A STUDY OF THE SORPTION CAPACITY OF LECITHIN MODIFIED NATURAL SORBENT RELATIVE TO NATIVE PROTEIN

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Neurofibromas in otorhinolaryngology. Literature review presentation of a rare clinical case of intramastoid solitary neurofibroma

Neurofibromas are precancerous neoplasms originating from the sheaths of peripheral nerves with a slow growth rate. A large proportion of cases (90%) are solitary tumors, while the rest (10%) are associated with the manifestation of neurofibromatosis type 1 (Morbus Recklinghausen) - an autosomal dominant genetic inherited disease. This type of tumor is relatively rare in the head and neck region. It involves mainly the skin and subcutaneous tissue of the trunkus, and represents about 5% of all benign soft tissue neoplasms. In the available english articles 22 cases of intratemporal solitary neurofibroma have been reported of which only 2 were intramastoid. We present a rare clinical case of a solitary intramastoid neurofibroma in a 39-year-old woman mimicking the clinical representation of latent mastoiditis with a brief literature review

Historical development of methods for diagnosis and treatment of OSA

Obstructive sleep apnea (OSA) has been known to mankind since ancient times. Medical  documents from 2000 years ago that have been found contain information describing severe snoring (apnea) characteristic of OSA. In order to obtain the information targeted research was carried out in the Scientific databases PubMed, Scopus, ScienceDirect, Web of Science. „History of OSA”, „CPAP”, „Polysomnography” keywords were used in for the search.The aim of this article is to present the historical development of methods for diagnosis and treatment of OSA. In 1981 Sullivan et al. published in the Lancet scientific paper on Obstructive Sleep Apnea “ Reversal of obstructive sleep apnea by continuous airway pressure applied through the nares “ . At the end of the XIX th century, the term “Pickwickian syndrome” was introduced in the medical literature. In 1965, the polysomnographic unit was created and for the first time, with the help of electronic device, sleep apnea was registered in patients. Eventually ambulatory sleep testing was introduced as an alternative to polysomnography. Apnea Graph is a new innovative ambulatory sleep analysis tool that identifies the location of snoring obstruction and OSA. It also determines the type of OSA. In 1981, the first CPAP for treatment OSA was created. Sullivan’s findings prove that CPAP is a very effective device for treating OSA

Artificial intelligence – the new suggestion for biomedicine, dentistry and healthcare

The development of technologies based on Artificial Intelligence (AI) and their application in medicine is growing rapidly. Innovations in digital technology, telemedicine, 5G technology and artificial intelligence (AI) create new opportunities for the development of the healthcare system. The aim of the present study is to explore the possibilities for the application of artificial intelligence in biomedicine, dentistry, healthcare and healthcare. In recent years there have been many major innovations, including the introduction of many new information and communication technologies. Digital innovations, including the further inclusion of telemedicine, the development of 5th generation wireless networks (5G) and artificial intelligence (AI) approaches, create an exceptional ecosystem for new health opportunities. The digital health sector creates a favorable environment for the provision of health services at a very high level

Age as a factor for cognitive decline in patients with glial tumors

Introduction: Cognitive impairment appears in almost all patients with glial tumors during the course of this neuro-oncological disease. There are various reasons for this in regards to the glial tumor: grade of malignancy, rate of growth, molecular nature, mass effect, and presence of perifocal edema. But these factors do not always correlate with the degree of patient’s cognitive impairment. The present study’s aim is to account for age as a factor in the occurrence of cognitive decline in patients with glial tumors.Materials and methods: The study includes thirty two patients diagnosed with a glial tumor, treated operatively in the Neurosurgery Clinic of University hospital „St. Marina“ in Varna between 2019 and 2022 year. Twenty nine of those patients are diagnosed with glioblastoma, two are diagnosed with diffuse astrocytoma and one with astrocytoma grade 3 according to WHO. The mean age of the patients is 58.4 ± 11.4 years. The youngest patient is 25 years old and the oldest is 78 years old. Preoperatively, all patients are subjected to a series of cognitive tests.Results: From the studied sample, patients diagnosed with glioblastoma showed lower cognitive scores compared to the patients diagnosed with other glial tumors. Patients diagnosed with glioblastoma are significantly older than the patients diagnosed with other glial tumors.Conclusion: The older age of patients affected by glioblastoma may be an additional reason beside tumor factors for lower cognitive test outcome compared to patients affected by lower-grade gliomas

Methods of cognitive status research in patients with glioblastoma

Introduction: Glioblastoma is a high-grade, aggressive central nervous system tumor with predominantly astrocytic differentiation, characterized by fast invasive growth into the surrounding brain parenchyma and aggressive clinical course. The short life expectancy of patients diagnosed with glioblastoma necessitates the need to maximize their quality of remaining life. One of the most common reasons for quality of life impairment in these patients is the cognitive deficit accompanying the disease. There is a lack of a unified and standardized method for the assessment of cognitive functions in these patients, which meets all the necessary criteria to be convenient and usable in the wide clinical practice.Aim: The aim of the present study is to compare the Montreal cognitive assessment (MoCA) brief screening test with an extended neuropsychological examination to determine its applicability in patients diagnosed with glioblastoma. Material and methods: The study includes 27 patients undergoing neurosurgical intervention for histologically proven IDH-wildtype glioblastoma in the Department of Neurosurgery, “St. Marina” University Hospital – a tertiary healthcare center, for the period January 2019 to December 2022. Preoperatively, patients were examined with the short MoCA screening test and an extended neuropsychological examination including the following subtests: Issac set test, Trail making test A and B, Luria test, Raven‘s color matrices, Stroop test and Bender test.Results: Of all the patients studied, those with a MoCA score below 26 points present at least one negative test of the extended neuropsychological examination. MoCA patients with scores of 26 or more do not demonstrate cognitive impairment in the extended neuropsychological impairment.Conclusion: The obtained results support the claim that the MoCA short screening test is applicable for preoperative diagnosis of cognitive disorders in patients with glioblastoma. Due to the study‘s small sample size, further research is needed to definitively prove this claim

Historical origin and meaning of the term „glial tumor“

In everyday neurosurgical practice, the term „glial tumor“ is associated with astrocytomas, glioblastomas, and oligodendrogliomas, although historically this has not always been the case. The term „glial tumor“ was first given by Virchow in the 19th century as a term initially combining all primary brain tumors under this name. It derives from the name of the group of „supporting“ nerve cells - glia or neuroglia (from the Greek glia - glue), a group which for many years was wrongly ascribed only a cohesive or supporting function.In 1926, in their classification of glial tumors - A Classification of the Tumors of the Glioma Group on a Histogenetic Basis with a Correlated Study of Prognosis, one of the founding fathers of neuropathology Percival Bailey and the founding father of modern neurosurgery – Harvey Cushing ascribed several different tumors in this group: in addition to neuroepithelioma, spongioblastoma multiforme, astrocytoma and ependymoma, they also add medulloblastoma, astroblastoma, oligodendroglioma and unipolar spongioblastoma. Since then, the classification of glial tumors has undergone many changes to its current form. In the latest classification of brain tumors published in 2021, glial tumors are united in a common group together with glioneuronal and neuronal tumors. Their extensive group includes tumors with different prognosis, age presentation, molecular profile and therapeutic response. From a neurosurgical point of view, the term „glial tumor“ does not carry a prognostic value, but only determines the belonging of the tumor to the astrocyte, oligodendrocyte cell line or their precursor cells. In relation to that an interesting question arises- why the remaining tumors originating from glial cells other than astrocytic, such as ependymomas, lost their belonging to the group of glial tumors, or such as intracranial schwannomas, are not included in it at all

Characterisation of the Cullin-3 mutation that causes a severe form of familial hypertension and hyperkalaemia

Deletion of exon 9 from Cullin‐3 (CUL3, residues 403–459: CUL3Δ403–459) causes pseudohypoaldosteronism type IIE (PHA2E), a severe form of familial hyperkalaemia and hypertension (FHHt). CUL3 binds the RING protein RBX1 and various substrate adaptors to form Cullin‐RING‐ubiquitin‐ligase complexes. Bound to KLHL3, CUL3‐RBX1 ubiquitylates WNK kinases, promoting their ubiquitin‐mediated proteasomal degradation. Since WNK kinases activate Na/Cl co‐transporters to promote salt retention, CUL3 regulates blood pressure. Mutations in both KLHL3 and WNK kinases cause PHA2 by disrupting Cullin‐RING‐ligase formation. We report here that the PHA2E mutant, CUL3Δ403–459, is severely compromised in its ability to ubiquitylate WNKs, possibly due to altered structural flexibility. Instead, CUL3Δ403–459 auto‐ubiquitylates and loses interaction with two important Cullin regulators: the COP9‐signalosome and CAND1. A novel knock‐in mouse model of CUL3WT/Δ403–459 closely recapitulates the human PHA2E phenotype. These mice also show changes in the arterial pulse waveform, suggesting a vascular contribution to their hypertension not reported in previous FHHt models. These findings may explain the severity of the FHHt phenotype caused by CUL3 mutations compared to those reported in KLHL3 or WNK kinases

A mechanism for the suppression of homologous recombination in G1 cells

DNA repair by homologous recombination (HR)(1) is highly suppressed in G1 cells(2,3) to ensure that mitotic recombination occurs solely between sister chromatids(4). Although many HR factors are cell cycle-regulated, the identity of the events that are both necessary and sufficient to suppress recombination in G1 cells is unknown. Here we report that the cell cycle controls the interaction of BRCA1 with PALB2-BRCA2 in order to constrain BRCA2 function to the S/G2 phases. We found that the BRCA1-interaction site on PALB2 is targeted by an E3 ubiquitin ligase composed of KEAP1, a PALB2-interacting protein(5), in complex with CUL3-RBX1(6). PALB2 ubiquitylation suppresses its interaction with BRCA1 and is counteracted by the deubiquitylase USP11, which is itself under cell cycle control. Restoration of the BRCA1-PALB2 interaction combined with the activation of DNA end resection is sufficient to induce HR in G1, as measured by RAD51 recruitment, unscheduled DNA synthesis and a CRISPR/Cas9-based gene targeting assay. We conclude that the mechanism prohibiting HR in G1 minimally consists of the suppression of DNA end resection coupled to a multi-step block to BRCA2 recruitment to DNA damage sites that involves the inhibition of BRCA1-PALB2-BRCA2 complex assembly. We speculate that the ability to induce HR in G1 cells with defined factors could spur the development of gene targeting applications in non-dividing cells

Giant intradiploic epidermoid cyst with large osteolytic lesions of the skull: a case report

<p>Abstract</p> <p>Introduction</p> <p>We report a case of tumor growth over a period of four decades, presenting with large multicentric lytic lesions of the skull and a profound mass effect, without neurological deficits. Clinical and radiological features of a patient with a giant intradiploic epidermoid and its impact on the choice of treatments are discussed.</p> <p>Case presentation</p> <p>An 81-year-old Caucasian man, who had first noticed a painless subcutaneous swelling over the left frontal scalp about 40 years ago, presented after a short episode of dizziness, which he experienced after treatment of focal retinal detachment. Computed tomography (CT) and magnetic resonance imaging (MRI) examinations revealed an exceptionally large tumor involving major parts of the skull with extensive destruction of the bone and distinct deformation of the brain. Considering his age and the absence of neurological deficits or pain, the patient refused the option of tumor removal and cranioplasty, yet agreed to a biopsy, which confirmed the suspected diagnosis.</p> <p>Conclusions</p> <p>The course of the disease demonstrates that even patients with large tumors, inducing distinct pathomorphological changes, do not necessarily experience significant impairment of their quality of life without surgery. This is an impressive example of the chance to lead a long and satisfying life without specific medical treatment, avoiding the inherent risks of these procedures. Yet, there is a clear indication for surgery of intradiploic epidermoids in most cases described in the literature.</p