bolus effect for both materials. 3DB reduced air gaps compared with PCB - particularly in irregular areas such as the ear, nose, and orbit. A dosimetric comparison of 3DB and PCB plans showed equivalent superficial homogeneity for 3DB and PCB (3DB median HI 1.249, range 1.111-1.300 and PCB median HI 1.165, range 1.094-1.279), but better conformity with 3DB (3DB median CI 0.993, range 0.962-0.993) versus PCB (PCB median CI 0.977, range 0.601-0.991). Patient dose measurements using 3DB confirm the delivered superficial dose was within 1% of the intended prescription (95% CI 97-102%; P = 0.11). CONCLUSIONS: 3DB improves radiotherapy plan conformity, reduces air gap volume in irregular superficial areas which could affect superficial dose delivery, and provides excellent dose coverage to irregular superficial targets.

Role of DNA damage in the progress of chronic tubule­interstitial injury.

Tubulointerstitial fibrosis (TIF) is a common final endpoint of chronic allograft nephropathy. Over the years, several hypotheses have been developed to explain the progression of TIF, including mechanisms such as inflammation, epithelial­mesenchymal transition, senescence, chronic hypoxia and reactive oxygen species. Furthermore, TIF is reportedly induced by the 'damage­proliferation­death' cycle. In the present study, an AA renal fibrosis model was established in vitro to investigate whether the vicious proliferation­death cycle is a pathophysiological process of TIF following chronic injury to the kidneys. Results from the present study revealed that cell death was associated with the entrance of cells into the cell cycle. Genetic knockdown of p21 was observed to increase cell cycle progression and the proliferative rate of cells, which overall promoted increased rates of cell death. In addition, the activation of the DNA damage response (DDR) signaling pathway was demonstrated to be crucial to the initiation of the vicious cycle of 'proliferation­death'. Ataxia telangiectasia mutated (ATM) is an important molecule of the DDR and the genetic knockdown of ATM induced apoptosis, increased cell proliferation and promoted cell death. The increase in apoptosis was suggested to be due to the decreased expression levels of p21 observed following the genetic knockdown of ATM. In conclusion, the present study suggested that the crosstalk between the ATM and p21 protein may serve an important role in the regulation of the 'proliferation­death' cycle in the progress of chronic tubulointerstitial injury.

Islet Transplantation Attenuating Testicular Injury in Type 1 Diabetic Rats Is Associated with Suppression of Oxidative Stress and Inflammation via Nrf-2/HO-1 and NF-κB Pathways.

Testicular structural and functional impairment is a serious complication in male diabetes mellitus (DM) patients that leads to impaired fertility in adulthood. In contrast to other endocrine therapies, islet transplantation (IT) can effectively prevent and even reverse diabetic nephropathy and myocardial damage. However, whether IT can alleviate diabetes-induced testicular injury remains unclear. In this study, we sought to investigate the effect of IT on diabetes-induced testicular damage. A diabetic rat model was established by streptozotocin injection. DM, IT, and insulin treatment (INS) groups were compared after 4 weeks of respective treatment. We confirmed that IT could effectively attenuate diabetes-induced testicular damage and recover sperm counts more extensively compared with INS in diabetic rats. In addition, significantly higher levels of superoxide dismutase (SOD) activity and lower contents of malondialdehyde (MDA) were detected in the testes of the IT group versus diabetic rats. Mechanism studies revealed that IT significantly activates the expression of Nrf-2, HO-1, and NQO-1 and inhibits upregulation of the NF-κB expression in response to DM, while INS only exhibit slight impact on the protein expression. Therefore, we speculate that IT may prevent the progression of testicular damage by downregulating oxidative stress and inhibiting inflammation via Nrf-2/HO-1 and NF-κB pathways.

Prognostic significance of mRNA expression of CASPs in gastric cancer.

Current studies suggest that the cysteinyl aspartate specific proteinase (caspase/CASP) family may be closely associated with apoptosis. Scientists have suggested that caspases may be a key to the development of more effective anti-cancer therapies. However, the prognostic value of CASP expression in gastric cancer (GC) remains unclear. Using a Kaplan-Meier plotter online database, the predictive prognostic significance of the expression of 12 CASPs genes (CASP1, CASP2, CASP3, CASP4, CASP5, CASP6, CASP7, CASP8, CASP9, CASP10, CASP12 and CASP14) to overall survival (OS) in different clinicopathological features, including Lauren classification, pathological stages, therapies employed and differentiation in gastric cancer patients was explored. The present study revealed that higher CASP1, 2, 3, 4, 5, 6, 7 and 8 mRNA expression was associated with better OS, whereas higher expression of CASP9, 10, 12 and 14 showed an unfavorable OS in all GC patients. Moreover, CASP1 to 8 were all associated with favorable OS in intestinal type and diffuse type classified by Lauren classification. Therefore, the results of the present study suggested that the CASP family may function as new prognostic indicators in GC and may be helpful in making treatment decisions.

High Glucose-Induced ROS Production Stimulates Proliferation of Pancreatic Cancer via Inactivating the JNK Pathway.

Aberrant glucose metabolism of diabetes mellitus or hyperglycemia stimulates pancreatic tumorigenesis and progression. Hyperglycemic environment can increase the ROS level of tumors, but the role of upregulation of ROS levels in pancreatic cancer (PC) still remains controversial. Here, the same as other reports, we demonstrate that high glucose promoted pancreatic cancer cell growth and resulted in an increase in the level of ROS. However, it is interesting that the phosphorylation of JNK was reduced. When treating PC cells with N-acetyl-L-cysteine (NAC), the intracellular ROS generation is repressed, but the expression of phosphorylation of JNK and c-Jun increased. Moreover, the JNK inhibitor SP600125 significantly promoted cell proliferation and suppressed cell apoptosis of pancreatic cancer cells under high glucose conditions. Collectively, high levels of ROS induced by high glucose conditions stimulated the proliferation of pancreatic cancer cells, and it may be achieved by inactivating the JNK pathway.

Islet transplantation attenuates cardiac fibrosis in diabetic rats through inhibition of TGF-ß1/Smad3 pathway.

Although islet transplantation has been identified as a promising endocrine replacement treatment for patient with diabetes mellitus (DM), it still remains unclear whether islet transplantation can inhibit the diabetic-induced myocardial injury and subsequent adverse ventricular remodeling. Here, we sought to explore the molecular mechanism underlying the cardioprotective effect of islet transplantation. We established the diabetic rat model by intraperitoneal injection of STZ, which was followed by either islet transplantation or conventional insulin treatment. Compared with insulin treatment, islet transplantation further reduced the elevated blood glucose which was nearly restored to normoglycaemia. In addition, islet transplantation attenuated the increased levels of cTn-I and CK-MB, cleaved-caspase-3 in response to DM, and ameliorated diabetic-induced cardiac hypertrophy and interstitial fibrosis, along with improved extracellular matrix (ECM) deposition. Moreover, diabetic rats that underwent islet transplantation had lower expression of TGF-ß1 and lower phosphorylation levels of Smad3. Therefore, islet transplantation exerted protective effect against diabetic-induced myocardial injury and fibrotic remodeling through deactivation of TGF-ß1/Smad3 signaling pathway.

Fluorescent Metal-Organic Framework (MOF) as a Highly Sensitive and Quickly Responsive Chemical Sensor for the Detection of Antibiotics in Simulated Wastewater.

A Zn(II)-based fluorescent metal-organic framework (MOF) was synthesized and applied as a highly sensitive and quickly responsive chemical sensor for antibiotic detection in simulated wastewater. The fluorescent chemical sensor, denoted FCS-1, exhibited enhanced fluorescence derived from its highly ordered, 3D MOF structure as well as excellent water stability in the practical pH range of simulated antibiotic wastewater (pH = 3.0-9.0). Remarkably, FCS-1 was able to effectively detect a series of sulfonamide antibiotics via photoinduced electron transfer that caused detectable fluorescence quenching, with fairly low detection limits. Two influences impacting measurements related to wastewater treatment and water quality monitoring, the presence of heavy-metal ions and the pH of solutions, were studied in terms of fluorescence quenching, which was nearly unaffected in sulfonamide-antibiotic detection. Additionally, the effective detection of sulfonamide antibiotics was rationalized by the theoretical computation of the energy bands of sulfonamide antibiotics, which revealed a good match between the energy bands of FCS-1 and sulfonamide antibiotics, in connection with fluorescence quenching in this system.

catena-Poly[[[tetra-aqua-cobalt(II)]-µ-4,4'-bipyridine-κN:N'] pyridine-3,5-dicarboxyl-ate trihydrate].

The crystal structure of the title compound, {[Co(C(10)H(8)N(2))(H(2)O)(4)](C(7)H(3)NO(4))·3H(2)O}(n), consists of Co(II) polymeric complex cations, uncoordinated pyridine-3,5-dicarboxyl-ate anions and lattice water mol-ecules. The Co(II) cation is coordinated by two N atoms from two 4,4'-bipyridine ligands and four water mol-ecules in a distorted octa-hedral geometry. The 4,4'-bipyridine ligands bridge Co cations, forming a polymeric chain running along the b axis. The two pyridine rings of the 4,4'-biyridine are twisted to each other by a dihedral angle of 8.95 (9)°. Extensive O-H⋯O hydrogen bonding network is present in the crystal structure.