循证医学大模型,实现文献来源引用

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https://www.openevidence.com/api/article/e317a509-a2d8-47d8-bb30-7031cf3abf29

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        "text": "REACTCOMPONENT!:!Thinking!:!{\"done\": true, \"summary\": \"Finished thinking\", \"steps\": [{\"kind\": \"reasoning\", \"label\": \"Analyzing query\"}, {\"kind\": \"search\", \"label\": \"Searching published medical literature, guidelines, FDA, CDC, and more\", \"queries\": []}, {\"label\": \"Synthesizing relevant information\", \"kind\": \"reasoning\"}]}\n\n\n<strong>发烧</strong>是指核心体温高于正常范围的状态,通常是由于体温调节中枢(下丘脑)对外源性或内源性致热原(如细菌、病毒、炎症介质等)产生反应,主动将体温设定点上调所致。发烧是机体对感染或炎症等刺激的适应性免疫反应,其机制主要涉及免疫细胞释放细胞因子(如IL-1、IL-6、TNF-α),这些细胞因子促使前列腺素E2在下丘脑前部产生,进而上调体温设定点,引发体温升高。[[[$$$Prajitha N, Athira SS, Mohanan PV. <a target=\"_blank\" href=\"https://pubmed.ncbi.nlm.nih.gov/30336182\">Pyrogens, a Polypeptide Produces Fever by Metabolic Changes in Hypothalamus: Mechanisms and Detections</a>. Immunology Letters. 2018;204:38-46. doi:10.1016/j.imlet.2018.10.006.$$$]!!![$$$Haidar G, Singh N. <a target=\"_blank\" href=\"https://www.nejm.org/doi/full/10.1056/NEJMra2111003\">Fever of Unknown Origin</a>. The New England Journal of Medicine. 2022;386(5):463-477. doi:10.1056/NEJMra2111003.$$$]!!![$$$Conti B, Tabarean I, Andrei C, Bartfai T. <a target=\"_blank\" href=\"https://pubmed.ncbi.nlm.nih.gov/14977558\">Cytokines and Fever</a>. Frontiers in Bioscience : A Journal and Virtual Library. 2004;9:1433-49. doi:10.2741/1341.$$$]]]\n\n在临床上,发烧的定义因人群和场景而异。美国疾病控制与预防中心(CDC)将体温超过38°C视为发烧,而美国感染病学会(IDSA)和美国重症医学会(SCCM)则在重症监护患者中将单次体温≥38.3°C定义为发烧。需要注意的是,发烧与被动性高热(如中暑、恶性高热)不同,后者是体温调节失控,体温升高但无体温设定点变化,且常对常规退热药无效。[[[$$$O'Grady NP, Alexander E, Alhazzani W, et al. <a target=\"_blank\" href=\"https://doi.org/10.1097/CCM.0000000000006022\">Society of Critical Care Medicine and the Infectious Diseases Society of America Guidelines for Evaluating New Fever in Adult Patients in the ICU</a>. Critical Care Medicine. 2023;51(11):1570-1586. doi:10.1097/CCM.0000000000006022.$$$]!!![$$$Sessler DI. <a target=\"_blank\" href=\"https://pubmed.ncbi.nlm.nih.gov/26775126\">Perioperative Thermoregulation and Heat Balance</a>. Lancet (London, England). 2016;387(10038):2655-2664. doi:10.1016/S0140-6736(15)00981-2.$$$]!!![$$$Mackowiak PA. <a target=\"_blank\" href=\"https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/10.1001/archinte.158.17.1870?utm_source=openevidence&utm_medium=referral\">Concepts of Fever</a>. Archives of Internal Medicine. 1998;158(17):1870-81. doi:10.1001/archinte.158.17.1870.$$$]]]\n\n发烧的临床意义在于提示机体可能存在感染、炎症或其他疾病过程,但并非所有感染患者都会出现发烧,且发烧的缺失在感染患者中与预后不良相关。[[[$$$O'Grady NP, Alexander E, Alhazzani W, et al. <a target=\"_blank\" href=\"https://doi.org/10.1097/CCM.0000000000006022\">Society of Critical Care Medicine and the Infectious Diseases Society of America Guidelines for Evaluating New Fever in Adult Patients in the ICU</a>. Critical Care Medicine. 2023;51(11):1570-1586. doi:10.1097/CCM.0000000000006022.$$$]]]\n\n\n我建议",
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                                    "text": "<strong>发烧</strong>",
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                                    "text": "是指核心体温高于正常范围的状态,通常是由于体温调节中枢(下丘脑)对外源性或内源性致热原(如细菌、病毒、炎症介质等)产生反应,主动将体温设定点上调所致。发烧是机体对感染或炎症等刺激的适应性免疫反应,其机制主要涉及免疫细胞释放细胞因子(如IL-1、IL-6、TNF-α),这些细胞因子促使前列腺素E2在下丘脑前部产生,进而上调体温设定点,引发体温升高。",
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                                                "snippet_text": "Title: Pyrogens, a Polypeptide Produces Fever by Metabolic Changes in Hypothalamus: Mechanisms and Detections\nJournal: Immunology letters\nPMID: 30336182\nPublication date: 2018-12-01\n----------\nFever is one of the cardinal symptoms of onset of an infection or inflammation and is the common clinical indicator for medical consultation in mammalian host worldwide. Simply, fever manifested with elevation of body temperature from normal physiological range represents adaptive response of immune system on challenge with an infectious and non-infectious circumstance. Fever usually initiated in the periphery as a result of interaction of immune cells with exogenous or endogenous pyrogens. Peripheral pyrogenic signals gain access to the central nervous system via humoral and neural route. Humoral pathway was initiated with production of pyrogenic cytokines and prostaglandins from immune cells of blood as well as liver, transmitted directly to pre-optic area of hypothalamus through the circumventricular organ of brain. On the other hand an alternative pathway was initiated by the same cytokines indirectly via stimulating the vagal sensory neurons result in pyrogenic fever; so-called neuronal pathway. If the magnitude of pyrogens associated fever is very high, it will lead to severe illness ranging from septic shock to death. So it is necessary to evaluate the presence of pyrogens in implants, medical devices, drugs and biological materials to ensure safety in biomedical applications and therapeutics. Classification, route of administration, mechanism of action and detection of pyrogens and associated products are the major subject of this review.",
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                                                    "title": "Pyrogens, a Polypeptide Produces Fever by Metabolic Changes in Hypothalamus: Mechanisms and Detections",
                                                    "authors_string": "Prajitha N, Athira SS, Mohanan PV.",
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                                                        "The Febrile Response"
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                                                "snippet_text": "Article Title: Fever of Unknown Origin\nJournal: The New England Journal of Medicine\nPublication Date: 2022-02-03\nSection: The Febrile Response\n----------\nThermometry did not become mainstream until Wunderlich’s pioneering work on temperature in 1868. Using a foot-long instrument that took 20 minutes to register, he recorded more than a million axillary readings and established normal body temperature as 37.0°C (98.6°F). Since the 19th century, however, human bodies appear to have gradually become colder. New population-based data show that body temperatures have been steadily declining at a rate of approximately 0.03 to 0.5°C per decade; currently, the normal range is 36.3 to 36.5°C. Inflammatory, environmental, and other changes during the previous two centuries are among the proposed reasons for these observations.\n\nThe preoptic area and anterior hypothalamus play key roles in thermal homeostasis. Induction of pyrogenic cytokines (e.g., interleukin-1 and interleukin-6) by pathogens or inflammatory stimuli triggers prostaglandin E2 production by brain endothelial cells, which resets the thermoregulatory set point in the preoptic area and thus elicits a febrile response. The preoptic area also controls other thermoregulatory responses, including cutaneous vasoconstriction, nonshivering thermogenesis in brown adipose tissue, and shivering thermogenesis in skeletal muscles. Fever-related anorexia is also prostaglandin-mediated. Whereas pyrogens induce fever, counterregulatory cytokines (e.g., interleukin-10) and other endogenous antipyretic mediators function as cryogens (inhibitors of fever) and prevent detrimental elevations of temperature.",
                                                "citation_detail": {
                                                    "title": "Fever of Unknown Origin",
                                                    "authors_string": "Haidar G, Singh N.",
                                                    "dt_published": "2022-02-03T00:00:00+00:00",
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                                                    "doi": "10.1056/NEJMra2111003",
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                                            "citation": "Haidar G, Singh N. <a target=\"_blank\" href=\"https://www.nejm.org/doi/full/10.1056/NEJMra2111003\">Fever of Unknown Origin</a>. The New England Journal of Medicine. 2022;386(5):463-477. doi:10.1056/NEJMra2111003."
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                                                "snippet_text": "Title: Cytokines and Fever\nJournal: Frontiers in bioscience : a journal and virtual library\nPMID: 14977558\nPublication date: 2004-05-01\n----------\nCytokines are highly inducible, secreted proteins mediating intercellular communication in the nervous and immune system. Fever is the multiphasic response of elevation and decline of the body core temperature regulated by central thermoregulatory mechanisms localized in the preoptic area of the hypothalamus. The discovery that several proinflammatory cytokines act as endogenous pyrogens and that other cytokines can act as antipyretic agents provided a link between the immune and the central nervous systems and stimulated the study of the central actions of cytokines. The proinflammatory cytokines interleukin 1 (IL-1), interleukin 6 (IL-6) and the tumor necrosis factor alpha (TNF) as well as the antiinflammatory cytokines interleukin 1 receptor antagonist (IL-1ra) and interleukin 10 (IL-10) have been most investigated for their pyrogenic or antipyretic action. The experimental evidence demonstrating the role of these secreted proteins in modulating the fever response is as follows: 1) association between cytokine levels in serum and CSF and fever; 2) finding of the presence of cytokine receptors on various cell types in the brain and demonstration of the effects of pharmacological application of cytokines and of their neutralizing antibodies on the fever response; 3) fever studies on cytokine- and cytokine receptor- transgenic models. Studies on the peripheral and the central action of cytokines demonstrated that peripheral cytokines can communicate with the brain in several ways including stimulation of afferent neuronal pathways and induction of the synthesis of a non cytokine pyrogen, i.e. PGE2, in endothelial cells in the periphery and in the brain. Cytokines synthesized in the periphery may act by crossing the blood brain barrier and acting directly via neuronal cytokine receptors. The mechanisms that ultimately mediate the central action of cytokines and of LPS on the temperature-sensitive neurons in the preoptic hypothalamic region involved in thermoregulation, directly or via second mediators, remain to be fully elucidated.",
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                                                    "title": "Cytokines and Fever",
                                                    "authors_string": "Conti B, Tabarean I, Andrei C, Bartfai T.",
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                                            "citation": "Conti B, Tabarean I, Andrei C, Bartfai T. <a target=\"_blank\" href=\"https://pubmed.ncbi.nlm.nih.gov/14977558\">Cytokines and Fever</a>. Frontiers in Bioscience : A Journal and Virtual Library. 2004;9:1433-49. doi:10.2741/1341."
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                                    "text": "在临床上,发烧的定义因人群和场景而异。美国疾病控制与预防中心(CDC)将体温超过38°C视为发烧,而美国感染病学会(IDSA)和美国重症医学会(SCCM)则在重症监护患者中将单次体温≥38.3°C定义为发烧。需要注意的是,发烧与被动性高热(如中暑、恶性高热)不同,后者是体温调节失控,体温升高但无体温设定点变化,且常对常规退热药无效。",
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                                                "snippet_text": "Guideline Title: Society of Critical Care Medicine and the Infectious Diseases Society of America Guidelines for Evaluating New Fever in Adult Patients in the ICU\nDate Published: 2023-11-01\nSocieties: Infectious Diseases Society of America; Society of Critical Care Medicine\nRegions: US\nSection Header: FEVER DEFINITION\nSection Path: FEVER DEFINITION\n----------\nThe normal body temperature range is subject to a variety of factors such as age, gender, diurnal variation, and sampling site (12). In addition, evidence indicates that the normal body temperature has been decreasing in the human population by 0.03°C per birth decade over the last 157 years (13).\nThe United States Centers for Disease Control and Prevention definition of fever in the diagnosis of hospital-acquired infections is a measured temperature of greater than 38°C (14). The Infectious Diseases Society of America (IDSA) has defined fever in individuals greater than 65 years old residing in long-term care facilities as a single oral temperature greater than 37.8°C, repeated temperature measurements greater than 37.2°C (oral) or greater than 37.5°C (rectal), or an increase from baseline greater than 1.1°C (15). In patients with neutropenia due to chemotherapy, fever is defined by both the IDSA and the National Comprehensive Cancer Network as a single oral temperature measurement greater than or equal to 38.3°C or greater than 38.0°C sustained over at least 1 hour (16). The SCCM and IDSA have previously defined fever in ICU patients as the presence of a single temperature measurement greater than or equal to 38.3°C (3). We used this SCCM/IDSA definition of fever for this guideline.\nNot all patients with infection manifest fever and, in fact, the absence of fever in patients with infection is associated with worse outcomes (17,18). Consequently, the recommendations in this guideline may generally apply to ICU patients with suspected infection regardless of the presence of temperature elevation.",
                                                "citation_detail": {
                                                    "title": "Society of Critical Care Medicine and the Infectious Diseases Society of America Guidelines for Evaluating New Fever in Adult Patients in the ICU",
                                                    "authors_string": "O'Grady NP, Alexander E, Alhazzani W, et al.",
                                                    "dt_published": "2023-11-01T00:00:00+00:00",
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                                            "citation": "O'Grady NP, Alexander E, Alhazzani W, et al. <a target=\"_blank\" href=\"https://doi.org/10.1097/CCM.0000000000006022\">Society of Critical Care Medicine and the Infectious Diseases Society of America Guidelines for Evaluating New Fever in Adult Patients in the ICU</a>. Critical Care Medicine. 2023;51(11):1570-1586. doi:10.1097/CCM.0000000000006022."
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                                                        "Hyperthermia and fever"
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                                                "snippet_text": "Article Title: Perioperative Thermoregulation and Heat Balance\nJournal: Lancet (London, England)\nPublication Date: 2016-06-25\nSection: Hyperthermia and fever\n----------\nHyperthermia is any elevation in core temperature. It can result from excessive heating, excessive heat production, inadequate heat loss, or setpoint elevation. Routine intraoperative warming systems can produce hyperthermia, especially during long operations. Hyperthermia is rare in adults using modern warming systems, but occasionally occurs in infants and children. Intraoperative hyperthermia can also result, either intentionally or not, from peritoneal lavage with heated chemotherapy solutions.\n\nExamples of excessive heat production include vigorous exercise and malignant hyperthermia. Inadequate heat loss can result from high ambient temperature, especially when combined with high humidity, but can also occur when sweating is prevented by moisture-impervious clothing such as hazardous material suits. Hyperthermia from most of these causes is usually easy to treat: eliminate excessive heating and promote heat loss.\n\nFever is a type of hyperthermia, but differs from other core temperature elevations in being a regulated increase. It is mediated by circulating pyrogenic cytokines including interleukins and interferon, which are largely released from mononuclear inflammatory cells. Endogenous pyrogens activate the vagus nerve, triggering release of prostaglandin E2 in the preoptic-anterior hypothalamus, which in turn increases the setpoint. Many drugs also provoke fever and hyperthermic syndromes.\n\nFever is rare during anaesthesia because both volatile anaesthetics and opioids blunt the febrile response, but can occur in response to infection, allergy, and mismatched blood transfusions. After surgery, when the thermoregulatory effects of anaesthesia dissipate, fever is more likely. Fever is also common in critical care patients.\n\nBy contrast with passive hyperthermia, fever can be challenging to manage. Because core temperature is highly regulated, simply promoting heat loss—and even vigorous cooling—often fails. Active cooling in patients with fever provokes thermal discomfort, autonomic nervous system activation, and shivering. Furthermore, it does not necessarily reduce core temperature, which remains regulated to a high temperature. Aggressive treatment of fever might worsen outcomes.\n\nA better strategy is to treat the underlying cause (ie, infection) or use drugs such as paracetamol to block fever centrally, thus converting fever to passive hyperthermia, which is easier to treat.",
                                                "citation_detail": {
                                                    "title": "Perioperative Thermoregulation and Heat Balance",
                                                    "authors_string": "Sessler DI.",
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                                                "snippet_text": "Article Title: Concepts of Fever\nJournal: JAMA Internal Medicine\nPublication Date: 1998-09-28\nSection: Definitions\n----------\nFever has been defined as \"a state of elevated core temperature, which is often, but not necessarily, part of the defensive responses of multicellular organisms (host) to the invasion of live (microorganisms) or inanimate matter recognized as pathogenic or alien by the host.\" The febrile response (of which fever is a component) is a complex physiologic reaction to disease, involving a cytokine-mediated rise in core temperature, generation of acute phase reactants, and activation of numerous physiologic, endocrinologic, and immunologic systems. The rise in temperature during fever is to be distinguished from that occurring during episodes of hyperthermia. Unlike fever, hyperthermia involves an unregulated rise in body temperature in which pyrogenic cytokines are not directly involved and against which standard antipyretics are ineffective. It represents a failure of thermoregulatory homeostasis, in which there is uncontrolled heat production, inadequate heat dissipation, or defective hypothalamic thermoregulation.\n\nIn the clinical setting, fever is typically defined as a pyrogen-mediated rise in body temperature above the normal range. Although useful as a descriptor for the febrile patient, the definition ignores the fact that a rise in body temperature is but one component of this multifaceted response. This standard clinical definition is further flawed, because it implies that \"body temperature\" is a single entity, when in fact, it is a pastiche of many different temperatures, each representative of a particular body part and each varying throughout the day in response to the activities of daily living and the influence of endogenous diurnal rhythms.",
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                                    "text": "发烧的临床意义在于提示机体可能存在感染、炎症或其他疾病过程,但并非所有感染患者都会出现发烧,且发烧的缺失在感染患者中与预后不良相关。",
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                                                "snippet_text": "Guideline Title: Society of Critical Care Medicine and the Infectious Diseases Society of America Guidelines for Evaluating New Fever in Adult Patients in the ICU\nDate Published: 2023-11-01\nSocieties: Infectious Diseases Society of America; Society of Critical Care Medicine\nRegions: US\nSection Header: FEVER DEFINITION\nSection Path: FEVER DEFINITION\n----------\nThe normal body temperature range is subject to a variety of factors such as age, gender, diurnal variation, and sampling site (12). In addition, evidence indicates that the normal body temperature has been decreasing in the human population by 0.03°C per birth decade over the last 157 years (13).\nThe United States Centers for Disease Control and Prevention definition of fever in the diagnosis of hospital-acquired infections is a measured temperature of greater than 38°C (14). The Infectious Diseases Society of America (IDSA) has defined fever in individuals greater than 65 years old residing in long-term care facilities as a single oral temperature greater than 37.8°C, repeated temperature measurements greater than 37.2°C (oral) or greater than 37.5°C (rectal), or an increase from baseline greater than 1.1°C (15). In patients with neutropenia due to chemotherapy, fever is defined by both the IDSA and the National Comprehensive Cancer Network as a single oral temperature measurement greater than or equal to 38.3°C or greater than 38.0°C sustained over at least 1 hour (16). The SCCM and IDSA have previously defined fever in ICU patients as the presence of a single temperature measurement greater than or equal to 38.3°C (3). We used this SCCM/IDSA definition of fever for this guideline.\nNot all patients with infection manifest fever and, in fact, the absence of fever in patients with infection is associated with worse outcomes (17,18). Consequently, the recommendations in this guideline may generally apply to ICU patients with suspected infection regardless of the presence of temperature elevation.",
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                                                    "authors_string": "O'Grady NP, Alexander E, Alhazzani W, et al.",
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                                            "citation": "O'Grady NP, Alexander E, Alhazzani W, et al. <a target=\"_blank\" href=\"https://doi.org/10.1097/CCM.0000000000006022\">Society of Critical Care Medicine and the Infectious Diseases Society of America Guidelines for Evaluating New Fever in Adult Patients in the ICU</a>. Critical Care Medicine. 2023;51(11):1570-1586. doi:10.1097/CCM.0000000000006022."
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