咏芯 48 呂
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on the atlas — 31
- Types of HIV Tests | Testing | HIV Basics | HIV/AIDS | CDC1 savers
- Some Perspectives on Hypersensitivity to Coronary Stents - PMC1 savers
- 2023 ESC Guidelines for the management of acute coronary syndromes | European Heart Journal | Oxford Academic1 savers
- Stroke of Genius: A Customizable Card Game Structure to Exercise Differential Diagnostic Skills - PMC1 savers
- Tabes Dorsalis - Physiopedia1 savers
- PI3K/Akt signaling transduction pathway, erythropoiesis and glycolysis in hypoxia (Review)1 savers
- Metformin and Its Benefits for Various Diseases - PMC1 savers
- The development and benefits of metformin in various diseases | SpringerLink1 savers
- Fig. 1: Proposed mechanisms for metformin-induced reductions in blood levels of glucose. | Nature Reviews Endocrinology1 savers
- Arrhythmogenic Right Ventricular Cardiomyopathy | Cedars-Sinai1 savers
- 【CV】心肌病變 Cardiomyopathy @ 小節的醫學筆記 :: 痞客邦 ::1 savers
- Contemporary Definitions and Classification of the Cardiomyopathies | Circulation1 savers
- Central Control of the Autonomic Nervous System and Thermoregulation (Section 4, Chapter 3) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy - The University of Texas Medical School at Houston1 savers
- Hypothalamus: Structural Organization (Section 4, Chapter 1) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy - The University of Texas Medical School at Houston1 savers
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highlights — 943
antibody tests, antigen/antibody tests, and nucleic acid tests (NAT)
Types of HIV Tests | Testing | HIV Basics | HIV/AIDS | CDCSirolimus is an unlikely cause of hypersensitivity because it typically reduces eosinophilic infiltration and histamine release and has been associated with low rates of hypersensitivity,33 but the incidence of allergic reactions to Paclitaxel itself is not known.
Some Perspectives on Hypersensitivity to Coronary Stents - PMCSecondary prevention therapies should be considered for those with evidence of coronary atherosclerotic disease and to control risk factors. The management of takotsubo syndrome is not informed by any prospective RCTs, and treatment is largely supportive and empiric.546,547 The treatment of patients with myocarditis has been covered by previous ESC documents.548,549 Ischemia with non-obstructive coronary arteries (INOCA) has also been described in the context of CCS
2023 ESC Guidelines for the management of acute coronary syndromes | European Heart Journal | Oxford Academicnon-invasive imaging (i.e. echocardiography, CMR, CT) is recommended, as clinically appropriate. CMR is one of the key diagnostic tools to determine the underlying cause of MINOCA
2023 ESC Guidelines for the management of acute coronary syndromes | European Heart Journal | Oxford AcademicMINOCA patients require follow-up review (3) and may require repeat assessment using echocardiography and magnetic resonance imaging, depending on the initial findings. aOptions for adjunctive tests. Patients will not require all investigations but instead the appropriate tests should be selected based on their presentation and clinical course. bExamples of potential blood tests include: full blood count, renal profile, troponin, C-reactive protein, D-dimer, NT-pro BNP.
2023 ESC Guidelines for the management of acute coronary syndromes | European Heart Journal | Oxford AcademicPatients presenting with NSTE-ACS or UA are often stabilized on the ward (2) prior to transfer to the cath lab (1). In this context the order in which the investigations are carried out will vary depending on the location these patients are managed during first contact
2023 ESC Guidelines for the management of acute coronary syndromes | European Heart Journal | Oxford AcademicPatients presenting with STEMI present directly to catheter lab as per the current standard of care pathway
2023 ESC Guidelines for the management of acute coronary syndromes | European Heart Journal | Oxford Academicleft ventriculography (including measurement of LV end-diastolic pressure), functional assessment with measurement of microvascular function/coronary reactivity, and intravascular imaging can be useful to identify the underlying cause.
2023 ESC Guidelines for the management of acute coronary syndromes | European Heart Journal | Oxford AcademicICA is the recommended definitive diagnostic test for ACS patients.
2023 ESC Guidelines for the management of acute coronary syndromes | European Heart Journal | Oxford AcademicIt is vital for clinicians to perform further assessments and investigations to establish the underlying cause of the MINOCA, which will allow a final diagnosis to be established and patients to be managed appropriately.
2023 ESC Guidelines for the management of acute coronary syndromes | European Heart Journal | Oxford AcademicThe first includes presenting symptoms, such as “Weakness.” The second contains 4 types of cards: Anatomy, such as “Precentral Gyrus”; Predisposing Condition, such as a tracing of atrial fibrillation; Pathology, such as a CT scan of a stroke; and Pathophysiology, such as “Cardioembolism.”
Stroke of Genius: A Customizable Card Game Structure to Exercise Differential Diagnostic Skills - PMCThe neurologic presentation is one of ongoing loss of pain sensation, loss of peripheral reflexes, impairment of vibration and position senses, and progressive ataxia.
Tabes Dorsalis - PhysiopediaFurthermore, PI3K/Akt can reduce the synthesis of glycogen and increase glycolysis. Inhibition of glycogen synthase kinase 3β activity by phosphorylation of its N‑terminal serine increases accumulation of cyclin D1, which promotes the cell cycle and improves cell proliferation through the PI3K/Akt signaling pathway.
PI3K/Akt signaling transduction pathway, erythropoiesis and glycolysis in hypoxia (Review)PI3K/Akt regulates fructose 2,6-bisphosphatase (PFKFB2) expression and strengthens glycolysis
PI3K/Akt signaling transduction pathway, erythropoiesis and glycolysis in hypoxia (Review)PI3K-dependent Akt is activated by insulin and growth factors that cause GSK-3β N terminal serine phosphorylation to inhibit GSK-3β activity
PI3K/Akt signaling transduction pathway, erythropoiesis and glycolysis in hypoxia (Review)increasing metabolic activity of brown adipose tissue (BAT), a tissue with abundant mitochondria. Through the action of UCP1 (uncoupling protein 1), BAT is able to dissipate chemically bound energy as heat, a process known as thermogenesis.
Metformin and Its Benefits for Various Diseases - PMCexert weak but beneficial effects on weight loss.
Metformin and Its Benefits for Various Diseases - PMCMetformin also inhibits mTORC1, a key regulator of cell growth that can integrate intracellular and extracellular stimuli (58), in an AMPK-independent manner (59). Additionally, metformin suppresses mitochondrial complex I, thereby preventing the generation of reactive oxygen species (ROS) and further decreasing DNA damage, suppressing cancer development
Metformin and Its Benefits for Various Diseases - PMCMetformin activates AMPK and then induces p53 phosphorylation to prevent cell invasion and metastasis
Metformin and Its Benefits for Various Diseases - PMCMetformin activates AMPK, which leads to the inhibition of mTOR signaling, and as a result, protein synthesis is disturbed, and cell growth and proliferation is suppressed
Metformin and Its Benefits for Various Diseases - PMCdecreases glucose levels through increasing (i) GLUT4(glucose transporter 4) mediated glucose uptake in skeletal muscles (46) and (ii) absorption of glucose in the intestines (47). Metformin also stimulates GLP-1 (glucagon-like-peptide-1) release, thereby enhancing insulin secretion and lowering plasma glucose levels
Metformin and Its Benefits for Various Diseases - PMCactivation of AMPK leads to the inhibition of mTORC1 (mammalian target of rapamycin complex I), which also results in the suppression of gluconeogenesis (42). On the other hand, metformin inhibits hepatic glucose production in an AMPK-independent manner
Metformin and Its Benefits for Various Diseases - PMCMetformin exerts its anti-hyperglycemic effects mostly by suppressing hepatic glucose production through AMPK-dependent (36, 37) or -independent pathways (38, 39). On the one hand, metformin inhibits gluconeogenesis through AMPK-dependent activation of SHP (small heterodimer partner) and inhibition of phosphorylation of CBP (CREB binding protein) (40), thus suppressing the expression of gluconeogenic genes, such as G6Pase (glucose 6 phosphatase), PEPCK (phosphoenolpyruvate carboxykinase), and PC (pyruvate carboxylase)
Metformin and Its Benefits for Various Diseases - PMCmetformin improves insulin sensitivity and decreases fasting insulin levels in cognitive impairment patients with abnormal glucose metabolism
Metformin and Its Benefits for Various Diseases - PMCmetformin could activate AMPK via the lysosomal pathway, i.e., the AXIN/LKB1-v-ATPase-Regulator pathway (17). AMPK is a key regulator of numerous metabolic pathways, including glucose metabolism, lipid metabolism, and energy homeostasis
Metformin and Its Benefits for Various Diseases - PMCMetformin inhibits mitochondrial complex I (13, 14), which leads to AMPK (adenosine 5′- monophosphate—activated protein kinase) activation
Metformin and Its Benefits for Various Diseases - PMCmetabolic associated diseases, cancer, aging and age-related diseases, neurological disorders
The development and benefits of metformin in various diseases | SpringerLinkmetformin-activated AMPK from lysosomes reduces lipid accumulation in the liver via acetyl-CoA carboxylase (ACC) inhibition and increases glucagon-like peptide 1 (GLP1) secretion in the gut
Fig. 1: Proposed mechanisms for metformin-induced reductions in blood levels of glucose. | Nature Reviews Endocrinologyinhibits mitochondrial respiratory chain complex IV, which can also result in an indirect inhibition of mGPDH activity.
Fig. 1: Proposed mechanisms for metformin-induced reductions in blood levels of glucose. | Nature Reviews Endocrinologythrough an increase in the glutathione to oxidized glutathione ratio (GSH:GSSG), leading to inhibition of genes encoding enzymes involved in gluconeogenesis through a let-7–TET3–HNF-4α pathway
Fig. 1: Proposed mechanisms for metformin-induced reductions in blood levels of glucose. | Nature Reviews Endocrinologydirectly inhibits mGPDH, resulting in an increased cytosolic redox state (NADH:NAD+), reduced gluconeogenesis from lactate and reduced activity of the glycerol–phosphate shuttle (which transfers NADH from the cytosol to mitochondria
Fig. 1: Proposed mechanisms for metformin-induced reductions in blood levels of glucose. | Nature Reviews Endocrinologyincrease in cellular redox potential (NADH:NAD+)
Fig. 1: Proposed mechanisms for metformin-induced reductions in blood levels of glucose. | Nature Reviews Endocrinologyactivates AMP-activated protein kinase (AMPK), but this has no direct effect on the regulation of glucose production.
Fig. 1: Proposed mechanisms for metformin-induced reductions in blood levels of glucose. | Nature Reviews Endocrinologyincreased AMP levels lead to inhibition of the activity of enzymes that are regulated by AMP and are involved in gluconeogenesis, such as adenylate cyclase and fructose-1-6-bisphosphatase (FBP1), which contributes to decreased glucose output.
Fig. 1: Proposed mechanisms for metformin-induced reductions in blood levels of glucose. | Nature Reviews Endocrinologymild inhibition of mitochondrial respiratory chain complex I, leading to a moderate decrease in ATP synthesis and a concomitant increase in cellular levels of AMP. The metformin-induced decrease in hepatic gluconeogenic flux, an ATP-dependent metabolic process, could result from this reduction in ATP levels.
Fig. 1: Proposed mechanisms for metformin-induced reductions in blood levels of glucose. | Nature Reviews EndocrinologyArrhythmogenic right ventricular cardiomyopathy (ARVC) is a disease of the heart muscle. In this disease, fatty fibrous tissue replaces normal heart muscle. This interrupts normal electrical signals in the heart and may cause irregular and potentially life-threatening heart rhythms.
Arrhythmogenic Right Ventricular Cardiomyopathy | Cedars-SinaiThese disorders are now part of a subgroup of previously described infiltrative forms of LV hypertrophy such as Pompe disease, a glycogen storage disease caused by α-1,4 glycosidase (acid maltase deficiency) in infants
Contemporary Definitions and Classification of the Cardiomyopathies | Circulationneuromuscular disorders such as Duchenne/Becker and Emery-Dreifuss muscular dystrophies
Contemporary Definitions and Classification of the Cardiomyopathies | CirculationNoncompaction of ventricular myocardium is a recently recognized congenital cardiomyopathy characterized by a distinctive (“spongy”) morphological appearance of the LV myocardium. Noncompaction involves predominantly the distal (apical) portion of the LV chamber with deep intertrabecular recesses (sinusoids) in communication with the ventricular cavity, resulting from an arrest in the normal embryogenesis.
Contemporary Definitions and Classification of the Cardiomyopathies | CirculationARVC/D involves predominantly the right ventricle with progressive loss of myocytes and fatty or fibrofatty tissue replacement, resulting in regional (segmental) or global abnormalities. Although frequently associated with myocarditis (enterovirus or adenovirus in some cases), ARVC/D is not considered a primary inflammatory cardiomyopathy.
Contemporary Definitions and Classification of the Cardiomyopathies | Circulationrelatively new clinical entity associated with sudden cardiac death in young people
Contemporary Definitions and Classification of the Cardiomyopathies | CirculationHCM is caused by a variety of mutations encoding contractile proteins of the cardiac sarcomere
Contemporary Definitions and Classification of the Cardiomyopathies | CirculationHCM is a clinically heterogeneous but relatively common autosomal dominant genetic heart disease
Contemporary Definitions and Classification of the Cardiomyopathies | Circulationperiaqueductal gray, the parabrachial nucleus, the mesencephalic raphe nuclei, and the locus ceruleus rostrally and the dorsal motor nucleus of the vagus, the nucleus ambiguous and the medullary raphe
Central Control of the Autonomic Nervous System and Thermoregulation (Section 4, Chapter 3) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy - The University of Texas Medical School at HoustonAfferent inputs from the periaqueductal gray, parabrachial nucleus, and the locus ceruleus ascend through the DLF to the hypothalamus
Central Control of the Autonomic Nervous System and Thermoregulation (Section 4, Chapter 3) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy - The University of Texas Medical School at Houstoncentral autonomic network is the dorsal longitudinal fasciculus
Central Control of the Autonomic Nervous System and Thermoregulation (Section 4, Chapter 3) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy - The University of Texas Medical School at Houstonvisceral and somatic input to the hypothalamus from the nucleus of the solitary tract, the parabrachial nuclei, the reticular formation and the periaqueductal gray.
Hypothalamus: Structural Organization (Section 4, Chapter 1) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy - The University of Texas Medical School at HoustonThe bi-directional pathways in this circuitry include the medial forebrain bundle noted as part of limbic circuitry above, as well as the dorsal longitudinal fasciculus. Whereas the medial forebrain bundle runs laterally through the brainstem and hypothalamus, the dorsal longitudinal fasciculus runs medially through the periventricular and periaqueductal gray matter.
Hypothalamus: Structural Organization (Section 4, Chapter 1) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy - The University of Texas Medical School at Houstonsitting w/o back support may elevate BP by 5-10mmHg
Pulsus Paradoxus and Blood Pressure Measurement Techniques | Stanford Medicine 25 | Stanford MedicineSpeaking may elevate BP by 8-15mmHg
Pulsus Paradoxus and Blood Pressure Measurement Techniques | Stanford Medicine 25 | Stanford Medicine