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#DianaDevi #antiaging #lookyounger #argentinetangodancer #Nutrition&Movement #selfhypnosis #meditation #anagelesslife #DrKimberleyLinert #IncrediblelifecreatorDiana Devi helps you look 10 Years Younger! She works with successful professionals who lack confidence in their appearance. Looking older steals opportunities and money. Diana's clients look and feel rejuvenated, energized and younger. Diana combines her over 30 years experience in the medical field with her passion for dancing Argentine tango so that you reap the benefits as her client. Background : Clinical pharmacist for over 30 years Argentine Tango Dancer and Instructor for over 15 years ( pre-Covid of course) Studied nutrition, movement ( all types from dance to body re-education to remove blocks), self hypnosis and meditation. Contact Diana Devi: Website https://anagelesslife.comFacebook : https://www.facebook.com/anagelesslife/IG : https://www.instagram.com/anagelesslife/Linked In https://www.linkedin.com/in/diana-devi-a6111728/Youtube: https://www.youtube.com/channel/UC9RMEbTnK8ZltLQvhUpEsNQ Dr. Kimberley Linert Speaker, Author, Broadcaster, Mentor, Trainer, Behavioral Optometrist Event Planners- I am available to speak at your event. Here is my media kit: https://brucemerrinscelebrityspeakers.com/portfolio/dr-kimberley-linert/To book Dr. Linert on your podcast, television show, conference, corporate training or as an expert guest please email her at incrediblelifepodcast@gmail.com or Contact Bruce Merrin at Bruce Merrin's Celebrity Speakers at merrinpr@gmail.com 702.256.9199 Host of the Podcast Series: Incredible Life Creator Podcast Available on... Apple: https://podcasts.apple.com/us/podcast/incredible-life-creator-with-dr-kimberley-linert/id1472641267Spotify: https://open.spotify.com/show/6DZE3EoHfhgcmSkxY1CvKf?si=ebe71549e7474663 and on 9 other podcast platforms Author of Book: "Visualizing Happiness in Every Area of Your Life" Get on Amazon: https://amzn.to/3srh6tZ Website: https://www.DrKimberleyLinert.com incrediblelifepodcast@gmail.com Social Media Links LinkedIn: https://www.linkedin.com/in/dr-kimberley-linert-incredible-life-creator/Facebook: https://www.facebook.com/kimberley.linert/Instagram: https://www.instagram.com/drkimberleylinert/Twitter: https://twitter.com/LifeKimberleyTumblr: https://www.tumblr.com/settings/blog/incrediblelifecreatorPinterest: https://www.pinterest.com/lifekimberley/_saved/ Please subscribe, share & LISTEN! Thanks.

Background: Clinical trials evaluating anti-CD20-mediated B-cell depletion in multiple sclerosis (MS) and neuromyelitis optica (NMO) generated encouraging results. Our recent studies in the MS model experimental autoimmune encephalomyelitis (EAE) attributed clinical benefit to extinction of activated B-cells, but cautioned that depletion of naive B-cells may be undesirable. We elucidated the regulatory role of un-activated B-cells in EAE and investigated whether anti-CD20 may collaterally diminish regulatory B-cell properties in treatment of neuroimmunological disorders. Methods: Myelin oligodendrocyte glycoprotein (MOG) peptide-immunized C57Bl/6 mice were depleted of B-cells. Functional consequences for regulatory T-cells (Treg) and cytokine production of CD11b(+) antigen presenting cells (APC) were assessed. Peripheral blood mononuclear cells from 22 patients receiving anti-CD20 and 23 untreated neuroimmunological patients were evaluated for frequencies of B-cells, T-cells and monocytes; monocytic reactivity was determined by TNF-production and expression of signalling lymphocytic activation molecule (SLAM). Results: We observed that EAE-exacerbation upon depletion of un-activated B-cells closely correlated with an enhanced production of pro-inflammatory TNF by CD11b(+) APC. Paralleling this pre-clinical finding, anti-CD20 treatment of human neuroimmunological disorders increased the relative frequency of monocytes and accentuated pro-inflammatory monocyte function; when reactivated ex vivo, a higher frequency of monocytes from B-cell depleted patients produced TNF and expressed the activation marker SLAM. Conclusions: These data suggest that in neuroimmunological disorders, pro-inflammatory APC activity is controlled by a subset of B-cells which is eliminated concomitantly upon anti-CD20 treatment. While this observation does not conflict with the general concept of B-cell depletion in human autoimmunity, it implies that its safety and effectiveness may further advance by selectively targeting pathogenic B-cell function.

Background: Clinical presentation, diagnosis, management and outcome of molecularly defined congenital pulmonary alveolar proteinosis (PAP) due to mutations in the GM-CSF receptor are not well known. Case presentation: A 2 1/2 years old girl was diagnosed as having alveolar proteinosis. Whole lung lavages were performed with a new catheter balloon technique, feasible in small sized airways. Because of some interstitial inflammation in the lung biopsy and to further improve the condition, empirical therapy with systemic steroids and azathioprin, and inhaled and subcutaneous GMCSF, were used. Based on clinical measures, total protein and lipid recovered by whole lung lavages, all these treatments were without benefit. Conversely, severe respiratory viral infections and an invasive aspergillosis with aspergilloma formation occurred. Recently the novel homozygous stop mutation p.Ser25X of the GMCSF receptor alpha chain was identified in the patient. This mutation leads to a lack of functional GMCSF receptor and a reduced response to GMCSF stimulation of CD11b expression of mononuclear cells of the patient. Subsequently a very intense treatment with monthly lavages was initiated, resulting for the first time in complete resolution of partial respiratory insufficiency and a significant improvement of the overall somato-psychosocial condition of the child. Conclusions: The long term management from early childhood into young adolescence of severe alveolar proteinosis due to GMCSF receptor deficiency requires a dedicated specialized team to perform technically demanding whole lung lavages and cope with complications.

Background: Clinical subtypes of mild cognitive impairment (MCI) may represent different underlying aetiologies. Methods: This European, multicentre, memory clinic based study (DESCRIPA) of non-demented subjects investigated whether MCI subtypes have different brain correlates on MRI and whether the relation between subtypes and brain pathology is modified by age. Using visual rating scales, medial temporal lobe atrophy (MTA) (0–4) and white matter hyperintensities (WMH) (0–30) were assessed. Results: Severity of MTA differed between MCI subtypes (p,0.001), increasing from a mean of 0.8 (SD 0.7) in subjective complaints (n=77) to 1.3 (0.8) in nonamnestic MCI (n=93), and from 1.4 (0.9) in single domain amnestic MCI (n=70) to 1.7 (0.9) in multiple domain amnestic MCI (n=89). The association between MCI subtype and MTA was modified by age and mainly present in subjects .70 years of age. Severity of WMH did not differ between MCI subtypes (p=0.21). However, the combination of MTA and WMH differed between MCI subtypes (p=0.02) Conclusion: We conclude that MCI subtypes may have different brain substrates, especially in older subjects. Isolated MTA was mainly associated with amnestic MCI subtypes, suggesting AD as the underlying cause. In nonamnestic MCI, the relatively higher prevalence of MTA in combination with WMH may suggest a different pathophysiological origin.

Background: Clinical chemical blood analysis including plasma electrolytes is routinely carried out for the diagnosis of various organ diseases. Phenotype-driven N-ethyl-N-nitrosourea (ENU) mouse mutagenesis projects used plasma electrolytes as parameters for the generation of novel animal models for human diseases. Methods: Here, we retrospectively evaluated the use of the plasma electrolytes calcium, chloride, inorganic phosphorus, potassium and sodium in the Munich ENU mouse mutagenesis project where clinical chemical blood analysis was carried out on more than 20,000 G1 and G3 offspring of chemically mutagenized inbred C3H mice to detect dominant and recessive mutations leading to deviations in various plasma parameter levels. Results: We identified a small number of animals consistently exhibiting altered plasma electrolyte values. Transmission of the phenotypic deviations to the subsequent generations led to the successful establishment of mutant lines for the parameters calcium and potassium. Published data from other phenotype-driven ENU projects also included only a small number of mutant lines which were generated according to altered plasma electrolyte levels. Conclusion: Thus, use of plasma electrolytes detected few mouse mutants in ENU projects compared to other clinical chemical blood parameters.

Background: Clinical outcome of patients with head and neck squamous cell carcinoma (SCCHN) depends on several risk factors like the presence of locoregional lymph node or distant metastases, stage, localisation and histologic differentiation of the tumour. Circulating tumour cells in the bone marrow indicate a poor prognosis for patients with various kinds of malignoma. The present study examines the clinical relevance of occult tumour cells in patients suffering from SCCHN. Patients and Methods: Bone marrow aspirates of 176 patients suffering from SCCHN were obtained prior to surgery and stained for the presence of disseminated tumour cells. Antibodies for cytokeratin 19 were used for immunohistochemical detection with APAAP on cytospin slides. Within a clinical follow-up protocol over a period of 60 months, the prognostic relevance of several clinicopathological parameters and occult tumour cells was evaluated. Results: Single CK19-expressing tumour cells could be detected in the bone marrow of 30.7% of the patients. There is a significant correlation between occult tumour cells in the bone marrow and relapse. Uni- and multivariate analysis of all clinical data showed the metastases in the locoregional lymph system and detection of disseminated tumour cells in the bone marrow to be statistically highly significant for clinical prognosis. Conclusion: The detection of minimal residual disease underlines the understanding of SCCHN as a systemic disease. Further examination of such cells will lead to a better understanding of the tumour biology, as well as to improvement of diagnostic and therapeutic strategies.