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排序方式: 共有362条查询结果,搜索用时 15 毫秒
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Teimourian S Rezvani Z Badalzadeh M Kannengiesser C Mansouri D Movahedi M Zomorodian E Parvaneh N Mamishi S Pourpak Z Moin M 《International journal of hematology》2008,87(4):398-404
Chronic granulomatous disease (CGD) is an inherited disorder of pathogen killing by phagocytic leukocytes caused by mutations
in NADPH oxidase subunits. Patients with CGD have life-threatening bacterial and fungal infections. Children’s Medical Center
at Tehran University is the referral center for immunodeficiency in Iran. During 2 years of study, 11 non-consanguineous families
with clinically diagnosed CGD were referred to this center. In functional assays performed on neutrophils from affected children
and their mothers; no activity or strongly decreased oxidase activity was detected in the patients’ cells. In oxidase tests
that scored this activity on a per-cell basis, a mosaic pattern was detected in the neutrophils from all 11 mothers. Western
blot analysis revealed an X91° phenotype in all patients. Mutation screening in the CYBB gene encoding gp91phox by SSCP analysis followed by sequencing showed nine different mutations, including two novel mutations. The present survey
is the first study aimed to analyze the clinical features and the molecular diagnosis of X-CGD in Iranian patients. 相似文献
3.
Malvi Surti Mitesh Patel Mohd Adnan Afrasim Moin Syed Amir Ashraf Arif Jamal Siddiqui Mejdi Snoussi Sumukh Deshpande Mandadi Narsimha Reddy 《RSC advances》2020,10(62):37707
The outbreak of novel coronavirus, SARS-CoV-2, has infected more than 36 million people and caused approximately 1 million deaths around the globe as of 9 October 2020. The escalating outspread of the virus and rapid rise in the number of cases require the instantaneous development of effectual drugs and vaccines. Presently, there are no approved drugs or vaccine available to treat the infection. In such scenario, one of the propitious therapeutic approaches against viral infection is to explore enzyme inhibitors amidst natural compounds, utilizing computational approaches aiming to get products with negligible side effects. In the present study, the inhibitory prospects of ilimaquinone (marine sponge metabolite) were assessed in comparison with hydroxychloroquine, azithromycin, favipiravir, ivermectin and remdesivir at the active binding pockets of nine different vital SARS-CoV-2 target proteins (spike receptor binding domain, RNA-dependent RNA polymerase, Nsp10, Nsp13, Nsp14, Nsp15, Nsp16, main protease, and papain-like-protease), employing an in silico molecular interaction based approach. In addition, molecular dynamics (MD) simulations of the SARS-CoV-2 papain-like protease (PLpro)–ilimaquinone complex were also carried out to calculate various structural parameters including root mean square fluctuation (RMSF), root mean square deviation (RMSD), radius of gyration (Rg) and hydrogen bond interactions. PLpro is a promising drug target, due to its imperative role in viral replication and additional function of stripping ubiquitin and interferon-stimulated gene 15 (ISG15) from host-cell proteins. In light of the possible inhibition of all vital SARS-CoV-2 target proteins, our study has emphasized the importance to study in depth ilimaquinone actions in vivo.Inhibitory potential of ilimaquinone (marine sponge metabolite) against nine essential SARS-CoV-2 target proteins, employing a molecular interaction and dynamics simulation approach. 相似文献
4.
Afrasim Moin N. K. Famna Roohi Syed Mohd Danish Rizvi Syed Amir Ashraf Arif Jamal Siddiqui Mitesh Patel S. M. Ahmed D. V. Gowda Mohd Adnan 《RSC advances》2020,10(57):34869
Three drugs namely caffeine, paracetamol, and aceclofenac are commonly used for treating various acute and chronic pain related ailments. These 3 drugs have varied solubility profiles, and formulating them into a single tablet did not have the desired dissolution profile for drug absorption. The objective of the present research was to tailor the drug release profile by altering drug solubility. This was achieved by loading the drug into nanosponges. Here, three-dimensional colloidal nanosponges were prepared using β-cyclodextrin with dimethyl carbonate as a cross-linker using the hot-melt compression method. The prepared nanosponges were characterized by FTIR, 1H NMR spectroscopy, DSC, XRPD studies and SEM. The FTIR and DSC results obtained indicated polymer-drug compatibility. The 1H NMR spectroscopy results obtained indicated the drug entrapment within nanosponges with the formation of the inclusion complex. XRPD studies showed that the loaded drug had changed crystalline properties altering drug solubility. SEM photographs revealed the porous and spongy texture on the surface of the nanosponge. Box–Behnken experimental design was adopted for the optimization of nanosponge synthesis. Among the synthesized nanosponges containing paracetamol, aceclofenac and caffeine, batch F3–P31, F3–A31 and F3–C31 were considered optimized. Their particle size was 185, 181 and 199 nm with an entrapment efficiency of 81.53, 84.96, and 89.28% respectively. These optimized nanosponges were directly compressed into tablets and were studied for both pre and post-compression properties including in vitro drug release. The prepared tablet showed desired drug dissolution properties compared to the pure drug. The above outcomes indicated the applicability of nanosponges in modulating the drug release with varied solubility for combination therapy.Polymeric nanosponges as potential carriers for successful combination therapy of poorly soluble drugs (paracetamol, aceclofenac, caffeine). 相似文献
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Moin A. Saleem 《Pediatric nephrology (Berlin, Germany)》2013,28(5):699-709
Nephrotic syndrome is a disorder of the glomerular filtration barrier, a highly specialised tri-layer structure with unique functional properties. Recent advances emanating from the field of molecular genetics have revealed the podocyte as probably the central player in the control of glomerular filtration. More specifically, the cell–cell junction between adjacent podocyte foot processes, namely, the slit diaphragm, has been revealed to be made up of a sophisticated multi-protein complex which dynamically controls foot process architecture via signalling to the actin cytoskeleton. Key genes that have been identified from the study of inherited nephrotic syndromes include those encoding nephrin, podocin, TRPC6 (transient receptor potential canonical channel-6) and α-actinin-4, and more remain to be found. It is now possible to identify genetic causes underlying a proportion of nephrotic syndromes presenting at any age. The next big challenge for clinicians and researchers is to translate the molecular information learnt into the understanding of acquired, non-inherited forms of the disease and to guide therapeutic options. In this regard several exciting advances have been made, both in understanding the molecular mechanisms of current therapies and in revealing circulating plasma factors and the molecular pathways they trigger in the podocyte, that could be targeted by novel therapies. 相似文献
7.
Takuji Ishimoto Gabriel Cara-Fuentes Heiman Wang Michiko Shimada Clive H. Wasserfall William E. Winter Christopher J. Rivard Carlos E. Araya Moin A. Saleem Peter W. Mathieson Richard J. Johnson Eduardo H. Garin 《Pediatric nephrology (Berlin, Germany)》2013,28(9):1803-1812
Background
Minimal change disease (MCD) is the most common cause of nephrotic syndrome in children and is associated with the expression of CD80 in podocytes and the increased excretion of CD80 in urine. We hypothesized that serum from patients with MCD might stimulate CD80 expression in cultured podocytes.Methods
Sera and peripheral blood mononuclear cells (PBMCs) were collected from subjects with MCD in relapse and remission and from normal controls. Immortalized human podocytes were incubated with culture media containing patient sera or supernatants from patient and control PBMC cultures. CD80 expression was measured by quantitative PCR and western blot analysis.Results
Sera collected from patients with MCD in relapse, but not in remission, significantly increased CD80 expression (mean ± standard deviation: 1.8?±?0.7 vs. 0.8?±?0.2; p?<?0.004) and CD80 protein secretion by podocytes (p?<?0.05 between relapse and normal controls). No such CD80 increase was observed when podocytes were incubated with supernatants of PBMC cultures from patients in relapse.Conclusions
Sera from MCD patients in relapse, but not in remission, stimulated CD80 expression in cultured podocytes. Identifying this factor in sera could provide insights into the pathogenesis of this disorder. No role in CD80 expression by podocytes was found for cytokines released by PBMCs. 相似文献8.
9.
Sogole Moin Zana Kalajzic Achint Utreja Jun Nihara Sunil Wadhwa Flavio Uribe Ravindra Nanda 《The Angle orthodontist》2014,84(6):1086
Objective:To investigate the time course of osteocyte death in a mouse model of orthodontic tooth movement (OTM) and its association to the caspase-3 activation pathway and osteoclast formation.Materials and Methods:Twenty-five male wild type CD-1 mice (8–12 weeks old) were loaded with an orthodontic appliance. A spring delivering 10–12 g of force was placed between the right first molar and the incisor to displace the first molar mesially. The contralateral unloaded sides served as the control. The animals were equally divided into five different time points: 6, 12, 24, and 72 hours and 7 days of orthodontic loading. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, caspase-3 immunostaining, and tartrate-resistant acid phosphatase (TRAP) staining was performed on histologic sections of the first molars. The labeling was quantified in osteocytes on the compression side of the alveolar bone at each time point.Results:TUNEL labeling significantly increased at 12, 24, and 72 hours after orthodontic loading; the peak was observed at 24 hours. Elevated caspase-3 labeling was noted at 12, 24, and 72 hours and 7 days after loading, although the increase was not significant. Significant osteoclast formation was initially evident after 72 hours and progressively increased up to 7 days.Conclusions:Osteocyte death during OTM peaks at 24 hours, earlier than initial osteoclast activation. However, only a slight trend for increased caspase-3 activity suggests that other mechanisms might be involved in osteocyte death during OTM. 相似文献
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