We present a case and literature review regarding posterior ischemic optic neuropathy (PION) in the context of orbital hemorrhage following cosmetic blepharoplasty. A 49-year-old male patient, who underwent resection of residual fat from a previous blepharoplasty, developed acute orbital hemorrhage six hours postoperatively, with sudden visual loss, painful proptosis, and a relative afferent pupillary defect. Urgent decompressive surgery was performed. Ultimately, the patient did not experience visual improvement, and optic atrophy was evident one month later, confirming the diagnosis of PION. Potential pathophysiological mechanisms include direct nerve compression, venous stasis, epinephrine-induced vasoconstriction, vascular steal phenomena, orbital fat traction, and alterations in coagulation and blood pressure. The various hemodynamic, orbital, and systemic mechanisms demonstrate the importance of considering PION as a possible cause of acute visual loss after eyelid procedures.

Mechanisms of neurotransmitter detection using a two-dimensional MoS2 platform are discussed. Machine learning methods are applied to distinguish the spectra of structurally similar analytes. The attachment of catechol-containing neurotransmitter molecules to a defect-engineered MoS2 is demonstrated, leading to activation of SERS through molecular charge transfer. The SERS effect and selective docking of biomolecules are boosted through introducing sulfur vacancies in MoS2 monolayer films via soft plasma etching. The quality of the defect-engineered material was controlled by Raman, photoluminescence, AFM, and XPS characterization, thus allowing for optimization of the process of defect formation and achieving sensing selectivity. Defect-engineered MoS2 has enabled SERS detection of dopamine and epinephrine down to the sub-nanomolar range (5 × 10-10 M), with strong calibration reliability (R2 = 0.95 and 0.99 for pure samples). The sensor material showed no response to serotonin, confirming the specificity of attachment due to S vacancies, which enables catechol-specific molecular adsorption. PCA-LDA achieved 100% accuracy in distinguishing dopamine and epinephrine, establishing defect-engineered MoS2 as a tunable, low-cost SERS platform for future sensing applications.

Food Protein-Induced Enterocolitis Syndrome (FPIES) is a non-IgE-mediated food allergy marked by delayed vomiting and potential hypovolemic shock. This review by the French FPIES working group (SFA, GFRUP, Sp2A, SFP) analyzes recent literature on oral food challenges (OFC) adverse reactions and proposes a standardized protocol for OFC and emergency management. Early consensus OFC protocols from 2017 showed limitations-mainly short intervals between doses during OFC and high hospitalization burdens-leading to inconsistent practices. This narrative review of 2017-2025 studies shows that a single 25% age-appropriate portion generally suffices to trigger symptoms, typically within 1-4 h. This approach balances safety and feasibility while reducing hospital time. As part of the French FPIES monitoring register, and to easily apply this portion, the serving size for each food has been established with specialized dieticians. According to severity, acute reactions require prompt rehydration and ondansetron. Oral or sublingual ondansetron, effective for mild to moderate reactions, can limit dehydration and hospital transfers. In a hospital setting, oral rehydration is indicated in mild reactions, whereas vascular hydration (10 mL/kg over 5-20 min) is required for moderate to severe reactions. Corticosteroids may be added in severe cases. Adrenaline is unnecessary unless associated IgE-mediated symptoms are observed. The working group also proposes including oral rehydration solution and ondansetron in every home emergency kit. These proposals provide a national consensus on the management of FPIES by standardizing French practice from the OFC to the acute management of allergic reaction both in hospitals and at home.

Psychological stress exacerbates lower urinary tract symptoms (LUTS), including urinary frequency and bladder hypersensitivity. This study aimed to determine whether chronic oxytocin (OXT) administration mitigates stress-induced bladder dysfunction and modulates central stress pathways. Female Sprague–Dawley rats were assigned to control, stress, or stress/OXT groups (n = 14 each) and exposed to repeated variable stress (RVS) for one week. Mechanical sensitivity, cystometric parameters, plasma catecholamines and cortisol, bladder histology, paraventricular nucleus (PVN) c-Fos expression, and gene expression in bladder and brain regions were evaluated. RVS induced mechanical hypersensitivity, shortened intercontraction intervals, increased bladder weight, and elevated plasma adrenaline, dopamine, and cortisol levels. Bladder epithelial thickening, submucosal nerve hyperplasia, and upregulation of EP3 and ENaC were also observed. Stress significantly increased PVN activation and upregulated ChAT, CRF, and TH expression in the brainstem. OXT treatment normalized intercontraction intervals, reduced catecholamine and cortisol levels, attenuated PVN c-Fos activation, and increased OXTR and GAD expression in the hypothalamus and thalamus. IL-6 expression was unchanged by stress but decreased by OXT. Chronic OXT administration was associated with improvement of stress-induced urinary frequency and was associated with modulation of central stress pathways, with limited evidence of direct peripheral anti-inflammatory effects.

Zhibai Anshen (ZbAs) oral liquid is employed to alleviate insomnia. However, the neurotransmitters in this treatment are insufficiently investigated. This study aimed to establish a method based on liquid chromatography-tandem mass spectrometry (LC-MS/MS) for determination of 5-hydroxytryptamine (5-HT), dopamine (DA), epinephrine (E), and norepinephrine (NE) in the plasma of patients treated with ZbAs. Plasma samples were processed by protein precipitation with acetonitrile containing internal standard linezolid. Insomnia patients were enrolled and treated with ZbAs, and the plasma samples were collected at baseline and end of treatment. The Pittsburgh Sleep Quality Index (PSQI) was retrieved and the concentrations of neurotransmitters were quantified. The method was successfully developed and validated. It was successfully applied to analyzing plasma samples from 51 patients, revealing a significantly increased level of 5-HT and obviously decreased levels of NE and DA after treatment, while the E kept steady against ZbAs. The PSQI significantly decreased after ZbAs treatment (21.63 ± 6.94 vs. 16.44 ± 7.17, p = 0.0006). A rapid, simple, and sensitive LC-MS/MS method for the determination of four neurotransmitters was established. ZbAs showed satisfying efficacy in treating insomnia, accompanied by obvious alterations of three neurotransmitters, which may be regarded as indicators for efficacy assessment of ZbAs.

Over the last decade, the prevalence of IgE-mediated food allergies has increased, alongside therapeutic innovations such as oral immunotherapy (OIT), omalizumab, combination approaches, intranasal epinephrine, and emerging biomarker-guided strategies. This mini review synthesizes evidence published between 2019 and 2025 and evaluates how these advances intersect with persistent safety and clinical decision-making challenges. Although these therapies demonstrate promising efficacy, validated risk-stratification tools capable of guiding individual treatment selection are lacking. The proposed conceptual framework illustrates how patient characteristics, biomarkers, and treatment-specific risks may ultimately support individualized therapeutic decision-making.

Anaphylaxis is a sudden, life-threatening, and generalized allergic reaction that develops within minutes to hours following exposure to an allergen. Cutaneous, respiratory, and cardiovascular symptoms may occur in various combinations, and the severity of the reaction can vary, potentially leading to anaphylactic reactions, which, if untreated with epinephrine, may be fatal. Although anaphylaxis is most commonly caused by allergic mechanisms, cofactors and comorbidities can contribute to increased severity. We present the case of a 34-year-old man who repeatedly experienced severe anaphylactic reactions after consuming products containing defensins. Comprehensive diagnostic evaluation confirmed an IgE-dependent allergic reaction to inhalant defensins. Additionally, histamine intolerance was suspected, and suspicion of systemic mastocytosis (SM) was raised. This study aims to describe the diagnostic process and highlight the challenges in differentiating clinical symptoms arising from overlapping pathophysiological mechanisms in these conditions.

Anaphylaxis is a rapid-onset, life-threatening systemic hypersensitivity reaction. Insufficient awareness of this condition in China and delayed or inappropriate use of epinephrine-the core treatment-are major causes of severe outcomes. Based on two clinical cases and the latest domestic and international guidelines, this article systematically describes early recognition and diagnosis of anaphylaxis in children, epinephrine-centered emergency management strategies, and the treatment protocol for refractory anaphylaxis. For classic anaphylaxis, early intramuscular injection of epinephrine into the anterolateral thigh is lifesaving. For refractory anaphylaxis, intravenous continuous infusion of epinephrine should be initiated promptly after two ineffective intramuscular injections, combined with aggressive fluid resuscitation and, if necessary, second-line vasoactive drugs. Antihistamines and corticosteroids are only adjunctive therapies and cannot replace epinephrine. Standardized post-discharge long-term management and the promotion of novel noninvasive delivery routes will further improve prognosis of pediatric anaphylaxis.