• Title/Summary/Keyword: mortality function

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Brain consequences of acute kidney injury: Focusing on the hippocampus

  • Malek, Maryam
    • Kidney Research and Clinical Practice
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    • v.37 no.4
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    • pp.315-322
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    • 2018
  • The high mortality rates associated with acute kidney injury are mainly due to extra-renal complications that occur following distant-organ involvement. Damage to these organs, which is commonly referred to as multiple organ dysfunction syndrome, has more severe and persistent effects. The brain and its sub-structures, such as the hippocampus, are vulnerable organs that can be adversely affected. Acute kidney injury may be associated with numerous brain and hippocampal complications, as it may alter the permeability of the blood-brain barrier. Although the pathogenesis of acute uremic encephalopathy is poorly understood, some of the underlying mechanisms that may contribute to hippocampal involvement include the release of multiple inflammatory mediators that coincide with hippocampus inflammation and cytotoxicity, neurotransmitter derangement, transcriptional dysregulation, and changes in the expression of apoptotic genes. Impairment of brain function, especially of a structure that has vital activity in learning and memory and is very sensitive to renal ischemic injury, can ultimately lead to cognitive and functional complications in patients with acute kidney injury. The objective of this review was to assess these complications in the brain following acute kidney injury, with a focus on the hippocampus as a critical region for learning and memory.

Pharmacophore Based Screening and Molecular Docking Study of PI3K Inhibitors

  • Rupa, Mottadi;Madhavan, Thirumurthy
    • Journal of Integrative Natural Science
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    • v.9 no.1
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    • pp.41-61
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    • 2016
  • Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related mortality worldwide. Phosphoinositide 3-kinases (PI3Ks) play important role in Non-Small Cell Lung Cancer. PI3Ks constitute a lipid kinase family which modulates the function of numerous substrates involved in the regulation of cell survival, cell cycle progression and cellular growth. Herein, we describe the ligand based pharmacophore combined with molecular docking studies methods to identify new potent PI3K inhibitors. Several pharmacophore models were generated and validated by Guner-Henry scoring Method. The best models were utilized as 3D pharmacophore query to screen against ZINC database (Chemical and Natural) and the retrieved hits were further validated by fitness score, Lipinski's rule of five. Finally four compounds were found to have good potential and they may act as novel lead compounds for PI3K inhibitor designing.

Risk Factors for the Progression of Chronic Kidney Disease in Children

  • Ahn, Yo Han;Kang, Hee Gyung;Ha, Il-Soo
    • Childhood Kidney Diseases
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    • v.25 no.1
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    • pp.1-7
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    • 2021
  • Chronic kidney disease (CKD) in children is associated with various complications, including poor growth and development, mineral bone disorder, cardiovascular disease, kidney failure, and mortality. Slowing down the progression of CKD is important since CKD is often not curable. Prospective cohort studies have been conducted to understand the progression and outcomes of CKD in children, and these studies have identified non-modifiable and modifiable risk factors. Recognition of known risk factors and early intervention are important to delay the progression of kidney function decline in children.

Clinical features and molecular mechanism of muscle wasting in end stage renal disease

  • Sang Hyeon Ju;Hyon-Seung Yi
    • BMB Reports
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    • v.56 no.8
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    • pp.426-438
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    • 2023
  • Muscle wasting in end-stage renal disease (ESRD) is an escalating issue due to the increasing global prevalence of ESRD and its significant clinical impact, including a close association with elevated mortality risk. The phenomenon of muscle wasting in ESRD, which exceeds the rate of muscle loss observed in the normal aging process, arises from multifactorial processes. This review paper aims to provide a comprehensive understanding of muscle wasting in ESRD, covering its epidemiology, underlying molecular mechanisms, and current and emerging therapeutic interventions. It delves into the assessment techniques for muscle mass and function, before exploring the intricate metabolic and molecular pathways that lead to muscle atrophy in ESRD patients. We further discuss various strategies to mitigate muscle wasting, including nutritional, pharmacological, exercise, and physical modalities intervention. This review seeks to provide a solid foundation for future research in this area, fostering a deeper understanding of muscle wasting in ESRD, and paving the way for the development of novel strategies to improve patient outcomes.

Computational approaches for molecular characterization and structure-based functional elucidation of a hypothetical protein from Mycobacterium tuberculosis

  • Abu Saim Mohammad, Saikat
    • Genomics & Informatics
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    • v.21 no.2
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    • pp.25.1-25.12
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    • 2023
  • Adaptation of infections and hosts has resulted in several metabolic mechanisms adopted by intracellular pathogens to combat the defense responses and the lack of fuel during infection. Human tuberculosis caused by Mycobacterium tuberculosis (MTB) is the world's first cause of mortality tied to a single disease. This study aims to characterize and anticipate potential antigen characteristics for promising vaccine candidates for the hypothetical protein of MTB through computational strategies. The protein is associated with the catalyzation of dithiol oxidation and/or disulfide reduction because of the protein's anticipated disulfide oxidoreductase properties. This investigation analyzed the protein's physicochemical characteristics, protein-protein interactions, subcellular locations, anticipated active sites, secondary and tertiary structures, allergenicity, antigenicity, and toxicity properties. The protein has significant active amino acid residues with no allergenicity, elevated antigenicity, and no toxicity.

A rare and unique experience of a blunt intrathoracic traumatic injury of the trachea and its management in South Africa: a case report

  • Rudo Mutsa Vanessa Pswarayi;Anna Katariina Kerola
    • Journal of Trauma and Injury
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    • v.36 no.4
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    • pp.416-420
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    • 2023
  • Blunt intrathoracic tracheal injuries are rare, even among blunt chest trauma patients. An early diagnosis based on a high index of suspicion allows for timely surgical management of potentially fatal airway trauma, thereby improving overall outcomes. Diagnosing these injuries can be difficult due to their nonspecific clinical features and the occasional difficulty in radiologic diagnosis. If a patient exhibits respiratory compromise with difficult ventilation and poor lung expansion, despite the insertion and management of an intercostal drain following high-energy blunt trauma, there should be a heightened suspicion of potential airway trauma. The aim of primary repair is to restore airway integrity and to minimize the loss of pulmonary parenchyma function. This case report discusses the rare clinical presentation of a patient with blunt trauma to the intrathoracic airway, the surgical management thereof, and his overall outcome. Although blunt traumatic injuries of the trachea are extremely rare and often fatal, early surgical intervention can potentially reduce the risk of mortality.

The underlying mechanism of calcium toxicity-induced autophagic cell death and lysosomal degradation in early stage of cerebral ischemia

  • Jirakhamon Sengking;Pasuk Mahakkanukrauh
    • Anatomy and Cell Biology
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    • v.57 no.2
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    • pp.155-162
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    • 2024
  • Cerebral ischemia is the important cause of worldwide disability and mortality, that is one of the obstruction of blood vessels supplying to the brain. In early stage, glutamate excitotoxicity and high level of intracellular calcium (Ca2+) are the major processes which can promote many downstream signaling involving in neuronal death and brain tissue damaging. Moreover, autophagy, the reusing of damaged cell organelles, is affected in early ischemia. Under ischemic conditions, autophagy plays an important role to maintain energy of the brain and its function. In the other hand, over intracellular Ca2+ accumulation triggers excessive autophagic process and lysosomal degradation leading to autophagic process impairment which finally induce neuronal death. This article reviews the association between intracellular Ca2+ and autophagic process in acute stage of ischemic stroke.

What is the disease burden from childhood and adolescent obesity?: a narrative review

  • Eun Byoul Lee
    • Journal of Yeungnam Medical Science
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    • v.41 no.3
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    • pp.150-157
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    • 2024
  • The prevalence of childhood and adolescent obesity has increased and exacerbated during the coronavirus disease 2019 pandemic, both in Korea and globally. Childhood and adolescent obesity poses significant risks for premature morbidity and mortality. The development of serious comorbidities depends not only on the duration of obesity but also on the age of onset. Obesity in children and adolescents affects almost all organ systems, including the endocrine, cardiovascular, gastrointestinal, reproductive, nervous, and immune systems. Obesity in children and adolescents affects growth, cognitive function, and psychosocial interactions during development, in addition to aggravating known adult comorbidities such as type 2 diabetes mellitus, hypertension, dyslipidemia, nonalcoholic fatty liver disease, obstructive sleep apnea, and cancer. Childhood and adolescent obesity are highly associated with increased cardiometabolic risk factors and prevalence of metabolic syndrome. The risk of cardiovascular and metabolic diseases in later life can be considerably decreased by even a small weight loss before the onset of puberty. Childhood and adolescent obesity is a disease that requires treatment and is associated with many comorbidities and disease burdens. Therefore, early detection and therapeutic intervention are crucial.

Middle East Respiratory Syndrome-Coronavirus Infection into Established hDPP4-Transgenic Mice Accelerates Lung Damage Via Activation of the Pro-Inflammatory Response and Pulmonary Fibrosis

  • Kim, Ju;Yang, Ye Lin;Jeong, Yongsu;Jang, Yong-Suk
    • Journal of Microbiology and Biotechnology
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    • v.30 no.3
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    • pp.427-438
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    • 2020
  • Middle East respiratory syndrome coronavirus (MERS-CoV) infects the lower respiratory airway of humans, leading to severe acute respiratory failure. Unlike human dipeptidyl peptidase 4 (hDPP4), a receptor for MERS-CoV, mouse DPP4 (mDPP4) failed to support MERS-CoV infection. Consequently, diverse transgenic mouse models expressing hDPP4 have been developed using diverse methods, although some models show no mortality and/or only transient and mild-to-moderate clinical signs following MERS-CoV infection. Additionally, overexpressed hDPP4 is associated with neurological complications and breeding difficulties in some transgenic mice, resulting in impeding further studies. Here, we generated stable hDPP4-transgenic mice that were sufficiently susceptible to MERS-CoV infection. The transgenic mice showed weight loss, decreased pulmonary function, and increased mortality with minimal perturbation of overexpressed hDPP4 after MERS-CoV infection. In addition, we observed histopathological signs indicative of progressive pulmonary fibrosis, including thickened alveolar septa, infiltration of inflammatory monocytes, and macrophage polarization as well as elevated expression of profibrotic molecules and acute inflammatory response in the lung of MERS-CoV-infected hDPP4-transgenic mice. Collectively, we suggest that this hDPP4-transgenic mouse is useful in understanding the pathogenesis of MERS-CoV infection and for antiviral research and vaccine development against the virus.

Reconstructive Procedures Combined with or Without Prosthetic Valve Replacement for Cardiac Valvular Lesions (심장판막 질환 성형술에 대한 임상적 고찰)

  • Kim, Y.;Cho, B.K.;Hong, S.N.
    • Journal of Chest Surgery
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    • v.9 no.2
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    • pp.207-214
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    • 1976
  • Operations for cardiac valvular disease has been progressed in various ways. Since 1949 when Lord Russel operated mitral stenosis by closed technique at Johns Hopkins Hospital then much progress has been achieved and that nowadays severely diseased cardiac valve has been replaced by prosthetic valve, which is almost ideal in hemodynamic aspect, but still it has many problems such as thromboembolism, destruction of red blood cell, pressure gradient, and disturbance of left ventricular function, so in case of delicate situations, valve replacement should be decided carefully. Besides prosthetic valve, there are some kinds of reconstructive procedures and these have been resulted in better prognosis than prosthetic valve replacement in selected cases. So, authors have reviewed 61 Cases of cardiac patients who have been operated reconstructive valvular surgery by cardiopulmonary bypass, at Yonsei University, from Jan. 1963 to Mar. 1976. Out of 61 cases, 9 patients were replaced by prosthetic valve and rest of the patients were operated upon in various reconstructive procedures such as commissurotomy, valvotomy, valvuloplasty, and annuloplasty. Twenty cases of congenital heart diseases with valvular lesion, which had been operated for valvular lesion were also included in this statistics. Out of 9 cases of prosthetic valvular replacement five cases of prosthetic valvular replacement was done combined with other reconstructive procedures after attempted valvuloplasty. Comparative prognosis of both procedures are somewhat variable by reporters, average 19% of mortality after reconstructive surgery and 38% of mortality after prosthetic valve replacement in long term results. Most common cause of death in postoperative period was low output syndrome in both cases. It seems that good preoperative evaluation and proper reconstructive surgery will afford good prognosis in selected cardiac valvular diseased patient.

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