Characterization of ornithine decarboxylase with histidine decarboxylase activity in natural histidine decarboxylase gene deletion Enterobacter hormaechei RH3.

Histamine is predominantly produced in sausages via the decarboxylation of histidine by bacteria. Furthermore, histamine-producing bacteria usually possess the enzyme histidine decarboxylase (hdc). Enterobacter hormaechei RH3 isolated from sausages exhibited significant levels of histamine production despite the absence of hdc. In this study, we elucidated the previously unidentified mechanism underlying histamine production by RH3. We identified an enzyme, NehdX-772, exhibiting the hdc activity from the cell lysate supernatant of RH3, which was annotated as ornithine decarboxylase. The optimal activity of NehdX-772 was recorded at 35 °C and pH 6.0, and it could tolerate a salt concentration of 2.5% (w/v) NaCl. Moreover, artificial inoculation revealed that NehdX-772 was synthesized at significant levels in sausages, leading to an increase in histamine levels. The discovery of NehdX-772 explains the underlying mechanism of histamine production by RH3 and can be applied to decrease histamine production in sausages.

Efficacy and safety of switching to bilastine, an H1-antihistamine, in patients with refractory chronic spontaneous urticaria (H1-SWITCH): a multicenter, open-label, randomized, parallel-group comparative study.

Background: For treating patients with refractory chronic spontaneous urticaria (CSU) resistant to standard doses of 2nd generation H1-antihistamines (H1AH) the International and Japanese guidelines recommend increasing H1AH dose. The latter also recommends switching to a different H1AH. This study explored if the efficacy of the standard dose of bilastine 20 mg is non-inferior to that of double-dose of H1AH in patients with refractory CSU. Methods: This phase IV, multicenter, open-label, randomized, parallel-group trial evaluated the efficacy and safety of switching treatment to bilastine compared to treatment with a 2-fold dose of H1AH in patients with CSU refractory to standard dose H1AH. The primary endpoint was the mean total symptom score (TSS) at Day 5-7 after the start of administration. Results: Treatment efficacy and safety were evaluated in 128 patients (bilastine, n=64; 2-fold dose of H1AH, n=64). The mean TSS at Day 5-7 after the start of administration was smaller than the non-inferiority margin of 0.8, demonstrating non-inferiority of the bilastine switching group to the double-dose H1AH group (0.17 (95% CI -0.32, 0.67)). No difference in Japanese version of Epworth Sleepiness Scale (JESS), DLQI, and urticaria activity score over 7 consecutive days (UAS7) was observed between the two groups. There were no serious adverse events in either group. H1AH-related adverse events occurred in 5 subjects (8 cases) and 2 subjects (3 cases) in the double-dose H1AH and bilastine groups, respectively. Conclusions: Switching treatment to bilastine demonstrated non-inferiority to a double-dose of H1AH in terms of efficacy in patients with CSU refractory to standard dose H1AH with a favorable safety profile. Clinical trial registration: https://jrct.niph.go.jp/latest-detail/jRCTs051180105, identifier jRCTs051180105.

Histamine H1-receptor-mediated modulation of NMDA receptors signaling responses.

This study attempted to clarify the role of histamine H1 receptors in epilepsy by exploring the effects of agonists and inverse agonists on the rundown of the current induced by iterative applications of NMDA or GABA in primary neuronal culture. Mepyramine, a classical H1-receptor antagonist/inverse agonist, increased the NMDA current by about 40% during the first minutes of recording. This effect was concentration-dependent, maximal at 10 nM, and mimicked by triprolidine, another antagonist/inverse agonist. No endogenous histamine was detected in the cultures by a selective immunoassay; both compounds were acting as inverse agonists. Indicating a high constitutive activity of the H1 receptor in this system, histamine did not affect the NMDA rundown, including its settlement, but significantly reversed the effect of mepyramine. A similar pattern was obtained with 2,3 bromophenyl histamine, a selective H1-receptor agonist. The initial increase induced by the two inverse agonists was followed by the same rundown as in controls. H1- and NMDA receptors are colocalized in most cultured neuronal cells. Mepyramine and histamine did not affect the GABA rundown. Our findings suggest an interaction between H1- and NMDA receptors. Inactivation of the H1-receptor by its inverse agonists delays the settlement of the NMDA rundown, which may underlie their proconvulsant effect reported in clinics. Therefore, H1-receptor constitutive activity and the effect of histamine revealed in its absence, tend to facilitate the initiation of the rundown, which is consistent with the anticonvulsant properties of histamine via activation of H1-receptors reported in many studies.

Electrochemical detection of glutamate and histamine using redox-labeled stimuli-responsive polymer as a synthetic target receptor.

Glutamate (Glu) and histamine (His) are two major neurotransmitters that play many critical roles in brain physiological functions and neurological disorders. Therefore, specific and sensitive monitoring of Glu and His is essential in the diagnosis and treatment of various mental health and neurodegenerative disorders. Both being non-electroactive species, direct electrochemical detection of Glu and His has been challenging. Herein, we report a stimuli-responsive polymer-based biosensor for the electrochemical detection of Glu and His. The polymer-based target receptors consist of a linear chain stimuli-responsive templated polymer hybrid that is labeled with an osmium-based redox-active reporter molecules to elicit conformation-dependent electrochemical responses. The polymers are then attached to a gold electrode to implement an electrochemical sensor. The cyclic voltammetry (CV) and square-wave voltammetry (SWV) results confirmed the polymers' conformational changes due to the specific target (i.e., Glu and His) recognition and the corresponding electrochemical detection capabilities. The voltammetry results indicate that this biosensor can be used as a 'signal-on' and 'signal-off' sensors for the detection of Glu and His concentrations, respectively. The developed biosensor also showed excellent regeneration capability by fully recovering the initial current signal after rinsing with deionized water. To further validate the polymer's utility as a target bioreceptor, the surface plasmon resonance (SPR) technique was used to characterize the binding affinity between the designed polymers and the target chemical. The SPR results exhibited the equilibrium dissociation constants (KD) of 2.40 µM and 1.54 µM for the polymer-Glu and polymer-His interactions, respectively. The results obtained this work strongly suggest that the proposed sensing technology could potentially be used as a platform for monitoring non-electroactive neurochemicals from animal models.

Hospitalized patients on proton pump inhibitors for stress ulcer prophylaxis have a higher risk of Clostridioides difficile infection compared with those on histamine-2 receptor antagonists.

BACKGROUND: Previous studies on Clostridioides difficile infection (CDI) in proton pump inhibitor (PPI) users generally enrolled a heterogeneous population and did not include a control group of histamine H2 receptor antagonists (H2RAs) users or adjust for confounding variables, such as previous antibiotics. It is uncertain whether hospitalized patients using PPIs for stress ulcer prophylaxis (SUP) are at a higher risk of CDI compared with those using H2RAs. This study aimed to compare the association between CDI and the usage of antisecretory drugs (ASDs): PPIs and H2RAs, for SUP among hospitalized patients, and the impact of the duration of their use on CDI. METHODS: In this nationwide population-based cohort study using the Taiwan National Health Insurance Database, hospitalized patients using ASDs for SUP were identified between 2017 and 2018. A total of 63,266 and 69,269 individuals were included in the PPI and H2RA groups, respectively. The primary endpoint was a 90-day monitoring of CDI occurrence. FINDINGS: The incidences of CDI were 1.6/10,000 and 0.5/10,000 person-days in the PPIs and H2RAs groups, respectively. After adjusting for confounding factors, the risk of infection in the PPIs group remained significantly higher than in the H2RAs group (hazard ratio (HR), 2.49; 95% confidence interval (CI), 1.63-3.81). In the subgroup analysis, during hospitalization, the risk of CDI for patients using high-risk antibiotics or admitted to the intensive care unit (ICU), as well as patients with immunodeficiency, using PPIs for SUP, was higher than using H2RAs. Furthermore, the risk of CDI was higher in patients using ASDs for durations >14 days than in those using them for <7 days (adjusted HR, 3.66; 95% CI, 2.34-5.75). CONCLUSIONS: The risk of occurrence CDI for hospitalized patients using PPIs for SUP was higher than using H2RAs. It is recommended not to exceed 14 days of any gastric ASDs for SUP during hospitalization, especially for patients who have used high-risk antibiotics, have been admitted to the ICU, or have immunodeficiency.

Rapid, Sensitive, and Specific Microbial Whole-Cell Biosensor for the Detection of Histamine: A Potential Food Toxin.

Histamine is a biogenic amine; its level indicates food quality, as elevated levels cause food poisoning. Therefore, monitoring food at each step during processing until it reaches the consumer is crucial, but current techniques are complicated and time-consuming. Here, we designed a Pseudomonas putida whole-cell biosensor using a histamine-responsive genetic element expressing a fluorescent protein in the presence of the cognate target. We improved the performance of the proposed biosensor by optimizing the chassis, genetic regulatory element, and reporter gene. A sensitive and rapid biosensor variant was obtained with a limit of detection (LOD) of 0.39 ppm, manifesting a linear response (R2 = 0.98) from 0.28 to 18 ppm in 90 min. The biosensor showed minimal cross-reactivity with other biogenic amines and amino acids prevalent in food, making it highly specific. The biosensor effectively quantified histamine in spiked fish, prawn, and wine samples with a satisfactory recovery. Additionally, a colorimetric sensor variant PAlacZ was developed enabling histamine quantification in seafood via a smartphone application, with an LODgray of 0.23 ppm, exhibiting a linear response from 0 to 2.24 ppm. Overall, this study reports an efficient, specific, and highly sensitive biosensor with strong potential for the on-site detection of histamine, ensuring food safety.

Pharmacological inhibition of histamine N-methyltransferase extends wakefulness and suppresses cataplexy in a mouse model of narcolepsy.

Histamine, a neurotransmitter, plays a predominant role in maintaining wakefulness. Further, our previous studies showed that histamine N-methyltransferase (HNMT), a histamine-metabolising enzyme, is important for regulating brain histamine concentration. However, the effects of pharmacological HNMT inhibition on mouse behaviour, including the sleep-wake cycle and cataplexy, in a mouse model of narcolepsy have not yet been investigated. In the present study, we investigated the effects of metoprine, an HNMT inhibitor with high blood-brain barrier permeability, in wild-type (WT) and orexin-deficient (OxKO) narcoleptic mice. Metoprine increased brain histamine concentration in a time- and dose-dependent manner without affecting peripheral histamine concentrations. Behavioural tests showed that metoprine increased locomotor activity in both novel and familiar environments, but did not alter anxiety-like behaviour. Sleep analysis showed that metoprine increased wakefulness and decreased non-rapid eye movement (NREM) sleep through the activation of the histamine H1 receptor (H1R) in WT mice. In contrast, the reduction of rapid eye movement (REM) sleep by metoprine occurred independent of H1R. In OxKO mice, metoprine was found to prolong wakefulness and robustly suppress cataplexy. In addition, metoprine has a greater therapeutic effect on cataplexy than pitolisant, which induces histamine release in the brain, and has been approved for patients with narcolepsy. These data demonstrate that HNMT inhibition has a strong effect on wakefulness, demonstrating therapeutic potential against cataplexy in narcolepsy.

Integrative phosphoproteomic analysis reveal hemostatic-endothelial signaling interplay.

BACKGROUND: The vascular endothelial cell (EC) monolayer plays a crucial part in maintaining hemostasis. An extensive array of G protein-coupled receptors (GPCRs) allows ECs to dynamically act on key hemostatic stimuli such as thrombin and histamine. The impact of these individual stimuli on EC signal transduction has been the subject of various studies, but insight into discordant and concordant EC signaling between different GPCRs remain limited. OBJECTIVES: To elucidate histamine and protease activated receptor (PAR1-4) signaling cascades in endothelial cells, discern overlapping and diverging regulation between these stimuli and their effect on the EC monolayer. METHODS: We employed stable isotope labelling by amino acids in cell culture (SILAC) mass spectrometry-based phosphoproteomics on in vitro cultured BOECs, stimulated with histamine and different protease activated receptor peptides (PAR1-4). We investigated key phosphosites through immuno(fluorescence)- staining and determined effects on barrier function through trans endothelial resistance assays. RESULTS: EC histamine activation initiated an extensive (kinase-) signaling network (among which, MAPK3, STAT3 and CTNND1). PAR1 and PAR2 receptors induced highly similar signaling cascades, wheras PAR3 and PAR4 induced minimal phospho-regulation. Integration of all applied stimuli indicated uniquely activated proteins between both stimuli, as well as a general overlapping activation of cell-junction and actin cytoskeletal proteins. CONCLUSION: We provide an integrative phosphoproteomic analysis of histamine and PAR agonists in the endothelium that highlights the endothelial response programs that are at the bases of regulating hemostasis.

Histamine stimulates human microglia to alter cellular prion protein expression via the HRH2 histamine receptor.

Although the cellular prion protein (PrPC) has been evolutionarily conserved, the role of this protein remains elusive. Recent evidence indicates that PrPC may be involved in neuroinflammation and the immune response in the brain, and its expression may be modified via various mechanisms. Histamine is a proinflammatory mediator and neurotransmitter that stimulates numerous cells via interactions with histamine receptors 1-4 (HRH1-4). Since microglia are the innate immune cells of the central nervous system, we hypothesized that histamine-induced stimulation regulates the expression of PrPC in human-derived microglia. The human microglial clone 3 (HMC3) cell line was treated with histamine, and intracellular calcium levels were measured via a calcium flux assay. Cytokine production was monitored by enzyme-linked immunosorbent assay (ELISA). Western blotting and quantitative reverse transcription-polymerase chain reaction were used to determine protein and gene expression of HRH1-4. Flow cytometry and western blotting were used to measure PrPC expression levels. Fluorescence microscopy was used to examine Iba-1 and PrPC localization. HMC3 cells stimulated by histamine exhibited increased intracellular calcium levels and increased release of IL-6 and IL-8, while also modifying PrPC localization. HMC3 stimulated with histamine for 6 and 24 hours exhibited increased surface PrPC expression. Specifically, we found that stimulation of the HRH2 receptor was responsible for changes in surface PrPC. Histamine-induced increases in surface PrPC were attenuated following inhibition of the HRH2 receptor via the HRH2 antagonist ranitidine. These changes were unique to HRH2 activation, as stimulation of HRH1, HRH3, or HRH4 did not alter surface PrPC. Prolonged stimulation of HMC3 decreased PrPC expression following 48 and 72 hours of histamine stimulation. HMC3 cells can be stimulated by histamine to undergo intracellular calcium influx. Surface expression levels of PrPC on HMC3 cells are altered by histamine exposure, primarily mediated by HRH2. While histamine exposure also increases release of IL-6 and IL-8 in these cells, this cytokine release is not fully dependent on PrPC levels, as IL-6 release is only partially reduced and IL-8 release is unchanged under the conditions of HRH2 blockade that prevent PrPC changes. Overall, this suggests that PrPC may play a role in modulating microglial responses.

Effect of Aerobic Exercise with Blood Flow Restriction on Postexercise Hypotension in Young Adults: The Role of Histamine Receptors.

We tested hypothesis that aerobic exercise with blood flow restriction (BFR) induced postexercise hypotension (PEH), and the reduction in blood pressure (BP) was due to peripheral vasodilation via the histamine receptors. Ten male subjects participated in this study. The subjects were randomly assigned to walk for 10 min at 6.4 km/h, 0% grade with or without BFR after taking histamine receptor blockade. Following exercise, BP was measured at 10 min interval for 60 min. Heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), and total peripheral resistance (TPR) were evaluated. Our results indicated that MAP was significantly lowered immediately after exercise at 20 min, 30 min, and 40 min before the blockade as opposed to after the blockade. A significant reduction in diastolic BP (DBP) occurred. There were no significant differences in HR, SV, CO, and TPR between before the blockade and after the blockade. MAP was substantially decreased at 20 min, 30 min, and 40 min before the blockade compared to resting (-3.2 ± 2.2, -3.3 ± 2.8, and -2.9 ± 2.5, respectively) while increasing MAP after the blockade. The current study demonstrated that low-intensity aerobic exercise with BFR lowered MAP via histamine receptor-induced peripheral vasodilation. In conclusion, BFR exercise training using short periods and low intensity would be greatly beneficial as a potential treatment to lower BP.

Targeting histamine in metabolic syndrome: Insights and therapeutic potential.

Metabolic syndrome is a complex disorder defined by a cluster of interconnected factors including obesity, insulin resistance, hypertension, hyperlipidemia and hyperglycemia which increase the risk of cardiovascular disease, non-alcoholic fatty liver disease, type 2 diabetes mellitus and other related diseases. Histamine, as a biogenic amine, participates in various physiological processes. Increasing evidence suggests histamine plays critical roles in Metabolic syndrome as well as its associated diseases by interacting with four histamine receptors. In this review, we summarize the functions and mechanisms of histamine in Metabolic syndrome, indicating histamine as a possible target in treating Metabolic syndrome and its associated diseases.

Association between gastroprotective agents and acute kidney injury in patients receiving non-steroidal anti-inflammatory drugs: Analysis of a Japanese hospital-based database.

INTRODUCTION: The concomitant use of non-steroidal anti-inflammatory drugs (NSAIDs) and proton pump inhibitors (PPIs) potentially increases the risk of acute kidney injury (AKI). However, the risk of AKI has not been comprehensively assessed for the concomitant use of NSAIDs with gastroprotective agents such as misoprostol and PPIs. The objective of this study was to evaluate whether the use of various gastroprotective agents affects the risk of AKI in patients receiving NSAIDs. METHODS: The data analyzed were obtained from the JMDC hospital-based administrative claims database between April 2014 and August 2022. Histamine-2 receptor antagonists (H2RAs) were compared with PPIs or misoprostol in patients receiving NSAIDs. The primary outcome was the incidence of AKI. The covariates considered were age and sex, admission to intensive care unit, presence of comorbidities based on the modified Charlson Comorbidity Index, and use of renin-angiotensin system inhibitors, loop diuretics, other diuretics, and lithium. AKI was identified by changes in serum creatinine. The distribution of AKI was analyzed using the log-rank test, and estimates of the incidence of AKI were compared among the groups using a Cox proportional hazards model with time-varying variables. Models were adjusted using a doubly robust method that accounts for the inverse probability of treatment weighting at baseline while adjusting for covariates. RESULTS: After screening, 11,688 patients were eligible for inclusion (1729 for H2RAs, 368 for misoprostol, and 9591 for PPIs). AKI occurred in 0.5% of H2RA recipients and 1.1% of PPI recipients; no AKI was observed in the misoprostol group. Compared with H2RAs, the risk of AKI tended to be higher with PPIs (adjusted hazard ratio 1.83, 95% confidence interval 0.92-3.63, p = 0.08). CONCLUSION: Compared with H2RAs, PPIs may increase the risk of AKI in patients receiving NSAIDs, although no statistically significant difference was observed. Further research is required to assess the risk trade-off with consideration of both peptic ulcer prevention and the increased risk of AKI in patients concurrently treated with NSAIDs and H2RAs, misoprostol, or PPIs.

Classics in Chemical Neuroscience: Deliriant Antihistaminic Drugs.

Antihistaminic drugs are widely used clinically and have long been primarily known for their use to treat severe allergic conditions caused by histamine release. Antihistaminic drugs also exert central nervous system (CNS) effects, acting as anxiolytics, hypnotics, and neuroleptics. However, these drugs also have multiple serious neuropharmacological side-effects, inducing delirium, hyperarousal, disorganized behavior, and hallucinations. Due to their robust CNS effects, antihistamines are also increasingly abused, with occasional overdoses and life-threatening toxicity. Here, we discuss chemical and neuropharmacological aspects of antihistaminic drugs in both human and animal (experimental) models and outline their current societal and mental health importance as neuroactive substances.

Black and white truffles as a source of neuroactive biogenic amines.

This study reports the first data about content of serotonin, histamine, and dopamine in black and white truffles fruiting body based on UHPLC-ESI-QqQ-MS/MS. Here we have demonstrated that black (Tuber macrosporum) and white (T. magnatum) truffles are a source of biogenic amines. Also, we demonstrated the absence of correlation between the quality of truffles and the content of biogenic amines.

Seizure and Takotsubo Cardiomyopathy Due to Proton Pump Inhibitor.

Proton Pump Inhibitor (PPI)-induced hypomagnesemia, first described in 2006, has gained increasing recognition in recent years as a potentially life-threatening adverse event. In comparison to histamine-2 receptor antagonists (H2RA), PPIs exhibit a higher frequency of electrolyte abnormalities, including hypomagnesemia, hypocalcemia, hypokalemia, and hyponatremia; hypomagnesemia is the most common. We report a case of an 80-year-old woman who presented with generalized weakness and diarrhea. She was found to have multiple electrolyte abnormalities that failed to resolve even after the resolution of diarrhea and resumption of feeding. However, her condition improved within one week of discontinuing PPI medication. Her hospital course was complicated by a seizure, attributed to alterations in ionic gradients across cellular membranes affecting neuronal discharge and facilitating epileptiform activities. Additionally, she experienced Takotsubo cardiomyopathy due to decreased myocardial contractility, both in the context of electrolyte imbalance induced by prolonged PPI use.

Famotidine increases cellular phospho-tyrosine levels.

While vaccines were being developed, the SARS-CoV-2 pandemic triggered a race to find known drugs that could be quickly repurposed to treat patients. One such candidate was famotidine, which retrospective cohort studies had shown increased survival in hospitalized patients. Computational studies had suggested that famotidine may target early viral proteases; however, ultimately, famotidine was shown not to function as a viral inhibitor. In contrast, we have observed a change in the cellular levels of phospho-tyrosine in A549 lung epithelial cells following treatment with famotidine. This quick change in phosphorylation was due mainly to a dose-dependent increase in cellular production of H2O2. Notably, these changes in phospho-tyrosine levels were able to affect cell signaling; we detected an increased short- and long-term response to IFNα stimulation. Our results suggest that famotidine can increase the anti-viral state of non-infected cells thereby potentially increasing viral resistance.

Simple design of fluorescein-based probe for rapid and in situ visual monitoring of histamine levels in food spoilage.

With the emergence of numerous food safety problems, rapid and accurate detection of histamine in food spoilage remains a challenge. To this end, we developed a simple design and easy synthesis of fluorescein-based probe FCHO to achieve specific and rapid (<1 s) quantitative detection of histamine through "imine formation" reaction. Significant enhanced fluorescence signal in response to histamine enabled our probe with high sensitivity as low as 51 nM. Utilizing the visualized fluorescence color changes of the probe as histamine increasing, we combined it with paper-based test chip to construct a color-resolved and highly selective recognition system. In addition, our proposed probe has been successfully used to visually imaging histamine changes in fish samples. Finally, for the first time, we have proved it possesses reliable ability to directly in situ imaging the distribution of histamine in whole spoiled fish. Thus, our strategy will provide great potential for monitoring food spoilage.

Structural Basis for Histaminergic Regulation of Neural Circuits in the Mouse Olfactory Bulb.

Odor information is modulated by centrifugal inputs from other brain regions to the olfactory bulb (OB). Neurons containing monoamines, such as serotonin, acetylcholine, and noradrenaline, are well known as centrifugal inputs; however, the role of histamine, which is also present in the OB, is not well understood. In this study, we examined the histaminergic neurons projecting from the hypothalamus to the OB. We used an antibody against histidine decarboxylase (HDC), a synthesizing enzyme of histamine, to identify histaminergic neurons and assess their localization within the OB and the ultrastructure of their fibers and synapses using multiple immunostaining laser microscopy, ultra-high voltage electron microscopy (EM), and EM to confirm their relationships with other neurons. To further identify the origin nucleus of the histaminergic neurons projecting to the OB, we injected the retrograde tracer FluoroGold and analyzed the pathway to the OB anterogradely. HDC-immunoreactive (-ir) fibers were abundant in the olfactory nerve (ON) layer compared to other monoamines. HDC-ir neurons received asymmetrical synapses from ONs and formed synapses containing pleomorphic vesicles with variable postsynaptic densities to non-ON elements, thus forming serial synapses. We also confirmed that histaminergic neurons project from the rostral ventral tuberomammillary nucleus to the granule cell layer of the OB and, for the first time, successfully visualized their axons from the hypothalamus to the OB. These findings indicate that histamine may regulate odor discrimination in the OB, suggesting a regulatory relationship between hypothalamic function and olfaction. We thus elucidate morphological mechanisms with tuberomammillary nucleus-derived histaminergic neurons involved in olfactory information.

Ultrasensitive detection of histamine in spoiled meat employing silver nanoparticles decorated Perylene: An experimental-computational conjugation.

Meat spoilage has been acquiring increasing attention recently and is directly associated with food safety and human health. Biogenic amines are the spying organic compounds fostered from the microorganism-mediated decarboxylation of amino acids during meat spoilage. Histamine, a biogenic amine acts as a model analyte and is toxic if consumed substantially. It is crucial to monitor histamine levels in meat due to its adverse effects. In this study, a simple and quick fluorescent sensor was fabricated for sensitive and selective detection of histamine. Citrate-capped silver nanoparticles (AgNP) were loaded onto Perylene (PER) to develop a sensing probe that was characterized using UV-visible, FTIR, XRD, and FESEM, and its optical behavior toward histamine was investigated. Moreover, the binding affinity between histamine and PER@AgNP was assessed using a DFT-based computer simulation. Under optimal conditions, the sensor showed linear relationships for histamine concentrations from 25 µM to 3200 µM with LOD 13.52 µM.

Fexofenadine As Successful Adjunctive Treatment of Rheumatoid Arthritis and Trochanteric Bursitis: A Case Report.

Rheumatoid arthritis (RA) is a chronic inflammatory joint disease that results in cartilage and bone damage, primarily involving synovial joints. The hallmark feature of this condition is inflammatory polyarthritis which can be associated with other joint pathologies, including bursitis. Many treatment options help relieve joint pain and slow down damage to the joints in both RA and bursitis. However, not all treatments are effective or affordable. These treatments include non-steroidal anti-inflammatory drugs (NSAIDs), biologic disease-modifying antirheumatic drugs (bDMARDS), conventional DMARDS (cDMARDS), and corticosteroids. This is a case of trochanteric bursitis in the setting of RA, which was subjectively and objectively treated using the histamine receptor antagonist fexofenadine.