18 research outputs found
1-ChloroÂacetyl-2,6-bisÂ(2-chloroÂphenÂyl)-3,5-dimethylÂpiperidin-4-one
In the title compound, C21H20Cl3NO2, the piperidin-4-one ring adopts a boat conformation. The two 2-chloroÂphenyl groups are approximately perpendicular to each other, making a dihedral angle of 74.07 (8)°
Hypofractionated Radiotherapy for Stage I Squamous Cell Carcinoma Glottis: An Experience with 60Gy in 20 Fractions
Introduction: Early-stage glottic cancer has a high cure rate with definitive radiotherapy. Historical reports show excellent local control. The present study evaluated the outcomes of early glottic cancer patients treated with a hypofractionated radiotherapy schedule of 60Gy in 20 fractions.Material and Methods: This is a retrospective study of patients with stage I glottic cancer who received radical intent LINAC-based hypo-fractionated 3D conformal radiotherapy with a dose 60Gy in 20 fractions. The primary objective was to assess the locoregional control (LRC), and secondary objectives were to determine disease-free survival (DFS), overall survival (OS), and toxicity.Results: The analysis included 105 patients from the age range of 35-88 years. About 69% of patients were over 60 years of age. The median overall treatment time (OTT) was 26 days (24 – 30 days). The mean follow-up was 74 months, ranging from 9 to 135 months. Seven patients had locoregional recurrence after an initial complete clinical response. Six had local, and one had a regional nodal recurrence. DFS at five years and ten years were 83% and 69%, and OS at five years and ten years were 87% and 80%, respectively. Most patients reported grade I skin reactions and tolerated the treatment well. We did not observe any late adverse events such as persistent laryngeal edema or radiation necrosis.Conclusion: The radiotherapy schedule of 60Gy in 20 fractions over four weeks offers comparable local disease control with reasonable long-term side effects in T1 glottic cancer
Effect of dexamethasone implant on intraocular cytokines in diabetic macular edema
Purpose: Our primary aim was to evaluate intraocular cytokines (IC) before and after dexamethasone in diabetic macular edema (DME). Our secondary aim was to study the early and late effects of single dexamethasone implant in DME. Methods: This before and after comparative study was conducted at the Department of Ophthalmology and Centre for Nanosciences at a quaternary referral center in Kerala, India, from September 2016 to September 2018. Patients underwent complete ophthalmological examination and cytokine analysis before and after dexamethasone implant. Levels of cytokines at baseline and repeat sample were studied. Results: Twenty-seven eyes (21 patients) were divided into two groups depending on time from baseline to second injection. Group 1 included patients with 3 months between the two samples –15 (55.6%). Best corrected visual acuity (BCVA) and central macular thickness (CMT) improved significantly post-dexamethasone in group 1, but not in group 2. Interleukin (IL)-4, IL-6, IL-10, vascular endothelial growth factor (VEGF), IL-1β, interferon-gamma inducible protein-10 (IP-10), monocyte chemoattractant protein-1 (MCP-1), and IL-2 decreased post-injection in group 1. But cytokines increased post-dexamethasone in group 2, except IL-10. When compared to baseline, IL-6 reduced to half in group 1 (P-value 0.814) and it tripled in group 2 ( P-value 0.009). The level of VEGF in the first and second samples was not different in either group. Conclusion: Our study suggests that dexamethasone acts more on IC than VEGF in DME. This is significant in the first 3 months with a rebound effect on IL-6 after 3 months. Our study also suggests that repeat injection of DEX in DME should be done at 3 months to prevent deterioration of visual acuity (VA) and worsening of CMT
A novel bio-physical approach for perchlorate contaminated well water treatment
A novel bio-physical approach for treating well water contaminated with perchlorate (ClO4¯) at 15 mg/L is reported in this study. In this process, the ClO4¯ was initially treated in an anaerobic fixed-film bioreactor (55 L), followed by a ceramic Micro-Filtration (MF) unit (1.5 μm pore size, 0.12 m2 surface area) and a Reverse Osmosis (RO) unit (0.38 m2 surface area) connected in series. The bioreactor inoculated with a ClO4¯ reducing bacterium Serratia marcescens (Gen bank no. JQ807993) removed ~97% of the ClO4¯ using acetate as substrate (acetate/ClO4¯ ratio = 4). Subsequently, the MF and RO units removed ClO4¯ to <10 μg/L, Total Dissolved Solids (TDS) to <25 mg/L and Total Chemical Oxygen Demand (TCOD) to below detection Limit. The fouling associated with membranes was controlled (88–100%) through hourly manual backwashing with 2 L pure water at 25 L/h, and 60 psi, and forward flushing with 1 L pure water at 30 L/h and 3–5 psi for MF and RO units, respectively. The rejects and membrane wash water were also treated in the bioreactor, resulted in complete removal of ClO4¯ through this approach. This is the first report where biotreatment is adopted as a pre- and post-treatment to membrane process for removing ClO4¯, and this will find field application for treating ClO4¯ contaminated ground as well as surface water sources
Active DNA demethylation in post-mitotic neurons: A reason for optimism
Over the last several years proteins involved in base excision repair (BER) have been implicated in active DNA demethylation. We review the literature supporting BER as a means of active DNA demethylation, and explain how the various components function and cooperate to remove the potentially most enduring means of epigenetic gene regulation. Recent evidence indicates that the same pathways implicated during periods of widespread DNA demethylation, such as the erasure of methyl marks in the paternal pronucleus soon after fertilization, are operational in post-mitotic neurons. Neuronal functional identities, defined here as the result of a combination of neuronal subtype, location, and synaptic connections are largely maintained through DNA methylation. Chronic mental illnesses, such as schizophrenia, may be the result of both altered neurotransmitter levels and neurons that have assumed dysfunctional neuronal identities. A limitation of most current psychopharmacological agents is their focus on the former, while not addressing the more profound latter pathophysiological process. Previously, it was believed that active DNA demethylation in post-mitotic neurons was rare if not impossible. If this were the case, then reversing the factors that maintain neuronal identity, would be highly unlikely. The emergence of an active DNA demethylation pathway in the brain is a reason for great optimism in psychiatry as it provides a means by which previously pathological neurons may be reprogrammed into a more favorable role. Agents targeting epigenetic processes have shown much promise in this regard, and may lead to substantial gains over traditional pharmacological approaches