No abstract available.
Pyloric Stenosis*

Nitric oxide (NO) production by endothelial nitric oxide synthase (eNOS) plays a protective role in cerebral ischemia by maintaining vascular permeability, whereas NO derived from neuronal and inducible NOS is neurotoxic and can participate in neuronal damage occurring in ischemia. Matrix metalloproteinases (MMPs) are up-regulated by ischemic injury and degrade the basement membrane if brain vessels to promote cell death and tissue injury. We previously reported that agmatine, synthesized from L-arginine by arginine decarboxylase (ADC) which is expressed in endothelial cells, has shown a direct increased eNOS expression and decreased MMPs expression in bEnd3 cells. But, there are few reports about the regulation of eNOS by agmatine in ischemic animal model. In the present study, we examined the expression of eNOS and MMPs by agmatine treatment after transient global ischemia in vivo. Global ischemia was induced with four vessel occlusion (4-VO) and agmatine (100 mg/kg) was administered intraperitoneally at the onset of reperfusion. The animals were euthanized at 6 and 24 hours after global ischemia and prepared for other analysis. Global ischemia led severe neuronal damage in the rat hippocampus and cerebral cortex, but agmatine treatment protected neurons from ischemic injury. Moreover, the level and expression of eNOS was increased by agmatine treatment, whereas inducible NOS (iNOS) and MMP-9 protein expressions were decreased in the brain. These results suggest that agmatine protects microvessels in the brain by activation eNOS as well as reduces extracellular matrix degradation during the early phase of ischemic insult.
Agmatine ; Animals ; Arginine ; Basement Membrane ; Brain ; Brain Ischemia ; Capillary Permeability ; Carboxy-Lyases ; Cell Death ; Cerebral Cortex ; Endothelial Cells ; Extracellular Matrix ; Glycosaminoglycans ; Hippocampus ; Ischemia ; Matrix Metalloproteinases ; Microvessels ; Models, Animal ; Neurons ; Nitric Oxide ; Nitric Oxide Synthase Type III ; Rats ; Reperfusion

In ischemic strokes, apoptosis is caused by excitotoxicity, ionic imbalance, oxidative/nitrosative stress, and apoptotic-like pathways. Nitric oxide (NO), a free radical, is elevated after ischemic insult. NO, which is generated primarily by neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS), promotes neuronal damage following ischemia. Evidence obtained in recent years has demonstrated that endoplasmic reticulum (ER)-mediated cell death plays an important role in cerebral ischemia. Agmatine is an endogenous substance synthesized from L-arginine by arginine decarboxylase (ADC) and is present in mammalian brain. We had previously reported that agmatine contributes to neuroprotection against ischemic injury. In continuation of our earlier work, we intended to investigate whether agmatine protects brain from transient global ischemia, and also tried to determine the neuroprotective mechanism of agmatine. Twenty minutes of transient global ischemia was induced by 4 vessel occlusion (4-VO). Agmatine (100 mg/kg, IP) was administered simultaneously with reperfusion. Samplings of brain were done at 6, 24, 48, and 72 h after reperfusion to determine the effect of agmatine on ischemic injured hippocampus. ER-damage was also investigated using electron microscope. Results showed that agmatine treatment prevented delayed neuronal cell death in hippocampal CA1 neurons after global cerebral ischemia. It also blocked NOS expression in the rat brain. Agmatine induced the increased expression of glucose-regulated protein 78 (Grp78). These results suggest that agmatine inhibits the production of NO by decreasing the expression of nNOS and iNOS on global forebrain ischemia and the neuroprotective effect of agmatine were concerned with the ER stress-mediated condition.
Agmatine ; Animals ; Apoptosis ; Arginine ; Brain ; Brain Ischemia ; Carboxy-Lyases ; Cell Death ; Electrons ; Endoplasmic Reticulum ; Glycosaminoglycans ; Hippocampus ; Ischemia ; Neurons ; Neuroprotective Agents ; Nitric Oxide ; Nitric Oxide Synthase ; Nitric Oxide Synthase Type I ; Nitric Oxide Synthase Type II ; Prosencephalon ; Rats ; Reperfusion ; Stroke

PURPOSE: To investigate the feasibility and accuracy of Proton Resonance Frequency (PRF) shift based magnetic resonance (MR) temperature mapping utilizing the selfdeveloped center array-sequencing phase unwrapping (PU) method for non-invasive temperature monitoring. MATERIALS AND METHODS: The computer simulation was done on the PU algorithm for performance evaluation before further application to MR thermometry. The MR experiments were conducted in two approaches namely PU experiment, and temperature mapping experiment based on the PU technique with all the image postprocessing implemented in MATLAB. A 1.5T MR scanner employing a knee coil with T2* GRE (Gradient Recalled Echo) pulse sequence were used throughout the experiments. Various subjects such as water phantom, orange, and agarose gel phantom were used for the assessment of the self-developed PU algorithm. The MR temperature mapping experiment was initially attempted on the agarose gel phantom only with the application of a custom-made thermoregulating water pump as the heating source. Heat was generated to the phantom via hot water circulation whilst temperature variation was observed with T-type thermocouple. The PU program was implemented on the reconstructed wrapped phase images prior to map the temperature distribution of subjects. As the temperature change is directly proportional to the phase difference map, the absolute temperature could be estimated from the summation of the computed temperature difference with the measured ambient temperature of subjects. RESULTS: The PU technique successfully recovered and removed the phase wrapping artifacts on MR phase images with various subjects by producing a smooth and continuous phase map thus producing a more reliable temperature map. CONCLUSION: This work presented a rapid, and robust self-developed center arraysequencing PU algorithm feasible for the application of MR temperature mapping according to the PRF phase shift property.
Artifacts ; Citrus sinensis ; Computer Simulation ; Heating ; Hot Temperature ; Knee ; Magnetic Resonance Spectroscopy ; Protons ; Sepharose ; Thermography ; Thermometry ; Water

Agmatine is a decarboxylated arginine by arginine decarboxylase. Agmatine is known to be a neuroprotective agent. It has been reported that agmatine works as a NMDA receptor blocker or a competitive nitric oxide synthase inhibitor in CNS injuries. In spinal cord injury, agmatine showed reduction of neuropathic pain, improvement of locomotor function, and neuroprotection. Macrophage is a key cellular component in neuroinflammation, a major cause of impairment after spinal cord injury. Macrophage has subtypes, M1 and M2 macrophages. M1 macrophage induces a pro-inflammatory response, but M2 inspires an anti-inflammatory response. In this study, it was clarified whether the neuroprotective effect of agmatine is related with the modulation of macrophage subdivision after spinal cord injury. Spinal cord injury was induced in rats with contusion using MASCIS. Animals received agmatine (100 mg/kg, IP) daily for 6 days beginning the day after spinal cord injury. The proportion of M1 and M2 macrophages are confirmed with immunohistochemistry and FACS. CD206+ & ED1+ cells were counted as M2 macrophages. The systemic treatment of agmatine increased M2 macrophages caudal side to epicenter 1 week after spinal cord injury in immunohistochemistry. M2 macrophage related markers, Arginase-1 and CD206 mRNA, were increased in the agmatine treatment group and M2 macrophage expressing and stimulated cytokine, IL-10 mRNA, also was significantly overexpressed by agmatine injection. Among BMPs, BMP2/4/7, agmatine significantly increased only the expression of BMP2 known to reduce M1 macrophage under inflammatory status. These results suggest that agmatine reduces impairment after spinal cord injury through modulating the macrophage phenotype.
Agmatine* ; Animals ; Arginine ; Contusions ; Immunohistochemistry ; Interleukin-10 ; Macrophages* ; N-Methylaspartate ; Neuralgia ; Neuroprotection ; Neuroprotective Agents ; Nitric Oxide Synthase ; Phenotype* ; Rats* ; RNA, Messenger ; Spinal Cord Injuries* ; Spinal Cord*

Objective: Bipolar disorder displays a spectrum of manifestations, including manic, hypomanic, depressive, mixed, psychotic, and atypical episodes, contributing to its chronic nature and association with heightened suicide risk. Creating effective pharmacotherapy guidelines is crucial for managing bipolar disorder and reducing its prevalence. Treatment algorithms grounded in science have improved symptom management, but variations in recommended medications arise from research differences, healthcare policies, and cultural nuances globally. Methods: This study compares Korea’s bipolar disorder treatment algorithm with guidelines from the UK, Australia, and an international association. The aim is to uncover disparities in key recommended medications and their underlying factors. Differences in CYP450 genotypes affecting drug metabolism contribute to distinct recommended medications. Variances also stem from diverse guideline development approaches—expert consensus versus metaanalysis results—forming the primary differences between Korea and other countries. Results: Discrepancies remain in international guidelines relying on meta-analyses due to timing and utilized studies. Drug approval speeds further impact medication selection. However, limited high-quality research results are the main cause of guideline variations, hampering consistent treatment conclusions. Conclusion Korea’s unique Delphi-based treatment algorithm stands out. To improve evidence-based recommendations, large-scale studies assessing bipolar disorder treatments for the Korean population are necessary. This foundation will ensure future recommendations are rooted in scientific evidence.

A beneficial radioprotective agent has been used to treat the radiation-induced lung injury. This study was performed to investigate whether curcumin, which is known to have anti-inflammatory and antioxidant properties, could ameliorate radiation-induced pulmonary inflammation and fibrosis in irradiated lungs. Rats were given daily doses of intragastric curcumin (200 mg/kg) prior to a single irradiation and for 8 weeks after radiation. Histopathologic findings demonstrated that macrophage accumulation, interstitial edema, alveolar septal thickness, perivascular fibrosis, and collapse in radiation-treated lungs were inhibited by curcumin administration. Radiation-induced transforming growth factor-beta1 (TGF-beta1), connective tissue growth factor (CTGF) expression, and collagen accumulation were also inhibited by curcumin. Moreover, western blot analysis revealed that curcumin lowered radiation-induced increases of tumor necrosis factor-alpha (TNF-alpha), TNF receptor 1 (TNFR1), and cyclooxygenase-2 (COX-2). Curcumin also inhibited the nuclear translocation of nuclear factor-kappa B (NF-kappaB) p65 in radiation-treated lungs. These results indicate that long-term curcumin administration may reduce lung inflammation and fibrosis caused by radiation treatment.
Animals ; Blotting, Western ; Collagen ; Connective Tissue Growth Factor ; Curcumin ; Cyclooxygenase 2 ; Edema ; Fibrosis ; Inflammation ; Lung ; Lung Injury ; Macrophages ; Pneumonia ; Rats ; Receptors, Tumor Necrosis Factor ; Tumor Necrosis Factor-alpha