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Model Estimation and Evaluation
Published in Douglas D. Gunzler, Adam T. Perzynski, Adam C. Carle, Structural Equation Modeling for Health and Medicine, 2021
Douglas D. Gunzler, Adam T. Perzynski, Adam C. Carle
If the CFI index is greater than one, it is set at one and if less than zero, it is set to zero. The closer the CFI index is to one, the better the model fit. As a rule of thumb, a CFI ≥ 0.90 is considered an acceptable fit, while a CFI ≥ 0.95 is considered an excellent fit [54].
Pragmatism or Principle? Continuity and Change in the British Approach to Treatment and Control
Published in Ross Coomber, The Control of Drugs and Drug Users, 2020
Response came in the form of the Central Funding Initiative (CFI) which was to change radically the landscape of drugs services in England. This was part of the government’s response to the ACMD Report of 1982 on Treatment and Rehabilitation, which had recommended the injection of new monies on a pump-priming basis to ensure the development of an adequate treatment and rehabilitation service. A comprehensive response involving both the statutory and non-statutory, the specialist and the non-specialist agencies was said to be needed. It was hoped that the CFI would be a way of remedying old problems such as lack of service co-ordination, inadequate treatment and rehabilitation resources, and absence of training for staff, while also rising to new challenges, such as providing a more comprehensive response, generating public awareness at the local level and promoting better joint planning. £17.5 million was provided to pump-prime new services or to develop further existing ones. Almost half of existing services received some additional funds and, in addition, a crucial new layer of services was developed — a layer of community-based services to complement hospital and residential rehabilitation provision. Services became more accessible and some major gaps were filled.
Combined hormonal contraception
Published in John Guillebaud, Contraception Today, 2019
Lengthening of the CFI may be caused either side of the “horseshoe” in Figure 8 from omissions, malabsorption as from vomiting, or enzyme-inducing drug interactions that inactivate pills either at the start or especially at the end of a packet.
The Complement System in Retinal Detachment with Choroidal Detachment
Published in Current Eye Research, 2022
Shasha Luo, Yanghao Chen, Lufei Yang, Xuechun Gong, Zhifeng Wu
Complement regulatory protein DAF is a glycosylated membrane protein.15 To the best of our knowledge, this may be the first quantitative measurement of sDAF in the vitreous fluid of eyes with either RRDCD or RRD. An elegant study has shown that sDAF in urine has C4bp (or factor H) activity, indicating that it can inhibit the liquid phase activation of the complement cascade, which is equivalent to the role of serum C4–binding protein.16 Complement factor I (C3bINH) is an esterase that is a C3b inhibitory factor that can cleave and inactivate C3b to become the ineffective iC3B. It can also cleave C4b into C4d and C4c, thereby inhibiting the activation of the complement system.17 In the RRDCD group, the levels of sDAF and CFI in the vitreous humor were significantly increased, further indicating that eyes with RRDCD may still have normal complement regulation mechanisms, but that some persistent inflammatory mechanisms cause the continuous activation of the complement pathway and the level of complement inhibitory factors increase accordingly. Interestingly, the CFD and C2 were higher in the RRD group than in the control group, and the downstream components were not activated. This phenomenon may occur due to the increased levels of CFI.
Anti-complement factor H (CFH) antibodies and a novel CFH gene mutation in an atypical hemolytic uremic syndrome patient with complement activation of the classical pathway
Published in Immunological Medicine, 2021
Sonoko Minato, Hiroyuki Iijima, Hiro Nakao, Kentaro Nishi, Yoshihiko Hidaka, Norimitsu Inoue, Mitsuru Kubota, Akira Ishiguro
Several causative genetic variants for aHUS have been identified. Approximately 50% of aHUS patients have loss-of-function variants in complement regulatory genes (CFH, MCP, CFI) or gain-of-function variants of complement factors (C3, CFB). In our patient, a single novel missense mutation, p.Glu1172Ala in the CFH gene, was found in a heterozygous state. No other mutations were found in complement genes. The majority of the reported CFH mutations are heterozygous likely pathogenic variants [9]. Previous reports have shown that only 9.2% of aHUS patients with CFH mutation carried abnormalities in other complement genes, suggesting that a mutation in the CFH gene alone may be sufficient to cause aHUS [9]. In addition, in silico analysis algorithms suggested the pathogenicity of the mutation. This mutation (exon 22 of CFH gene) is located in the major functional region C-terminal SCR 20, which is the recognition region and binding sites for the surface of endothelial cells. The exon 20–22 of the CFH gene is known as a hotspot for mutations in aHUS [10]. Therefore, the heterozygous CFH mutation in our case may be a cause of aHUS. Further studies are needed to elucidate this association.
Severe acute kidney injury following Sri Lankan Hypnale spp. envenoming is associated with thrombotic microangiopathy
Published in Clinical Toxicology, 2021
Eranga S. Wijewickrama, Lalindra V. Gooneratne, Ariaranee Gnanathasan, Indika Gawarammana, Mangala Gunatilake, Geoffrey K. Isbister
The pathophysiology of TMA and its association with AKI in snakebites is poorly understood. Thrombotic thrombocytopaenic purpura (TTP) and haemolytic uraemic syndrome (HUS) are the prototype diseases associated with TMA [27]. TTP is caused by the reduction in the amount or the function of ADAMTS13, which is an enzyme, required to cleave the giant multimers of von Willebrand Factor (vWF). Increase in the circulating multimers of vWF lead to excessive platelet adhesion in arterioles and capillaries leading to thrombi formation. The disease is characterized by fever, neurological dysfunction and acute kidney injury in addition to MAHA and thrombocytopenia. The classic form of HUS follows a diarrhoeal illness due to Shiga toxin producing serotypes of E. coli or Shigella species and is associated with normal ADAMTS13 activity. Shiga toxin triggers a cascade of signalling events resulting in loss of anti-adhesive, anti-inflammatory and thromboresistant properties of glomerular endothelial cells leading to platelet adhesion and thrombus formation causing TMA [28]. In the atypical form of HUS (aHUS), which may or not be associated with diarrhoea, the endothelial cell damage and subsequent glomerular microthrombi formation is caused by dysregulation of the alternative complement pathway leading to excessive activation of the terminal complement pathway [29]. Complement abnormalities have been detected in about 50% of patients with aHUS including loss of function mutations in membrane co-factor protein, complement factor H, complement factor I and autoantibodies to factors H and I.