Abnormal Activity Research Articles

The Pencil Exercise

Background: Voluntary posterior shoulder instability is a rare condition, with a prevalence of 0.5% to 2.6% in young adults, in which the patient is able to provoke a dislocation or subluxation through voluntary activation of the muscles. Studies have shown results that highlight the importance of abnormal cortical activation in this population and suggest physiotherapeutic treatment as first line. Indications: Currently, there are a wide range of options of physiotherapeutic treatment for this condition, such as muscle reinforcement, scapulohumeral coordination, and/or muscle activation with electrodes, all with acceptable results. Simple, low-cost neuromotor rehabilitation is based on the simplicity of a different approach. We believe that with distal-proximal neuromotor rehabilitation we can improve a physiological muscle function. Technique Description: The goal of the pencil exercise is to stimulate the cerebral cortex by making circular movements with a pen between the fingers, bridging abnormal voluntary stimulation and activation of the shoulder muscles, allowing the patient to focus, by the view, only on hand movements. Results: In this case, we have achieved the bypass of the abnormal voluntary stimulation and activation of the shoulder muscles and improve the patient's physiological shoulder function with the implementation of the pencil exercise. Conclusion: This technique may be an effective option for the treatment of voluntary posterior shoulder dislocation because it is based on the stimulation of the cerebral cortex and not on traditional physiotherapeutic or surgical interventions. It is important to note that more research is needed to validate the results of this technique and determine its long-term efficacy. Patient Consent Disclosure Statement: The author(s) attests that consent has been obtained from any patient(s) appearing in this publication. If the individual may be identifiable, the author(s) has included a statement of release or other written form of approval from the patient(s) with this submission for publication.

The use of ibuprofen as an anti-seizure medication: a systematic review

Summary Background Epileptic seizure is a transient period of signs and symptoms resulting from the abnormal excessive and synchronous neuronal activity in the brain, resulting in brain damage. To prevent complications, the antiseizure medication is needed. Several agents have a potency of anti-seizure effect, including ibuprofen. Unfortunately, there are few studies regarding the anti-seizure effect of ibuprofen. Aim To determine the anti-seizure effect of ibuprofen to reduce the symptoms of epileptic seizures. Materials and Methods A systematic review using the databases ScienceDirect, SpringerLink, Nature, and Pubmed. The article was obtained using the keywords “ibuprofen” and (“epilepsy” or “anticonvulsant” or “antiseizure” or “epileptic” or “neuroinflammation”) in the period 2012 to 2022 and screened with inclusion and exclusion criteria. Out of the 1376 articles screened, there are three studies included in this review. The SYRCLE Risk of Bias Tool was used to assess the risk of bias, and the data was synthesised using SWiM guidelines. Results Ibuprofen affects seizures by reducing the number, grade, and duration of seizure intensity in the PTZ-induced rats. Despite the risk of bias assessment revealing some potential bias in the studies, our study shows that ibuprofen has potency as an additional agent for epileptic seizures among febrile convulsive patients. Conclusion In animal models of seizures, ibuprofen has an antiseizure effect by reducing the number, grade, and duration of seizures.

Fungal-bacteria interactions provide shelter for bacteria in Caesarean section scar diverticulum.

Caesarean section scar diverticulum (CSD) is a significant cause of infertility among women who have previously had a Caesarean section, primarily due to persistent inflammatory exudation associated with this condition. Even though abnormal bacterial composition is identified as a critical factor leading to this chronic inflammation, clinical data suggest that a long-term cure is often unattainable with antibiotic treatment alone. In our study, we employed metagenomic analysis and mass spectrometry techniques to investigate the fungal composition in CSD and its interaction with bacteria. We discovered that local fungal abnormalities in CSD can disrupt the stability of the bacterial population and the entire microbial community by altering bacterial abundance via specific metabolites. For instance, Lachnellula suecica reduces the abundance of several Lactobacillus spp., such as Lactobacillus jensenii, by diminishing the production of metabolites like Goyaglycoside A and Janthitrem E. Concurrently, Clavispora lusitaniae and Ophiocordyceps australis can synergistically impact the abundance of Lactobacillus spp. by modulating metabolite abundance. Our findings underscore that abnormal fungal composition and activity are key drivers of local bacterial dysbiosis in CSD.

Structural and functional brain alterations in subthreshold depression: A multimodal coordinate-based meta-analysis.

Imaging studies of subthreshold depression (StD) have reported structural and functional abnormalities in a variety of spatially diverse brain regions. However, there is no consensus among different studies. In the present study, we applied a multimodal meta-analytic approach, the Activation Likelihood Estimation (ALE), to test the hypothesis that StD exhibits spatially convergent structural and functional brain abnormalities compared to healthy controls. A total of 31 articles with 25 experiments were included, collectively representing 1001 subjects with StD. We found consistent differences between StD and healthy controls mainly in the left insula across studies with various neuroimaging methods. Further exploratory analyses found structural atrophy and decreased functional activities in the right pallidum and thalamus in StD, and abnormal spontaneous activity converged to the middle frontal gyrus. Coordinate-based meta-analysis found spatially convergent structural and functional impairments in StD. These findings provide novel insights for understanding the neural underpinnings of subthreshold depression and enlighten the potential targets for its early screening and therapeutic interventions in the future.

LncRNAs in Immune and Stromal Cells Remodel Phenotype of Cancer Cell and Tumor Microenvironment.

Emerging studies suggest that long non-coding RNAs (lncRNAs) participate in the mutual regulation of cells in tumor microenvironment, thereby affecting the anti-tumor immune activity of immune cells. Additionally, the intracellular pathways mediated by lncRNAs can affect the expression of immune checkpoints or change the cell functions, including cytokines secretion, of immune and stromal cells in tumor microenvironment, which further influences cancer patients' prognosis and treatment response. With the in-depth research, lncRNAs have shown great potency as a new immunotherapy target and predict immunotherapy response. The research on lncRNAs provides us with a new insight into developing new immunotherapy drugs and predicting the outcome of immunotherapy. With development of RNA sequencing technology, amounts of lncRNAs were found to be dysregulated in immune and stromal cells rather than tumor cells. These lncRNAs function through ceRNA network or regulating transcript factor activity, thus leading abnormal differentiation and activation of immune and stromal cells. Here, we review the function of lncRNAs in the immune microenvironment and focus on the alteration of lncRNAs in immune and stromal cells, and discuss how these alterations affect tumor growth, metastasis and treatment response.

Fungal–bacteria interactions provide shelter for bacteria in Caesarean section scar diverticulum

Caesarean section scar diverticulum (CSD) is a significant cause of infertility among women who have previously had a Caesarean section, primarily due to persistent inflammatory exudation associated with this condition. Even though abnormal bacterial composition is identified as a critical factor leading to this chronic inflammation, clinical data suggest that a long-term cure is often unattainable with antibiotic treatment alone. In our study, we employed metagenomic analysis and mass spectrometry techniques to investigate the fungal composition in CSD and its interaction with bacteria. We discovered that local fungal abnormalities in CSD can disrupt the stability of the bacterial population and the entire microbial community by altering bacterial abundance via specific metabolites. For instance, Lachnellula suecica reduces the abundance of several Lactobacillus spp., such as Lactobacillus jensenii, by diminishing the production of metabolites like Goyaglycoside A and Janthitrem E. Concurrently, Clavispora lusitaniae and Ophiocordyceps australis can synergistically impact the abundance of Lactobacillus spp. by modulating metabolite abundance. Our findings underscore that abnormal fungal composition and activity are key drivers of local bacterial dysbiosis in CSD.

Assessment of Oculomotor Functions as a Biomarker in Mild Traumatic Brain Injury.

Mild traumatic brain injury (mTBI), or concussion, is a major public health problem, and ambiguity still exists regarding its diagnosis. While functional magnetic resonance imaging (fMRI) has been identified as a helpful screening tool for concussion, its limited accessibility in clinical or field settings necessitates a more efficient alternative. Oculomotor function deficit is an often-reported pathology in mTBI. Due to the neuroanatomical overlap between eye-movement circuitry and mTBI pathophysiology, visual deficits are expected. In this study, we investigate the possibility of using an oculomotor assessment tool for finding biomarkers in concussion. We used fMRI with tasks evaluating oculomotor functions: smooth pursuit (SP), saccades, anti-saccades, and optokinetic nystagmus (OKN). Before the scanning, the testing with a system of virtual reality goggles with integrated eye- and head-tracking was used where subjects performed the same tasks as those used in fMRI. Twenty-nine concussed symptomatic adults (CSA) within 1-month postconcussion and 29 age- and sex-matched healthy controls (HCS) were tested to examine blood oxygen level-dependent (BOLD) fMRI alterations associated with performances in oculomotor function after mTBI and evaluate the efficacy of the oculomotor assessment in detecting oculomotor and gaze deficits following mTBI. Comparing CSA with HCS, significant differences were observed in anti-saccades and OKN performance. CSA group exhibited elevated %BOLD signal change on each task compared with HCS: in the superior frontal gyrus during the smooth pursuit, inferior frontal gyrus during the saccades, putamen and dorsolateral prefrontal cortex (DLPFC) during the anti-saccades, and lingual gyrus and IFG during the OKN. Key findings include the following: (1) oculomotor deficits in concussed subjects compared with controls, (2) abnormal activation patterns in areas related to the regulation and control of oculomotor movements, suggesting concussion-induced disruptions, and (3) the potential of oculomotor assessment as a promising approach for mTBI biomarkers, with anti-saccades and OKN identified as the most sensitive tasks.

Cinnamaldehyde, A Bioactive Compound from the Leaves of Cinnamomum osmophloeum Kaneh, Ameliorates Dextran Sulfate Sodium-Induced Colitis in Mice by Inhibiting the NLRP3 Inflammasome.

Inflammatory bowel disease (IBD) comprises a group of idiopathic intestinal disorders, including ulcerative colitis and Crohn's disease, significantly impacting the quality of life for affected individuals. The effective management of these conditions remains a persistent challenge. The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, a complex molecular structure, regulates the production of pro-inflammatory cytokines such as interleukin-1β. Abnormal activation of the NLRP3 inflammasome plays a pivotal role in the development of IBD, making it a compelling target for therapeutic intervention. Our research revealed that cinnamaldehyde (CA), a major bioactive compound found in the leaves of Cinnamomum osmophloeum kaneh, demonstrated a remarkable ability to alleviate colitis induced by dextran sulfate sodium (DSS) in a mouse model. This effect was attributed to CA's ability to downregulate the activation of the NLRP3 inflammasome and reduce the expression of pro-inflammatory mediators in the colon. In the mechanism study, we observed that CA inhibited the NLRP3 inflammasome in macrophages, at least partially, by enhancing the autophagic response, without reducing mitochondrial damage. These findings collectively suggest that CA holds significant potential as a therapeutic agent for enhancing the management of IBD, offering a promising avenue for further research and development.

Mechanism of Chaijin Jieyu Anshen Tablets in regulating abnormal ACC-vHPC glutaminergic neural circuit to alleviate synaptic remodeling of ventral hippocampal neurons in depressed rats

This study aims to reveal the molecular mechanism of Chaijin Jieyu Anshen Tablets(CJJYAS) in regulating the abnormal anterior cingulate cortex(ACC)-ventral hippocampus(vHPC) glutaminergic neural circuit to alleviate synaptic remodeling of ventral hippocampal neurons in depressed rats. Firstly, the study used chemogenetics to localize glutaminergic adeno-associated virus(AAV) into the ACC brain region of rats. The model of depressed rats was established by chronic unpredictable mild stress(CUMS) combined with independent feeding. The rats were randomly divided into control group, model group, AAV empty group, AAV group, AAV+ glucocorticoid receptors(GR) blocker group, AAV+chemokine receptor 1(CX3CR1) blocker group, and AAV+CJJYAS group. Depressive-like behaviors of rats were evaluated by open-field, forced-swimming, and Morris water maze tests, combined with an animal behavior analysis system. The morphological and structural changes of ACC and vHPC neurons in rats were observed by hematoxylin-eosin(HE) staining. Immunofluorescence and nuclear phosphoprotein(c-Fos) were used to detect glutaminergic neural circuit activation of ACC-vHPC in rats. The changes in dendrites, synaptic spines, and synaptic submicrostructure of vHPC neurons were observed by Golgi staining and transmission electron microscopy, respectively. The expressions of synaptic remodeling-related proteins N-methyl-D-asprtate receptor 2A(GRIN2A), N-methyl-D-asprtate receptor 2B(GRIN2B), Ca~(2+)/calmodulin-dependent protein kinase Ⅱ(CaMKⅡ), mitogen-activated protein kinase-activated protein kinase 2(MK2), and a ubiquitous actin-binding protein(cofilin) in vHPC glutaminergic neurons of rats were detected by immunofluorescence and Western blot, respectively. The results indicated that the activated glutaminergic AAV aggravated the depressive-like behaviors phenotype of rats in the model group and deteriorated the damage of morphology and structure of ACC and vHPC neurons and synaptic ultrastructure. However, both GR and CX3CR1 bloc-kers could reverse the abnormal changes to varying degrees, suggesting that the abnormal activation of ACC-vHPC glutaminergic neural circuit mediated by GR/CX3CR1 signals in gliocytes in the ACC brain region may be closely related to the occurrence and development of depression. Interestingly, CJJYAS significantly inhibited the activation of the ACC-vHPC glutaminergic neural circuit induced by AAV and the elevated Glu level. Furthermore, CJJYAS could also effectively reverse the aggravation of depressive-like behaviors and synaptic remodeling of vHPC neurons of rats in the model group induced by the activated AAV. Additionally, the findings suggested that the molecular mechanism of CJJYAS in improving synaptic damage of vHPC neurons might be related to the regulation of synaptic remodeling-related signals such as NR/CaMKⅡ and MK2/cofilin. In conclusion, this research confirms that CJJYAS effectively regulates the abnormal ACC-vHPC glutaminergic neural circuit and alleviates the synaptic remodeling of vHPC glutaminergic neurons in depressed rats, and the molecular mechanism might be associated with the regulation of synapse-related NR/CaMKⅡ and MK2/cofilin signaling pathways, which may be the crucial mechanism of its antidepressant effect.

Short report: Twins with 20p13 duplication. Case report and comprehensive literature review.

Trisomy 20p is a rare genetic condition caused by a duplication of the short arm of chromosome 20. We employed clinical observation and molecular genetic testing (SNP microarray), to study identical twin males with an unknown dysmorphic syndrome. We conducted a literature review of trisomy 20p and collated the clinical and molecular genetic findings on 20 affected subjects reported since 2000. Identical twin males, whose prenatal course was complicated by a twin-to-twin transfusion, manifested profound language and neurocognitive delays as well as distinctive facial dysmorphisms when evaluated at 2 years of age. SNP microarray identified identical duplications of 20p13 with no other chromosomal aberrations. A literature survey of 20p trisomy syndrome identified 20 other examples of this condition reported since 2000, which we collated with 33 summarized by Sidwell etal. (2000). Within the combined total of 55 affected individuals, we found a distinctive clinical phenotype that provides insight on the effects of abnormal dosage of genes in 20p13. These loci include FAM110A (OMIM 611393), ANGPT4 (OMIM 603705), RSPO4 (OMIM 610573), PSMF1 (OMIM 617858), SNPH (OMIM 604942), SDCBP2 (OMIM 617358), FKBP1A (OMIM 186945), TMEM74B, C20orf202, and RAD21L1 (OMIM 619533). Gene profiling highlighted that syntaphilin (SNPH) is highly expressed in mammalian brain, where it is considered critical for mitochondrial transport in neuronal axons, and to directly influence axonal morphogenesis and function. We propose that abnormal activity of syntaphilin engendered by the trisomy is primarily responsible for the language, neurocognitive, and gross motor delays reported in individuals with 20p trisomy. Additional studies, for example, characterization of cerebral organoids generated from affected patients may help to better understand this condition, and potentially suggest rational remedies to improve the lives of affected individuals and their families.

RASopathies for Radiologists.

RASopathies are a heterogeneous group of genetic syndromes caused by germline mutations in a group of genes that encode components or regulators of the Ras/mitogen-activated protein kinase (MAPK) signaling pathway. RASopathies include neurofibromatosis type 1, Legius syndrome, Noonan syndrome, Costello syndrome, cardiofaciocutaneous syndrome, central conducting lymphatic anomaly, and capillary malformation-arteriovenous malformation syndrome. These disorders are grouped together as RASopathies based on our current understanding of the Ras/MAPK pathway. Abnormal activation of the Ras/MAPK pathway plays a major role in development of RASopathies. The individual disorders of RASopathies are rare, but collectively they are the most common genetic condition (one in 1000 newborns). Activation or dysregulation of the common Ras/MAPK pathway gives rise to overlapping clinical features of RASopathies, involving the cardiovascular, lymphatic, musculoskeletal, cutaneous, and central nervous systems. At the same time, there is much phenotypic variability in this group of disorders. Benign and malignant tumors are associated with certain disorders. Recently, many institutions have established multidisciplinary RASopathy clinics to address unique therapeutic challenges for patients with RASopathies. Medications developed for Ras/MAPK pathway-related cancer treatment may also control the clinical symptoms due to an abnormal Ras/MAPK pathway in RASopathies. Therefore, radiologists need to be aware of the concept of RASopathies to participate in multidisciplinary care. As with the clinical manifestations, imaging features of RASopathies are overlapping and at the same time diverse. As an introduction to the concept of RASopathies, the authors present major representative RASopathies, with emphasis on their imaging similarities and differences. ©RSNA, 2024 Test Your Knowledge questions for this article are available in the supplemental material.

THERAPEUTIC OPTIONS IN CALCIFIC ROTATOR CUFF TENDINOPATHY OF THE SHOULDER

Calcific tendinopathy in the tendons of the rotator cuff muscles of the shoulder is an increasingly common and disabling pathology. Calcific tendinopathy is a common disease that mainly affects people aged between 40 and 60. Women seem to be more affected than men. It has been suggested that various factors play a role in the condition, such as abnormal thyroid gland activity, metabolic diseases (e.g. gout, diabetes) and genetic predisposition. Various aetiological hypotheses have been put forward: the degenerative and multiphasic theories are the two most widely accepted. Clinically, calcific tendonitis is characterised by severe, disabling pain, often occurring spontaneously, usually in the morning or following exertion disproportionate to subsequent symptoms. There may be concomitant stiffness, giving rise to a clinical picture resembling frozen shoulder or hyperalgesic painful shoulder. Conventional radiography of the shoulder is the most appropriate imaging approach, but perfectly complemented by soft tissue ultrasound. Most acute painful episodes resolve spontaneously symptomatically. Numerous conservative treatments have been reported in the literature with varying levels of evidence of efficacy. In the present study we tried to evaluate which therapeutic option could give superior results both from a functional, lesional architectural and causal point of view in terms of reduction of callus size, but also from an imaging point of view. The use of various therapeutic protocols have shown a significant benefit of the association of ESWT with conventional FKT, and intra-articular infiltration, with a plus for the association of Corticosteroids and Sodium Hyaluronate regarding the speed of achieving the desired results. Similar results were obtained with the intra-articular shoulder PRP technique, but with slower achievement of the desired results. Arthroscopic surgery is the orthopaedic specialist's last option. Keywords: Calcific tendinopathy, rotator cuff muscles, shoulder, intra-articular infiltration.

Diagnostic and therapeutic approach to patients with first seizure episode

Seizures are transient episodes of signs and/or symptoms resulting from abnormal, excessive or synchronous neuronal activity in the brain. About 8% to 10% of people will experience a seizure at some point in their lives, and of that group, about 2% to 3% will develop epilepsy. Given the impact that epilepsy can have on a person's quality of life and related medical, cognitive, or psychiatric conditions, it is crucial to perform a detailed evaluation when a patient presents an unprovoked first seizure episode. A seizure crisis must be distinguished from other events with a similar presentation, as the possible causes must be determined, to establish the need for adequate treatment, and establish a long-term prognosis.

Executive function deficits in patients with the first episode of late-life depression before and after SSRI treatment: A pilot fMRI study.

Executive function deficits (EFD) in late-life depression (LLD) has been reported to be associated with antidepressant treatment resistance, increased disability, and poor quality of life. However, the underlying neutral mechanisms of EFD in patients with the first episode of LLD remains unclear. A total of 27 patients with first-episode, drug-naive LLD and 27 non-depressed controls (NC) were recruited for the present research. Participants underwent the Trail Making Test, the 17-item Hamilton depression rating scale (HAMD-17) test, and task-state functional magnetic resonance imaging scans under the neutral Stroop task. LLD patients' executive functions, depressive symptoms, and brain activity were examined again after 6months of antidepressant treatment. Of the 27 LLD patients, 16 cases completed 6-month follow-ups. Patients in the LLD baseline group spent more time on the Trail Making Test A test than those in the NC group (p<0.05). In the presence of an incongruency between the word color and meaning, the accuracy rate of the neutral Stroop task in the LLD baseline group was lower, and the reaction time was greater than that in the NC group, with statistically significant difference (p<0.05). The HAMD-17 score in the LLD follow-up group was significantly lower than that in the LLD baseline group (p<0.05). More activated brain regions were present in the LLD baseline group than in the NC group when performing the neutral Stroop task. Compared with the LLD baseline group, abnormal activation of relevant brains in the cingulate-prefrontal-parietal network of LLD patients still existed in the LLD follow-up group. LLD patients engaged more brain areas than the NC group while performing the neutral Stroop task. Abnormal activation of the cingulate-prefrontal-parietal network could be a contributing factor to EFD in LLD. ChiCTR, ChiCTR2100042370 (Date of registration: 21/01/2021). We didn't enroll enough first-episode, LLD patients, the robustness of the findings need to be confirmed by large sample clinical trials.

Identification of Novel STAT3 Dimerization Inhibitor Through Structure-Based Virtual Screening for Cancer Management

Background: Signal transducer and activator of transcription 3 (STAT3) is a transcription factor that controls cell proliferation, differentiation, angiogenesis, and immunological responses. In many human malignancies, abnormal STAT3 activation promotes tumor growth via oncogenic gene expression, resulting in tumor malignancy. Many drugs with clinically authorized analogues that are used as STAT3 inhibitors for cancer therapy have several drawbacks in terms of stability and toxicity.Methods: This study used PyRx 0.8 tool to screen the Traditional Chinese Medicine (TCM) database of about 32,364 commercially available natural compounds in order to identify new STAT3 inhibitors. Physicochemical and ADME properties of selected compounds were estimated using Datawarrior and SwissADME.Result: The top 20 compounds were initially chosen based on their strong binding affinities with STAT3. Lipinski and Vaber tools were used to filter the top 20 compounds, yielding the top 6 compounds. The compounds ZINC85542844, ZINC4098720, ZINC85543599, ZINC85593523, ZINC85593528, and ZINC85593537 were passed through these filters. These compounds were found to interact with active site STAT3 residues and have several amino acid interactions in common with the control compound (STX0119).Conclusion: This study suggests that the compounds ZINC85542844, ZINC4098720, ZINC85543599, ZINC85593523, ZINC85593528, and ZINC85593537 could be used as a lead for the development of novel STAT3 inhibitors. However, further experimental validation is required to optimized them as STAT3 inhibitors.Keywords: STAT3; Transcription factor; Natural compounds; Cancer; Virtual screening

Insights into metastatic roadmap of head and neck cancer squamous cell carcinoma based on clinical, histopathological and molecular profiles.

The incidence of head and neck cancer (HNC), constituting approximately one in ten cancer cases worldwide, affects approximately 644,000 individuals annually. Managing this complex disease involves various treatment modalities such as systemic therapy, radiation, and surgery, particularly for patients with locally advanced disease. HNC treatment necessitates a multidisciplinary approach due to alterations in patients' genomes affecting their functionality. Predominantly, squamous cell carcinomas (SCCs), the majority of HNCs, arise from the upper aerodigestive tract epithelium. The epidemiology, staging, diagnosis, and management techniques of head and neck squamous cell carcinoma (HNSCC), encompassing clinical, image-based, histopathological and molecular profiling, have been extensively reviewed. Lymph node metastasis (LNM) is a well-known predictive factor for HNSCC that initiates metastasis and significantly impacts HNSCC prognosis. Distant metastasis (DM) in HNSCC has been correlated to aberrant expression of cancer cell-derived cytokines and growth factors triggering abnormal activation of several signaling pathways that boost cancer cell aggressiveness. Recent advances in genetic profiling, understanding tumor microenvironment, oligometastatic disease, and immunotherapy have revolutionized treatment strategies and disease control. Future research may leverage genomics and proteomics to identify biomarkers aiding individualized HNSCC treatment. Understanding the molecular basis, genetic landscape, atypical signaling pathways, and tumor microenvironment have enhanced the comprehension of HNSCC molecular etiology. This critical review sheds light on regional and distant metastases in HNSCC, presenting major clinical and laboratory features, predictive biomarkers, and available therapeutic approaches.

Methionine-choline deficient diet deteriorates DSS-induced murine colitis through disturbance of gut microbes and infiltration of macrophages.

Ulcerative colitis (UC) is associated with changed dietary habits and mainly linked with the gut microbiota dysbiosis, necroptosis of epithelial cells, and mucosal ulcerations. Liver dysfunction and abnormal level of liver metabolism indices were identified in UC patients, suggesting a close interaction between gut and liver disorders. Methionine-choline deficient diet (MCD) has been shown to induce persistent alterations of gut microbiota and metabolome during hepatitis. In this study we further explored the disease phenotypes in UC patients and investigated whether MCD functioned as a trigger for UC susceptibility. After assessing 88 serum specimens from UC patients, we found significant liver dysfunction and dyslipidemia including abnormal ALT, AST, TG, TC, LDL-c and HDL-c. Liver dysfunction and dyslipidemia were confirmed in DSS-induced colitis mice. We fed mice with MCD for 14 days to cause mild liver damage, and then treated with DSS for 7 days. We found that MCD intake significantly exacerbated the pathogenesis of mucosal inflammation in DSS-induced acute, progressive, and chronic colitis, referring to promotion of mucosal ulcers, colon shortening, diarrhea, inflammatory immune cell infiltration, cytokines release, and abnormal activation of inflammatory macrophages in colon and liver specimens. Intraperitoneal injection of clodronate liposomes to globally delete macrophages dramatically compromised the pathogenesis of MCD-triggering colitis. In addition, MCD intake markedly changed the production pattern of short-chain fatty acids (SCFAs) in murine stools, colons, and livers. We demonstrated that MCD-induced colitis pathogenesis largely depended on the gut microbes and the disease phenotypes could be transmissible through fecal microbiota transplantation (FMT). In conclusion, this study supports the concept that intake of MCD predisposes to experimental colitis and enhances its pathogenesis via modulating gut microbes and macrophages in mice.

Combined EEG-tDCS approach in resting state to reduce comorbid anxiety and depressive symptoms in affective disorders: A sham-controlled pilot study

Continuous challenges have been imposed on mental health science by Anxiety and Depression disorders as the most prevalent and debilitating psychiatric conditions worldwide. Pharmacologic and cognitive behavioral therapies, either alone or in combination, have been considered as the first-line therapies, however, resistant symptomatology is prevalent in comorbid conditions with symptoms remaining after interventions. The demand for new therapeutic solutions has given space to the development of non-invasive brain stimulation techniques (NIBS), and the transmagnetic direct current stimulation (tDCS) has been reported as a safe and well-tolerated technique for the treatment of several mental health conditions, including Anxiety and Depression disorders. Relying on quantitative electroencephalography(qEEG)- tDCS approach, the current study aims to inspect the effect of tDCS intervention on patients who suffer from anxiety-depression comorbidity, in particular, the impact of tDCS intervention on qEEG spectral power activity and resting-state connectivity organization during eyes closed and eyes open protocols. QEEG data were acquired from eight patients suffering from moderate to severe anxiety-depression comorbid symptoms along with poor coping skills to manage stress and negative affect. Twelve control subjects allocated in the control group exhibiting low to moderate symptoms in both anxiety and depression conditions went also through the qEEG data acquisition. In addition, a sham-controlled study was conducted, and the patient group went through resting-state qEEG-tDCS neuromodulation once a week for ten weeks. Various-stage qEEG recordings were performed to inspect the efficacy of tDCS treatment during the modulation of brain regions involved in the regulation of affective responses. Our results demonstrated that after tDCS neuromodulation, the patients' groups exhibited decreased absolute power abnormalities over the left anterior cingulate cortex and reduced abnormal activity in the alpha band over posterior regions; improved functional connectivity indexes; decreased anxiety and depressive scores while positive affect score was improved. Besides the promising improvements, our study did not find a significant tDCS effect on perceived stress and negative affect scores. Consistently, significant differences in absolute spectral power over the left anterior cingulate cortex were detected among the patient group, as compared to the controls, as expected. Therefore, our study offers preliminary data to understand the neuroplasticity changes that potentially result from the manipulation of cortical excitability during affective regulation protocols followed by the consequent decrease of comorbid anxiety and depressive symptomatology. The pilot study was followed by prospective registration with ChiCTR2200062142.

A hybrid 1D CNN-BiLSTM model for epileptic seizure detection using multichannel EEG feature fusion

Epilepsy, a chronic non-communicable disease is characterized by repeated unprovoked seizures, which are transient episodes of abnormal electrical activity in the brain. While Electroencephalography (EEG) is considered as the gold standard for diagnosis in current clinical practice, manual inspection of EEG is time consuming and biased. This paper presents a novel hybrid 1D CNN-Bi LSTM feature fusion model for automatically detecting seizures. The proposed model leverages spatial features extracted by one dimensional convolutional neural network and temporal features extracted by bi directional long short-term memory network. Ictal and inter ictal data is first acquired from the long multichannel EEG record. The acquired data is segmented and labelled using small fixed windows. Signal features are then extracted from the segments concurrently by the parallel combination of CNN and Bi-LSTM. The spatial and temporal features thus captured are then fused to enhance classification accuracy of model. The approach is validated using benchmark CHB-MIT dataset and 5-fold cross validation which resulted in an average accuracy of 95.90%, with precision 94.78%, F1 score 95.95%. Notably model achieved average sensitivity of 97.18% with false positivity rate at 0.05/hr. The significantly lower false positivity and false negativity rates indicate that the proposed model is a promising tool for detecting seizures in epilepsy patients. The employed parallel path network benefits from memory function of Bi-LSTM and strong feature extraction capabilities of CNN. Moreover, eliminating the need for any domain transformation or additional preprocessing steps, model effectively reduces complexity and enhances efficiency, making it suitable for use by clinicians during the epilepsy diagnostic process.

Epilepsy Unveiled using a Multi-Classifier Approach integrated in EAS system for Enhanced Detection Using EEG Signal Analysis.

The study focuses on the advantages of using non-invasive approaches to detect epileptic seizures, aiming to prevent injuries from sudden falls and improve medical diagnosis and management. It presents an EEG Acquisition System (EAS) that integrates a multi-level amplifier with four machine learning algorithms—K-Nearest Neighbors (KNN), Support Vector Machine (SVM), Multilayer Perceptron Neural Networks (MLPNN), and Convolutional Neural Network (CNN)—for signal classification. These methods are chosen for their accuracy and rapid processing, making them ideal for real-time use. The research analyzed data from 310 participants to detect epileptic patterns under various conditions. The results show that the SVM model achieved the highest accuracy at 96.37%±2.68 in the small data, followed by the CNN with 95.25%±2.25 in real-time detection, MLPNN at 89.87%, and KNN with 86.37% . This demonstrates CNN's strong performance in seizure detection, complemented by a detailed comparison of sensitivity and specificity across all models to assess their predictive efficiency. The system tells the scientist if there is an epilepsy , dementia ,or a normal brain activity, if the system detects the abnormal activities, it could map it on the brain map with a precision of 98%.