Publications by authors named "Haider Cheema"

Diabetic macular edema (DME) is a major cause of vision impairment in diabetic individuals, characterized by fluid accumulation in the macula due to a breakdown of the blood-retinal barrier (BRB). This review article explores the role of anti-vascular endothelial growth factor (anti-VEGF) therapies in the management of DME. Anti-VEGF treatments, including ranibizumab, bevacizumab, and aflibercept, have revolutionized DME management by targeting VEGF, a key mediator in DME pathogenesis.

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This review examines the evolution, current status, and future potential of minimally invasive glaucoma surgeries (MIGS), a significant advancement in the treatment of glaucoma, a leading cause of irreversible blindness. MIGS offer a less invasive alternative to traditional glaucoma surgeries, primarily aimed at reducing intraocular pressure, minimizing tissue trauma, and providing a safer profile. With the emergence of devices such as the Trabectome, iStent, and others, MIGS have expanded the surgical toolkit, allowing personalized, patient-centered care.

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Sarcoid-like granulomas are a rare adverse effect of TNF-α inhibitors that are becoming increasingly reported in the literature. A retrospective study in France estimated this adverse effect to occur in 0.04% patients.

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Aims: To determine the short-term efficacy of corneal collagen crosslinking (CXL) treatment in patients with progressive Keratoconus (KCN) in comparison with no treatment.

Settings And Design: This controlled clinical trial study was carried out at a tertiary eye hospital, Eastern Province, Saudi Arabia.

Methods And Material: A prospective controlled clinical study of patients being treated for Keratoconus at a tertiary eye care hospital in the Eastern province of Saudi Arabia.

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The aim of this communication is to report the incidence of endophthalmitis following the use of intravitreal Bevacizumab (IVB) at a tertiary care hospital in the Eastern province of Saudi Arabia. A total of 2769 intravitreal Bevacizumab injections were carried out between January 2009 and April 2014. During this period, one case of endophthalmitis following IVB injection occurred.

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Aim: To report the visual outcome based on various patterns of optical coherence tomography (OCT) morphology in diabetic macular edema (DME), following treatment with anti-VEGF intravitreal bevacizumab (IVB) injection.

Methods: Sixty-seven consecutive subjects with centre involving DME underwent intravitreal injection of Bevacizumab (1.25 mg/0.

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Purpose: We report our experience in treating 2 patients of idiopathic retinal vasculitis, aneurysm, and neuroretinitis (IRVAN) syndrome with antitumor necrosis factor agent, infliximab, who showed a very favorable response to treatment.

Methods: Two patients with clinical diagnosis of IRVAN syndrome were included in the study. The visual acuity was affected due to ocular inflammation and presence of macular edema due to exudation around the optic nerve.

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The phenotypic change characteristic of Aurora B inhibition is the induction of polyploidy. Utilizing specific siRNA duplexes and a selective small molecule inhibitor (AZD1152) to inhibit Aurora B activity in tumor cells, we sought to elucidate the mechanism by which Aurora B inhibition results in polyploidy. Cells treated with AZD1152 progressed through mitosis with misaligned chromosomes and exited without cytokinesis and subsequently underwent endoreduplication of DNA despite activation of a p53-dependent pseudo G1 checkpoint.

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Malignant peripheral nerve sheath tumors (MPNST) are soft-tissue tumors with a very poor prognosis and largely resistant to chemotherapy. MPNSTs are characterized by activation of the Ras pathway by loss of tumor suppressor neurofibromatosis type 1. In view of this, MPNST may be susceptible to inhibition of the activated Ras/Raf/mitogen-activated protein kinase pathway by the B-Raf inhibitor sorafenib.

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Purpose: Chk1 kinase is a critical regulator of both S and G(2)-M phase cell cycle checkpoints in response to DNA damage. This study aimed to evaluate the biochemical, cellular, and antitumor effects of a novel Chk1 inhibitor, CHIR124.

Experimental Design: CHIR-124 was evaluated for its ability to abrogate cell cycle checkpoints, to potentiate cytotoxicity, and to inhibit Chk1-mediated signaling induced by topoisomerase I poisons in human tumor cell line and xenograft models.

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