13 results on '"Jahangir Syed"'
Search Results
2. A Survey on RFID based School Bus Monitoring and Attendance System
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Jahangir, Syed Mobin, primary
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- 2019
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3. Histone deacetylase inhibitors restore toxic BH3 domain protein expression in anoikis-resistant mammary and brain cancer stem cells, thereby enhancing the response to anti-ERBB1/ERBB2 therapy
- Author
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Hossein A. Hamed, Laurence Booth, Seyedmehrad Tavallai, Andrew Poklepovic, Nichola Cruickshanks, Jahangir Syed, Gangadharan B. Sajithlal, Paul Dent, and Steven Grant
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Cancer Research ,Indoles ,Receptor, ErbB-2 ,Cell ,Gene Expression ,Epigenesis, Genetic ,necrosis ,Mice ,0302 clinical medicine ,anoikis ,Anoikis ,RNA, Small Interfering ,ERBB1 ,bcl-2-Associated X Protein ,BH3 domain ,0303 health sciences ,biology ,Brain Neoplasms ,3. Good health ,ErbB Receptors ,Gene Expression Regulation, Neoplastic ,bcl-2 Homologous Antagonist-Killer Protein ,Cell killing ,medicine.anatomical_structure ,Proto-Oncogene Proteins c-bcl-2 ,Oncology ,Gene Knockdown Techniques ,030220 oncology & carcinogenesis ,Neoplastic Stem Cells ,Molecular Medicine ,Female ,Stem cell ,signaling ,Bcl-2 Homologous Antagonist-Killer Protein ,Research Paper ,autophagy ,tumor ,Programmed cell death ,Antineoplastic Agents, Hormonal ,Cell Survival ,NOXA ,bcl-X Protein ,Mice, Nude ,Breast Neoplasms ,03 medical and health sciences ,Bcl-2-associated X protein ,Proto-Oncogene Proteins ,medicine ,Animals ,Humans ,Pyrroles ,030304 developmental biology ,Pharmacology ,Valproic Acid ,BAK ,Lapatinib ,Xenograft Model Antitumor Assays ,Molecular biology ,Histone Deacetylase Inhibitors ,Drug Resistance, Neoplasm ,Quinazolines ,biology.protein ,Cancer research ,Myeloid Cell Leukemia Sequence 1 Protein ,Histone deacetylase ,MCL-1 ,Apoptosis Regulatory Proteins - Abstract
The present studies focused on defining the mechanisms by which anoikis-resistant (AR) mammary carcinoma cells can be reverted to a therapy-sensitive phenotype. AR mammary carcinoma cells had reduced expression of the toxic BH3 domain proteins BAX, BAK, NOXA, and PUMA. In AR cells expression of the protective BCL-2 family proteins BCL-XL and MCL-1 was increased. AR cells were resistant to cell killing by multiple anti-tumor cell therapies, including ERBB1/2 inhibitor + MCL-1 inhibitor treatment, and had a reduced autophagic flux response to these therapies, despite similarly exhibiting increased levels of LC3II processing. Knockdown of MCL-1 and BCL-XL caused necro-apoptosis in AR cells to a greater extent than in parental cells. Pre-treatment of anoikis-resistant cells with histone deacetylase inhibitors (HDACIs) for 24 h increased the levels of toxic BH3 domain proteins, reduced MCL-1 levels, and restored/re-sensitized the cell death response of AR tumor cells to multiple toxic therapies. In vivo, pre-treatment of AR breast tumors in the brain with valproate restored the chemo-sensitivity of the tumors and prolonged animal survival. These data argue that one mechanism to enhance the anti-tumor effect of chemotherapy could be HDACI pre-treatment.
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- 2013
4. Sorafenib/Regorafenib and Phosphatidyl Inositol 3 Kinase/Thymoma Viral Proto-Oncogene Inhibition Interact to Kill Tumor Cells
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Laurence Booth, Paul Dent, Hossein A. Hamed, Steven Grant, Jahangir Syed, Gangadharan B. Sajithlal, Nichola Cruickshanks, Seyedmehrad Tavallai, and Andrew Poklepovic
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Niacinamide ,Sorafenib ,Thymoma ,Pyridines ,Cell Communication ,Gonanes ,Pharmacology ,Biology ,Proto-Oncogene Mas ,Mice ,Phosphatidylinositol 3-Kinases ,chemistry.chemical_compound ,GSK-3 ,Cell Line, Tumor ,Regorafenib ,medicine ,Animals ,Humans ,Protein kinase B ,PI3K/AKT/mTOR pathway ,Phosphoinositide-3 Kinase Inhibitors ,Cell Death ,Kinase ,Phenylurea Compounds ,Drug Synergism ,Hep G2 Cells ,Thymus Neoplasms ,Articles ,Perifosine ,Xenograft Model Antitumor Assays ,Cell killing ,chemistry ,Molecular Medicine ,Female ,Proto-Oncogene Proteins c-akt ,medicine.drug - Abstract
The present studies were undertaken to determine whether the multikinase inhibitors sorafenib/regorafenib cooperated with clinically relevant , phosphatidyl inositol 3 kinase (PI3K)-thymoma viral proto-oncogene (AKT) inhibitors to kill tumor cells. In liver, colorectal, lung, breast, kidney, and brain cancer cells, at clinically achievable doses, sorafenib/regorafenib and the PI3K inhibitor acetic acid (1S,4E,10R,11R,13S,14R)-[4-diallylaminomethylene-6-hydroxy-1-methoxymethyl-10,13-dimethyl-3,7,17-trioxo-1,3,4,7,10,11,12,13,14,15,16,17-dodecahydro-2-oxa-cyclopenta[a]phenanthren-11-yl ester (PX-866) cooperated in a greater than additive fashion to kill tumor cells. Cells lacking phosphatase and tensin homolog were as sensitive to the drug combination as cells expressing the protein. Similar data were obtained using the AKT inhibitors perifosine and 8-[4-(1-aminocyclobutyl)phenyl]-9-phenyl-1,2,4-triazolo[3,4-f] [1,6]naphthyridin-3(2H)-one hydrochloride (MK2206). PX-866 treatment abolished AKT/glycogen synthase kinase 3 (GSK3) phosphorylation, and cell killing correlated with reduced activity of AKT and mammalian target of rapamycin (mTOR). Expression of activated AKT and to a lesser extent activated mTOR reduced drug combination lethality. Expression of B-cell lymphoma–extra large or dominant negative caspase 9, but not cellular FLICE (FADD-like IL-1b–converting enzyme)-inhibitory protein short, protected cells from the drug combination. Treatment of cells with PX-866 increased protein levels of p62, lysosome-associated membrane protein 2 (LAMP2), and microtubule-associated protein light chain (LC) 3 and LC3II that correlated with a large increase in LC3–green fluorescent protein (GFP) vesicle numbers. Exposure of PX-866 treated cells to sorafenib reduced p62 and LAMP2 levels, decreased the ratio of LC3 to LC3II, and reduced LC3-GFP vesicle levels. Knockdown of Beclin1 or autophagy-related 5 suppressed drug toxicity by ∼40%. In vivo, sorafenib and PX-866 or regorafenib and MK2206 cooperated to suppress the growth of established HuH7 and HCT116 tumors, respectively. Collectively our data demonstrate that the combination of sorafenib family kinase inhibitors with inhibitors of the PI3K/AKT pathway kills tumor cells in vitro and in vivo.
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- 2013
5. CHRONIC HEPATITIS C
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Salim Rind, Muhammad, primary, Iqbal shah, Muhammad, additional, Suthar, Ramesh Kumar, additional, and Jahangir, Syed, additional
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- 2016
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6. CHRONIC HEPATITIS C; “APRI SCORE A NONINVASIVE MARKER, ITS PREDICTIVE VALUE FOR DETERMINATION OF HEPATIC FIBROSIS AND LIVER CIRRHOSIS AT TERTIARY CARE HOSPITAL HYDERABAD/ JAMSHORO”
- Author
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Salim Rind, Dr. Muhammad, primary, Iqbal Shah, Dr. Muhammad, additional, Kumar Suthar, Dr. Ramesh, additional, and Jahangir, Syed, additional
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- 2016
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7. Biomarkers for virus-induced hepatocellular carcinoma (HCC)
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Mathew, Shilu, primary, Ali, Ashraf, additional, Abdel-Hafiz, Hany, additional, Fatima, Kaneez, additional, Suhail, Mohd, additional, Archunan, Govindaraju, additional, Begum, Nargis, additional, Jahangir, Syed, additional, Ilyas, Muhammad, additional, Chaudhary, Adeel G.A., additional, Al Qahtani, Mohammad, additional, Mohamad Bazarah, Salem, additional, and Qadri, Ishtiaq, additional
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- 2014
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8. In Silico Studies of Medicinal Compounds against Hepatitis C Capsid Protein from North India
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Mathew, Shilu, primary, Faheem, Muhammad, additional, Archunan, Govindaraju, additional, Ilyas, Muhammad, additional, Begum, Nargis, additional, Jahangir, Syed, additional, Qadri, Ishtiaq, additional, Qahtani, Mohammad Ai, additional, and Mathew, Shiny, additional
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- 2014
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9. Abstract 2690: Sorafenib/regorafenib and phosphatidyl inositol 3 kinase/thymoma viral proto-oncogene inhibition interact to kill tumor cells
- Author
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Nichola Cruickshanks, Jahangir Syed, Larry A. Booth, Seyedmehrad Tavallai, Andrew Poklepovic, Hossein A. Hamed, Gangadharan B. Sajithlal, Steven Grant, and Paul Dent
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Sorafenib ,Cancer Research ,Oncogene ,biology ,business.industry ,Kinase ,Pharmacology ,Perifosine ,chemistry.chemical_compound ,Oncology ,chemistry ,Regorafenib ,biology.protein ,medicine ,PTEN ,business ,Protein kinase B ,PI3K/AKT/mTOR pathway ,medicine.drug - Abstract
The present study aimed to determine whether the multikinase inhibitors, sorafenib/regorafenib, worked in conjunction with PI3K/AKT inhibitors to enhance tumor cell death. It has been noted that combination of sorafenib/regorafenib with a PI3K inhibitor acetic acid (PX-866) resulted in tumor cell death, in a greater than additive fashion, in liver, colorectal, lung, breast, kidney and brain cancer cells. Similar data was obtained using AKT inhibitors perifosine and MK2206. Furthermore, even cells lacking PTEN remained as sensitive to this combinational approach as cells expressing PTEN. PX-866 treatment abolished AKT/GSK3 phosphorylation, with tumor cell death correlating with reduced activity of AKT and mTOR. Expression of activated AKT and to a lesser extent activated mTOR reduced drug combination lethality. Expression of B-cell lymphoma-extra large or dominant negative caspase 9, but not cellular FLICE-inhibitory protein short, protected cells from the drug combination. Treatment of cells with PX-866 increased protein levels of p62, LAMP2 and LC3/LC3II which correlated with the resulting increase in LC3-GFP vesicle numbers. Exposure of PX-866 treated cells to sorafenib reduced p62 and LAMP2 levels, decreased the ratio of LC3 to LC3II and reduced LC3-GFP vesicle levels. Knockdown of Beclin1 or ATG5 suppressed drug toxicity by ∼40%. In vivo, combination of either sorafenib and PX-866 or regorafenib and MK2206 cooperated to suppress the growth of established HuH7 and HCT116 tumors, respectively. Collectively our data demonstrates that the combination of sorafenib family kinase inhibitors with inhibitors of the PI3K/AKT pathway kills tumor cells in vitro and in vivo. Citation Format: Larry A. Booth, Nichola A. Cruickshanks, G B. Sajithlal, Hossein A. Hamed, Seyedmehrad Tavallai, J Syed, Steven Grant, Andrew Poklepovic, Paul Dent. Sorafenib/regorafenib and phosphatidyl inositol 3 kinase/thymoma viral proto-oncogene inhibition interact to kill tumor cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2690. doi:10.1158/1538-7445.AM2014-2690
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- 2014
10. CHRONIC HEPATITIS C; "APRI SCORE A NONINVASIVE MARKER, ITS PREDICTIVE VALUE FOR DETERMINATION OF HEPATIC FIBROSIS AND LIVER CIRRHOSIS AT TERTIARY CARE HOSPITAL HYDERABAD/JAMSHORO".
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Rind, Muhammad Salim, Suthar, Ramesh Kumar, Jahangir, Syed, and shah, Muhammad Iqbal
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HEPATITIS C risk factors ,HEPATIC fibrosis ,CIRRHOSIS of the liver - Abstract
The major causative factor of hepatic cirrhosis and its complications in chronic hepatitis C is due to presence of liver fibrosis. To assess prognosis and management related decisions, the exact staging of liver fibrosis is of greatest importance. Now, liver biopsy is the inexact gold standard for this purpose. APRI or AST to platelet ratio Index is the best noninvasive marker which can predict presence of fibrosis in majority of chronic hepatitis C patients without the need of biopsy. It is also cost effective and only depends on routine testing (Platelet count and serum AST). Objectives: To determine the positive predictive value of APRI Score for the prediction of fibrosis and cirrhosis in chronic hepatitis C patients. Study design: Cross sectional study. Setting: Medical wards and Out Patient Medicine Department of Liaquat University Hospital Hyderabad / Jamshoro. Period: 6 months. Methodology: A total of 51 patients of either gender, age >14 years presenting to Medical wards and OPD for the evaluation of chronic hepatitis were enrolled in this research study after giving preference and avoiding criteria. Clinical data was collected at the time of liver biopsy and blood samples for liver function tests, blood glucose and complete blood picture with platelet count were collected before the biopsy (only AST and platelet count are needed for APRI score) a core biopsy needle of 14 gauge was used and the procedure was conducted under ultrasound guidance. Fibrosis stage was determined according to the METAVIR group scoring system. The patients were examined in a very comfortable manner and all the information collected from the patients was kept confidential and entered in the predesigned proforma. Results: A total of 51 patients were selected for this study. Out of these 31 (60.78%) were male and 20(39.22%) were female. The mean age was 42.53 years (±11.2 SD). The positive predictive value for APRI score between 0.5 to 1.0 was 58.82% whereas the positive predictive values for APRI score 1.1-1.5 was 70.58%. Conclusion: The positive predictive values of APRI score in the ranges of 0.5 to 1.5 were not indicative of the presence of significant liver fibrosis in this research study. However, additional data are required to authenticate or disprove the usefulness of APRI score for the prediction of significant hepatic fibrosis in chronic hepatitis C patients. [ABSTRACT FROM AUTHOR]
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- 2016
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11. EFFECTS OF EDUCATIONAL ATTAINMENT ON DENTITION STATUS IN SOCIOECONOMICALLY DEPRIVED POPULATION OF KARACHI.
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MOHAMMAD, TAQI, MIRZA, ASAAD JAVAID, and JAHANGIR, SYED MOHAMMAD
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EDUCATIONAL attainment research ,DENTITION ,SOCIOECONOMIC factors ,MOUTH examination ,DENTAL caries research - Abstract
The objective of this study was to evaluate the relationship between educational attainment and dentition status. A cross sectional survey was conducted. The total number of participants in this study was 408. The subjects of age 15 years to 65 years were included in this survey. To record subjects own educational attainment, education level was divided into levels which are Primary school (1-5 grade), Middle (6-8 Grade), Secondary or High school (9-10 Grade), Higher Secondary and highly educated which include Tertiary School (Bachelors). To record dentition status, DMFT index was used. The DMFT score of 0 indicates minimum risk of caries, DMFT score between 1-4 indicates moderate risk of decay and DMFT score greater than 4 indicates high risk of dental decay. The data was collected through intra oral examination of subjects. The test indicates that association exists between level of education and DMFT scores. However, the strength of association is not very strong. The correlation value for spearman's rho was (.116) and (P= .01). The impact of poor oral health in low educated people can be reduced by the developing policies related to building healthy public policy, strengthening community actions, and developing personal skills. To improve the knowledge, attitudes and oral health of people with low educational status, it is necessary to increase the oral health promotion activities. [ABSTRACT FROM AUTHOR]
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- 2014
12. To examine delayed PTSD symptomatology over time among trauma survivors in Pakistan.
- Author
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Khalily, Muhammad Tahir, Gul, Seema, Mushtaq, Rabia, and Jahangir, Syed Farhana
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POST-traumatic stress disorder ,TRAUMATIC psychoses ,PSYCHOLOGY ,SYMPTOMS - Abstract
This study investigates the presence of delayed PTSD symptoms after a period of twenty months in individuals who had an exposure to a traumatic event and to distinguish them from individuals who had no direct exposure but were affected indirectly. A purposive sample of fifty one individuals comprising Group 1 (Female N=30) and Group 2 (Male N=21) examined in this study. Two standardised psychological tests known as Clinician- Administered PTSD Scale (CAPS) and PTSD Checklist - Civilian Version (PCL-C) were used for this purpose. Our results indicated a significant difference (P<.001) between Group 1 and Group 2 and distinguished Group 1 (Individuals with direct exposure to trauma) from Group 2 (Individuals with indirect exposure to trauma) on the basis of PTSD symptomatology. This suggests the presence of delayed PTSD symptoms in individuals who were exposed to a traumatic event than the individuals with no direct exposure to a traumatic event after a long period of a recovery phase. Our results were found consistent with the previous studies and add the findings of this study to the scientific literature in the context of developing delayed PTSD symptoms in response to a traumatic event [ABSTRACT FROM AUTHOR]
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- 2012
13. SERIAL ORDER IN SHORT-TERM MEMORY: A COMPARATIVE STUDY BETWEEN DEMENTIA PATIENTS AND NORMAL INDIVIDUALS.
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Um-e-Kalsoom, Jahangir, Syed Farhana, and Khalily, Muhammad Tahir
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SHORT-term memory , *DEMENTIA patients , *PSYCHIATRIC hospitals , *EDUCATION - Abstract
The present study is designed to investigate the impact of three different types of short term memory models on serial recall. It also aims to see the impact of these different memory models on different levels of neurological functioning. Fifty four demented patients were selected from Khyber Teaching Hospital, Lady Reading Hospital and Mental hospital Peshawar, Pakistan. Mini Mental State Examination was used for screening as well as for measuring the intensity of dementia. On the basis of these scores, patients were bifurcated into two experimental groups of an equal number portraying severe dementia and moderate dementia. The control group (n=27) was selected from the normal population having no neurological dysfunction, and was matched on the basis of age, education and socioeconomic status. In order to explore the difference among the groups t-test was used. Results indicated a significant difference among the groups, which subsequently supports the hypothesis framed for this study. [ABSTRACT FROM AUTHOR]
- Published
- 2011
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