Drug induced Parkinson’s: A comprehensive review of the issues and measures required to tackle the same

Drug-inducedParkinsonism(DIP) closelyresemblesParkinson'sdisease(PD)inmotorsymptoms butiscausedbyspecificmedicationsdisruptingdopaminereceptorsandneurotransmitterbalance. PD involves a complex interplay of genetic, environmental, and biochemical factors resulting in the gradual degeneration of dopaminergic neurons. Environmental toxins and genetic mutations, such as LRRK2 and SNCA, contribute to the risk of developing PD. DIP primarily occurs due to the obstruction of dopamine receptors by certain drugs, notably antipsychotics and antiemetics, affecting dopamine transmission and causing Parkinsonian symptoms. Toxin-induced Parkinsonism(TIP)arisesfromexposuretosubstanceslikemanganese,herbicides,pesticides,and specific drugs, disrupting dopaminergic pathways and altering neurotransmission. This study examines various cases of DIP, emphasizing the significance of timely identification and intervention. A thorough understanding and proactive management of DIP are crucial for alleviatingsymptomsandimprovingpatientoutcomes.Healthcareprofessionalsneedtodiligently monitor patients using medications associated with DIP, adjust treatment plans, and educate patientsaboutpotentialsideeffects. Further researchisimperativetounravelthepathophysiology of DIP, considering genetic, environmental, and drug-related factors, to enhance clinical practices and optimize patient care. Addressing DIP requires a multifaceted approach, including early recognition, thoughtful management, and patient-centred care

Data for engineering lipid metabolism of Chinese hamster ovary (CHO) cells for enhanced recombinant protein production

The data presented in this article relates to the manuscript entitled ‘Engineering of Chinese hamster ovary cell lipid metabolism results in an expanded ER and enhanced recombinant biotherapeutic protein production’, published in the Journal Metabolic Engineering [1]. In the article here, we present data examining the overexpression of the lipid metabolism modifying genes SCD1 and SREBF1 in CHO cells by densitometry of western blots and by using mass spectrometry to investigate the impact on specific lipid species. We also present immunofluorescence data at the protein level upon SCD1 and SREBF1 overexpression. The growth profile data during batch culture of control CHO cells and CHO cells engineered to overexpress SCD1 and SREBF1 during batch culture are also reported. Finally, we report data on the yields of model secretory recombinant proteins produced from control, SCD1 or SREBF1 engineered cells using a transient expression systems

The oxysterol 27-hydroxycholesterol increases β-amyloid and oxidative stress in retinal pigment epithelial cells

<p>Abstract</p> <p>Background</p> <p>Alzheimer's disease (AD) and age-related macular degeneration (AMD) share several pathological features including β-amyloid (Aβ) peptide accumulation, oxidative damage, and cell death. The causes of AD and AMD are not known but several studies suggest disturbances in cholesterol metabolism as a culprit of these diseases. We have recently shown that the cholesterol oxidation metabolite 27-hydroxycholesterol (27-OHC) causes AD-like pathology in human neuroblastoma SH-SY5Y cells and in organotypic hippocampal slices. However, the extent to which and the mechanisms by which 27-OHC may also cause pathological hallmarks related to AMD are ill-defined. In this study, the effects of 27-OHC on AMD-related pathology were determined in ARPE-19 cells. These cells have structural and functional properties relevant to retinal pigmented epithelial cells, a target in the course of AMD.</p> <p>Methods</p> <p>ARPE-19 cells were treated with 0, 10 or 25 μM 27-OHC for 24 hours. Levels of Aβ peptide, mitochondrial and endoplasmic reticulum (ER) stress markers, Ca²⁺homeostasis, glutathione depletion, reactive oxygen species (ROS) generation, inflammation and cell death were assessed using ELISA, Western blot, immunocytochemistry, and specific assays.</p> <p>Results</p> <p>27-OHC dose-dependently increased Aβ peptide production, increased levels of ER stress specific markers caspase 12 and gadd153 (also called CHOP), reduced mitochondrial membrane potential, triggered Ca²⁺dyshomeostasis, increased levels of the nuclear factor κB (NFκB) and heme-oxygenase 1 (HO-1), two proteins activated by oxidative stress. Additionally, 27-OHC caused glutathione depletion, ROS generation, inflammation and apoptotic-mediated cell death.</p> <p>Conclusions</p> <p>The cholesterol metabolite 27-OHC is toxic to RPE cells. The deleterious effects of this oxysterol ranged from Aβ accumulation to oxidative cell damage. Our results suggest that high levels of 27-OHC may represent a common pathogenic factor for both AMD and AD.</p

A class of estimators with estimated optimum values in sample surveys

Srivastava and Jhajj (1981) proposed a class of estimators for population mean of a character using auxiliary information and optimum values involving unknown parameters. From the practical point of view, their results have very little utility. In view of practical utility, we propose a class of estimators with estimated optimum values. Further, it is shown that the proposed class with estimated optimum values attains the same minimum mean square error of the class of estimators based on optimum values.class of estimators mean square error estimated optimum values unbiased estimators

Drug induced Parkinson’s: A comprehensive review of the issues and measures required to tackle the same

Drug-inducedParkinsonism(DIP) closelyresemblesParkinson'sdisease(PD)inmotorsymptoms butiscausedbyspecificmedicationsdisruptingdopaminereceptorsandneurotransmitterbalance. PD involves a complex interplay of genetic, environmental, and biochemical factors resulting in the gradual degeneration of dopaminergic neurons. Environmental toxins and genetic mutations, such as LRRK2 and SNCA, contribute to the risk of developing PD. DIP primarily occurs due to the obstruction of dopamine receptors by certain drugs, notably antipsychotics and antiemetics, affecting dopamine transmission and causing Parkinsonian symptoms. Toxin-induced Parkinsonism(TIP)arisesfromexposuretosubstanceslikemanganese,herbicides,pesticides,and specific drugs, disrupting dopaminergic pathways and altering neurotransmission. This study examines various cases of DIP, emphasizing the significance of timely identification and intervention. A thorough understanding and proactive management of DIP are crucial for alleviatingsymptomsandimprovingpatientoutcomes.Healthcareprofessionalsneedtodiligently monitor patients using medications associated with DIP, adjust treatment plans, and educate patientsaboutpotentialsideeffects. Further researchisimperativetounravelthepathophysiology of DIP, considering genetic, environmental, and drug-related factors, to enhance clinical practices and optimize patient care. Addressing DIP requires a multifaceted approach, including early recognition, thoughtful management, and patient-centred care

The draft genome sequence of Mangrovibacter sp. strain MP23, an endophyte isolated from the roots of Phragmites karka

Till date, only one draft genome has been reported within the genus Mangrovibacter. Here, we report the second draft genome shotgun sequence of a Mangrovibacter sp. strain MP23 that was isolated from the roots of Phargmites karka (P. karka), an invasive weed growing in the Chilika Lagoon, Odisha, India. Strain MP23 is a facultative anaerobic, nitrogen-fixing endophytic bacteria that grows optimally at 37 °C, 7.0 pH, and 1% NaCl concentration. The draft genome sequence of strain MP23 contains 4,947,475 bp with an estimated G + C content of 49.9% and total 4392 protein coding genes. The genome sequence has provided information on putative genes that code for proteins involved in oxidative stress, uptake of nutrients, and nitrogen fixation that might offer niche specific ecological fitness and explain the invasive success of P. karka in Chilika Lagoon. The draft genome sequence and annotation have been deposited at DDBJ/EMBL/GenBank under the accession number LYRP00000000