Gene therapy has been one of the most researched topics in the last decade. It has now become a revolutionized therapeutic tool of modern medicine. Gene therapy is the alteration of the defective gene involved in the disease process in the host cells. It delivers therapeutic genetic information via modified viral or non-viral vectors. Ocular gene therapy, in particular, has progressed in treating inherited retinal diseases since the eye is a favourable organ for gene therapy development. The advantage of the eye as a target for gene therapy is attributed to its easy accessibility and blood-ocular barrier. Several ongoing clinical trials are investigating various gene therapies for other ocular diseases, including neovascular agerelated macular degeneration, retinitis pigmentosa (RP), Usher syndrome, glaucoma, and several others. However, there are challenges such as ocular inflammation and humoral response, infection by the viral vectors, and insertional mutagenesis. These limitations depend on several factors; whether viral or non-viral vectors are used, which viral vectors were used, the route of administration, whether subretinal, intravitreal, or suprachoroidal, and the dose of vectors and the target tissue. These complications may lead to therapeutic failure and vision loss due to intraocular inflammation. This review aims to summarize existing knowledge about ocular gene therapy and the associated limitations we face, with a special focus on a few ongoing clinical trials.
A variant of autism spectrum disorder (ASD) known as Asperger syndrome (AS) is characterized by severe issues with interpersonal, verbal, and nonverbal communication as well as restricted and repetitive patterns of behavior and activities. Although there is no known cause for ASD, various genetic as well as non-genetic risk factors that may act either alone or in combination to induce ASD have been identified. The occurrence of ASD has been increasing worldwide. Co-occurring neuropsychological diseases are frequently present as well. The premise for diagnosis is the observation of abnormal conduct, with diagnostic criteria emphasizing limitations in social interaction and communication as well as constrained, repetitive behavioral patterns, activities, or hobbies. The degree of the illness and the presence of intellectual impairment have a significant impact on the prognosis. Like autism, Asperger's can neither be prevented nor treated. There is no specific medical therapy that can effectively cure all of the symptoms of autism. However, medications may be used as adjuvant therapy for maladaptive behaviors and co-occurring mental problems. The treatment aims to reduce core impairments, increase functional ability, and reduce harmful behaviors that could limit functional skills. It is crucial to provide proper care, establish supportive networks for individuals who are affected and their families, and use effective therapies to enhance functioning and results.
BACKGROUND Retinopathy and nephropathy are chronic vascular complications of type 2 diabetes mellitus, this eventually leads to end stage renal disease and blindness. Diabetic retinopathy is an important cause of legal blindness in 20 - 70 years. The purpose of the study was to establish association between severity of diabetic retinopathy with systemic levels of glycosylated haemoglobin and renal function test. METHODS This is a cross sectional study conducted among 75 patients with type 2 diabetes mellitus attending the ophthalmology out-patient department (OPD) of Acharya Vinoba Bhave Hospital, Wardha and patients referred from the hospital. Detailed fundus examination and staging of diabetic retinopathy (DR) was done. Glycosylated haemoglobin levels, serum creatinine and blood urea nitrogen were measured. RESULTS Majority of patients were in the age range of 61 to 70 years. Mean ± SD of 3 parameters in patients with no DR, mild non-proliferative diabetic retinopathy (NPDR), moderate NPDR, severe NPDR and proliferative diabetic retinopathy (PDR) were as follows: Serum creatinine 1.12 ± 0.41, 1.21 ± 0.53, 1.35 ± 0.49, 1.55 ± 0.22 and 1.70 ± 0.23 respectively. P = 0.007. Blood urea nitrogen (BUN) 28.62 ± 4.20, 31.83 ± 7.20, 37.31 ± 12.57, 44.21 ± 7.53 and 48.76 ± 5.08 respectively. P = 0.0001. HbA1c l, 6.72 ± 0.60, 8.14 ± 0.98, 8.52 ± 2.67, 9.96 ± 1.22 and 12.14 ± 1.96 respectively. P = 0.0001. All the 3 parameters were statistically significant. 40 % of cases had clinically significant macular oedema. CONCLUSIONS Poor glycaemic control as seen by higher levels of glycosylated haemoglobin and deranged renal function is associated with severe form of DR. KEY WORDS Diabetes Mellitus, Diabetic Retinopathy, Serum Creatinine HbA1c and BUN
Gefitinib is a selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor. It is used for treating locally advanced or metastatic non-small cell lung carcinoma and is well tolerated systemically. However, sight-threatening ocular adverse effects, like corneal ulcer and perforation, can occur due to the expression of EGFR on limbal and conjunctival epithelia. In this report, we describe a case of a 36-year-old female who presented with loss of eyebrow hair and eyelashes of both eyes and blurring of vision in the right eye. On ocular examination, the patient had anterior blepharitis, madarosis, punctuate epithelial erosions and reduced corneal sensation in both eyes, and corneal thinning in the right eye. On specular microscopy, there was decreased central corneal thickness in both eyes. Treatment with topical antibiotics and lubricating drops led to the resolution of blepharitis and punctate epithelial erosions. This case report aims to create awareness among ophthalmologists and oncologists about the early detection of gefitinib-related ocular adverse effects and timely intervention in patients.
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