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  1. Article ; Online: Hypertriglyceridemia-induced acute necrotizing pancreatitis: Poor clinical outcomes requiring revisiting management modalities.

    Abboud, Yazan / Shah, Meet / Simmons, Benjamin / Mandava, Kranthi / Morales, John E M / Jaber, Fouad / Alsakarneh, Saqer / Ismail, Mohamed / Hajifathalian, Kaveh

    JGH open : an open access journal of gastroenterology and hepatology

    2024  Volume 8, Issue 4, Page(s) e13061

    Abstract: Hypertriglyceridemia-induced acute pancreatitis (HTG-AP) is the third most common cause of AP after gallstones and alcohol. Supportive measures, intravenous insulin, and plasmapheresis are possible treatment modalities for HTG-AP; however, definitive ... ...

    Abstract Hypertriglyceridemia-induced acute pancreatitis (HTG-AP) is the third most common cause of AP after gallstones and alcohol. Supportive measures, intravenous insulin, and plasmapheresis are possible treatment modalities for HTG-AP; however, definitive guidelines evaluating the best therapeutic approach are not clearly established. We present a rare case of a 42-year-old male without known comorbidities who was found to have HTG-AP. Despite early initiation of intravenous insulin and plasmapheresis and the initial decline in his triglycerides level, his condition was complicated by necrotizing pancreatitis and subsequent multi-organ failure. Future studies are warranted to evaluate the role of plasmapheresis in HTG-AP and its efficacy.
    Language English
    Publishing date 2024-04-13
    Publishing country Australia
    Document type Case Reports
    ISSN 2397-9070
    ISSN (online) 2397-9070
    DOI 10.1002/jgh3.13061
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Neonatal Fc Receptor Inhibitor Therapeutics in Neuromuscular Disease.

    Jaffry, Mustafa / Menkes, Daniel L / Shaikh, Anam / Mandava, Kranthi / Kothari, Om / Jaffry, Kazim / Souayah, Nizar

    Journal of clinical neuromuscular disease

    2023  Volume 24, Issue 4, Page(s) 188–198

    Abstract: Abstract: The Neonatal Fc Receptor (FcRn) is integral to a wide variety of processes including IgG recycling, serum albumin turnover, and bacterial opsonization. Thus, targeting FcRn will increase antibody degradation including pathogenic IgGs. FcRn ... ...

    Abstract Abstract: The Neonatal Fc Receptor (FcRn) is integral to a wide variety of processes including IgG recycling, serum albumin turnover, and bacterial opsonization. Thus, targeting FcRn will increase antibody degradation including pathogenic IgGs. FcRn inhibition provides a novel therapeutic mechanism by which autoantibody titers are reduced resulting in clinical improvement and disease abatement. The FcRn targeting mechanism is similar to that of intravenous immunoglobulin (IVIg) in which saturated FcRn facilitates accelerated pathogenic IgG degradation. Recently, the FcRn inhibitor efgartigimod was approved for the treatment of myasthenia gravis. Subsequently, clinical trials of this agent have been conducted for numerous inflammatory conditions involving pathogenic autoantibodies. These disorders include the Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy, and inflammatory myositis. Other disorders traditionally treated with IVIg may also benefit from FcRn inhibition in certain contexts. This manuscript discusses the mechanism of FcRn inhibition, preclinical data, and the results of clinical trials of this agent for a wide range of neuromuscular diseases.
    MeSH term(s) Humans ; Autoantibodies ; Immunoglobulins, Intravenous ; Myasthenia Gravis ; Neuromuscular Diseases
    Chemical Substances Autoantibodies ; Fc receptor, neonatal (TW3XAW0RCY) ; Immunoglobulins, Intravenous
    Language English
    Publishing date 2023-05-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1454947-5
    ISSN 1537-1611 ; 1522-0443
    ISSN (online) 1537-1611
    ISSN 1522-0443
    DOI 10.1097/CND.0000000000000451
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5293: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Optic Neuritis After COVID-19 Vaccination: An Analysis of the Vaccine Adverse Event Reporting System.

    Jaffry, Mustafa / Aftab, Owais M / Mostafa, Fahad B / Faiz, Iqra / Jaffry, Kazim / Mandava, Kranthi / Rosario, Sanjana / Jedidi, Kamel / Khan, Hafiz / Souayah, Nizar

    Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society

    2023  Volume 43, Issue 4, Page(s) 499–503

    Abstract: Background: To investigate the association of optic neuritis (ON) after the COVID-19 vaccines.: Methods: Cases of ON from Vaccine Adverse Event Reporting System (VAERS) were collected and divided into the prepandemic, COVID-19 pandemic, and COVID-19 ... ...

    Abstract Background: To investigate the association of optic neuritis (ON) after the COVID-19 vaccines.
    Methods: Cases of ON from Vaccine Adverse Event Reporting System (VAERS) were collected and divided into the prepandemic, COVID-19 pandemic, and COVID-19 vaccine periods. Reporting rates were calculated based on estimates of vaccines administered. Proportion tests and Pearson χ 2 test were used to determine significant differences in reporting rates of ON after vaccines within the 3 periods. Kruskal-Wallis testing with Bonferroni-corrected post hoc analysis and multivariable binary logistic regression was used to determine significant case factors such as age, sex, concurrent multiple sclerosis (MS) and vaccine manufacturer in predicting a worse outcome defined as permanent disability, emergency room (ER) or doctor visits, and hospitalizations.
    Results: A significant increase in the reporting rate of ON after COVID-19 vaccination compared with influenza vaccination and all other vaccinations (18.6 vs 0.2 vs 0.4 per 10 million, P < 0.0001) was observed. However, the reporting rate was within the incidence range of ON in the general population. Using self-controlled and case-centered analyses, there was a significant difference in the reporting rate of ON after COVID-19 vaccination between the risk period and control period ( P < 0.0001). Multivariable binary regression with adjustment for confounding variables demonstrated that only male sex was significantly associated with permanent disability.
    Conclusions: Some cases of ON may be temporally associated with the COVID-19 vaccines; however, there is no significant increase in the reporting rate compared with the incidence. Limitations of this study include those inherent to any passive surveillance system. Controlled studies are needed to establish a clear causal relationship.
    MeSH term(s) Humans ; Male ; Adverse Drug Reaction Reporting Systems ; COVID-19/epidemiology ; COVID-19/prevention & control ; COVID-19 Vaccines/adverse effects ; Optic Neuritis/etiology ; Pandemics ; United States ; Vaccination/adverse effects ; Vaccines/adverse effects
    Chemical Substances COVID-19 Vaccines ; Vaccines
    Language English
    Publishing date 2023-06-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1189901-3
    ISSN 1536-5166 ; 1070-8022
    ISSN (online) 1536-5166
    ISSN 1070-8022
    DOI 10.1097/WNO.0000000000001900
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1670: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Optic Neuritis After COVID-19 Vaccination: Response.

    Jaffry, Mustafa / Aftab, Owais M / Mostafa, Fahad B / Faiz, Iqra / Jaffry, Kazim / Mandava, Kranthi / Rosario, Sanjana / Jedidi, Kamel / Khan, Hafiz / Souayah, Nizar

    Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society

    2023  

    Language English
    Publishing date 2023-10-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1189901-3
    ISSN 1536-5166 ; 1070-8022
    ISSN (online) 1536-5166
    ISSN 1070-8022
    DOI 10.1097/WNO.0000000000002016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1670: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Gain of function mutant p53 protein activates AKT through the Rac1 signaling to promote tumorigenesis.

    Yue, Xuetian / Wu, Fangnan / Li, Yanchen / Liu, Juan / Boateng, Michael / Mandava, Kranthi / Zhang, Cen / Feng, Zhaohui / Gao, Jimin / Hu, Wenwei

    Cell cycle (Georgetown, Tex.)

    2020  Volume 19, Issue 11, Page(s) 1338–1351

    Abstract: Tumor suppressor p53 is the most frequently mutated gene in human cancer. Mutant p53 (mutp53) not only loses the tumor suppressive activity of wild type p53, but often gains new oncogenic activities to promote tumorigenesis, defined as mutp53 gain of ... ...

    Abstract Tumor suppressor p53 is the most frequently mutated gene in human cancer. Mutant p53 (mutp53) not only loses the tumor suppressive activity of wild type p53, but often gains new oncogenic activities to promote tumorigenesis, defined as mutp53 gain of function (GOF). While the concept of mutp53 GOF is well-established, its underlying mechanism is not well-understood. AKT has been suggested to be activated by mutp53 and contribute to mutp53 GOF, but its underlying mechanism is unclear. In this study, we found that the activation of the Rac1 signaling by mutp53 mediates the promoting effect of mutp53 on AKT activation. Blocking Rac1 signaling by RNAi or a Rac1 inhibitor can inhibit AKT activation by mutp53. Importantly, targeting Rac1/AKT can greatly compromise mutp53 GOF in tumorigenesis. Results from this study uncover a new mechanism for AKT activation in tumors, and reveal that activation of AKT by mutp53
    MeSH term(s) Breast Neoplasms/genetics ; Carcinogenesis/genetics ; Carcinogenesis/pathology ; Cell Proliferation/genetics ; Cohort Studies ; Enzyme Activation ; Female ; Gain of Function Mutation/genetics ; Humans ; Mutant Proteins/metabolism ; Phosphorylation ; Protein Binding ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Sumoylation ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; rac1 GTP-Binding Protein/antagonists & inhibitors ; rac1 GTP-Binding Protein/metabolism ; ras GTPase-Activating Proteins/metabolism
    Chemical Substances DAB2IP protein, human ; Mutant Proteins ; Tumor Suppressor Protein p53 ; ras GTPase-Activating Proteins ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; rac1 GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2020-04-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2020.1749790
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5881: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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