Hasil Pencarian  ::  Simpan CSV :: Kembali

Hasil Pencarian

Ditemukan 3251 dokumen yang sesuai dengan query
cover
Askandar Tjokroprawiro
"Many persons have a constellation of major risk/actors, life-habit risk factors, and emerging risk factors that constitute a condition called the Metabolic Syndrome. Eight components characteristic of the Metabolic Syndrome are: I. insulin resistance (with or without glucose intolerance), 2. hyperinsulinemia, 3. abdominal obesity, 4. raised blood pressure, 5. atherogenic dyslipidemia (T Triglyceride, T Postprandial lipemia, Small dense LDL or Type B pattern), 6. procoagulant state (t Fibrinogen, T PAI-1), 7. hyperuricemia, 8. endothelial dysfunction ft Albumin excretion rate, etc).
Among the single etiologic factors being considered are: 1. a genetic defect in one or more components of the insulin action cascade leading to insulin resistance, 2. malnutrition during fetal development, and 3. abdominal obesity. It is possible that these three factors could be in some way interrelated. Several mechanisms implicated in the development of insulin resistance in obesity can be shortly postulated below. TNF-a oversecreted by the enlarged fat cells impairs insulin action by inhibiting insulin receptor signaling, possibly by increasing IRS-l serine phosphorylation GLUT-4 expression and translocation to the cell surface will be impaired by TNF-a.
Leptin released from visceral adipocytes may inhibit insulin action in the liver by impairing insulin receptor signaling, leading to reduced down-regulation of PEPCK, the rate-limiting enzyme in gluconeogenesis. Glucose-stimulated insulin released from pancreatic fi-cell is also impaired by leptin through STAT-3 production stimulated by leptin via leptin receptor on the surface membrane of fl-cell, and then STAT-3 stimulates the opening of K+Arp-channels, and consequently insulin release will be inhibited.
Resistin, as well as TNF-a and leptin released by adipocytes, decrease insulin sensitivity and to be suggested to inhibit adipogenesis; insulin administration rapidly increases resistin levels to normal in adipose tissue. Potential therapeutic beneficial effects of metformin for obesity and insulin resistance may be selectively categorized into 3 groups. In carbohydrate metabolism, metformin prevents pancreatic j3-cellfrom gluco-and lipotoxicity, increases insulin receptor binding, and increases insulin receptor tyrosine kinase (IRTK) activity.
Metformin increases oral glucose-induced GLP-l amide levels in obese non-diabetic subjects; metformin is able to inhibit GLP-l degradation induced by dipeptidyl-peptidase IV. GLP-l is a gastrointestinal hormone, which stimulates insulin secretion and promotes satiety, and hence GLP-l and dipeptyl-peptidase IV-inhibitor can be proposed as therapeutic goals for the treatment of patients with Type 2-DM (T2DM) and obesity.
In lipid metabolism, metformin may improve lipid profile. Several vasoprotective effects also belong to Metformin, f.e. 4. Hyperinsulinemia, J- Fibrinogen, -I PAl-I, -I FactorXHIa which functions to stabilize fibrin, 4- Platelet aggregation, i Capillary permeability, -I SMC-Fibroblast activity, and i Carbonyl stress (pathway to AGE formation).
Conclusion: Obesity and insulin resistance are two major components of the metabolic syndrome, which predispose individuals to the development of T2DM and coronary heart disease. TNF-a and leptin, which are oversecreted by enlarged fat cells, play pivotal roles in the molecular defects of insulin action in obesity-linked insulin resistance. Pleio-tropic properties (vasoprotective effects) of metformin beyond carbohydrate and lipid effects may contribute to the beneficial therapeutic tools for obesity-linked insulin resistance."
2002
AMIN-XXXIV-4-OktDes2002-146
Artikel Jurnal  Universitas Indonesia Library
cover
cover
Elwood, Mark
"Summary:
Critical appraisal is now accepted as central to the development of rational health care and evidence-based medicine, by applying it to questions of aetiology, clinical therapy, and health care management. The reader will learn how to assess the strengths and weaknesses of new studies, and how to conduct their own studies"
New York: Oxford University Press, 2010
614.402 ELW c
Buku Teks SO  Universitas Indonesia Library
cover
Elwood, Mark
"This book presents a system of critical appraisal applicable to clinical, epidemiological and public health studies and to many other fields. It assumes no prior knowledge. The methods are relevant to students, practitioners and policymakers. The book shows how to assess if the results of one study or of many studies show a causal effect. The book discusses study designs: randomised and non-randomised trials, cohort studies, case-control studies, and surveys, showing the presentation of results including person-time and survival analysis, and issues in the selection of subjects. The system shows how to describe a study, how to detect and assess selection biases, observation bias, confounding, and chance variation, and how to assess internal validity and external validity (generalisability). Statistical methods are presented assuming no previous knowledge, and showing applications to each study design. Positive features of causation including strength, dose-response, and consistency are discussed. The book shows how to do systematic reviews and meta-analyses, and discusses publication bias. Systems of assessing all evidence are shown, leading to a general method of critical appraisal based on 20 key questions in five groups, which can be applied to any type of study or any topic. Six chapters show the application of this method to randomised trials, prospective and retrospective cohort studies, and case-control studies. An appendix summarises key statistical methods, each with a worked example. Each main chapter has self-test questions, with answers provided."
Oxford: Oxford University Press, 2017
e20511936
eBooks  Universitas Indonesia Library
cover
Elwood, Mark
Oxford: Oxford University Press, 2017
614.4 ELW c
Buku Teks SO  Universitas Indonesia Library
cover
Muhammad Hanafi
"Insul1n adalah suatu harmon yang dihasilkan oleh sel beta pulau Langerhans, dan berfungsi mengatur kadar glukosa darah kebutuhan insulin pada umumnya diperoleh dari hasil 10 ekstrasi pankreas babi dan sapi jumlah produksi tersebut belum mencukupi, mengingat kebutuhan insulin meningkat terus dengan diketemukan teknik rekombinasi DNA, insulin dapat dihasilkan oleh bakteri F coli bahan-bahan yang diperlukan untuk rekombinasi tersebut adalah plasmid pBR322, Xplac5, 2 enzim restriksi, DNA ligase dan gen insulin."
Depok: Fakultas Matematika dan Ilmu Pengetahuan Alam Universitas Indonesia, 1984
S-Pdf
UI - Skripsi Membership  Universitas Indonesia Library
cover
Paul Kosma, editor
"Anticarbohydrate antibodies provides a cohesive overview of current knowledge on the immunological recognition of carbohydrates by the adaptive immune system. The text provides fundamental insight needed for advancing clinically relevant diagnostics and therapeutic applications. "
Wien: [, Springer], 2012
e20417995
eBooks  Universitas Indonesia Library
cover
Levitt, Seymour H., editor
"This well-received book, now in its fifth edition, is unique in providing a detailed examination of the technological basis of radiation therapy. Another unique feature is that the chapters are jointly written by North American and European authors. This considerably broadens the book’s contents and increases its applicability in daily practice throughout the world. The book is divided into two sections. The first section covers basic concepts in treatment planning and explains the various approaches to radiation therapy, such as intensity-modulated radiation therapy, tomotherapy, stereotactic radiotherapy, and high and low dose rate brachytherapy. The second discusses in depth the practical clinical applications of the different radiation therapy techniques in a wide range of cancer sites. All chapters have been written by leaders in the field. "
Berlin : Springer, 2012
e20425949
eBooks  Universitas Indonesia Library
cover
Norton, Barbara A.
Norwalk, Connecticut: Appleton-Century-Crofts , 1986
610.73 NOR s
Buku Teks SO  Universitas Indonesia Library
cover
Muhammad Dzaky Abdillah
"Latar Belakang
Pandemi COVID-19 merupakan kejadian luar biasa yang berdampak secara global. Pandemi ini sudah banyak memakan korban terutama pada pasien yang memiliki komorbiditas. Salah satu komorbiditas tersering adalah diabetes melitus tipe 2 (DMT2). Kondisi hiperglikemia pada pasien DMT2 akan meningkatkan tingkat mortalitas pasien sehingga diperlukan suatu tatalaksana, yaitu insulin. Namun, beberapa studi melaporkan bahwa insulin ternyata berkaitan dengan meningkatnya angka mortalitas pada pasien yang mendapatkannya, tetapi masih banyak perselisihan mengenai efek dari insulin ini sendiri. Salah satu penyebab yang diduga adalah penggunaan insulin sebelum dirawat. Dalam penelitian ini, penulis secara khusus ingin melihat hubungan penggunaan insulin sebelum dirawat dengan perburukan klinis pasien DMT2 yang terinfeksi COVID-19 dan mendapatkan terapi insulin selama rawatan.
Metode
Studi kasus kontrol dengan total subjek penelitian 270 pasien yang mengalami DMT2 dan COVID-19 yang diberikan insulin. 110 subjek mengalami perburukan klinis dan 160 lainnya tidak mengalami perburukan klinis. Studi dilakukan dengan menggunakan data sekunder yang berasal dari data rekam medis pasien di RSCM Jakarta pada periode Maret 2020 – Maret 2023.
Hasil
Tidak terdapat hubungan yang signifikan antara penggunaan insulin sebelum dirawat dengan perburukan profil klinis pasien (p = 0,517) dengan nilai OR 0,839 (0,493 – 1,428). Kesimpulan
Penggunaan insulin sebelum dirawat tidak berhubungan dengan perburukan klinis pada pasien DMT2 dengan infeksi COVID-19.

Introduction
The COVID-19 pandemic is a remarkable occurrence with worldwide implications. Numerous people have died as a result of this pandemic, particularly patients with comorbidities. One of the most common comorbidities is type 2 diabetes mellitus (T2DM). The high mortality risk associated with hyperglycemia in T2DM patients necessitates the use of insulin as a treatment. However, several studies indicate that insulin use is linked to higher patient death rates, yet, there is still some disagreement over the effects of insulin itself. Insulin before treatment is one of the possible causes. The study aimed to examine the link between preadmission use of insulin and clinical deterioration in T2DM patients who have COVID-19 infection and are getting insulin therapy during treatment.
Method
A case-control study included 270 research participants with COVID-19 and T2DM who received insulin. 160 patients did not have clinical deterioration, while 110 subjects did. The study was conducted using secondary data originating from patient medical records at RSCM Jakarta from March 2020 – March 2023.
Results
There was no significant relationship between insulin use before treatment and the worsening of the patient’s clinical profile (p = 0,517) with an OR value of 0,839 (0,493 – 1,428).
Conclusion
Preadmission use of insulin did not associate with clinical deterioration in T2DM patients with COVID-19 infection.
"
Jakarta: Fakultas Kedokteran Universitas Indonesia, 2024
S-pdf
UI - Skripsi Membership  Universitas Indonesia Library
<<   1 2 3 4 5 6 7 8 9 10   >>