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Article ; Online: Clinical pharmacist interventions in an intensive care unit reduces ICU mortality at a tertiary hospital in Dubai, United Arab Emirates.

Ali Hussain Alsayed, Hawra / Saheb Sharif-Askari, Fatemeh / Saheb Sharif-Askari, Narjes / Halwani, Rabih

Exploratory research in clinical and social pharmacy

2024 Volume 14, Page(s) 100431

Abstract: Background: Drug-related problems (DRPs) are prevalent in critical care settings and can be life-threatening. Involving clinical pharmacists (CP) within the critical care team is recommended to optimize therapy and improve patient survival.: Objective! ...

Abstract	Background: Drug-related problems (DRPs) are prevalent in critical care settings and can be life-threatening. Involving clinical pharmacists (CP) within the critical care team is recommended to optimize therapy and improve patient survival. Objective: To classify DRPs identified by a CP in the Intensive Care Unit (ICU) and to assess the impact of CP interventions accepted by physicians on the length of ICU stay and in-hospital survival. Methods: This study was conducted prospectively at the Medical ICU of Rashid Hospital, a tertiary hospital in Dubai, over a 16-month period from September 2021 to December 2022. The study included patients admitted to ICU during the study period. CP interventions were documented, and DRPs were classified using the modified Pharmaceutical Care Network Europe V.9.1. Results: During the study period, 1004 interventions were recommended for 200 patients. The majority of these interventions, 92% ( Conclusion: The study emphasizes the critical role of CP in the ICU, addressing DRPs, and enhancing overall patient care. Furthermore, it highlights the potential impact of pharmacist interventions in improving patient survival outcomes. This underscores the importance of implementing CP services in ICUs across the UAE.
Language	English
Publishing date	2024-03-09
Publishing country	United States
Document type	Journal Article
ISSN	2667-2766
ISSN (online)	2667-2766
DOI	10.1016/j.rcsop.2024.100431
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Article ; Online: Hemizygous BTK Gene Variant Causing X-Linked Agammaglobulinemia in Two Siblings.

Saheb Sharif-Askari, Narjes / Hafezi, Shirin / Saheb Sharif-Askari, Fatemeh / Frommenwiler, Naomi / Halwani, Rabih

Journal of clinical immunology

2023 Volume 43, Issue 7, Page(s) 1533–1536

MeSH term(s)	Humans ; Siblings ; Protein-Tyrosine Kinases/genetics ; Agammaglobulinaemia Tyrosine Kinase/genetics ; Agammaglobulinemia/diagnosis ; Agammaglobulinemia/genetics ; Genetic Diseases, X-Linked/diagnosis ; Genetic Diseases, X-Linked/genetics ; Mutation/genetics
Chemical Substances	Protein-Tyrosine Kinases (EC 2.7.10.1) ; Agammaglobulinaemia Tyrosine Kinase (EC 2.7.10.2)
Language	English
Publishing date	2023-06-21
Publishing country	Netherlands
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-023-01534-3
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Article: Unraveling the gut-Lung axis: Exploring complex mechanisms in disease interplay.

Eladham, Mariam Wed / Selvakumar, Balachandar / Saheb Sharif-Askari, Narjes / Saheb Sharif-Askari, Fatemeh / Ibrahim, Saleh Mohamed / Halwani, Rabih

Heliyon

2024 Volume 10, Issue 1, Page(s) e24032

Abstract: The link between gut and lung starts as early as during organogenesis. Even though they are anatomically distinct, essential bidirectional crosstalk via complex mechanisms supports GLA. Emerging studies have demonstrated the association of gut and lung ... ...

Abstract	The link between gut and lung starts as early as during organogenesis. Even though they are anatomically distinct, essential bidirectional crosstalk via complex mechanisms supports GLA. Emerging studies have demonstrated the association of gut and lung diseases via multifaceted mechanisms. Advancements in omics and metagenomics technologies revealed a potential link between gut and lung microbiota, adding further complexity to GLA. Despite substantial studies on GLA in various disease models, mechanisms beyond microbial dysbiosis regulating the interplay between gut and lung tissues during disease conditions are not thoroughly reviewed. This review outlines disease specific GLA mechanisms, emphasizing research gaps with a focus on gut-to-lung direction based on current GLA literature. Moreover, the review discusses potential gut microbiota and their products like metabolites, immune modulators, and non-bacterial contributions as a basis for developing treatment strategies for lung diseases. Advanced experimental methods, modern diagnostic tools, and technological advancements are also highlighted as crucial areas for improvement in developing novel therapeutic approaches for GLA-related diseases. In conclusion, this review underscores the importance of exploring additional mechanisms within the GLA to gain a deeper understanding that could aid in preventing and treating a wide spectrum of lung diseases.
Language	English
Publishing date	2024-01-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2024.e24032
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Article ; Online: Risk factors and early preventive measures for long COVID in non-hospitalized patients: analysis of a large cohort in the United Arab Emirates.

Saheb Sharif-Askari, Fatemeh / Ali Hussain Alsayed, Hawra / Saheb Sharif-Askari, Narjes / Saddik, Basema / Al Sayed Hussain, Ali / Halwani, Rabih

Public health

2024 Volume 230, Page(s) 198–206

Abstract: Objectives: Long COVID is characterized by persistent symptoms lasting for 4 weeks or more following the acute infection with SARS-CoV-2. Risk factors for long COVID and the impact of pre-COVID vaccination and treatment during acute COVID-19 remain ... ...

Abstract	Objectives: Long COVID is characterized by persistent symptoms lasting for 4 weeks or more following the acute infection with SARS-CoV-2. Risk factors for long COVID and the impact of pre-COVID vaccination and treatment during acute COVID-19 remain uncertain. This study aimed to investigate patient-specific factors associated with long COVID in a large cohort of non-hospitalized adult patients with mild to moderate COVID-19 in Dubai. Study design: Cohort study. Methods: The study included 28,375 non-hospitalized adult patients diagnosed with mild to moderate COVID-19 between January 1, 2021, and September 31, 2022, in Dubai, who were followed up for 90 days. The presence of long COVID symptoms was documented by physicians during patient visits to the family medicine department. Furthermore, long COVID-related risk factors were collected and analyzed, including patient demographics, comorbidities, pre-COVID vaccination status, and the COVID-related treatments received during the acute phase of the illness. Cox proportional hazard models were applied for the statistical analysis. Results: Among the cohort, 2.8% of patients experienced long COVID symptoms during the 90-day follow-up. Patients with long COVID tended to be younger, female, and of Caucasian race. Common symptoms included fatigue, muscle pain, respiratory symptoms, abdominal and neurological symptoms, allergic reactions, skin rashes, and hair loss. Risk factors for long COVID were identified as diabetes mellitus, asthma, and Vitamin D deficiency. Females and Caucasians had a higher risk of long COVID during the pre-Omicron period compared to the Omicron period. Pre-COVID vaccination was associated with a reduced risk of long COVID in all patient subgroups. Treatment with favipiravir or sotrovimab during the acute phase of COVID-19 was linked to a decreased risk of long COVID, although favipiravir showed limited effectiveness in the high-risk group. Conclusion: This study contributes to the existing knowledge by identifying risk factors for long COVID among non-hospitalized patients and emphasizing the potential benefits of pre-COVID vaccination and timely treatment.
MeSH term(s)	Adult ; Humans ; Female ; Post-Acute COVID-19 Syndrome ; COVID-19/epidemiology ; COVID-19/prevention & control ; United Arab Emirates/epidemiology ; SARS-CoV-2 ; Cohort Studies ; Risk Factors ; Amides ; Pyrazines
Chemical Substances	favipiravir (EW5GL2X7E0) ; Amides ; Pyrazines
Language	English
Publishing date	2024-04-03
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	427333-3
ISSN	1476-5616 ; 0033-3506
ISSN (online)	1476-5616
ISSN	0033-3506
DOI	10.1016/j.puhe.2024.02.031
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Article: Multiple inborn errors of type I IFN immunity in a 33-year-old male with a fatal case of COVID-19.

Saheb Sharif-Askari, Narjes / Hafezi, Shirin / Saheb Sharif-Askari, Fatemeh / Ali Hussain Alsayed, Hawra / B M Ahmed, Samrein / Alsafar, Habiba S / Halwani, Rabih

Heliyon

2024 Volume 10, Issue 8, Page(s) e29338

Abstract: The host genetic inborn errors of immunity (IEIs) have been shown to contribute to susceptibility to life-threatening coronavirus disease 2019 (COVID-19), as it had been associated previously with other viral infections. Most genetic association studies ... ...

Abstract	The host genetic inborn errors of immunity (IEIs) have been shown to contribute to susceptibility to life-threatening coronavirus disease 2019 (COVID-19), as it had been associated previously with other viral infections. Most genetic association studies have described IEIs as a monogenic defect, while there have been no reports of patients with multiple inherited immune deficiencies. This is a complex case of IEIs predisposing to severe viral infections in an unvaccinated 33-year-old male patient. The patient was admitted with no respiratory symptoms, showed a SARS-CoV-2 PCR positive test on the second day of admission, started developing progressive lung consolidation within three days of hospitalization, and was moved from non-invasive to mechanical ventilation within 12 days of hospitalization. Impaired production of type I IFN was detected in patient PBMCs treated with poly(I:C), at both mRNA and protein levels. Whole exome sequencing revealed three mutations across type I IFN production pathway, which were predicted to be loss-of-function (pLOF). The three mutations were predicted to predispose to severe viral infections: monoallelic R488X TLR3, monoallelic His684Arg TLR3, and biallelic Val363Met IRF3. Functional analysis confirmed that all these mutations dysregulated the type I IFN pathway. Evaluation of TLR3 and IRF3 IFN-β1 luciferase reporter activity showed a hypomorphic suppression of function. TOPO TA cloning was used to ascertain the positioning of both TLR3 variants, indicating that both variants were on the same allele. We have described a unique complex IEI patient with multiple mutations, particularly along type I IFN production pathway.
Language	English
Publishing date	2024-04-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2024.e29338
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Article ; Online: Unraveling the gut-Lung axis

Mariam Wed Eladham / Balachandar Selvakumar / Narjes Saheb Sharif-Askari / Fatemeh Saheb Sharif-Askari / Saleh Mohamed Ibrahim / Rabih Halwani

Heliyon, Vol 10, Iss 1, Pp e24032- (2024)

Exploring complex mechanisms in disease interplay

2024

Abstract	The link between gut and lung starts as early as during organogenesis. Even though they are anatomically distinct, essential bidirectional crosstalk via complex mechanisms supports GLA. Emerging studies have demonstrated the association of gut and lung diseases via multifaceted mechanisms. Advancements in omics and metagenomics technologies revealed a potential link between gut and lung microbiota, adding further complexity to GLA. Despite substantial studies on GLA in various disease models, mechanisms beyond microbial dysbiosis regulating the interplay between gut and lung tissues during disease conditions are not thoroughly reviewed. This review outlines disease specific GLA mechanisms, emphasizing research gaps with a focus on gut-to-lung direction based on current GLA literature. Moreover, the review discusses potential gut microbiota and their products like metabolites, immune modulators, and non-bacterial contributions as a basis for developing treatment strategies for lung diseases. Advanced experimental methods, modern diagnostic tools, and technological advancements are also highlighted as crucial areas for improvement in developing novel therapeutic approaches for GLA-related diseases. In conclusion, this review underscores the importance of exploring additional mechanisms within the GLA to gain a deeper understanding that could aid in preventing and treating a wide spectrum of lung diseases.
Keywords	GLA ; Microbiota ; Gut ; Lung ; Dysbiosis ; Metabolites ; Science (General) ; Q1-390 ; Social sciences (General) ; H1-99
Subject code	610
Language	English
Publishing date	2024-01-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Salivary autoantibodies to type I IFNs: Mirror plasma levels, predispose to severe COVID-19, and enhance feasibility for clinical screening.

Saheb Sharif-Askari, Narjes / Saheb Sharif-Askari, Fatemeh / Bayram, Ola Salam / Hafezi, Shirin / Alsayed, Hawra Ali Hussain / Kasim, Fathima / Mdkhana, Bushra / Selvakumar, Balachandar / Alsafar, Habiba S / Halwani, Rabih

Heart & lung : the journal of critical care

2024 Volume 66, Page(s) 31–36

Abstract: Background: Autoantibodies have been demonstrated to dampen the interferon (IFN) response in viral infections. Elevated levels of these preexisting autoantibodies (aAbs) decrease basal interferon levels, increasing susceptibility to severe infections.!## ...

Abstract	Background: Autoantibodies have been demonstrated to dampen the interferon (IFN) response in viral infections. Elevated levels of these preexisting autoantibodies (aAbs) decrease basal interferon levels, increasing susceptibility to severe infections. Objectives: This study aimed to evaluate the prevalence of type I IFN aAbs in both plasma and saliva from COVID-19 patients, analyze their neutralizing activity, and examine their associations with clinical outcomes, including the need for mechanical ventilation and in-hospital mortality. Methods: Prospective analyses of patients admitted to intensive care units in three UAE hospitals from June 2020 to March 2021 were performed to measure aAbs using enzyme-linked immunosorbent assay (ELISA), assess aAbs activity via neutralization assays, and correlate aAbs with clinical outcomes. Results: Type I IFN aAbs (α2 and/or ω) were measured in plasma samples from 213 ICU patients, and positive results were obtained for 20 % (n = 42) of the patients, with half exhibiting neutralizing activity. Saliva samples from a subgroup of 24 patients reflected plasma levels. In multivariate regression analyses, presence of type I IFN aAbs was associated with a higher need for mechanical ventilation (OR 2.58; 95 % CI 1.07-6.22) and greater in-hospital mortality (OR 2.40; 95 % CI 1.13 - 5.07; P = 0.022). Similarly, positive neutralizing aAbs (naAbs) were associated with a greater need for mechanical ventilation (OR 4.96; 95 % CI 1.12-22.07; P = 0.035) and greater odds of in-hospital mortality (OR 2.87; 95 % CI 1.05-7.89; P = 0.041). Conclusions: Type I IFN autoantibodies can be detected in noninvasive saliva samples, alongside conventional plasma samples, from COVID-19 patients and are associated with worse outcomes, such as greater mechanical ventilation needs and in-hospital mortality.
Language	English
Publishing date	2024-03-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	193129-5
ISSN	1527-3288 ; 0147-9563
ISSN (online)	1527-3288
ISSN	0147-9563
DOI	10.1016/j.hrtlng.2024.03.005
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Article: PRMT5 Mediated HIF1α Signaling and Ras-Related Nuclear Protein as Promising Biomarker in Hepatocellular Carcinoma.

Abumustafa, Wafaa / Castven, Darko / Sharif-Askari, Fatemeh Saheb / Abi Zamer, Batoul / Hamad, Mawieh / Marquardt, Jens-Uwe / Muhammad, Jibran Sualeh

Biology

2024 Volume 13, Issue 4

Abstract: Protein arginine N-methyltransferase 5 (PRMT5) has been identified as a potential therapeutic target for various cancer types. However, its role in regulating the hepatocellular carcinoma (HCC) transcriptome remains poorly understood. In this study, ... ...

Abstract	Protein arginine N-methyltransferase 5 (PRMT5) has been identified as a potential therapeutic target for various cancer types. However, its role in regulating the hepatocellular carcinoma (HCC) transcriptome remains poorly understood. In this study, publicly available databases were employed to investigate PRMT5 expression, its correlation with overall survival, targeted pathways, and genes of interest in HCC. Additionally, we utilized in-house generated NGS data to explore
Language	English
Publishing date	2024-03-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology13040216
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Article ; Online: Increased blood immune regulatory cells in severe COVID-19 with autoantibodies to type I interferons.

Saheb Sharif-Askari, Fatemeh / Saheb Sharif-Askari, Narjes / Hafezi, Shirin / Alsayed, Hawra Ali Hussain / Selvakumar, Balachandar / Eladham, Mariam Wed Abdelaziz / Mdkhana, Bushra / Bayram, Ola Salam / Temsah, Mohamad-Hani / Halwani, Rabih

Scientific reports

2023 Volume 13, Issue 1, Page(s) 17344

Abstract: The hallmark of severe COVID-19 is an uncontrolled inflammatory response, resulting from poorly understood immunological dysfunction. While regulatory T (Treg) and B (Breg) cells, as the main elements of immune homeostasis, contribute to the control of ... ...

Abstract	The hallmark of severe COVID-19 is an uncontrolled inflammatory response, resulting from poorly understood immunological dysfunction. While regulatory T (Treg) and B (Breg) cells, as the main elements of immune homeostasis, contribute to the control of hyperinflammation during COVID-19 infection, we hypothesized change in their levels in relation to disease severity and the presence of autoantibodies (auto-Abs) to type I IFNs. Cytometric analysis of blood of 62 COVID-19 patients with different severities revealed an increased proportion of conventional (cTreg; CD25
MeSH term(s)	Humans ; Interleukin-10 ; T-Lymphocytes, Regulatory ; Autoantibodies ; COVID-19 ; Cytokines ; B-Lymphocytes, Regulatory ; Forkhead Transcription Factors
Chemical Substances	Interleukin-10 (130068-27-8) ; Autoantibodies ; Cytokines ; Forkhead Transcription Factors
Language	English
Publishing date	2023-10-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-43675-w
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Article ; Online: Nucleic acid sensor STING drives remodeling and its inhibition enhances steroid responsiveness in chronic obstructive pulmonary disease.

Mdkhana, Bushra / Saheb Sharif-Askari, Narjes / Ramakrishnan, Rakhee K / Al-Sheakly, Baraa Khalid / Hafezi, Shirin / Saheb Sharif-Askari, Fatemeh / Bajbouj, Khuloud / Hamid, Qutayba / Halwani, Rabih

PloS one

2023 Volume 18, Issue 7, Page(s) e0284061

Abstract: Background: Chronic obstructive pulmonary disease (COPD) is progressive and irreversible chronic lung inflammatory disease. Cigarette smoke, the main cause of COPD, is often associated with double-stranded DNA release which potentially activates DNA- ... ...

Abstract	Background: Chronic obstructive pulmonary disease (COPD) is progressive and irreversible chronic lung inflammatory disease. Cigarette smoke, the main cause of COPD, is often associated with double-stranded DNA release which potentially activates DNA-sensing pathways, such as STING. This study, therefore, analyzed the role of STING pathway in inducing pulmonary inflammation, steroid resistance, and remodeling in COPD. Methods: Primary cultured lung fibroblasts were isolated from healthy non-smoker, healthy smoker, and smoker COPD individuals. The expression of STING pathway, remodeling, and steroid resistance signatures were investigated in these fibroblasts upon LPS stimulation and treatment with dexamethasone and/or STING inhibitor, at both mRNA and protein levels using qRT-PCR, western blot, and ELISA. Results: At baseline, STING was elevated in healthy smoker fibroblasts and to a higher extent in smoker COPD fibroblasts when compared to healthy non-smoker fibroblasts. Upon using dexamethasone as monotherapy, STING activity was significantly inhibited in healthy non-smoker fibroblasts but showed resistance in COPD fibroblasts. Treating both healthy and COPD fibroblasts with STING inhibitor in combination with dexamethasone additively inhibited STING pathway in both groups. Moreover, STING stimulation triggered a significant increase in remodeling markers and a reduction in HDAC2 expression. Interestingly, treating COPD fibroblasts with the combination of STING inhibitor and dexamethasone alleviated remodeling and reversed steroid hyporesponsiveness through an upregulation of HDAC2. Conclusion: These findings support that STING pathway plays an important role in COPD pathogenesis, via inducing pulmonary inflammation, steroid resistance, and remodeling. This raises the possibility of using STING inhibitor as a potential therapeutic adjuvant in combination with common steroid treatment.
MeSH term(s)	Humans ; Nucleic Acids/metabolism ; Pulmonary Disease, Chronic Obstructive ; Lung/pathology ; Pneumonia/pathology ; DNA/metabolism ; Dexamethasone/pharmacology ; Dexamethasone/therapeutic use ; Dexamethasone/metabolism ; Steroids/metabolism
Chemical Substances	Nucleic Acids ; DNA (9007-49-2) ; Dexamethasone (7S5I7G3JQL) ; Steroids
Language	English
Publishing date	2023-07-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0284061
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