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Heart failure (HF) is a structural and functional disease that affects millions of people worldwide. The role of inflammation has been demonstrated in many diseases. However, the impact of the Systemic Inflammatory Response Index (SIRI) and the Systemic Immuno-Inflammation Index (SII) on mortality in HF patients has not been adequately investigated. Therefore, in this study, we aimed to demonstrate the effect of SIRI and SII on mortality in patients diagnosed with HF.

Background: Renal colic is a frequently encountered condition in the emergency department (ED), characterized by the sudden and severe onset of flank pain. To assess the risk of cardiac arrhythmia in patients with renal colic, electrocardiography (ECG) was used to investigate several ventricular arrhythmia characteristics, such as the Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio.Objective: This study aimed to investigate the role of the Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio as cardiac arrhythmia stimulators in patients with renal colic. By evaluating these parameters, the risk of developing cardiac arrhythmia in individuals with renal colic could be better understood.Methods: The study included patients who presented to the tertiary emergency department with renal colic over a period of six months, from June 10, 2022, to December 31, 2022. Upon admission, all patients underwent an ECG, and measurements of QT interval and Tp-e interval were conducted in leads D2 and V5. These measurements served as indicators for assessing the potential risk of cardiac arrhythmia in patients with renal colic.Results: The levels of D2 TPE were significantly elevated in patients experiencing renal colic attacks compared to both the pain-free period and the control group (p=0.036). Additionally, the levels of D2 Tpe and QTc were significantly higher during the renal colic attack period as well as the pain-free period when compared to the control group (p=0.041).Conclusions: The Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio may potentially be associated with fatal ventricular arrhythmias in patients who present to emergency departments with renal colic pain.

Introduction: Scombroid poisoning is a condition that occurs after ingestion of seafood and can cause cardiac and respiratory effects, shock, and life-threatening conditions, as well as gastrointestinal findings caused by increased histamine levels. Case Report: The detailed history of the 80-year-old male patient who presented to the emergency department with chest pain, nausea and vomiting revealed that he had consumed an excessive amount of anchovies 10 hours prior to admission. On follow-up, the patient's blood pressure was 142/66 mmHg and heart rate was 48/min. Bradycardia, PR interval prolongation and ST depressions were observed on the initial ECG. No troponin elevation was observed during the patient's follow-up in the emergency department, and the patient was treated with antihistamines, steroids, and fluid resuscitation, and his condition was assessed as scombroid toxicity. The follow-up ECG of the patient whose symptoms resolved after treatment showed that the bradycardia had resolved, the heart rhythm was 65 bpm, the PR interval prolongation had returned to normal, and the signs of first-degree AV block had resolved. Conclusion: While tachycardia and bronchospasm have been observed in scambroid poisoning in the literature, in our case bradycardia was observed to develop as a result of vagal stimulation due to increased histamine. Increased histamine levels can cause life-threatening situations by producing bradycardia, which can develop into asystole with vagal nerve impulses. The use of antihistamines in the treatment of bradycardia, which is one of the effects of histamine, shows a good prognosis, as in our case.

Abstract Norepinephrine (NE) is a well-known appetite regulator, and the nor/adrenergic system is targeted by several anti-obesity drugs. To better understand the circuitry underlying adrenergic appetite control, here we investigated the paraventricular hypothalamic nucleus (PVN), a key brain region that integrates energy signals and receives dense nor/adrenergic input, using a mouse model. We found that PVN NE level increases with signals of energy deficit and decreases with food access. This pattern is recapitulated by the innervating catecholaminergic axon terminals originating from NTSTH-neurons. Optogenetic activation of rostral-NTSTH → PVN projection elicited strong motivation to eat comparable to overnight fasting whereas its inhibition attenuated both fasting-induced & hypoglycemic feeding. We found that NTSTH-axons functionally targeted PVNMC4R-neurons by predominantly inhibiting them, in part, through α1-AR mediated potentiation of GABA release from ARCAgRP presynaptic terminals. Furthermore, glucoprivation suppressed PVNMC4R activity, which was required for hypoglycemic feeding response. These results define an ascending nor/adrenergic circuit, NTSTH → PVNMC4R, that conveys peripheral hunger signals to melanocortin pathway.

Objective: The prevalence of obesity has increased over the past three decades. Proopiomelanocortin (POMC) neurons in the hypothalamic arcuate nucleus (ARC) play a vital role in induction of satiety. Chronic consumption of high-fat diet is known to reduce hypothalamic neuronal sensitivity to hormones like leptin, thus contributing to the development and persistence of obesity. The functional and morphological effects of a high-calorie diet on POMC neurons and how these effects contribute to the development and maintenance of the obese phenotype are not fully understood. For this purpose, POMC-Cre transgenic mice model was exposed to high-fat diet (HFD) and at the end of a 3- and 6-month period, electrophysiological and morphological changes, and the role of POMC neurons in homeostatic nutrition and their response to leptin were thoroughly investigated. Methods: Effects of HFD on POMC-satiety neurons in transgenic mice models exposed to chronic high-fat diet were investigated using electrophysiological (patch-clamp), chemogenetic and Cre recombinase advanced technological methods. Leptin, glucose and lipid profiles were determined and analyzed. Results: In mice exposed to a high-fat diet for 6 months, no significant changes in POMC dendritic spine number or projection density from POMC neurons to the paraventricular hypothalamus (PVN), lateral hypothalamus (LH), and bed nucleus stria terminalis (BNST) were observed. It was revealed that leptin hormone did not change the electrophysiological activities of POMC neurons in mice fed with HFD for 6 months. In addition, chemogenetic stimulation of POMC neurons increased HFD consumption. In the 3-month HFD-fed group, POMC activation induced an orexigenic response in mice, whereas switching to a standard diet was found to abolish orexigenic behavior in POMC mice. Conclusions: Chronic high fat consumption disrupts the regulation of POMC neuron activation by leptin. Altered POMC neuron activation abolished the neuron's characteristic behavioral anorexigenic response. Change in nutritional content contributes to the reorganization of developing maladaptations.

Summary: Opioids are generally known to promote hedonic food consumption. Although much of the existing evidence is primarily based on studies of the mesolimbic pathway, endogenous opioids and their receptors are widely expressed in hypothalamic appetite circuits as well; however, their role in homeostatic feeding remains unclear. Using a fluorescent opioid sensor, deltaLight, here we report that mediobasal hypothalamic opioid levels increase by feeding, which directly and indirectly inhibits agouti-related protein (AgRP)-expressing neurons through the μ-opioid receptor (MOR). AgRP-specific MOR expression increases by energy surfeit and contributes to opioid-induced suppression of appetite. Conversely, its antagonists diminish suppression of AgRP neuron activity by food and satiety hormones. Mice with AgRP neuron-specific ablation of MOR expression have increased fat preference without increased motivation. These results suggest that post-ingestion release of endogenous opioids contributes to AgRP neuron inhibition to shape food choice through MOR signaling.

Summary: Resting metabolic rate (RMR) adaptation occurs during obesity and is hypothesized to contribute to failed weight management. Angiotensin II (Ang-II) type 1 (AT1A) receptors in Agouti-related peptide (AgRP) neurons contribute to the integrative control of RMR, and deletion of AT1A from AgRP neurons causes RMR adaptation. Extracellular patch-clamp recordings identify distinct cellular responses of individual AgRP neurons from lean mice to Ang-II: no response, inhibition via AT1A and Gαi, or stimulation via Ang-II type 2 (AT2) receptors and Gαq. Following diet-induced obesity, a subset of Ang-II/AT1A-inhibited AgRP neurons undergo a spontaneous G-protein “signal switch,” whereby AT1A stop inhibiting the cell via Gαi and instead begin stimulating the cell via Gαq. DREADD-mediated activation of Gαi, but not Gαq, in AT1A-expressing AgRP cells stimulates RMR in lean and obese mice. Thus, loss of AT1A-Gαi coupling within the AT1A-expressing AgRP neuron subtype represents a molecular mechanism contributing to RMR adaptation.

Objective: Serotonin (5HT) is a well-known anorexigenic molecule, and 5HT neurons of dorsal raphe nucleus (DRN) have been implicated in suppression of feeding; however, the downstream circuitry is poorly understood. Here we explored major projections of DRN5HT neurons for their capacity to modulate feeding. Methods: We used optogenetics to selectively activate DRN5HT axonal projections in hypothalamic and extrahypothalamic areas and monitored food intake. We next used fiber photometry to image the activity dynamics of DRN5HT axons and 5HT levels in projection areas in response feeding and metabolic hormones. Finally, we used electrophysiology to determine how DRN5HT axons affect downstream neuron activity. Results: We found that selective activation of DRN5HT axons in (DRN5HT → LH) and (DRN5HT → BNST) suppresses feeding whereas activating medial hypothalamic projections has no effect. Using in vivo imaging, we found that food access and satiety hormones activate DRN5HT projections to LH where they also rapidly increase extracellular 5HT levels. Optogenetic mapping revealed that DRN5HT → LHvGAT and DRN5HT → LHvGlut2 connections are primarily inhibitory and excitatory respectively. Further, in addition to its direct action on LH neurons, we found that 5HT suppresses GABA release from presynaptic terminals arriving from AgRP neurons. Conclusions: These findings define functionally redundant forebrain circuits through which DRN5HT neurons suppress feeding and reveal that these projections can be modulated by metabolic hormones.

Gold nanoparticles (AuNPs) can cross the blood brain barrier, thus can be used as nanocarriers in brain drug delivery. However, the effect of bare and polyethylene glycol-modified (PEGylated) AuNPs on normal neural function has not been extensively investigated. In this study, bioelectrical properties of neuronal functions of male BALB/c mice were explored ex vivo and in vivo by using 5 nm bare AuNPs and PEGylated AuNPs. Electrophysiological properties of neurons from hippocampal CA1 region sections were recorded by patch clamp method. Ex vivo, firing rate of action and membrane potentials in response to negative current stimuli significantly altered only after bare AuNP exposure compared to control (p < 0.05). After in vivo injections, anxiety levels of animals were similar. Amplitude of action potentials reduced only in bare AuNP group (p < 0.05). In conclusion, excitability of hippocampal neurons is increasing with bare AuNP exposure, and PEGylation might be more biocompatible for medical applications.

Prader-Willi and the related Schaaf-Yang Syndromes (PWS/SYS) are rare neurodevelopmental disorders characterized by overlapping phenotypes of high incidence of autism spectrum disorders (ASD) and neonatal feeding difficulties. Based on clinical and basic studies, oxytocin pathway defects are suggested to contribute disease pathogenesis but the mechanism has been poorly understood. Specifically, whether the impairment in oxytocin system is limited to neuropeptide levels and how the functional properties of broader oxytocin neuron circuits affected in PWS/SYS have not been addressed. Using cell type specific electrophysiology, we investigated basic synaptic and cell autonomous properties of oxytocin neurons in the absence of MAGEL2; a hypothalamus enriched ubiquitin ligase regulator that is inactivated in both syndromes. We observed significant suppression of overall ex vivo oxytocin neuron activity, which was largely contributed by altered synaptic input profile; with reduced excitatory and increased inhibitory currents. Our results suggest that dysregulation of oxytocin system goes beyond altered neuropeptide expression and synaptic excitation inhibition imbalance impairs overall oxytocin pathway function.

Opioids are generally known to promote hedonic food consumption. Although much of the existing evidence is primarily based on studies of the mesolimbic pathway, endogenous opioids and their receptors are widely expressed in hypothalamic appetite circuits as well; however, their role in homeostatic feeding remains unclear. Using a fluorescent opioid sensor, deltaLight, here we report that mediobasal hypothalamic opioid levels increase by feeding, which directly and indirectly inhibits agouti-related protein (AgRP)-expressing neurons through the μ-opioid receptor (MOR). AgRP-specific MOR expression increases by energy surfeit and contributes to opioid-induced suppression of appetite. Conversely, its antagonists diminish suppression of AgRP neuron activity by food and satiety hormones. Mice with AgRP neuron-specific ablation of MOR expression have increased fat preference without increased motivation. These results suggest that post-ingestion release of endogenous opioids contributes to AgRP neuron inhibition to shape food choice through MOR signaling.

Introduction: Postweaning social isolation (PWSI) in rodents is an advanced psychosocial stress model in early life. Some psychosocial stress, such as restrain and isolation, disrupts reproductive physiology in young and adult periods. Mechanisms of early-life stress effects on central regulation of reproduction need to be elucidated. We have investigated the effects of PWSI on function of arcuate kisspeptin (ARCKISS1) neurons by using electrophysiological techniques combining with monitoring of puberty onset and estrous cycle in male and female Kiss1-Cre mice. Methods: Female mice were monitored for puberty onset with vaginal opening examination during social isolation. After isolation, the estrous cycle of female mice was monitored with vaginal cytology. Anxiety-like behavior of mice was determined by an elevated plus maze test. Effects of PWSI on electrophysiology of ARCKISS1 neurons were investigated by the patch clamp method after intracranial injection of AAV-GFP virus into arcuate nucleus of Kiss1-Cre mice after the isolation period. Results: We found that both male and female isolated mice showed anxiety-like behavior. PWSI caused delay in vaginal opening and extension in estrous cycle length. Spontaneous-firing rates of ARCKISS1 neurons were significantly lower in the isolated male and female mice. The peak amplitude of inhibitory postsynaptic currents to ARCKISS1 neurons was higher in the isolated mice, while frequency of excitatory postsynaptic currents was higher in group-housed mice. Conclusion: These findings demonstrate that PWSI alters pre- and postpubertal reproductive physiology through metabolic and electrophysiological pathways. [ABSTRACT FROM AUTHOR]

Introduction: Scombroid poisoning is a condition that occurs after ingestion of seafood and can cause cardiac and respiratory effects, shock, and life-threatening conditions, as well as gastrointestinal findings caused by increased histamine levels. Case Report: The detailed history of the 80-year-old male patient who presented to the emergency department with chest pain, nausea and vomiting revealed that he had consumed an excessive amount of anchovies 10 hours prior to admission. On follow-up, the patient's blood pressure was 142/66 mmHg and heart rate was 48/min. Bradycardia, PR interval prolongation and ST depressions were observed on the initial ECG. No troponin elevation was observed during the patient's follow-up in the emergency department, and the patient was treated with antihistamines, steroids, and fluid resuscitation, and his condition was assessed as scombroid toxicity. The follow-up ECG of the patient whose symptoms resolved after treatment showed that the bradycardia had resolved, the heart rhythm was 65 bpm, the PR interval prolongation had returned to normal, and the signs of first-degree AV block had resolved. Conclusion: While tachycardia and bronchospasm have been observed in scambroid poisoning in the literature, in our case bradycardia was observed to develop as a result of vagal stimulation due to increased histamine. Increased histamine levels can cause lifethreatening situations by producing bradycardia, which can develop into asystole with vagal nerve impulses. The use of antihistamines in the treatment of bradycardia, which is one of the effects of histamine, shows a good prognosis, as in our case. [ABSTRACT FROM AUTHOR]

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Gold nanoparticles (GNPs) have been widely used in medicine such as imaging, drug delivery and therapeutics due to their multifunctional properties. Alterations in neuronal function may contribute to various neurological diseases. Transferrin plays a primary role in iron transportation and delivery and has recently been utilized for drug delivery to the brain. We have investigated effects of transferrin-conjugated GNPs (Tf-GNPs) on anxiety and locomotor behavior in vivo and also hippocampal neuronal activity ex vivo. Electrophysiological effects of Tf-GNP on hippocampal neurons were determined by patch clamp method. Fifteen male young adult C57BL/6 mice were randomly divided into three groups as control (200 µL PBS), GNP (bare GNP; 2.2 μg/g in PBS) and Tf-GNPs (2.2 μg/g Tf-GNP). Animals intraperitoneally received the respective treatments for seven consecutive days and were subjected to elevated plus maze (EPM) and open field tests (OFT). Ex vivo, firing frequency of the neurons significantly increased by GNP treatment (p < 0.001). In vivo, animals in Tf-GNP group showed significantly longer distance in open arms but significantly lower number of entries to the open arms in EPM (p < 0.05). Mice received bare GNPs had significantly higher locomotor activity in OFT (p < 0.05), while Tf-GNP did not alter the locomotor activity significantly (p = 0.051). Animals in Tf-GNP group spent significantly longer time in the peripheral zone in OFT (p < 0.05). The present findings have shown that Tf-GNP induces anxiety-like behavior without altering spontaneous firing rate of hippocampal neurons. We suggest that neurobiological effects of Tf-GNP should be pre-determined before using in medical applications. [ABSTRACT FROM AUTHOR]

In the emergency department, there are many symptoms patients present. One of the major symptoms is fever which could be the only symptom, as our patient had. Not only do infections, drugs, trauma, etc., cause fever, but also undetermined cancer types do. In this case, we are presenting a 28-year-old male coming with a 3-week duration of fever and being admitted with the diagnosis of pulmonary artery intimal sarcoma as generally misconceived with pulmonary thromboembolism, to raise awareness of this fatal cancer. [ABSTRACT FROM AUTHOR]

A Motor Vehicle Accident (MVA) can result in death or serious injury to the driver and passengers in case the airbags are not deployed. However, airbags can themselves cause ocular injuries of a varying degree of severity. We report the case of a 41-year-old female patient who reported facial bone fractures and a retinal detachment after her air bag deflated during a car accident. On admission to the Emergency Department (ED) the patient complained of facial pain, swelling and redness in the eye. Orbital CT imaging documented a fragmented fracture line displaced into the maxillary sinus at the floor of right orbit, post-traumatic changes in preorbital skin and in the right globe vitreous, an appearance thought to belong to hyperdense hemorrhage. The patient was taken to emergency operation due to retinal detachment in her right eye. [ABSTRACT FROM AUTHOR]