Atypical Forms Research Articles

Clinical and biological underpinnings of longitudinal atrophy pattern progression in Alzheimer's disease.

Magnetic resonance imaging (MRI) has recently enabled to identify four distinct Alzheimer's disease (AD) subtypes: hippocampal sparing (HpSp), typical AD (tAD), limbic predominant (Lp), and minimal atrophy (MinAtr). To date, however, the natural history of these subtypes, especially regarding the presence of subjects switching to other MRI patterns and their clinical and biological differences, remains poorly understood. To investigate the clinical and biological underpinnings of longitudinal atrophy pattern progression in AD. 251 AD patients (16 with significant memory concern, 66 with early mild cognitive impairment (MCI), 125 with late MCI, and 44 with AD dementia) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database were assigned to their baseline MRI atrophy subtype using Freesurfer-derived cortical:hippocampal volumes ratio. Switching to other MRI patterns was investigated on longitudinal scans, and patients were accordingly classified as "switching" and "stable". Logistic regression models were applied to identify predictors of switching to other MRI patterns. 40% of Lp, 26% of HpSp, and 35% of MinAtr cases switched to other MRI patterns, with tAD representing the destination subtype of all switching HpSp and Lp, and the majority of MinAtr. At baseline significant clinical, cognitive and biomarkers differences were observed across the four subtypes. Only clinical and cognitive variables, however, were significantly associated with switch to other MRI patterns. Our results suggest convergent directions of disease progression across atypical and typical AD forms, at least in a subset of AD subjects, and highlight the importance of deep-phenotyping approaches to understand AD heterogeneity.

Apparent lncRNAs involvement in pathogenesis of endometriosis

Endometriosis is an estrogen-dependent, debilitating gynecologic disease impacting millions of women globally. One of the main characteristics of this benign condition is the presence of endometrial-like tissue outside the uterus, causing dysmenorrhea, chronic pelvic pain, and infertility. However, despite many reports on the origin and molecular pathogenesis of endometriosis, the etiology of this disease has not been fully explored yet. Recently, significant attention has been paid to long noncoding RNAs (lncRNAs). Numerous studies focused on exploring the association between lncRNAs and the progression of various human diseases. LncRNAs function as competing endogenous RNAs (ceRNAs) interacting with microRNAs as a “sponge” to regulate cell functions. According to multiple studies, lncRNAs seem to have the potential as markers for diagnosing, and monitoring progression and staging in endometriosis. In this review, we summarized the lncRNAs that were found to influence the pathogenesis of endometriosis. Furthermore, we tried to assess its potential in the process of endometriosis transition from benign through atypical forms, up to EAOC (Endometriosis Associated Ovarian Cancer).

ЛИЧНОСТЬ В СИТУАЦИИ АТИПИЧНОЙ ЗАНЯТОСТИ: АНАЛИЗ С ПОЗИЦИЙ СУБЪЕКТНОГО ПОДХОДА

The article examines the phenomenon of atypical employment from the point of view of a subjective approach. The purpose of the article is to describe the psychological characteristics of individuals in a situation of atypical forms of employment. By atypical employment we mean a form of employment that, in comparison with traditional work, has other (distinctive) characteristics (involves working on short-term, non-permanent conditions not guaranteed by the organization). The focus of our research is informal and distance employment as options for atypical employment. There are options for combining forms of employment: office-official, remote-official, office-unofficial, remote-unofficial. The article provides a comparative analysis of atypical and precarious employment. The importance of taking into account subjective and objective signs of precarity in studies of atypical employment is emphasized. The results obtained make it possible to conduct empirical studies of the personality as a subject of work, the situation of typical and atypical employment, as well as the development of programs for psychological support of persons in a situation of precarious employment.

Atypical Cogan syndrome: a case report

BackgroundCogan syndrome is a rare autoimmune systemic vasculitis presenting with interstitial keratitis and audiovestibular symptoms. The atypical form, characterized by more extensive ocular lesions with audiovestibular symptoms appearing with a longer delay and more frequent systemic features, is usually underdiagnosed, delaying treatment.Case presentationWe report the case of a 30-year-old Mediterranean female who presented recurrent left red and painful eye. The evolution in flare-ups during 3 years, associated with a nonspecific biological inflammatory response, motivated ocular biopsies demonstrating diffuse inflammatory changes from the cornea to the sclera. Since Morocco is an endemic region for tuberculosis, the laboratory tests were expanded to identify the latent forms based on the tuberculin skin test and QuantiFERON TB Gold in tube assay, both positive for Mycobacterium tuberculosis infection. Thus, antibacillary chemotherapy was started for 6 months, with reappearance of the symptoms at the end of treatment. Three years later, the patient presented isolated and fluctuating audiovestibular Ménière-like symptoms, with progressive sensorineural hearing loss. The nonstabilization under usual medical treatment along with her diffuse inflammatory ocular lesions led to the diagnosis of atypical Cogan syndrome. The patient received long-term corticosteroid with notable improvement.ConclusionCogan syndrome is a rare autoimmune disease that should be considered when faced with ocular and audiovestibular manifestations, even in its atypical form, to provide early and adequate treatment, which is the main prognosis factor in the control of irreversible lesions. Thus, interdisciplinary collaboration is fundamental along with screening for other infectious and systemic disorders that should include tuberculosis.

Fabry Disease - literature review

Introduction and objective: Fabry disease (FD) is a rare lysosomal storage disorder that can manifest in classical and atypical forms, with the latter being more common. It results from deficient alpha-galactosidase activity, leading to the accumulation of globotriaosylceramide (Gb3), causing inflammation, cellular damage, and mitochondrial dysfunction. The aim of this publication is to discuss various aspects of Fabry disease based on the latest literature. Review Methods: The PubMed database was searched for scientific articles where the terms "Fabry disease" or "FD" appear in the title, abstract, or keywords. The focus was on articles published between 2017 and 2024, although in some cases, older sources were consulted when more recent data was lacking.Brief Description of the State of Knowledge: The Fabry disease occurs with a frequency between 1:40,000 and 1:117,000 live male births. Symptoms include proteinuria, kidney failure, hypertrophic cardiomyopathy, valve defects, peripheral neuropathy, and gastrointestinal issues. The disease affects life expectancy, primarily due to cardiovascular complications. Early diagnosis is often delayed due to non-specific symptoms, and prognosis tends to be worse in males. Current treatments include enzyme replacement therapy (ERT), chaperone therapy with migalastat, and second-generation ERT.Summary: Given the rarity of Fabry disease, research is limited, and there is a need for more studies to explore novel therapeutic options that could improve patient quality of life and mitigate the disease's complications.

The role of the co-chaperone DNAJB11 in polycystic kidney disease: Molecular mechanisms and cellular origin of cyst formation.

Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in PKD1 and PKD2, encoding polycystin-1 (PC1) and polycystin-2 (PC2), which are required for the regulation of the renal tubular diameter. Loss of polycystin function results in cyst formation. Atypical forms of ADPKD are caused by mutations in genes encoding endoplasmic reticulum (ER)-resident proteins through mechanisms that are not well understood. Here, we investigate the function of DNAJB11, an ER co-chaperone associated with atypical ADPKD. We generated mouse models with constitutive and conditional Dnajb11 inactivation and Dnajb11-deficient renal epithelial cells to investigate the mechanism underlying autosomal dominant inheritance, the specific cell types driving cyst formation, and molecular mechanisms underlying DNAJB11-dependent polycystic kidney disease. We show that biallelic loss of Dnajb11 causes cystic kidney disease and fibrosis, mirroring human disease characteristics. In contrast to classical ADPKD, cysts predominantly originate from proximal tubules. Cyst formation begins in utero and the timing of Dnajb11 inactivation strongly influences disease severity. Furthermore, we identify impaired PC1 cleavage as a potential mechanism underlying DNAJB11-dependent cyst formation. Proteomic analysis of Dnajb11- and Pkd1-deficient cells reveals common and distinct pathways and dysregulated proteins, providing a foundation to better understand phenotypic differences between different forms of ADPKD.

A Bullous Variant of Central Serous Chorioretinopathy Treated With Sclerotomy.

Bullous serous central chorioretinopathy (bCSCR) is an atypical form of CSCR characterized by large serous detachment. This variant presents significant diagnostic challenges, and optimal treatment strategies are not well defined. This report presents a case of a 31-year-old man with bCSRC treated with scleral thinning surgery in four quadrants with scleral windows created in the two inferior quadrants. The etiology, pathogenesis, and optimal treatment of bCSCR are not fully understood. Various therapeutic options, including photocoagulation and photodynamic therapy, have been employed with varying degrees of success. We describe a case of scleral thinning (sclerectomy) with two inferior sclerotomies without subretinal drainage, which resulted in a positive outcome.[Ophthalmic Surg Lasers Imaging Retina 2024;55:XX-XX.].

A phenomap of TTR amyloidosis to aid diagnostic screening.

Cardiac amyloidosis due to transthyretin (ATTR) remains an underdiagnosed cause of cardiomyopathy. As awareness of the disease grows and referrals for ATTR increase, clinicians are likely to encounter more atypical forms of the condition in clinical practice. Therefore, physicians and treating cardiologists should be aware of the full phenotypic spectrum of ATTR. The phenotypic manifestation of ATTR varies depending on the stage of the disease, the presence and type of TTR mutation and the patient's comorbidities. ATTR findings can be grouped into four major categories: clinical profile and cardiac phenotype, extra-cardiac findings, electrocardiogram and imaging findings, which cumulatively form the full phenomap of ATTR. Results from any diagnostic test for ATTR should be interpreted in light of the pre-test probability for the disease. Findings that suggest negative markers for ATTR can point towards other forms of amyloidosis (such as AL amyloidosis) or alternate causes of left ventricular hypertrophy, including hypertrophic cardiomyopathy or Fabry disease. The rising number of referrals for ATTR cardiomyopathy presents a challenge in daily clinical practice. To prevent an increase in false-positive diagnostic test results, an ATTR phenomap can serve as a valuable tool for guiding diagnostic assessments, interpreting test outcomes and prioritizing appropriate referrals for ATTR screening.

Concomitant primary and secondary syphilis: a case series from a reference center in Mexico

Primary syphilis is characterized by the presence of a chancre and secondary syphilis by the presence of syphilis. The presence of chancres within secondary syphilis have been reported, however, this form of presentation is rare. Patients with synchronous diagnosis of primary and secondary syphilis were included. They underwent a reverse sequence algorithm for syphilis diagnosis with a rapid syphilis test, if positive, a rapid plasma reagin (RPR) or venereal disease research laboratory (VDRL) tests were performed. A total of 15 patients were included. All were men. In primary syphilis, penile chancre predominated in 13 patients (86.6%), and one (6.7%) was in the tongue. In secondary syphilis syphilitic roseola was the most common type of presentation in 10 patients (66.6%), followed by the palmoplantar plaques in 6 patients (40%) and condyloma lata in 2 patients (13.3%). One patient presented alopecia in a “moth-eaten” pattern and this presentation coexisted with a condyloma lata and the palmoplantar plaques. Other patient presented with syphilitic roseola, palmoplantar plaques and condyloma lata. Clinical presentation as coexistent primary-secondary syphilis will become more frequent. First contact physicians and dermatologists would have to take more in consideration infrequent and atypical clinical forms of this disease.

The effect of Trimetazidine on the left ventricular global longitudinal strain assessed by cardiac magnetic resonance in stable angina patients with previous myocardial infarction and left ventricular

Abstract Introduction Trimetazidine (TMZ) is an anti-ischemic metabolic agent that is indicated in adults as add-on therapy for the symptomatic treatment of patients with stable angina pectoris (SA). Global left ventricular (LV) systolic function is an important predictor of outcomes in patients after myocardial infarction (MI). Cardiac magnetic resonance (CMR) imaging has now evolved into a major tool for the evaluation of patients with LV dysfunction, providing precise measurements of ejection fraction (EF) and viability assessment but also now allowing assessment of global longitudinal strain (GLS) from standard cine CMR images. We hypothesized that the use of TMZ 80 mg as an anti-ischemic agent in patients with SA, history of MI, reduced EF and in the presence of viable myocardium may produce an early modification of GLS. Methods TRIM-AZ - was a non-interventional, prospective Azerbaijan study to analyze the capacity of short-term therapy with TMZ 80 mg on LV GLS evaluated by CMR in patients with previous MI. Patients with a confirmed diagnosis of heart failure (HF) with impaired LV systolic function and SA in the presence of viable myocardium were included. The treatment of all patients was optimized according to the latest ESC guidelines before entry in the study. Patients were randomized into two groups, one received TMZ 80 mg on top of guidelines directed medical therapies, and the other was the control group. A CMR as well as a transthoracic echography were performed for all patients at the inclusion visit and 8 weeks later. Results 52 patients were included in the study, 30 patients in the TMZ group and 22 in the control group,. At baseline, the mean age was 62±7 years , 63% were smokers, 60% hypertensive, 60% diabetics, 48% had a family history of MI, 12% had typical symptoms of SA while 88% had atypical form (e.g. like shortness of breath). All patients received baseline therapy with ARNI/ACE-i, SGLT2 inhibitors, beta-blockers, MRA, ASA, and statin. 8 weeks after the initiation of TMZ, there were no significant changes in LVEF assessed both by Echo and CMR (29,8%±3,2% vs 30,1%±3,5% by echo in TMZ group; 31,3%±2,7% vs 31,6%±2,7% by echo in the control group; 25,9%±3,1% vs 26,9±4,1% by CMR in TMZ group; 26,9%±2,1% vs 30,1%±2,3% by CMR in the control group), however GLS was significantly improved in TMZ group (-9,9%±1,1% to -12,7%±1,2%, p=0,00), but not in control group (-9,3%±1,3% vs -10,3%±1,4% p=0,3). No adverse event related to TMZ use was reported during the study. Conclusion These findings suggest that the use of trimetazidine in patients with stable angina , previous MI and heart failure in the presence of viable myocardium could improve the left ventricular global longitudinal strain assessed by CMR.

Neuroleptic malignant syndrome in Huntington disease.

Despite the wide use of dopamine receptor blocking agents (DRBAs) in Huntington disease (HD), neuroleptic malignant syndrome (NMS) is rarely described in this population. The aim of this study was to assess NMS prevalence in a large cohort of HD patients and explore the main associated risk factors. In 2023, an HD patient was admitted to our neurology department due to NMS. Starting from the case description, we performed a narrative review of the literature of NMS cases in HD, reviewed data from the fifth dataset of the Enroll-HD (a longitudinal, observational, global study of families with HD) study (PDS5) selecting HD patients treated with DRBAs and/or tetrabenazine (TBZ) who presented at least one of the core symptoms of NMS (rigidity and hyperthermia), and collected data to investigate prevalence of NMS and identify risk factors. In the Enroll-HD PDS5 dataset, we identified 5108 of 11,569 HD patients who were undergoing DRBA and/or TBZ treatment. Only one patient, a Caucasian man of 46 years, undergoing clozapine and valproate treatment, had a registered diagnosis of NMS. NMS in HD patients is seldom described. This could be due to an underestimation of this condition. There are no available objective NMS diagnostic criteria at present, and the existence of atypical forms of NMS further complicates diagnosis. Advanced disease stage, rigid-akinetic phenotype, abrupt therapy changes, polytherapy, and dehydration are key risk factors, most of which are preventable through awareness and caution in managing medications in the HD population.

Celiac disease in the aspect of comorbidity: facets and boundaries

Celiac disease poses a serious diagnostic problem due to significant clinical polymorphism with a high frequency of atypical forms. The problem of comorbidity for celiac disease is relevant due to the possible involvement of almost all organs and systems in the pathological process. In this regard, the question arises of which symptoms are a manifestation of the disease, which are complications, and which symptoms are associated with comorbid conditions. The clinical polymorphism of celiac disease is obviously associated with damage to many organs in this disease. They all have a common starting point - an immunopathological process leading to malabsorption and secondary metabolic disorders, which are essentially a manifestation of the disease, but not complications, as is sometimes interpreted. A complication can be considered the oncological consequences of the disease, which develop after prolonged non-compliance of a gluten-free diet. The combination of celiac disease with associated diseases, primarily autoimmune diseases, should be considered as a manifestation of comorbidity.

Shared Jobs, Shared Trajectories? Employer Groups and the Regulation of Part-time Work in Germany and the Netherlands

ABSTRACT To explain cross-national variation in the regulation of atypical forms of employment, including measures aimed at protecting the employment conditions of nonstandard workers, existing studies have typically emphasised the importance of labour's relative power resources and insider-outsider dynamics. This article shows that differences in employer stances can also be of key importance in explaining this type of variation. Moreover, it shows that employer support for regulatory efforts to improve quality of atypical employment neither have to result from a perceived need to seek strategic accommodation nor from a positive assessment of the costs and benefits of regulation. It does so by comparing the very different responses of Dutch and German employer groups to regulatory attempts to improve the quality of part-time employment. It illustrates their importance and attributes them to strategic choices that were a logical outcome of the different institutional environments in which Dutch and German employer groups operated.

Default mode network tau predicts future clinical decline in atypical early Alzheimer's disease.

Identifying individuals with early-stage Alzheimer's disease (AD) at greater risk of steeper clinical decline would enable better-informed medical, support, and life planning decisions. Despite accumulating evidence on the clinical prognostic value of tau positron emission tomography (PET) in typical late-onset amnestic AD, its utility in predicting clinical decline in individuals with atypical forms of AD remains unclear. Across heterogeneous clinical phenotypes, patients with atypical AD consistently exhibit abnormal tau accumulation in the posterior nodes of the default mode network of the cerebral cortex. This evidence suggests that tau burden in this functional network could be a common imaging biomarker for prognostication across the syndromic spectrum of AD. Here, we examined the relationship between baseline tau PET signal and the rate of subsequent clinical decline in a sample of 48 A+/T+/N+ patients with mild cognitive impairment or mild dementia due to AD with atypical clinical phenotypes: Posterior Cortical Atrophy (n = 16), logopenic variant Primary Progressive Aphasia (n = 15), and amnestic syndrome with multi-domain impairment and young age of onset < 65 years (n = 17). All patients underwent magnetic resonance imaging (MRI), tau PET, and amyloid PET scans at baseline. Each patient's longitudinal clinical decline was assessed by calculating the annualized change in the Clinical Dementia Rating Sum-of-Boxes (CDR-SB) scores from baseline to follow-up (mean time interval = 14.55 ± 3.97 months). Atypical early AD patients showed an increase in CDR-SB by 1.18 ± 1.25 points per year: t(47) = 6.56, p < .001, Cohen's d = 0.95. Across clinical phenotypes, baseline tau in the default mode network was the strongest predictor of clinical decline (R2 = .30), outperforming a simpler model with baseline clinical impairment and demographic variables (R2 = .10), tau in other functional networks (R2 = .11-.26), and the magnitude of cortical atrophy (R2 = .20) and amyloid burden (R2 = .09) in the default mode network. Overall, these findings point to the contribution of default mode network tau to predicting the magnitude of clinical decline in atypical early AD patients one year later. This simple measure could aid the development of a personalized prognostic, monitoring, and treatment plan, which would help clinicians not only predict the natural evolution of the disease but also estimate the effect of disease-modifying therapies on slowing subsequent clinical decline given the patient's tau burden while still early in the disease course.

Not All Therapy-Related Neoplasms are Myeloid: A Case Report of Rare B-ALL With t(5;14) Following Alkylating Agent Treatment

Abstract Introduction/Objective Most therapy-related hematologic neoplasms are myeloid (t-MN). Although not recognized as a distinct entity in the WHO classification of hematologic neoplasms, therapy-related acute lymphoblastic leukemia (t- ALL) cases have been previously reported. ALL incidence increases with any previous malignancy and is higher in those with previous treatment, supporting the concept of therapy-related ALL. B lymphoblastic leukemia/lymphoma (B- ALL) with t(5:14) is a rare subtype of the ALL (&amp;lt;1%) harboring a IL-3/IGH gene translocation. We present the first case of B-ALL with t(5;14) following treatment with alkylating agents for breast carcinoma. Methods/Case Report A 79-year-old female received docetaxel, carboplatin, trastuzumab, pertuzumab, Herceptin and radiotherapy for an invasive ductal breast carcinoma. Two years later, she developed progressive pancytopenia requiring a bone marrow biopsy. Results (if a Case Study enter NA) The bone marrow aspirate smears demonstrated B-ALL with 25% blasts, limited neutrophilic maturation, moderate erythroid dysplasia, and decreased megakaryocytes with occasional atypical forms. On the biopsy, atypical megakaryocytes and lymphoblasts were positive for TP53 immunohistochemical stain. On flow cytometry, blasts were positive for CD19, cCD79a, CD22, CD10, TdT, and HLA-DR and only 6% were positive for CD34. Next generation sequencing showed TP53 and NRAS mutation. Karyotyping revealed 46, XX, t (5;14) (q33; q13) and trisomy 21. Conclusion B-ALL with t (5;14); IGH/IL3 fusion has not been previously reported following treatment with alkylating agents. The presence of morphologic myeloid dysplasia developing after chemotherapy with alkylating agents support causality being therapy related rather than an independent process. The case expands the breadth of known therapy- related hematologic neoplasms and raises questions regarding the mechanisms of leukemogenesis.

Analysis and comparison of post-translational modifications of α-synuclein filaments in multiple system atrophy and dementia with Lewy bodies

Our previous cryogenic electron microscopy (cryoEM) analysis showed that the core structures of α-synuclein filaments accumulated in brains of patients diagnosed with dementia with Lewy bodies (DLB) and multiple system atrophy (MSA) patients are different. We analyzed the post-translational modifications (PTMs) in these filaments , and examined their relationship with the core filament structures and pathological features. Besides the common PTMs in MSA and DLB filaments, acetylation, methylation, oxidation and phosphorylation were frequently detected in MSA filaments, but not in DLB filaments. Furthermore, in DLB filament cases, the processing occurred at the C-terminal side of Asp at 119 residue and Asn at 122 residue, while in MSA cases, the processing occurred at multiple sites between residues 109–123. We have previously reported that PTMs in tau filaments depend on the filament core structure. This was considered to apply to α-synuclein filaments as well. As an example, PTMs including processing sites detected in α-synuclein filaments in early-onset DLB (an atypical form, now named juvenile-onset α-synucleinopathy) brain also supported this idea. These suggests that PTMs appeared to be closely related to the specific filament core structures.

A novel KCNC3 gene variant in the voltage-dependent Kv3.3 channel in an atypical form of SCA13 with dominant central vertigo.

Potassium channel mutations play an important role in neurological diseases, such as spinocerebellar ataxia (SCA). SCA is a heterogeneous autosomal-dominant neurodegenerative disorder with multiple sub-entities, such as SCA13, which is characterized by mutations in the voltage-gated potassium channel Kv3.3 (KCNC3). In this study, we present a rare and atypical case of SCA13 with a predominant episodic central rotational vertigo, while the patient suffered only from mild progressive cerebellar symptoms, such as dysarthria, ataxia of gait and stand, and recently a cognitive impairment. In this patient, we identified a heterozygous variant in KCNC3 (c.2023G > A, p.Glu675Lys) by next-generation sequencing. This Kv3.3E675K variant was studied using voltage-clamp recordings in Xenopus oocytes. While typical SCA13 variants are dominant-negative, show shifts in the voltage-dependence of activation or an altered TBK1 regulation, the Kv3.3E675K variant caused only a reduction in current amplitude and a more pronounced cumulative inactivation. Thus, the differences to phenotypes observed in patients with classical SCA13 mutations may be related to the mechanism of the observed Kv3.3 loss-of-function. Treatment of our patient with riluzole, a drug that is known to also activate potassium channels, turned out to be partly beneficial. Strikingly, we found that the Kv3.3 and Kv3.3E675K inactivation and the frequency-dependent cumulative inactivation was antagonized by increased extracellular potassium levels. Thus, and most importantly, carefully elevated plasma potassium levels in the physiological range, or novel drugs attenuating Kv3.3 inactivation might provide novel therapeutic approaches to rescue potassium currents of SCA13 variants per se. In addition, our findings broaden the phenotypic spectrum of Kv3.3 variants, expanding it to atypical phenotypes of Kv3.3-associated neurological disorders.

Comorbidity of Eating Disorder in Patients with Bipolar Mood Disorder Type I and Type II in Euthymic State, Case Control Study

Abstract Background Bipolar mood disorder it is one of the leading causes of disability worldwide. Bipolar disorders are furtherly classified as bipolar I disorder, bipolar II disorder, cyclothymia and other categories of atypical forms that do not fulfill the criteria for the abovementioned subtypes. There is growing recognition of the clinical significance of eating disorder (ED) comorbidity in patients with bipolar disorder (BD). The prevalence rate of EDs in BD vary substantially according to the studies in recent years. Patients and Methods This study is a case control study, the study conducted at psychiatric outpatient clinic in Ain Shams University Hospitals, starting from June 2022 till completion of the sample. Results This study shows that there is correlation between eating disorders and bipolar mood disorders where there was statistically significant difference on applying the eating disorder inventory (EDI) on both cases and controls with the cases having higher scores on the EDI total scores and severity. The study revealed the potential role of different risk factors on both eating disorders and bipolar mood disorder. Conclusion It is one of the preliminary studies done in Egypt aiming to investigate the correlation between eating disorders and bipolar mood disorders and that Screening for all individuals having bipolar mood disorders underlying eating disorders is essential for proper intervention and management.

Sarcomatoid Morphology in Pediatric Langerhans Cell Neoplasm Does Not Always Predict Aggressive Clinical Course.

Langerhans cell sarcoma (LCS), a rare malignant neoplasm in the general category of myeloid neoplasms characterized by overtly malignant Langerhans cells (LC) with conspicuous mitotic activity including atypical forms. Although most cases occur in adults, rare examples of LCS have been reported in children with variable clinical outcome. We present 2 childhood cases of Langerhans cell neoplasm with high grade sarcomatous features and OSBPL9::BRAF fusion and BRAF V600E mutation.

Phyto-nanotechnology: A novel beneficial strategy for Alzheimer's disease therapy

Alzheimer's disease, a neurodegenerative condition, is characterized by the slow and progressive deterioration of the cognitive functions of geriatric patients. It occurs due to exacerbation of neurons in the brain, indicated by loss of memory, mood instability, and even death. The aggregation of amyloid β protein and neurofibrillary tangles-atypical forms of tau protein is the major cause of this disease. Phytoconstituents have been frequently employed in treating Alzheimer's disease. These natural compounds act through different molecular mechanisms to treat the disease. However, their potential in Alzheimer's disease therapy may be limited due to poor blood-brain barrier permeability, off-target effects, low bioavailability, etc. In recent times, nanotechnology has gained attraction to overcome these challenges. This article focuses on the potential phytoconstituents for Alzheimer's disease treatment and the associated limitations. Moreover, it highlights various nanoformulation strategies employed to penetrate the blood-brain barrier effectively, avoid side effects, improve bioavailability, and target specificity in treating Alzheimer's disease. The integration of nanotechnology with plant-derived compounds has the potential to revolutionize the therapeutic landscape for Alzheimer's disease.