Shahana Urooj Kazmi

Dr. Shahana Urooj Kazmi


Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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17 October 2013 in BMC Ophthalmology
Verified
Journal Article
Open access
PDF file
SASyed Hani Abidi
Syed Hani Abidi
SSSikandar K Sherwani
Sikandar K Sherwani
TSTarrunum R Siddiqui
Tarrunum R Siddiqui
Asma BashirAsma Bashir
Asma Bashir
SKShahana Urooj Kazmi
Shahana Urooj Kazmi
The contaminated contact lens provides Pseudomonas aeruginosa an ideal site for attachment and biofilm production. Continuous contact of the eye to the biofilm-infested lens can lead to serious ocular diseases, such as keratitis (corneal ulcers). The biofilms also prevent effective penetration of the antibiotics, which increase the chances of antibiotic resistance.

25 March 2014 in Pathology and Oncology Research
Verified
Journal Article
Closed access
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YRYasir Raza
Yasir Raza
AKAdnan Khan
Adnan Khan
AFAmber Farooqui
Amber Farooqui
MMMuhammad Mubarak
Muhammad Mubarak
AFAlex Facista
Alex Facista
SKShahana Urooj Kazmi
Shahana Urooj Kazmi

18 December 2015 in BMC Medical Genetics
Verified
Journal Article
Open access
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SAShafqat Ahmad
Shafqat Ahmad
WZWei Zhao
Wei Zhao
FRFrida Renström
Frida Renström
ARAsif Rasheed
Asif Rasheed
MSMaria Samuel
Maria Samuel
DSDanish Saleheen
Danish Saleheen
Multiple genetic variants have been reliably associated with obesity-related traits in Europeans, but little is known about their associations and interactions with lifestyle factors in South Asians. In 16,157 Pakistani adults (8232 controls; 7925 diagnosed with myocardial infarction [MI]) enrolled in the PROMIS Study, we tested whether: a) BMI-associated loci, individually or in aggregate (as a genetic risk score - GRS), are associated with BMI; b) physical activity and smoking modify the association of these loci with BMI. Analyses were adjusted for age, age2, sex, MI (yes/no), and population substructure. Of 95 SNPs studied here, 73 showed directionally consistent effects on BMI as reported in Europeans. Each additional BMI-raising allele of the GRS was associated with 0.04 (SE = 0.01) kg/m2 higher BMI (P = 4.5 × 10−14). We observed nominal evidence of interactions of CLIP1 rs11583200 (P interaction = 0.014), CADM2 rs13078960 (P interaction = 0.037) and GALNT10 rs7715256 (P interaction = 0.048) with physical activity, and PTBP2 rs11165643 (P interaction = 0.045), HIP1 rs1167827 (P interaction = 0.015), C6orf106 rs205262 (P interaction = 0.032) and GRID1 rs7899106 (P interaction = 0.043) with smoking on BMI. Most BMI-associated loci have directionally consistent effects on BMI in Pakistanis and Europeans. There were suggestive interactions of established BMI-related SNPs with smoking or physical activity.

12 January 2010 in BMC Infectious Diseases
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Journal Article
Open access
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MRMohammad A Rai
Mohammad A Rai
VNVivek R Nerurkar
Vivek R Nerurkar
SKSuhail Khoja
Suhail Khoja
SKSaeed Khan
Saeed Khan
RYRichard Yanagihara
Richard Yanagihara
SASyed Asad Ali
Syed Asad Ali
Background: We have previously reported a HIV-1 subtype A infection in a community of injection drug users (IDUs) in Karachi, Pakistan. We now show that this infection among the IDUs may have originated from a single source. Methods: Phylogenetic analysis was performed of partial gag sequences, generated using PCR, from 26 HIV-positive IDU samples. Results: Our results showed formation of a tight monophyletic group with an intra-sequence identity of < 98% indicating a "founder effect". Our data indicate that the HIV-1 epidemic in this community of IDUs may have been transmitted by an HIV positive overseas contract worker who admitted to having contact with commercial sex workers during stay abroad. Conclusion: Specific measures need to implemented to control transmission of HIV infection in Pakistan through infected migrant workers.

27 October 2008 in BMC Infectious Diseases
Verified
Journal Article
Open access
PDF file
SKSaeed Khan
Saeed Khan
MRMohammad A Rai
Mohammad A Rai
AKAdnan Khan
Adnan Khan
AFAmber Farooqui
Amber Farooqui
SKShahana Urooj Kazmi
Shahana Urooj Kazmi
SASyed Asad Ali
Syed Asad Ali
Background: On October 8, 2005, an earthquake of magnitude 7.6 hit the Northern parts of Pakistan. In the post-earthquake scenario, overcrowding, improper sewage disposal, contamination of food and drinking water, hasty surgical procedures, and unscreened blood transfusions to earthquake victims most likely promotes the spread of infections already prevalent in the area.Objective: The objective of the study reported here was to determine the prevalence of Human Immunodeficiency and Hepatitis C viruses (respectively, HIV and HCV) in the earthquake-affected communities of Pakistan. The samples were analyzed 2 months and then again 11 months after the earthquake to estimate the burden of HIV and HCV in these areas, and to determine any rise in the prevalence of these viral infections as a result of the earthquake.Methods: Blood samples were initially collected during December, 2005 to March 2006, from 245 inhabitants of the earthquake-affected areas. These samples were screened for HCV and HIV, using immunochromatography and Enzyme-Linked Immuno-Sorbent Assay (ELISA).Results: Out of 245 samples tested, 8 (3.26%) were found positive for HCV, and 0 (0.0%) for HIV, indicating the existence of HCV infection in the earthquake-stricken areas. The same methods were used to analyze the samples collected in the second round of screening in the same area, in September, 2006 – 11 months after the earthquake. This time 290 blood samples were collected, out of which 16 (5.51%) samples were positive for HCV, and 0 for HIV.Conclusion: A slightly higher prevalence of HCV was recorded 11 months after the earthquake; this increase, however, was not statistically significant. None of the study participants was found HIV-infected.

1 May 2020 in DNA Repair
Verified
Journal Article
Open access
YRYasir Raza
Yasir Raza
AAAyaz Ahmed
Ayaz Ahmed
AKAdnan Khan
Adnan Khan
Arif Ali ChishtiArif Ali Chishti
Arif Ali Chishti
SASyed Shakeel Akhter
Syed Shakeel Akhter
SKShahana Urooj Kazmi
Shahana Urooj Kazmi
Gastric cancers are the third leading cause of cancer mortality in the world. Helicobacter pylori causes over 60 % of all stomach cancers. Colonization of the gastric mucosa by H. pylori results in increased DNA damage. Repair of DNA damage may also be reduced by H. pylori infection. Reduced DNA repair in combination with increased DNA damage can cause carcinogenic mutations. During progression to gastric cancer, gastric epithelium goes through stages of increasing pathology. Determining the levels of DNA repair enzymes during progression to gastric cancer could illuminate treatment approaches. Our aim is to determine the level of gastric expression of DNA repair proteins ERCC1 (a nucleotide excision repair enzyme) and PMS2 (a mismatch repair enzyme) in the presence of H. pylori infection at successive stages of gastric pathology and in gastric cancers. We analyzed gastric tissues of 300 individuals, including 30 without dyspepsia, 200 with dyspepsia and 70 with gastric cancers. The presence of H. pylori, gastric pathology and expression of DNA repair proteins ERCC1 and PMS2 were evaluated. Infection by H. pylori carrying the common cagA gene reduced median nuclear expression of ERCC1 and PMS2 to less than 20 % and 15 % of normal, respectively, in all pathologic stages preceding cancer. ERCC1 and PMS2 nuclear expression was 0-5 % of normal in gastric cancers. H. pylori can cause deficiency of ERCC1 and PMS2 protein expression. These deficiencies are associated with gastric pathology and cancer. This reduction in DNA repair likely causes carcinogenic mutations. Substantially reduced ERCC1 and PMS2 expression appears to be an early step in progression to H. pylori-induced gastric cancer.