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Background: As interest in health increases, the number of people engaging in weight training to enhance muscle strength and muscle mass is on the rise. High-intensity weight training has been reported to induce tooth clenching habits, leading to tooth damage and temporomandibular joint (TMJ) abnormalities. Consequently, it is essential to investigate the impact of weight training accompanied by tooth clenching on oral health and to develop guidelines based on these findings. Methods: The study included male participants aged 25 years and older, comprising 15 non-exercisers and 15 professional fitness trainers who have been engaged in weight training for over 5 years. Data were collected using a self-administered questionnaire to gather information on age, exercise experience, total weight lifted in three major weight training exercises (deadlift, bench press, and squat), and teeth clenching habits. Additionally, examinations for tooth cracks and fractures, TMJ noise and pain, maximum mouth opening, occlusal force, and occlusal contact area were conducted. Results: Compared to non-exercisers, professional fitness trainers who have been engaged in weight training for over 5 years exhibited a higher prevalence of teeth clenching habits. While there were no significant differences between the two groups in occlusal contact area and the extent of tooth fractures, there were significant differences in occlusal force and the degree of tooth cracks. Furthermore, unlike joint noise and TMJ pain, the maximum mouth opening was significantly reduced in professional fitness trainers compared to non-exercisers. Conclusion: Our study suggests that the continuation of high-intensity exercise, which induces teeth clenching habits, may cause tooth damage and TMJ disorders.

Glioblastoma (GBM) is the most aggressive and common malignant and CNS tumor, accounting for 47.7% of total cases. Glioblastoma has an incidence rate of 3.21 cases per 100,000 people. The regulation of autophagy, a conserved cellular process involved in the degradation and recycling of cellular components, has been found to play an important role in GBM pathogenesis and response to therapy. Autophagy plays a dual role in promoting tumor survival and apoptosis, and here we discuss the complex interplay between autophagy and GBM. We summarize the mechanisms underlying autophagy dysregulation in GBM, including PI3K/AKT/mTOR signaling, which is most active in brain tumors, and EGFR and mutant EGFRvIII. We also review potential therapeutic strategies that target autophagy for the treatment of GBM, such as autophagy inhibitors used in combination with the standard of care, TMZ. We discuss our current understanding of how autophagy is involved in TMZ resistance and its role in glioblastoma development and survival.

Cerebral small vessel disease (CSVD) is a group of pathologies that affect the cerebral blood vessels. CSVD accounts for 25% of strokes and contributes to 45% of dementia. However, the pathogenesis of CSVD remains unclear, involving a variety of complex mechanisms. CSVD may result from dysfunction in the glymphatic system (GS). The GS contains aquaporin-4 (AQP-4), which is in the perivascular space, at the endfeet of the astrocyte. The GS contributes to the removal of waste products from the central nervous system, occupying perivascular spaces and regulating the exchange and movement of cerebrospinal fluid and interstitial fluid. The GS involves astrocytes and aquaporin channels, which are components of the blood–brain barrier, and problems with them may constitute the pathogenesis of CSVD. Vascular risk factors, including diabetes, dilate the perivascular space, disrupting the glymphatic system and the active regulation of AQP-4. CSVD exacerbation due to disorders of the GS is associated with multiple vasculopathies. Dysfunction of the glymphatic system and AQP-4 interferes with the functioning of the blood–brain barrier, which exacerbates CSVD. In a long-term follow-up of CSVD patients with microbleeds, lacunar infarcts, and white matter hyperintensity, several vascular risk factors, including hypertension, increased the risk of ischemic stroke. Dysfunction of the GS may be the cause of CSVD; however, the underlying treatment needs to be studied further.

Current chemical treatments for cerebrovascular disease and neurological disorders have limited efficacy in tissue repair and functional restoration. Induced pluripotent stem cells (iPSCs) present a promising avenue in regenerative medicine for addressing neurological conditions. iPSCs, which are capable of reprogramming adult cells to regain pluripotency, offer the potential for patient-specific, personalized therapies. The modulation of molecular mechanisms through specific growth factor inhibition and signaling pathways can direct iPSCs’ differentiation into neural stem cells (NSCs). These include employing bone morphogenetic protein-4 (BMP-4), transforming growth factor-beta (TGFβ), and Sma-and Mad-related protein (SMAD) signaling. iPSC-derived NSCs can subsequently differentiate into various neuron types, each performing distinct functions. Cell transplantation underscores the potential of iPSC-derived NSCs to treat neurodegenerative diseases such as Parkinson’s disease and points to future research directions for optimizing differentiation protocols and enhancing clinical applications.

Abstract Background Malignant glioma is among the most lethal and frequently occurring brain tumors, and the average survival period is 15 months. Existing chemotherapy has low tolerance and low blood-brain barrier (BBB) permeability; therefore, the required drug dose cannot be accurately delivered to the tumor site, resulting in an insufficient drug effect. Methods Herein, we demonstrate a precision photodynamic tumor therapy using a photosensitizer (ZnPcS) capable of binding to albumin in situ, which can increase the permeability of the BBB and accurately target glioma. Albumin-binding ZnPcS was designed to pass through the BBB and bind to secreted protein acidic and rich in cysteine (SPARC), which is abundant in the glioma plasma membrane. Results When the upper part of a mouse brain was irradiated using a laser (0.2 W cm− 2) after transplantation of glioma and injection of ZnPcS, tumor growth was inhibited by approximately 83.6%, and the 50% survival rate of the treatment group increased by 14 days compared to the control group. In glioma with knockout SPARC, the amount of ZnPcS entering the glioma was reduced by 63.1%, indicating that it can target glioma through the SPARC pathway. Conclusion This study showed that the use of albumin-binding photosensitizers is promising for the treatment of malignant gliomas. Graphical Abstract

Methotrexate (MTX) is commonly used in intrathecal chemotherapy for patients with acute lymphocytic leukemia (ALL) to prevent central nervous system (CNS) involvement. However, the use of MTX-based chemotherapy can lead to rare yet severe complications, such as MTX-induced myelopathy. Here, we report the case of MTX-induced myelopathy initially misdiagnosed as Guillain–Barre syndrome, leading to a delay in diagnosis and treatment. We present a case of a 39-year-old male with a history of B-cell acute lymphoblastic leukemia (B-ALL) who experienced bilateral foot paresthesia and progressive lower extremity weakness after intrathecal methotrexate (MTX) treatment. Initially, the patient was suspected as having Guillain–Barre syndrome (GBS) due to similar clinical features and nerve conduction studies. The patient received intravenous immunoglobulin (IVIG) treatment, but his condition worsened. T2-weighted images of the thoracic spinal cord revealed high signal intensity in both lateral and posterior columns, typically associated with subacute combined degeneration. However, elevated vitamin B12 levels ruled out SCD in this case. Based on the aforementioned findings, intrathecal methotrexate-induced myelopathy was diagnosed. This case highlights the diagnostic challenge posed by the similarity in clinical presentation between MTX-induced myelopathy and GBS. Differentiating between these conditions is critical for appropriate management. Prompt recognition and treatment with folate metabolism compounds may mitigate neurological sequelae.

IntroductionRecent improvements in treatment for subarachnoid hemorrhage (SAH) have decreased the mortality rates; however, the outcomes of SAH management are dependent on many other factors. In this study, we used nationwide, large-scale, observational data to investigate short- and long-term mortality rates after SAH treatment and the influence of patient severity and hospital volume.Patients and methodsWe selected patients with SAH treated with clipping and coiling from the South Korean Acute Stroke Assessment Registry. High- and low-volume hospitals performed ≥20 clipping and coiling procedures and

IntroductionAdvances in the diagnosis and management of acute ischemic stroke (AIS) and the increased use of mechanical thrombectomy (MT) have improved the quality of care and prognosis of patients with AIS since 2015. We investigated the changing trends in mortality of patients with AIS in Korea before and after 2015.Materials and methodsA retrospective cohort study was conducted using combined anonymized data from the Acute Stroke Assessment Registry of Korea and the Health Insurance Review & Assessment Service database. Patients with ischemic stroke with precise onset time and initial National Institute of Health Stroke Scale records were included.ResultsPatients receiving MT treatment increased from 256 (2.7%) pre-2015 to 1,037 (3.9%) post-2015 (p < 0.001). Overall mortality significantly decreased from pre-2015 to post-2015. In pre-2015, intravenous thrombolysis (IVT) administered within 2 h significantly reduced 3-month mortality when compared with non-IVT. While, in post-2015, IVT administered within 2 h significantly reduced the 3-month, 1-year, 2-year, and 4-year mortality (p < 0.05). MT only reduced 1-year mortality pre-2015; however, MT significantly reduced the 3-month, 1-year, and 2-year mortality post-2015 (p < 0.05). Post-stroke antiplatelet and anticoagulant drugs significantly reduced the 3-month, 1-year, 2-year, and 4-year mortality post-2015.DiscussionSince 2015, faster IVT has significantly reduced the short- and long-term mortality in patients with AIS; MT reduced the 3-month, 1-year, and 2-year mortality. Post-stroke antithrombotic medication has significantly lowered the 2- and 4-year mortality since 2015.ConclusionsChanging trends in AIS management since 2015 have improved the prognosis of patients with AIS.

Stroke is the leading cause of death and neurological disorders worldwide. However, diagnostic techniques and treatments for stroke patients are still limited for certain types of stroke. Intensive research has been conducted so far to find suitable diagnostic techniques and treatments, but so far there has been no success. In recent years, various studies have drawn much attention to the clinical value of utilizing the mechanism of exosomes, low toxicity, biodegradability, and the ability to cross the blood–brain barrier. Recent studies have been reported on the use of biomarkers and protective and recovery effects of exosomes derived from stem cells or various cells in the diagnostic stage after stroke. This review focuses on publications describing changes in diagnostic biomarkers of exosomes following various strokes and processes for various potential applications as therapeutics.

Dementia is a disease in which memory, thought, and behavior-related disorders progress gradually due to brain damage caused by injury or disease. It is mainly caused by Alzheimer’s disease or vascular dementia and several other risk factors, including genetic factors. It is difficult to treat as its incidence continues to increase worldwide. Many studies have been performed concerning the treatment of this condition. Rho-associated kinase (ROCK) and phosphodiesterase-5 (PDE-5) are attracting attention as pharmacological treatments to improve the symptoms. This review discusses how ROCK and PDE-5 affect Alzheimer’s disease, vascular restructuring, and exacerbation of neuroinflammation, and how their inhibition helps improve cognitive function. In addition, the results of the animal behavior analysis experiments utilizing the Morris water maze were compared through meta-analysis to analyze the effects of ROCK inhibitors and PDE-5 inhibitors on cognitive function. According to the selection criteria, 997 publications on ROCK and 1772 publications on PDE-5 were screened, and conclusions were drawn through meta-analysis. Both inhibitors showed good improvement in cognitive function tests, and what is expected of the synergy effect of the two drugs was confirmed in this review.

Patients with vascular dementia, caused by cerebral ischemia, experience long-term cognitive impairment due to the lack of effective treatment. The mechanisms of and treatments for vascular dementia have been investigated in various animal models; however, the insufficient information on gene expression changes that define pathological conditions hampers progress. To investigate the underlying mechanism of and facilitate treatment development for vascular dementia, we established a mouse model of chronic cerebral hypoperfusion, including bilateral carotid artery stenosis, by using microcoils, and elucidated the molecular pathway underlying vascular dementia development. Rho-associated protein kinase (ROCK) 1/2, which regulates cellular structure, and inflammatory cytokines (IL-1 and IL-6) were upregulated in the vascular dementia model. However, expression of claudin-5, which maintains the blood–brain barrier, and MAP2 as a nerve cell-specific factor, was decreased in the hippocampal region of the vascular dementia model. Thus, we revealed that ROCK pathway activation loosens the tight junction of the blood–brain barrier and increases the influx of inflammatory cytokines into the hippocampal region, leading to neuronal death and causing cognitive and emotional dysfunction. Our vascular dementia model allows effective study of the vascular dementia mechanism. Moreover, the ROCK pathway may be a target for vascular dementia treatment development in the future.

Objective This study was conducted to investigate the effects of dietary supplementation with fermented and non-fermented brown algae by-products on the laying performance, egg quality, relative organ weight, and blood profile of laying hens. Methods Hy-Line Brown chickens (n = 180; 70-week-old) were randomly divided into 5 groups with 4 replicates per group (3 hens per cage, 4 cages per replicate), and fed with 5 experimental diets, namely the basal control diet (CON) or the control diet supplemented with 0.5% brown seaweed (BS), 0.5% seaweed fusiforme (SF), 0.5% fermented brown seaweed (FBS), or 0.5% fermented seaweed fusiforme (FSF), for 4 weeks. Results Egg production rate and egg mass were greater in the BS group than in the other groups (p

The effects of the manufacturing process and the regeneration of Shirasu porous glass (SPG) membranes were investigated on the reproducibility of protein precipitants, termed protein microbeads. Intravenous immunoglobulin (IVIG) was selected as a model protein to produce its microbeads in seven different cases. The results showed that the hydrophobically modified SPG membrane produced finer microbeads than the hydrophilic SPG membrane, but this was inconsistent when using the general regeneration method. Its reproducibility was determined to be mostly dependent on rinsing the SPG membrane prior to the modification and on the protein concentration used for emulsification. The higher concentration could foul and plug the membrane during protein release and thus the membrane must be washed thoroughly before hydrophobic modification. Moreover, the membrane regenerated by silicone resin dissolved in ethanol had better reproducibility than silicone resin dissolved in water. On the other hand, rinsing the protein precipitant with cold ethanol after the emulsification was not favorable and induced protein aggregation. With the addition of trehalose, the purity of the IVIG microbeads was almost the same as before microbeadification. Therefore, the regeneration method, protein concentration, and its stabilizer are key to the success of protein emulsification and precipitation using the SPG membrane.

Toxic epidermal necrolysis (TEN) is a drug-related fatal disease. Extensive necrosis of the epidermis can lead to serious complications. This report describes two cases of TEN, associated with deflazacort (DFZ), in two boys, aged 4 years and 14 years, with nephrotic syndrome (NS). The 14-year-old male teenager received DFZ following NS relapse. After 17 days, pruritic papules appeared on the lower extremities. Another case involved a 4-year-old boy receiving DFZ and enalapril. After a 41-day DFZ treatment period, erythematous papules appeared on the palms and soles. Within 3 days, both boys developed widespread skin lesions (>50%) and were admitted to the intensive care unit for resuscitative and supportive treatment. The patients showed improvement after intravenous immunoglobulin-G therapy. Owing to the rapid, fatal course of TEN, clinicians need to be aware of the adverse effects of this drug when treating cases of NS.

Objective: Markers of neuroinflammation during ischemic stroke are well characterized, but additional markers of neural damage are lacking. The study identified associations of behavioral disorders after stroke with histologic neural damage and molecular biological change. Methods: Eight-week-old, 25 g male mice of the C57BL/6J strain were subjected to middle cerebral artery occlusion (MCAO) to induce ischemic stroke. The control group was a healthy wild type (WT), and the experimental group were designed as a low severity MCAO1 and a high severity MCAO2 based on post-stroke neurological scoring. All groups underwent behavioral tests, realtime polymerase chain reaction, triphenyltetrazolium chloride (TTC) staining and Hematoxylin and Eosin staining. One-way analysis of variance was used to analyze statistical significance between groups. Results: In TTC staining, MCAO1 showed 29.02% and MCAO2 showed 38.94% infarct volume (p<0.0001). The pro-inflammatory cytokine interleukin (IL)-1ß was most highly expressed in MCAO2 (WT 0.44 vs. MCAO1 2.69 vs. MCAO2 5.02, p<0.0001). From the distance to target in the Barnes maze test, WT had a distance of 178 cm, MCAO1 had a distance of 276 cm, and MCAO2 had a distance of 1051 (p=0.0015). The latency to target was 13.3 seconds for WT, 27.9 seconds for MCAO1, and 87.9 seconds for MCAO2 (p=0.0007). Prospero homeobox 1 (Prox1) was most highly expressed in MCAO2 (p=0.0004). Doublecortin (Dcx) was most highly expressed in MCAO2 (p<0.0001). Conclusion: The study demonstrated that histological damage to neural cells and changes in brain mRNA expression were associated with behavioral impairment after ischemic stroke. Prox1 and Dcx may be biomarkers of neural damage associated with long-term cognitive decline, and increased expression at the mRNA level was consistent with neural damage and long-term cognitive dysfunction. [ABSTRACT FROM AUTHOR]

Objective: This study was conducted to investigate the effects of dietary supplementation with fermented and non-fermented brown algae by-products on the laying performance, egg quality, relative organ weight, and blood profile of laying hens. Methods: Hy-Line Brown chickens (n = 180; 70-week-old) were randomly divided into 5 groups with 4 replicates per group (3 hens per cage, 4 cages per replicate), and fed with 5 experimental diets, namely the basal control diet (CON) or the control diet supplemented with 0.5% brown seaweed (BS), 0.5% seaweed fusiforme (SF), 0.5% fermented brown seaweed (FBS), or 0.5% fermented seaweed fusiforme (FSF), for 4 weeks. Results: Egg production rate and egg mass were greater in the BS group than in the other groups (p<0.05), and the SF and FSF groups had greater egg production than the control group (p<0.05). Egg weight was higher in the BS group than in the other groups (p<0.05). There were no differences in eggshell color, egg yolk color, eggshell strength, or eggshell thickness among the groups. There was no difference in Haugh units among the treatment groups, except for the FSF group, which had a significantly lower value (p<0.05). The non-fermented groups had greater relative organ weights, particularly the liver and cecum, than the other groups (p<0.05). Regarding blood profile, the supplemented-diet groups had higher albumin levels than the control group (p<0.05). The FBS group had higher total cholesterol and triglyceride levels than the other groups (p<0.05). The BS and FBS groups had higher glutamic pyruvic transaminase levels than the other groups (p<0.05). Conclusion: This study demonstrated that dietary brown algae supplementation can improve egg-laying performance; however, supplementation with fermented seaweeds had no positive effect on the egg-laying performance of hens. [ABSTRACT FROM AUTHOR]

Purpose: Persistent pulmonary hypertension (PPHN) is considered an important prognostic factor in meconium aspiration syndrome (MAS). The aim of this study was to determine the comorbid risk factors for PPHN in infants with MAS. Methods: We retrospectively analyzed 60 infants diagnosed with MAS and admitted to the neonatal intensive care unit of the Sanggye Paik Hospital from January 2007 to April 2013. There were 28 infants (47%) with PPHN and 32 infants (53%) without PPHN. Clinical characteristics, laboratory findings within 24 hours after birth, and initial capillary blood gas analysis results were compared between infants with and without PPHN. Results: Incidence of PPHN was associated with the severity of MAS (P <0.001). The PPHN group had a greater incidence of hypotension and hypoxic-ischemic encephalopathy within 24 hours of birth compared to the non-PPHN group. The PPHN group also had a lower initial pH. However, there was no significant difference for laboratory findings within 24 hours of birth and initial capillary blood gas analysis. In the multivariate analysis, hypotension within 24 hours of birth (P =0.046, odds ratio 11.494, 95% confidence interval 1.048-125.00) was found to be a significant comorbid factor for PPHN in infants with MAS. Conclusion: Infants with MAS who develop hypotension within 24 hours of birth should be closely monitored for development of PPHN. [ABSTRACT FROM AUTHOR]