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Empirically-based developmental psychopathology approach identified three domains involved in the emergence of borderline personality disorder (BPD): i) underlying liabilities to develop psychopathology (i.e., early patterns of internalizing and externalizing manifestations); ii) invalidating relational experiences (e.g., childhood traumatic experiences, maladaptive parenting, problematic peer relationships); iii) regulatory mechanisms of emotions and behaviors. Nevertheless, no studies have quantitatively summarized empirical findings concerning how and to what extent these domains might be temporally associated to the emergence of BPD features from adolescence to adulthood. The current multi-level meta-analysis included 106 studies (N = 86,871 participants) assessing the role of previously mentioned antecedents and risk factors for BPD. The analysis showed moderate effect sizes capturing temporal associations between early internalizing/externalizing psychopathological manifestations, different invalidating relational experiences, emotion/behavior regulation processes with later BPD features. The effect sizes of these domains were not statistically different from each other. This evidence supports a transactional developmental model of BPD. Consistently, the emergence of BPD could be viewed in the light of dynamic interplays between an underlying liability to psychopathology and invalidating relational experiences across different stages of development, which are progressively reinforced through increasing alterations of emotion and behavior regulation mechanisms. • Antecedents and risk factors for BPD were meta-analyzed (prospective/retrospective studies) • Liabilities to psychopathology showed moderate associations with later BPD features • Invalidating experiences highlighted moderate relationships with later BPD features • Emotion/behavior regulation were moderately associated with later BPD features • Findings supported a transactional etiopathogenic model of BPD [ABSTRACT FROM AUTHOR]

Extensive research has been conducted on postpartum depression (PPD) over the past century, and yet no definitive answer regarding its etiopathogenesis, risk factors, genetic predilection, and treatment has been found. The few preclinical and clinical studies propose that maternal brain adaptations to the endocrinological, immunological, and behavioral changes and external sociodemographic risk factors in the perinatal period make women more vulnerable to anxiety and depression. Irrespective of the cause, a dilemma exists regarding the type of help to provide postpartum mothers. With very few treatment options at our disposal, deciding between psychotherapy, pharmacological, and non‐pharmacological therapy on a case‐by‐case basis is unproductive because in developing countries infrastructure is limited and the availability of medications, especially for psychiatric illnesses, is still evolving. Hence, regardless of psychotherapy, antidepressants remain the first line of treatment with selective serotonin reuptake inhibitors (SSRIs); sertraline has the best efficacy and safety profile in breastfeeding women. As endocrine factors play a significant role in etiopathogenesis, hormonal therapy with oxytocin has been shown to be efficacious, and studies investigating the role of testosterone in treating PPD are also under way. In 2019, the US Food and Drug Administration (FDA) approved the first and only drug for the sole purpose of treating PPD, brexanolone. Zuranolone, a drug recently approved by the FDA, has a similar mechanism of action to brexanolone. For breastfeeding mothers reluctant to use pharmacotherapy, somatic therapy has been studied, including bright light therapy, vagal nerve stimulation, and newer noninvasive interventions. This article encompasses a short note on PPD, including its etiopathogenesis and clinical characteristics, and recapitulates the various available and evolving pharmacological and nonpharmacological therapies. [ABSTRACT FROM AUTHOR]

Autoimmune polyglandular syndrome (APS) comprises a complex association of autoimmune pathological conditions. APS Type 1 originates from loss-of-function mutations in the autoimmune regulator (AIRE) gene. APS2, APS3 and APS4 are linked to specific HLA alleles within the major histocompatibility complex, with single-nucleotide polymorphisms (SNPs) in non-HLA genes also contributing to disease. In general, variability in the AIRE locus and the presence of heterozygous loss-of-function mutations can impact self-antigen presentation in the thymus. In this study, whole-exome sequencing (WES) was performed on a sixteen-year-old female APS3A/B patient to investigate the genetic basis of her complex phenotype. The analysis identified two variants (p.Arg111Trp and p.Thr101Ile) of the hepatitis A virus cell receptor 2 gene (HAVCR2) encoding for the TIM-3 (T cell immunoglobulin and mucin domain 3) protein. These variants were predicted, through in silico analysis, to impact protein structure and stability, potentially influencing the patient's autoimmune phenotype. While confocal microscopy analysis revealed no alteration in TIM-3 fluorescence intensity between the PBMCs isolated from the patient and those of a healthy donor, RT-qPCR showed reduced TIM-3 expression in the patient's unfractionated PBMCs. A screening conducted on a cohort of thirty APS patients indicated that the p.Thr101Ile and p.Arg111Trp mutations were unique to the proband. This study opens the pathway for the search of TIM-3 variants possibly linked to complex autoimmune phenotypes, highlighting the potential of novel variant discovery in contributing to APS classification and diagnosis. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is the most common type of dementia worldwide. The etiopathogenesis of this disease remains unknown. Currently, several hypotheses attempt to explain its cause, with the most well-studied being the cholinergic, beta-amyloid (Aβ), and Tau hypotheses. Lately, there has been increasing interest in the role of immunological factors and other proteins such as alpha-synuclein (α-syn) and transactive response DNA-binding protein of 43 kDa (TDP-43). Recent studies emphasize the role of tunneling nanotubes (TNTs) in the spread of pathological proteins within the brains of AD patients. TNTs are small membrane protrusions composed of F-actin that connect non-adjacent cells. Conditions such as pathogen infections, oxidative stress, inflammation, and misfolded protein accumulation lead to the formation of TNTs. These structures have been shown to transport pathological proteins such as Aβ, Tau, α-syn, and TDP-43 between central nervous system (CNS) cells, as confirmed by in vitro studies. Besides their role in spreading pathology, TNTs may also have protective functions. Neurons burdened with α-syn can transfer protein aggregates to glial cells and receive healthy mitochondria, thereby reducing cellular stress associated with α-syn accumulation. Current AD treatments focus on alleviating symptoms, and clinical trials with Aβ-lowering drugs have proven ineffective. Therefore, intensifying research on TNTs could bring scientists closer to a better understanding of AD and the development of effective therapies. [ABSTRACT FROM AUTHOR]

Nowadays, glaucoma is viewed as a multifactorial neurodegenerative condition that involves many factors affecting different cell types in a human body. As is known, increased intraocular pressure (IOP) is not the only threatening factor of ganglion cell apoptosis and glaucomatous optic neuropathy development; IOP can be associated with other factors, such as vascular, metabolic, neurotrophic, immune, inflammatory, etc. However, the treatment of glaucoma remains largely symptomatic, aimed almost exclusively at reducing IOP. Microbiotic dysbiosis is a newly developing research direction of the glaucomatous progress, showing that this mechanism may turn out to be an important factor of glaucoma development. There are reasons to believe that treatment strategies aimed at microbiota damage correction may contribute to a better efficiency of glaucoma management.

Background: Diffuse idiopathic skeletal hyperostosis (DISH) is a potentially serious osteopathic disorder associated with coalescing ossifications of the anterior vertebrae and may be concomitant with a constellation of symptomatology and systemic comorbidities. There is limited dental literature describing this finding on panoramic radiographs and cone beam computed tomography (CBCT) scans. Case presentations: Two case reports of DISH are provided. One patient manifested extensive ossifications along the cervical vertebrae and consequent episodes of dysphagia and hoarseness. The other affected patient's cervical ossification was found at an earlier stage of formation and without symptomatology. Panoramic radiography, cervical spine radiography, and CBCT examinations have been provided. Conclusion: Attending dental healthcare practitioners should carefully evaluate all areas of interest and surrounding fields of view when taking panoramic radiographs and CBCT scans for manifestations of DISH and other potential disorders of the cervical vertebrae. A suspected radiologic finding of DISH should prompt timely referral for comprehensive medical assessment to mitigate neurologic deficits and other comorbidities. [ABSTRACT FROM AUTHOR]

Background: Amenorrhea is defined as the cessation of menstruation; it is a significant clinical sign of reproductive dysfunction that affects 1.5-3% of women of childbearing age and is a leading cause of female infertility. The increasing incidence is attributed to better healthcare access and awareness. The Unani system of medicine offers a distinctive perspective on reproductive ailments, yet its terminology and concepts often diverge from modern medical understandings. Research Problem and Aim: This study aims to bridge the gap between classical Unani literature and contemporary medicine by exploring the etiopathogenesis (asbāb wa mahiyatul marazi) of Iβtibḥs al-Tamth (amenorrhea) and comparing it with conventional medical definition, types, causes and its pathogenesis, thereby enhancing understanding of it from both perspectives. Methodology: A systematic review was conducted in 2023, that includes: The primary and main sources of collection of material were from classical published books, manuscripts and their translations. The second type of sources of collection of material were from different types of available published and unpublished literature related to study topic i.e. journals, proceedings, thesis, reports, souvenir, dissertations etc. The third type of sources were from authentic digital material i.e. trusted online websites i.e. PubMed, internet archive etc. Results/Findings: The research revealed a structured understanding of Iḥtibās al-Tamth in Unani literature, highlighting its nuanced classification and etiological factors in comparison to conventional medicine. The findings underscore the potential for integrating Unani insights into contemporary gynaecological practices. Implications: This exploration contributes to a more comprehensive understanding of Iḥtibās al- Tamth (amenorrhea), suggesting that Unani medicine's holistic approach may offer alternative treatment avenues that could mitigate the side effects associated with conventional hormonal therapies. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a chronic, autoimmune rheumatic disease characterized by synovial joint inflammation with subsequent destruction as well as systemic manifestation, leading to impaired mobility and impaired quality of life. The etiopathogenesis of RA is still unknown, with genetic, epigenetic and environmental factors (incl. tobacco smoking) contributing to disease susceptibility. The link between genetic factors like "shared epitope alleles" and the development of RA is well known. However, why only some carriers have a break in self-tolerance and develop autoimmunity still needs to be clarified. The presence of autoantibodies in patients' serum months to years prior to the onset of clinical manifestations of RA has moved the focus to possible epigenetic factors, including environmental triggers that could contribute to the initiation and perpetuation of the inflammatory reaction in RA. Over the past several years, the role of microorganisms at mucosal sites (i.e., microbiome) has emerged as an essential mediator of inflammation in RA. An increasing number of studies have revealed the microbial role in the immunopathogenesis of autoimmune rheumatic diseases. Interaction between the host immune system and microbiota initiates loss of immunological tolerance and autoimmunity. The alteration in microbiome composition, the so-called dysbiosis, is associated with an increasing number of diseases. Immune dysfunction caused by dysbiosis triggers and sustains chronic inflammation. This review aims to provide a critical summary of the literature findings related to the hypothesis of a reciprocal relation between the microbiome and the immune system. Available data from studies reveal the pivotal role of the microbiome in RA pathogenesis. [ABSTRACT FROM AUTHOR]

The incidence of trigeminal neuralgia (TN) is 4–5 cases per 100,000 population per year, and the prevalence is about 20–50 cases per 100,000 population. According to the modern classification, the following types of TN are distinguished: classical, symptomatic and idiopathic. The cause of classical TN is a neurovascular conflict, of symptomatic TN – neoplasms in the petroclival area, vascular anomalies, multiple sclerosis, etc. In the absence of a reliable etiological factor, TN is considered idiopathic. TN pathogenesis remains one of the most challenging topics in neuroscience. Today, there are many theories and hypotheses regarding the peripheral and central mechanisms of trigeminal neuralgia. The most popular theory is the neurovascular conflict that occurs between the trigeminal nerve and the cerebral vessels, but this theory is not the only one. It is known that even after microvascular decompression, patients may continue to experience facial pain. Therefore, other pathogenetic mechanisms are discussed: short circuit theory, multineuronal mechanism, allergic and immune hypothesis, gate theory, bioresonance hypothesis, trigeminal convergence projection theory, “ignition” hypothesis and ion channel pathology. TN is a clinical diagnosis, and its establishing requires certain criteria proposed by the International Headache Society. Using instrumental research methods, namely magnetic resonance imaging of the brain, is necessary for the differential diagnosis of classical and symptomatic TN, and imaging results should always be interpreted in combination with clinical data to make correct decisions on further treatment tactics.

Background: Bipolar disorder is one of the severe mental disorders that are associated with significant morbidity of the patients. Despite advancements in our understanding about the disorder, it remains a challenging proposition to treat bipolar disorder, largely since the prophylactic treatment of the disorder requires assessment of complex clinical algorithms. The revisions of the classificatory systems have also changed the conceptualization of the disorder. In this background, we conducted a review of the Indian studies conducted on the clinical aspects of bipolar disorder. Methods: A narrative review was conducted with focus on the literature published from India. The databases searched included PubMed, Scopus, and Google Scholar, and articles published over the last 15 years by Indian authors were included for this review. Results: In our review, we could access a substantial volume of research published from India. We could identify studies that catered to most of the relevant themes in bipolar disorder including epidemiology, etiology, comorbidities, stigma, disability, clinical course, cognitive profile, pathways to care, and recovery. Conclusion: The research trajectory was in line with the research conducted elsewhere in the world. However, certain dissimilarities in terms of focus could also be observed. The possible reason behind this deviation could be the difference in clinical need and unique challenges faced in the management and rehabilitation of patients in bipolar disorder in Indian scenario.

Fibromyalgia (FM) is characterized by chronic widespread pain accompanied by fatigue, poor sleep quality, and numerous accompanying conditions. Its prevalence worldwide is around 2.7%, and it is more common in women. Although its epidemiology and pathophysiology cannot be precisely explained, it is known that various factors coexist. Over the years, guidelines containing various criteria have been established for the diagnosis of the disease. The goal of treatment in FM is to improve the patient’s quality of life and minimize symptoms as much as possible. The success of treatment in FM is limited. Many patients seek alternative treatment methods, including diet and lifestyle changes. Recently, medical nutritional therapies and phytotherapy products have been at the forefront of research in this area. Phytotherapy products can be added alone or in combination with other treatment methods and can enhance the success of treatment. In this article, the epidemiology, pathophysiology, diagnostic methods, pharmacological and non-pharmacological methods used in the treatment of FM syndrome will be discussed, and the most widely used phytotherapeutic products will be addressed.

Mounting evidence suggests that acute appendicitis (AA) is not one but two diseases: complicated appendicitis, which is associated with necrosis leading to perforation or periappendicular abscess, and uncomplicated appendicitis, which does not necessarily result in perforation. Even though AA is the most frequent cause of surgery from abdominal pain, little is known about the origins and etiopathogenesis of this disease, much less regarding the different disease types. In this study, we investigated the microbiome (inter-domain amplicon and metagenome sequencing) of samples from the appendix, rectum and peritoneum of 60 children and adolescents with AA to assess the composition and potential function of bacteria, archaea and fungi. The analysis of the appendix microbial community revealed a shift depending on the severity of the AA. This shift was reflected by two major community state types that represented the complicated and uncomplicated cases. We could demonstrate that complicated, but not uncomplicated, appendicitis is associated with a significant local expansion of oral, bacterial pathogens in the appendix, most strongly influenced by necrotizing Fusobacterium spp., Porphyromonas and Parvimonas. Uncomplicated appendicitis, however, was characterized by gut-associated microbiomes. Our findings support the hypothesis that two disease types exist in AA, which cannot be distinguished beyond doubt using standard clinical characterization methods or by analysis of the patients rectal microbiome. An advanced microbiome diagnosis, however, could improve non-surgical treatment of uncomplicated AA.

Several cases reported in the literature have confirmed the link between pulmonary aspergillosis and various malignant diseases. Furthermore, it has been observed that the correlation between carcinoid tumor and lung adenocarcinoma is quite uncommon. The etiopathogenic mechanisms underlying these correlations remain poorly defined. We present the case of a patient with three of these diseases: a lung adenocarcinoma with a lepidic pattern, a typical carcinoid, and pulmonary aspergillosis. An additional noteworthy aspect of this case pertains to the timely detection of both lung malignancies. Thus, the necessity for further investigation to ascertain the pathogenic connection among the three diseases is underscored. The ultimate objective is to enhance the prognosis of individuals diagnosed with lung cancer, which is a prevailing malignant disease on a global scale. [ABSTRACT FROM AUTHOR]

Background: Bipolar disorder is one of the severe mental disorders that are associated with significant morbidity of the patients. Despite advancements in our understanding about the disorder, it remains a challenging proposition to treat bipolar disorder, largely since the prophylactic treatment of the disorder requires assessment of complex clinical algorithms. The revisions of the classificatory systems have also changed the conceptualization of the disorder. In this background, we conducted a review of the Indian studies conducted on the clinical aspects of bipolar disorder. Methods: A narrative review was conducted with focus on the literature published from India. The databases searched included PubMed, Scopus, and Google Scholar, and articles published over the last 15 years by Indian authors were included for this review. Results: In our review, we could access a substantial volume of research published from India. We could identify studies that catered to most of the relevant themes in bipolar disorder including epidemiology, etiology, comorbidities, stigma, disability, clinical course, cognitive profile, pathways to care, and recovery. Conclusion: The research trajectory was in line with the research conducted elsewhere in the world. However, certain dissimilarities in terms of focus could also be observed. The possible reason behind this deviation could be the difference in clinical need and unique challenges faced in the management and rehabilitation of patients in bipolar disorder in Indian scenario. [ABSTRACT FROM AUTHOR]

Simple Summary: Circular bovine meat and milk factor (BMMF) DNAs have recently been identified in peritumoral tissues of human colon and breast cancers. Here we aimed to test the most common subtypes of renal cell carcinoma (RCC) for the prevalence of BMMF1 and BMMF2 DNA. We directly tested formalin-fixed and paraffin-embedded (FFPE) RCC and peritumoral tissues for BMMF1 and BMMF2 sequences by introducing novel consensus PCR primers. We demonstrate that BMMF1- and BMMF2- like DNA sequences can be reliably detected in FFPE tissues by consensus PCR. Our results demonstrate that BMMF1- and BMMF2- like sequences are frequently present in FFPE tissues of RCC and peritumoral tissues. Of interest, these sequences are more prevalent in peritumoral kidney tissues. These findings are potentially in line with the proposed model for BMMF-induced indirect colon carcinogenesis, which includes the presence of BMMFs in adjacent peritumoral tissues. Previous studies have indicated a potential role of diet in the pathogenesis of renal cell carcinoma (RCC). Recently, circular bovine meat and milk factor (BMMF) DNAs have been identified in peritumoral tissues of human colon and breast cancers. Here, we investigated the prevalence of the DNA of these novel human pathogenic infectious agents in RCC and adjacent peritumoral renal tissues. DNA was extracted from formalin-fixed and paraffin-embedded (FFPE) RCC and peritumoral kidney tissues, including a test (n = 11) and a validation (n = 152) collection. BMMF1 and BMMF2 consensus primers were designed to screen for the presence of BMMF1- and BMMF2-like DNA. In addition, BMMF-specific PCR was performed on selected cases to test for the presence of additional regions of BMMF1 and BMMF2 genomes. A reference collection of hepatocellular carcinomas (HCCs; n = 60) and adjacent peritumoral liver tissues (n = 50) was also included. Our results demonstrated that BMMF1 and BMMF2 DNAs are frequently found in human RCC tissues and are particularly more prevalent in peritumoral kidney tissues. Of note, BMMF1 and BMMF2 genotype heterogeneity was higher in peritumoral kidney tissues compared to RCC tissues. This is the first study to directly test human FFPE tissues for BMMF1- and BMMF2-like DNA using consensus PCR and demonstrate BMMF DNA in neoplastic and peritumoral kidney tissues. The findings are in line with the recently proposed indirect etiopathogenetic role of BMMFs in, e.g., colorectal carcinogenesis. Follow-up studies are needed to explore the potential role of BMMFs in the etiopathogenesis of RCC. [ABSTRACT FROM AUTHOR]

Fibromyalgia (FM) is characterized by chronic widespread pain accompanied by fatigue, poor sleep quality, and numerous accompanying conditions. Its prevalence worldwide is around 2.7%, and it is more common in women. Although its epidemiology and pathophysiology cannot be precisely explained, it is known that various factors coexist. Over the years, guidelines containing various criteria have been established for the diagnosis of the disease. The goal of treatment in FM is to improve the patient's quality of life and minimize symptoms as much as possible. The success of treatment in FM is limited. Many patients seek alternative treatment methods, including diet and lifestyle changes. Recently, medical nutritional therapies and phytotherapy products have been at the forefront of research in this area. Phytotherapy products can be added alone or in combination with other treatment methods and can enhance the success of treatment. In this article, the epidemiology, pathophysiology, diagnostic methods, pharmacological and non-pharmacological methods used in the treatment of FM syndrome will be discussed, and the most widely used phytotherapeutic products will be addressed. [ABSTRACT FROM AUTHOR]

Background: Inflammatory bowel disease (IBD) is an increasingly prevalent global health concern that has garnered substantial attention. However, the underlying mechanisms are still unclear and the current treatments have significant limitations. Intestinal organoids provide an in vitro model to explore the pathogenesis, test the therapeutic effects, and develop regenerative treatments as well as offer the potential to transform drug discovery of IBD. Methods: To advance our understanding of the whole story of IBD spanning from the pathogenesis to the current therapeutic strategies and latest advancements, a comprehensive search of major databases including PubMed, Scopus, and Web of Science was conducted to retrieve original articles and reviews related to IBD, organoids, pathogenesis and therapy. Results: This review deciphers the etiopathogenesis and the current therapeutic approaches in the treatment of IBD. Notably, critical aspects of intestinal organoids in IBD, such as their potential applications, viability, cell renewal ability, and barrier functionality are highlighted. We also discuss the advances, limitations, and prospects of intestinal organoids for precision medicine. Conclusion: The latest strides made in research about intestinal organoids help elucidate intricate aspects of IBD pathogenesis, and pave the prospective avenues for novel therapeutic interventions. [ABSTRACT FROM AUTHOR]

Background: The primary co-occurrence of gonadal and extragonadal central nervous system (CNS) germ cell tumors (GCTs) has rarely been reported in the literature, and a common opinion on the underlying etiopathogenetic mechanism is lacking. Objective: We aim to investigate the pathophysiological mechanisms and genetic pathways underlying the primary co-occurrence of gonadal and CNS GCTs. Methods: We reviewed data from 29 consecutive patients with a diagnosis of CNS GCT, evaluated in our Hospital over the past 23 years, and searched for those who had at least a primary gonadal co-occurrence of GCT. A systematic review of the literature according to the PRISMA guidelines was also conducted. For a comprehensive and detailed search, PubMed, Ovid MEDLINE, and Ovid EMBASE databases have been consulted. Boolean operators and MeSH terms were used to find studies. Only articles published between 2000 and 2023 were considered. Results: Including our Institutional case report, a total of 7 patients with both testicular NGGCTs and CNS GCTs were identified (5 patients with metachronous tumors and patients with synchronous presentation). The average age at tumor diagnosis was 17 years. The cerebral histotypes reported were mixed GCTs (3 cases; 43%), pure germinomas (3 cases, 43%), and one yolk sac tumor (14%). Two out of seven cases (29%) were syndromic, one suffering from Down Syndrome and the other from Testicular Dysgenesis Syndrome. Regarding the etiology and molecular mechanism of GCT development, several gene mutations have been reported in the literature. Particularly, genetic alterations in the MAPK and/or PI3K/AKT/mTOR pathway, together with mutations of the KIT gene, have been shown to guarantee survival and transformation of mismigrated totipotent primordial germ cells, while suppressor genes allow their resistance against apoptotic death. Aberrant chromosomes have also been reported to be responsible for oncogenic transformation. It is also known that CNS and testicular GCTs share some genetic/epigenetic profiles. Conclusions: The primary co-occurrence of testicular NGGCT and extragonadal CNS GCTs is extremely rare. Genetic factors seem to play a paramount role in their etiopathogenesis. Additional research is needed to elucidate molecular mechanisms of oncogenesis in such patients.

Ovarian tuberculosis is a rare entity with non-specific clinical manifestations, difficult diagnosis, and specific medical management. Ovarian involvement in tuberculosis (TB) may occur in two forms, namely, perioophoritis and oophoritis. The constitutional symptoms of tuberculosis such as anorexia, weight loss, night sweats, and evening rise in temperature have been reported in up to 45% of patients. Misdiagnosis and delayed diagnosis are common. A direct histopathological demonstration is the best diagnostic modality. Fine needle aspiration cytology (FNAC) is the study of choice and polymerase chain reaction (PCR) assay increases its sensitivity. The standard short-course antituberculous for 6 months is recommended for isolated ovarian tuberculosis and for widespread disease, 12 months of therapy is recommended. Surgery is reserved for failure of medical therapy and abscess formation. There are many studies on genito-urinary tuberculosis but a detailed study defining diagnostic studies and management guidelines is still lacking. This article aims to present and share a review of the English-language literature on ovarian tuberculosis to gain a better understanding of etiopathogenesis and diagnostic methods and to provide guidelines for its management.

Leprosy is an infectious disease caused by the acid-fast bacillus, namely Mycobacterium lepra. The entry of Mycobacterium leprae into the body can trigger various immune responses. in some individuals, an adequate immune response can prevent the development of this disease, but in other individuals it can develop into a severe form that can result in disability. Leprosy is widespread throughout the world, especially in tropical/subtropical areas. The highest incidence rates are in India, Brazil and India. Eradicating this disease is still a challenge, especially in endemic areas like Indonesia. Therefore, this article aims to review the basic concepts of leprosy, especially in the epidemiological and etiopathogenesis aspects of leprosy, so that it can be used as a reference for further research.

Necrobiosis lipoidica (NL) is a rare granulomatous disease of a not fully understood etiopathogenesis. Classically, NL is associated with insulin-dependent diabetes mellitus. The disease often fails to respond to conventional treatments and adversely affects patients' quality of life. First-line medications are usually topical corticosteroids, but patients respond to them with varying degrees of success. Other options include tacrolimus, phototherapy, cyclosporine, fumaric acid esters, and biologics (adalimumab, etanercept, and infliximab). Our review aims to present new therapeutic approaches potentially effective in patients with refractory lesions, describe the presumed etiopathogenesis, and provide diagnostic guidance for clinicians. The review concludes that Janus kinase inhibitors and biologics such as ustekinumab and secukinumab can be used effectively in patients with recalcitrant NL. Another promising treatment option is tapinarof (an aryl hydrocarbon receptor agonist). However, studies on larger groups of patients are still needed to evaluate the effectiveness of different therapeutic options and to define consistent treatment regimens for NL. It is advisable to improve the awareness of physicians of various specialties regarding necrobiosis lipoidica as lesions diagnosed earlier usually have a better response to treatment. [ABSTRACT FROM AUTHOR]

Background: The primary co-occurrence of gonadal and extragonadal central nervous system (CNS) germ cell tumors (GCTs) has rarely been reported in the literature, and a common opinion on the underlying etiopathogenetic mechanism is lacking. Objective: We aim to investigate the pathophysiological mechanisms and genetic pathways underlying the primary co-occurrence of gonadal and CNS GCTs. Methods: We reviewed data from 29 consecutive patients with a diagnosis of CNS GCT, evaluated in our Hospital over the past 23 years, and searched for those who had at least a primary gonadal co-occurrence of GCT. A systematic review of the literature according to the PRISMA guidelines was also conducted. For a comprehensive and detailed search, PubMed, Ovid MEDLINE, and Ovid EMBASE databases have been consulted. Boolean operators and MeSH terms were used to find studies. Only articles published between 2000 and 2023 were considered. Results: Including our Institutional case report, a total of 7 patients with both testicular NGGCTs and CNS GCTs were identified (5 patients with metachronous tumors and patients with synchronous presentation). The average age at tumor diagnosis was 17 years. The cerebral histotypes reported were mixed GCTs (3 cases; 43%), pure germinomas (3 cases, 43%), and one yolk sac tumor (14%). Two out of seven cases (29%) were syndromic, one suffering from Down Syndrome and the other from Testicular Dysgenesis Syndrome. Regarding the etiology and molecular mechanism of GCT development, several gene mutations have been reported in the literature. Particularly, genetic alterations in the MAPK and/or PI3K/AKT/mTOR pathway, together with mutations of the KIT gene, have been shown to guarantee survival and transformation of mismigrated totipotent primordial germ cells, while suppressor genes allow their resistance against apoptotic death. Aberrant chromosomes have also been reported to be responsible for oncogenic transformation. It is also known that CNS and testicular GCTs share some genetic/epigenetic profiles. Conclusions: The primary co-occurrence of testicular NGGCT and extragonadal CNS GCTs is extremely rare. Genetic factors seem to play a paramount role in their etiopathogenesis. Additional research is needed to elucidate molecular mechanisms of oncogenesis in such patients. [ABSTRACT FROM AUTHOR]

Background: Degeneration of the intervertebral disc (IVD), resulting from various factors, including genetic and environmental causes, is a significant musculoskeletal disorder. It is characterized by a gradual deterioration of the structure and a weakening in the function of the IVD, leading to a decline in the quality of life (QOL) or disability. Aim of the study: This study aimed to perform a review of scientific reports and a summary of the current knowledge regarding IVD degeneration in terms of etiopathogenesis, clinical symptoms, and various diagnostic methods. Materials and methods: The literature review was performed by searching key medical databases such as pubmed, MEDLINE, and Scopus. A search strategy was defined, encompassing keywords, synonyms, and controlled keywords (MeSH terms). The search included the last 20 years and focused on aspects of etiopathogenesis, clinical symptoms, and diagnostic methods. papers meeting the inclusion criteria underwent a full-text analysis. Data and information gathered from the literature analysis were synthesized to provide a comprehensive overview of the current state of knowledge on the researched subject. Results: The process of IVD degeneration is extremely complex, involving biochemical, metabolic, and morphological changes that impact its structure and function. It entails a gradual loss of water in the nucleus pulposus (dehydration), resulting in an impaired shock-absorbing function and leading to the formation of breaks in the annulus fibrosus, allowing herniation of the nucleus pulposus. for years, mechanical injuries, especially work-related injuries, have been considered the primary factors causing IVD degeneration. Recent findings emphasize the significant role of genetic factors, with the identification of several genes encoding structural proteins of the IVD. mutations in these genes may accelerate degeneration. Current clinical research results indicate a correlation between aortic calcifications and episodes of low back pain (LBP) and between lumbar artery stenosis, IVD degeneration, and subsequent LBP. Conclusions: understanding the complexity of IVD degeneration and its neurological consequences is crucial in planning effective treatment. It is essential to monitor the latest research to systematically update the etioknowledge and practical guidelines in the discussed area. Collaboration between an experienced neurosurgeon and an interdisciplinary team of medical specialists can achieve the best therapeutic outcomes. [ABSTRACT FROM AUTHOR]

Fibromyalgia (FM) is a highly prevalent chronic disease. About 4.7% of the world's population suffers from generalized pain and hypersensitivity, in addition to a wide range of physical and psychological symptoms. The etiopathogenesis of this disease is multifactorial, which makes its diagnosis and treatment challenging. Recently, the increase in the number of studies on microbiota has provided new data that can help to understand the onset and development of FM. An updated systematic review of the causes of FM has been carried out in this work. Particularly in the last decade, research has focused on the gut–brain axis, which has emerged as a crucial mechanism for microbiota‐host crosstalk. In FM patients, quantitative imbalances of the intestinal microbiota (dysbiosis) and bacterial metabolites with differential relative abundance have been found, especially short‐chain fatty acids and lipopolysaccharides. Furthermore, the microbiota has been found to indirectly influence host neurotransmitter mechanisms, mainly through the serotonin precursor, glutamate, and gamma‐aminobutyric acid. Thus, all these mechanisms and their influence on the etiopathogenesis of FM are discussed in this review. [ABSTRACT FROM AUTHOR]

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Abstract Objective: To compare Transforming growth factor beta-1 (TGF-β1) expression in patients with and without adenomyosis. Methods: A prospective design was performed including 49 patients submitted to hysterectomy. Immunohistochemistry was performed on anatomopathological samples staged in paraffin blocks from patients with and without adenomyosis. The sample contained 28 adenomyosis cases and 21 controls. Student's t-test and multivariate logistic regression tests were used for statistical analysis. Associations were considered significant at p < 0.05. Results: We found no significant association between adenomyosis and: smoking (p = 0.75), miscarriage (p = 0.29), number of previous pregnancies (p = 0.85), curettage (p = 0.81), pelvic pain (p = 0.72) and myoma (p = 0.15). However, we did find a relationship between adenomyosis and abnormal uterine bleeding (AUB) (p = 0.02) and previous cesarean section (p = 0.02). The mean TGF-β1 intensity (mean ± SD) in the ectopic endometrium of women with adenomyosis showed no significant association (184.17 ± 9.4 vs.184.66 ± 16.08, p = 0.86) from the topic endometrium of women without adenomyosis. Conclusion: TGF-β1 expression was not increased in the ectopic endometrium of women with adenomyosis.

Objective: The stroke-associated pneumonia (SAP) is considered an important risk factor for death following a stroke. It is important for clinicians to be able to recognize the causes of its occurrence, characteristic clinical and radiological signs and to be aware of treatment and prophylaxis in the early post-stroke period. This review article is devoted to the analysis and presentation of modern data on etiopathogenesis, modern strategies for early diagnosis and management of patients with stroke-associated pneumonia in the early post-stroke period. Design: Review of observational studies. Methods: We used following databases: PubMed, Web of Science, Scopus for the period of time 2019-2023 for studies search. Data from selected studies were extracted, including study design, data source, outcome definition, sample size, etiopathogenesis, diagnostic criteria and treatment strategies for stroke-associated pneumonia. Results: Totally 354 studies were reviewed, and after the selection process, 37 studies were included in this article. The incidence of stroke-associated pneumonia in patients with acute stroke ranged from 6.7 % to 37.98 %. Despite the abovementioned practical statements, there is currently no «gold standard» or generally accepted criteria for the diagnosis and treatment of SAP. As a rationale, detection of patients with the highest risk of SAP facilitates both prevention and treatment. The highest risks are associated with the age over 65, brain stem infarction with dysphagia, decreased throat and cough reflexes, impaired consciousness. Conclusion: The identification of high-risk patients requires knowledge of the modern criteria for diagnosing SAP. Since most SAP consists of aspiration pneumonia, hospital-acquired pneumonia, healthcare-associated pneumonia, pneumonia caused by artificial ventilation, partial diagnosis, treatment, rehabilitation, are related to the provision of medical care.

Due to the fact that arthrosis is a disease that affects a very large number of people, we felt that presenting some aspects of its pathophysiology and kinetoprophylaxis will be helpful to those working in the field of recovery and beyond. The literature also describes a rather complex clinical picture regarding the processes of degradation and deconditioning of the anatomical joint structures.The presentation of the factors of etiopathogenesis of gonarthrosis and the kinetoprophylactic means of preserving the function of the knee joint is the subject of the study that is intended to be presented. Analysis of the etiopathogenic factors and combating the effects of arthrosis installation through a model of analytical investigation of them, the results obtained from the analysis can be the basis for the realization of a kinetoprophylaxis program.

Venous trophic ulcers are one of the most common in the population, and costly in terms of treatment costs for complications of chronic venous insufficiency. The prevalence of venous trophic ulcers ranges from 0.18 to 1%. Over the age of 65 it increases to 4%. The cause of the formation of venous trophic ulcers is chronic diseases of the veins of the lower extremities. Chronic disease of the veins is a term that includes a wide range of morphological and functional disorders affecting the venous system. At the same time, even after conservative treatment, the level of recurrence of venous trophic ulcers remains extremely high, which leads to an increase in the duration of treatment for patients in the hospital, in some cases causing permanent disability in patients of working age. The literature has accumulated a huge volume of both fundamental and clinical research on the etiology, pathogenesis, diagnosis and treatment of venous ulcers. However, despite the numerous studies, the number of patients with this disease continues to steadily increase, and a number of important aspects of the pathogenesis have not yet been studied. In addition, these works do not allow us to formulate a unified concept of the pathogenesis of venous ulcers, which in turn affects the effectiveness of treatment of venous trophic ulcers. Our study highlights modern aspects of the pathogenesis of venous trophic ulcers, which may be of key importance in the treatment of this pathology. Promising directions of scientific research in this area are determined. This requires a more in-depth study of aspects of intercellular interactions, and also opens up the prospect of searching for new methods of influencing the pathogenesis of venous trophic ulcers, taking into account the presence of microflora resistant to standard antibacterial agents.

Abstract Background Myalgic encephalitis/chronic fatigue syndrome (ME/CFS) is a long-term disabling illness without a medically explained cause. Recently during COVID-19 pandemic, many studies have confirmed the symptoms similar to ME/CFS in the recovered individuals. To investigate the virus-related etiopathogenesis of ME/CFS, we conducted a systematic assessment of viral infection frequency in ME/CFS patients. Methods We conducted a comprehensive search of PubMed and the Cochrane Library from their inception through December 31, 2022, using selection criteria of viral infection prevalence in ME/CFS patients and controls. Subsequently, we performed a meta-analysis to assess the extent of viral infections' contribution to ME/CFS by comparing the odds ratio between ME/CFS patients and controls (healthy and/or diseased). Results Finally, 64 studies met our eligibility criteria regarding 18 species of viruses, including a total of 4971 ME/CFS patients and 9221 control subjects. The participants included healthy subjects and individuals with one of 10 diseases, such as multiple sclerosis or fibromyalgia. Two DNA viruses (human herpes virus (HHV)-7 and parvovirus B19, including their co-infection) and 3 RNA viruses (borna disease virus (BDV), enterovirus and coxsackie B virus) showed odds ratios greater than 2.0 compared with healthy and/or diseased subjects. Specifically, BDV exceeded the cutoff with an odds ratio of ≥ 3.47 (indicating a "moderate association" by Cohen’s d test) compared to both healthy and diseased controls. Conclusion This study comprehensively evaluated the risk of viral infections associated with ME/CFS, and identified BDV. These results provide valuable reference data for future studies investigating the role of viruses in the causation of ME/CFS.

Rheumatoid arthritis (RA) is a chronic, autoimmune rheumatic disease characterized by synovial joint inflammation with subsequent destruction as well as systemic manifestation, leading to impaired mobility and impaired quality of life. The etiopathogenesis of RA is still unknown, with genetic, epigenetic and environmental factors (incl. tobacco smoking) contributing to disease susceptibility. The link between genetic factors like “shared epitope alleles” and the development of RA is well known. However, why only some carriers have a break in self-tolerance and develop autoimmunity still needs to be clarified. The presence of autoantibodies in patients’ serum months to years prior to the onset of clinical manifestations of RA has moved the focus to possible epigenetic factors, including environmental triggers that could contribute to the initiation and perpetuation of the inflammatory reaction in RA. Over the past several years, the role of microorganisms at mucosal sites (i.e., microbiome) has emerged as an essential mediator of inflammation in RA. An increasing number of studies have revealed the microbial role in the immunopathogenesis of autoimmune rheumatic diseases. Interaction between the host immune system and microbiota initiates loss of immunological tolerance and autoimmunity. The alteration in microbiome composition, the so-called dysbiosis, is associated with an increasing number of diseases. Immune dysfunction caused by dysbiosis triggers and sustains chronic inflammation. This review aims to provide a critical summary of the literature findings related to the hypothesis of a reciprocal relation between the microbiome and the immune system. Available data from studies reveal the pivotal role of the microbiome in RA pathogenesis.

Copyright of Pediatrie pro Praxi is the property of SOLEN sro and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Urologie Pro Praxi is the property of SOLEN sro and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Myalgic encephalitis/chronic fatigue syndrome (ME/CFS) is a long-term disabling illness without a medically explained cause. Recently during COVID-19 pandemic, many studies have confirmed the symptoms similar to ME/CFS in the recovered individuals. To investigate the virus-related etiopathogenesis of ME/CFS, we conducted a systematic assessment of viral infection frequency in ME/CFS patients. Methods: We conducted a comprehensive search of PubMed and the Cochrane Library from their inception through December 31, 2022, using selection criteria of viral infection prevalence in ME/CFS patients and controls. Subsequently, we performed a meta-analysis to assess the extent of viral infections' contribution to ME/CFS by comparing the odds ratio between ME/CFS patients and controls (healthy and/or diseased). Results: Finally, 64 studies met our eligibility criteria regarding 18 species of viruses, including a total of 4971 ME/CFS patients and 9221 control subjects. The participants included healthy subjects and individuals with one of 10 diseases, such as multiple sclerosis or fibromyalgia. Two DNA viruses (human herpes virus (HHV)-7 and parvovirus B19, including their co-infection) and 3 RNA viruses (borna disease virus (BDV), enterovirus and coxsackie B virus) showed odds ratios greater than 2.0 compared with healthy and/or diseased subjects. Specifically, BDV exceeded the cutoff with an odds ratio of ≥ 3.47 (indicating a "moderate association" by Cohen's d test) compared to both healthy and diseased controls. Conclusion: This study comprehensively evaluated the risk of viral infections associated with ME/CFS, and identified BDV. These results provide valuable reference data for future studies investigating the role of viruses in the causation of ME/CFS. [ABSTRACT FROM AUTHOR]

Objective To characterize the demographic and the cutaneous features of pyoderma gangrenosum in large series of patients. Methods This is a case series cross sectional descriptive study with therapeutic trial where 53 patients with pyoderma gangrenosum were seen during the period from September 2013-January 2023.All patients were fully investigated and diagnosed as cases of pyoderma gangrenosum. Still full history and examination were carried out to characterize the clinical pictures. All patients were fully investigated to exclude any associated disease in doubtful diagnosis. Skin biopsy was performed when needed as exclusive measure. Triple therapeutic trial was tried using oral azathioprine, oral dapsone and oral prednisolone. Results Fifty-three patients were included, their ages ranged from 10-60 years with a mean 45 years, with 39 (73.58%) males and 14 (26.41%) females with ratio 2.78:1. The duration of lesions ranged from 4-12 weeks. The location of these lesions was mostly lower limbs in 31(58.49%) cases. For the rest of the cases, lesions appeared on the trunk including the groin and neck in 14 (26.41%), breast of the female in 3 (5.66%) cases, upper limbs in 2 (3.77%) cases, male genitalia in 2 (3.77%) cases and face in one (1.88%) case. The lesions were single in 36 (67.9.21%) patients while multiple in 17 (32%) cases. The rash had mostly painful ulcerative yellowish surface with undermined edges. The ulcerative subtype was the most frequently recorded in 48 (90.56%) patients. No associated underlying triggering pathologies were noticed during follow up except in seven (13.2%) patients. The therapeutic response was noticed after two weeks but complete clearance of ulcers took several weeks to months according to the size of ulceration. Conclusion This study showed that pyoderma gangrenosum is a disease of middle-aged males with no well-defined etiological triggering factors except in 13.2% of cases that have been associated with miscellaneous underlying diseases. Accordingly, the etiopathogenesis of pyoderma gangrenosum remains idiopathic, still long follow up might discover many other concealed etiologies. Effective triple therapy was tried and proved its effectiveness. [ABSTRACT FROM AUTHOR]

Oral squamous cell carcinoma (OSCC) is an extremely rare occurrence during pregnancy. OSCC accounts for less than 2% of all malignancies in pregnant women, with an average mortality rate of 36%. Understanding the features of this tumor during pregnancy is important; however, the paucity of reports in the literature makes this challenging. Case presentation: The following is a case presentation of a woman who was diagnosed with SCC of the tongue (TSCC) at 13 weeks gestation. The article also provides a review of the literature of TSCC affecting pregnant women aged 30 years and under. Conclusion: Although OSCC in young women of reproductive age is rare, recent literature suggests an increased risk for this age group. The rarity of OSCC in pregnancy may potentially lead to low clinical index of suspicion, misdiagnosis, and delay in treatment. Additionally, treatment modalities, prognosis, and the long-term impact on the developing fetus are not well established, due to rarity of OSCC in pregnancy. Further studies to identify specific etiologic factors are needed to establish the association of OSCC with pregnancy, aid in prevention, and improve treatment and outcome. [ABSTRACT FROM AUTHOR]

Background. The most frequent female reproductive system tumors are uterine leiomyoma (UL). They are benign monoclonal tumors of uterine smooth muscle. They affect reproductive-age women with a lifetime prevalence of 3070%. UL is a disease with complex etiology determined by many genetic and environmental factors. Despite the frequency of UL, there is no long-term, cost-effective or fertility-preserving therapy option for it. Aim. To summarize the available literature data on the etiopathogenesis of uterine fibroids as well as the risk factors for the development of this disease. Materials and methods. The PubMed, Scopus, and Web of science literature databases were searched for relevant articles using such keywords as uterine fibroids, UL, association, genetic and hormonal factors, gene, etiology in various combinations. Results. Genetic disorders and hormonal and growth factors all have a part in the etiology of UL, and studies have resulted to the use of hormone therapy for fibroids, with varying results. Recent findings on the etiopathogenesis of UL, as well as the introduction of relevant genetically modified mouse models of UL, have rekindled interest in the disease. In this review, the basic features of fibroids are discussed, as well as the primary contributors to UL etiopathogenesis, including as genetic, hormonal, and growth causes. Besides the risk factors that contribute to the development of UL. Conclusion. Many questions about the causes and mechanisms of development factors that predispose remain unanswered, necessitating the continuation of these studies in order to obtain new information. Prospective studies are needed to better understand the biology and epidemiological associations, both to better understand modifiable risk factors and to shed light on the etiopathogenesis of this disease.

Several cases reported in the literature have confirmed the link between pulmonary aspergillosis and various malignant diseases. Furthermore, it has been observed that the correlation between carcinoid tumor and lung adenocarcinoma is quite uncommon. The etiopathogenic mechanisms underlying these correlations remain poorly defined. We present the case of a patient with three of these diseases: a lung adenocarcinoma with a lepidic pattern, a typical carcinoid, and pulmonary aspergillosis. An additional noteworthy aspect of this case pertains to the timely detection of both lung malignancies. Thus, the necessity for further investigation to ascertain the pathogenic connection among the three diseases is underscored. The ultimate objective is to enhance the prognosis of individuals diagnosed with lung cancer, which is a prevailing malignant disease on a global scale.

Pemphigus is a life-threatening autoimmune blistering disease affecting skin and mucous membranes. Despite its etiopathogenesis remains largely unknown, several trigger and predisposing factors have been reported. Pemphigus is caused by autoantibodies that target desmoglein 1 and desmoglein 3, impacting desmosome function. However, circulating autoantibodies are often the consequence of a precipitating factor that occurs in predisposed individuals. This review aims to describe and discuss almost all trigger and predisposing factors reported as possible or probable cause of the disease. Among the reported trigger factors that may induce or exacerbate pemphigus, we have found of particular interest: drug intake (especially thiol- and phenol-containing compounds), vaccines, infections, as well as some reports about pregnancy, radiations, emotional stress, pesticides and physical trauma. Moreover, we discuss the possible role of food intake in pemphigus onset and particular attention is given to dietary factors containing thiol, phenol and tannin compounds. A trigger factor is “the straw that breaks the camel’s back,” and often acts together with predisposing factors. Here we discuss how pemphigus onset may be influenced by genetic susceptibility and comorbidities like thyroid diseases, malignancies and other autoimmune disorders.To identify other hitherto unknown trigger and predisposing factors, well designed prospective studies are needed. In this context, future research should explore their connection with the aim to advance our understanding of pemphigus pathogenesis.

ABSTRACTMounting evidence suggests that acute appendicitis (AA) is not one but two diseases: complicated appendicitis, which is associated with necrosis leading to perforation or periappendicular abscess, and uncomplicated appendicitis, which does not necessarily result in perforation. Even though AA is the most frequent cause of surgery from abdominal pain, little is known about the origins and etiopathogenesis of this disease, much less regarding the different disease types. In this study, we investigated the microbiome (inter-domain amplicon and metagenome sequencing) of samples from the appendix, rectum and peritoneum of 60 children and adolescents with AA to assess the composition and potential function of bacteria, archaea and fungi. The analysis of the appendix microbial community revealed a shift depending on the severity of the AA. This shift was reflected by two major community state types that represented the complicated and uncomplicated cases. We could demonstrate that complicated, but not uncomplicated, appendicitis is associated with a significant local expansion of oral, bacterial pathogens in the appendix, most strongly influenced by necrotizing Fusobacterium spp., Porphyromonas and Parvimonas. Uncomplicated appendicitis, however, was characterized by gut-associated microbiomes. Our findings support the hypothesis that two disease types exist in AA, which cannot be distinguished beyond doubt using standard clinical characterization methods or by analysis of the patient’s rectal microbiome. An advanced microbiome diagnosis, however, could improve non-surgical treatment of uncomplicated AA.

Neurology as a separate branch of clinical medicine was not yet formed in Europe in the early 19th century. However, in the medical writings of the Vilnius University (VU) authors of that time, the brain was already called the “noblest organ of the human body”, the seat of the soul, the centre of external senses, and the primary beginning of all bodily movements. The aim of the present study is to reveal various etiopathogenic theories of diseases of the nervous system (NS) in Vilnius region, since this knowledge may indicate that there were some beginnings of clinical neurology in the early 19th century in Vilnius. First, we analysed old doctoral dissertations on NS diseases defended at VU in 1803-1832; we then turned to Consessus Caesareae Societatis Medicae Vilnensis (The Protocols of Vilnius Medical Society) and analysed clinical reports recorded in 1806-1842. Our study revealed that although humoralism was the most popular system of medicine, the main causes of NS diseases were believed to be in the solid parts of the human body (influence of solidism theory). It was also assumed that some NS diseases may be inherited or caused by fetal diseases in utero. On the other hand, one of the oldest theories, imaginatio gravidarum, was still prevalent in Vilnius at the time. It was also stated that some NS diseases may be triggered by physical and mechanical causes, concomitant diseases, medications and drinks, strong emotions, or violation of sleep hygiene. “Inflammatory agents” were reported to cause traumatic tetanus as inflammation spread upwards from the nerve endings, tendons, and ligaments to the brain. The authors also described the theory of “poison, specifically acting on the NS” that was transmitted by a rabid animal to a bitten patient. To describe the etiopathogenesis of spinal cord diseases, the concept of “diminishing vital spirits through the loss of bodily matter” was used (it was claimed, e.g., that excessive number of sexual intercourses dried out the spinal cord). In addition, the astrological causes of NS diseases were also believed to be of great importance (“somnambulism, insanity, and epilepsy exacerbate when the moonlight shines”). Finally, cutting off the Polish plait (plica polonica) was considered to be an essential etiological factor of various NS diseases in Vilnius in the early 19th century.

Copyright of Medicina (Buenos Aires) is the property of Medicina (Buenos Aires) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Lung cancer is a serious health concern that is associated with a poor prognosis and low survival rate. It is widely recognized as one of the most common types of cancer, particularly among individuals in their third decade of life. Given the high incidence and severity of this disease, extensive research has been conducted in an effort to improve patient outcomes. The current study used a systematic approach to identify relevant studies, utilizing biomedical bibliographic databases as the primary sources of information. A thorough search was conducted, and 58 publications were initially identified. After a rigorous screening process, 25 of these studies were selected for further analysis. The chosen studies represent a diverse range of research on lung cancer, including investigations into epidemiology, pathogenesis, diagnosis, and treatment. The results of these studies provide a comprehensive overview of the current state of knowledge regarding lung cancer, and highlight key areas that require further investigation. This study underscores the need for continued research into the prevention and treatment of lung cancer, in order to improve the outcomes for patients and reduce the burden of this disease on society. The findings of this study can be used to guide future research efforts, and inform clinical practice, in order to help improve patient outcomes and reduce the impact of lung cancer. Goals: To describe and study certain aspects of lung cancer, focusing on its epidemiology, etiology, and lymph node staging. Improvement: It was updated with new categories of tumor components (T) and metastases (M), as well as the advent of new stages, but did not change the lymph node component (N) in its eighth version, which was released in 2016; Despite this, patients with non-small cell lung cancer should consider the prognostic and therapeutic implications of the assessment of the mediastina lymph node (pN)(Lopez et al., 2022). Conclusions: TNM staging is crucial in determining prognosis and therapeutic decisions because non-small cell lung cancer is the most prevalent and deadly cancer globally, affecting an elderly population. Environmental, genetic, and molecular factors are thought to play a role in its development. Affection is correctly identified. The lymph node is essential since it will decide the prognosis even if there are no metastases. With the advancement of modern science, the process used to construct the various TNM editions is continually changing. [ABSTRACT FROM AUTHOR]

In this contribution, the author explores the shift from viewing psychological issues as 'psychic pathology' to adopting a perspective of 'pathological psychology'. This transition underscores the need to consider the intricate interplay between individual and environmental factors in the development of psychological disorders. The author emphasizes the importance of understanding mental illness as a result of complex interactions and disruptions in equilibrium. Alongside neurobiological influences, life experiences and the environment also wield a pivotal role. A clinical case of a four-session-a week psychoanalysis illustrates the significance of the environment. This case highlights how the interplay between internal and relational-environmental factors is crucial not only in understanding symptoms but also in the interpretive process. [ABSTRACT FROM AUTHOR]

Background: Rapid hair loss is caused by the chronic inflammatory disorder alopecia areata, which destroys the hair follicle. It often affects the scalp, though it can also affect other hairy areas like the beard or eyebrow. There are numerous clinical types, including patchy, alopecia totalis, alopecia universalis, and ophiasis. It may be caused by genetic, immunological, endocrine, or psychological factors. Objective: Review of literature about Alopecia Areata etiopathogenesis, diagnosis and management. Methods: We searched Science Direct, Google Scholar as well as PubMed for relevant articles on Alopecia Areata as well as etiopathogenesis. However, only the most recent or thorough study was taken into account between October 2003 and January 2023. The authors also evaluated the value of resources culled from other works in the same genre. Documents written in languages other than English have been ignored due to a lack of translation funds. Unpublished works, oral presentations, conference abstracts, and dissertations were generally agreed upon not to qualify as scientific research. Conclusion: The primary effectors in the pathophysiology of alopecia areata condition are CD8 cytotoxic T cells. Additionally, Janus kinase (JAK) signaling pathways are upregulated. JAK inhibitors are utilized to block the signaling pathway downstream and novel therapeutic strategies that have been developed. The most prevalent place for sudden onset hair loss in alopecia areata is the scalp, and it most commonly affects adults. The absence of scales, erythema, or the exclamation marks that are pathognomonic for alopecia areata indicate that the skin is entirely healthy. Hair pull tests are often negative, with the exception of early active lesions near the periphery, which indicate disease activity and development. [ABSTRACT FROM AUTHOR]