Hastingsrohde2472
6%), and kidney weight (43.75%). Histological examination of the kidneys showed capillary congestion, tubular damage, glomerular distortion, and many oxalate crystals. Rats co-administered with EEATR 250 and 500 mg/kg had marked improvement (P ≤ 0.0001%) in all the above parameters with a marked reduction in size and number of oxalate crystals in the kidney. In the anti-oxidant assays, EEATR exhibited significant antioxidant activity.
EEATR was found to be an effective nephroprotective agent in adenine-induced chronic renal failure in Wistar albino rats.
EEATR was found to be an effective nephroprotective agent in adenine-induced chronic renal failure in Wistar albino rats.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with kidney damage. In India, only a few reports related to the risk of chronic kidney disease (CKD) with NSAIDs are available. The present study highlights the prevalence and pattern of NSAIDs-induced CKD adverse drug reactions in the Indian population.
The individual case safety reports (ICSRs) reported by the National Coordination Centre (NCC)-Pharmacovigilance Program of India to the Uppsala monitoring center Pharmacovigilance database system "VigiLyze" were analyzed by using the preferred term "Chronic Kidney Disease" and "NSAIDs" from July 1, 2011 to September 12, 2019. A total of 28 ICSRs of NSAIDs associated CKD ICSRs were analyzed retrospectively for age, gender, concomitant medication, seriousness, and other criteria.
About 82% of CKD cases due to NSAIDs were in the age group of 40-80 years, in which 54% belong to male. About 43% of the patients had CKD due to the use of diclofenac, and almost 96% of the patients had oral dosage forms of NSAIDs. The main indications of NSAIDs in these CKD cases were generalized body pain and joint pain. About 79% case of NSAID-induced CKD were serious, among which 54% led to the hospitalization and further use of NSAIDs discontinued in 86% of CKD cases.
The present study revealed that prolonged use of NSAIDs in chronic pain conditions was responsible for CKD. To reduce the risk of NSAIDs-induced CKD, health care professionals should take the necessary steps to improve patient safety.
The present study revealed that prolonged use of NSAIDs in chronic pain conditions was responsible for CKD. To reduce the risk of NSAIDs-induced CKD, health care professionals should take the necessary steps to improve patient safety.
Colorectal cancer (CRC) is one of the most common cancers worldwide. RNA-binding proteins (RBPs) regulate essential biological processes and play essential roles in a variety of cancers. The present study screened differentially expressed RBPs, analyzed their function and constructed a prognostic model to predict the overall survival of patients with CRC.
We downloaded CRC RNA-sequencing data from the Cancer Genome Atlas (TCGA) portal and screened differentially expressed RBPs. Then, functional analyses of these genes were performed, and a risk model was established by multivariate Cox regression.
We obtained 132 differentially expressed RBPs, including 66 upregulated and 66 downregulated RBPs. Functional analysis revealed that these genes were significantly enriched in RNA processing, modification and binding, ribosome biogenesis, post-transcriptional regulation, ribonuclease and nuclease activity. Additionally, some RBPs were significantly related to interferon (IFN)-alpha and IFN-beta biosynthetic processes and the Toll-like receptor signaling pathway. A prognostic model was constructed and included insulin like growth factor 2 messenger ribonucleic acid binding protein 3 (IGF2BP3), poly (A) binding protein cytoplasmic 1 like (PABPC1L), peroxisome proliferator activated receptor gamma coactivator 1 alpha (PPARGC1A), peptidyl- transfer ribonucleic acid hydrolase 1 homolog (PTRH1) and tudor domain containing 7 (TDRD7). The model is an independent risk factor for clinicopathological characteristics.
Our study provided novel insights into the pathogenesis of CRC and constructed a prognostic gene model, which may be helpful for determining the prognosis of CRC.
Our study provided novel insights into the pathogenesis of CRC and constructed a prognostic gene model, which may be helpful for determining the prognosis of CRC.In contrast to previous perceptions that inflammatory bowel disease (IBD) patients are generally malnourished and underweight, there is mounting evidence to suggest that rates of obesity in IBD now mirror that of the general population. IBD is an immune-mediated condition that appears to develop in individuals who have not only a genetic predisposition to immune dysregulation but also likely exposure to various environmental factors which further potentiate this risk. With the surge in obesity alongside the rising incidence of IBD, particularly in developing nations, the role that obesity may play, not only in the pathogenesis but also in the natural history of disease has become a topic of growing interest. Currently available data exploring obesity's impact on the natural history of IBD are largely conflicting, potentially limited by the use of body mass index as a surrogate measure of obesity at varying time points throughout the disease course. While there are pharmacokinetic data to suggest possible detrimental effects that obesity may have on the response to medical therapy, results in this realm are also inconsistent. Moreover, not only is it unclear whether weight loss improves IBD outcomes, little is known about the safety and efficacy of available weight-loss strategies in this population. For these reasons, it becomes increasingly important to further understand the nature of any interaction between obesity and IBD.The incidence of cerebral aneurysms is rare in children, and it has to be definitively ruled out in all cases of intracranial bleed even if there is associated history of trauma. We report a case of 11-month-old girl who presented with intracranial bleed after a history of minor trauma whose diagnosis of an intracranial aneurysm was initially missed which later led to a rebleed. Selleck GSK2795039 It was managed emergently with endovascular coiling and the patient showed incredible recovery in the post-operative period.Idiopathic trigeminal neuralgia (TN) due to an embedded arteriovenous malformation (AVM) on the trigeminal root entry zone (REZ) is rare but a potentially challenging condition to manage. Herein, we report such a case with an additional unruptured aneurysm on the feeding artery and highlight the role of a multimodality approach to their management. A 50-year-old female presented with drug-resistant right-sided trigeminal neuralgia for one year. The magnetic resonance imaging (MRI) suggested a possibility of AVM, the angiographic study showed an AVM nidus with feeders from the right anterior inferior cerebellar artery (AICA) and a dilated right intrinsic pontine artery, the latter showing a flow-related aneurysm towards its brainstem end. The flow-related aneurysm, as well as the dilated intrinsic pontine artery feeder, was embolized at first. During surgery, the AVM was found embedded inside the root entry zone. Parts of the AVM and its draining vein were partially coagulated followed by microvascular decompression of the AICA loop as well as a feeder emanating from it following which the patient recovered completely. She subsequently received gamma knife surgery (GKS) for the residual AVM and remained asymptomatic after 3.5 years of GKS. AVM-related TN are rare, and the additional presence of a feeding artery aneurysm increases the management complexity. Endovascular management of the aneurysm followed by microvascular decompression (MVD) and tailored AVM coagulation represent a prompt and effective means of pain control. Subsequent GKS is necessary to obliterate the AVM nidus.Primary central nervous system lymphoma (PCNSL) is a rare disease that can be confused with Wernicke encephalopathy (WE). We have reported here the case of a 31-year-old malnourished man who presented with headache, fever, vomiting, diarrhea, and confusion. His imaging and laboratory findings were indicative of WE. His condition improved after treatment with a high dose of vitamin B1 and intravenous administration of methylprednisolone. However, after continuing to take vitamin B1 for 2 weeks, his symptoms and neuroimaging findings worsened. Increased standardized uptake values of positron emission tomography with 2-deoxy-2-[fluorine-18]fluoro-D-glucose integrated with computed tomography (18F-FDG-PET) and interleukin-10 (IL-10) in the cerebrospinal fluid led to the diagnosis of PCNSL. After treatment with methotrexate and calcium leucovorin, the symptoms and neuroimaging abnormalities disappeared at the 6-month follow-up examination. The possibility of PCNSL should be considered if the routine treatment for WE are ineffective. 18F-FDG PET and IL-10 may provide a new method for the early diagnosis of PCNSL.
Mechanisms involved in the causation of sudden unexpected death in epilepsy (SUDEP) are not well understood. Ictal asystole has been identified as a cause of SUDEP in patients with temporal lobe epilepsy. Herein, we report a patient who developed cardiac arrest during the ictal period of frontal lobe epilepsy.
A 35-year-old man presented with a history of progressive nocturnal stiffness in the left lower extremity since 6 years and that of paroxysmal episodes of altered consciousness. In the last 2 years, he sustained epileptic seizures which presented as closed eyes, wheezy phlegm in the throat, facial pallor, moist cold skin, clenched fists, and limb stiffness; the episodes lasted 3-4 min. The seizures did not respond to antiepileptic therapy. Twenty four-hour electrocardiography monitoring showed transient atrial tachycardia, supraventricular premature beats, and cardiac arrest.
Frontal lobe epilepsy may be a potential cause of SUDEP. Clinician should be aware of this condition.
Frontal lobe epilepsy may be a potential cause of SUDEP. Clinician should be aware of this condition.
Non-convulsive status epileptics (NCSE) is a common neurological emergency necessitating rapid assessment and management, but is often underdiagnosed as it lacks specific electroencephalographic features. The diagnostic value of periodic lateralized epileptiform discharges (PLEDs) in NCSE is still unclear. Herein, we reported a case with NCSE manifesting as PLEDs and coma.
A 62-year-old man presented with epileptic seizures. Based on clinical and radiological profiles, he was diagnosed with frontal hemorrhage, coma, and NCSE. An electroencephalogram (EEG) revealed PLEDs. A combined antiepileptic regimen was initiated and, over a follow-up period of 2 months, a favorable outcome was achieved.
EEG may help identify potential NCSE in comatose patients, and PLEDs can be an atypical manifestation of NCSE, which can be effectively treated with antiepileptic drugs. The emphasis in NCSE is on early identification and individualized therapeutic regimens.
EEG may help identify potential NCSE in comatose patients, and PLEDs can be an atypical manifestation of NCSE, which can be effectively treated with antiepileptic drugs. The emphasis in NCSE is on early identification and individualized therapeutic regimens.
