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Article ; Online: Co-crystal of Tramadol-Celecoxib Versus Tramadol or Placebo for Acute Moderate-to-Severe Pain After Oral Surgery: Randomized, Double-Blind, Phase 3 Trial (STARDOM1).

Langford, Richard / Pogatzki-Zahn, Esther M / Morte, Adelaida / Sust, Mariano / Cebrecos, Jesús / Vaqué, Anna / Ortiz, Esther / Fettiplace, James / Adeyemi, Shola / López-Cedrún, José Luis / Bescós, Socorro / Gascón, Neus / Plata-Salamán, Carlos

Advances in therapy

2024 Volume 41, Issue 3, Page(s) 1025–1045

Abstract: Introduction: Co-crystal of tramadol-celecoxib (CTC) is the first analgesic co-crystal for acute pain. This completed phase 3 multicenter, double-blind trial assessed the efficacy and safety/tolerability of CTC in comparison with that of tramadol in the ...

Abstract	Introduction: Co-crystal of tramadol-celecoxib (CTC) is the first analgesic co-crystal for acute pain. This completed phase 3 multicenter, double-blind trial assessed the efficacy and safety/tolerability of CTC in comparison with that of tramadol in the setting of moderate-to-severe pain up to 72 h after elective third molar extraction requiring bone removal. Methods: Adults (n = 726) were assigned randomly to five groups (2:2:2:2:1): orally administered twice-daily CTC 100 mg (44 mg rac-tramadol hydrochloride/56 mg celecoxib; n = 164), 150 mg (66/84 mg; n = 160) or 200 mg (88/112 mg; n = 160); tramadol 100 mg four times daily (n = 159); or placebo four times daily (n = 83). Participants in CTC groups also received twice-daily placebo. The full analysis set included all participants who underwent randomization. The primary endpoint was the sum of pain intensity differences over 0 to 4 h (SPID Results: All CTC doses were superior to placebo (P < 0.001) for primary and key secondary endpoints. All were superior to tramadol for SPID Conclusions: CTC demonstrated superior pain relief compared with tramadol or placebo, as well as an improved benefit/risk profile versus tramadol. Trial registration: ClinicalTrials.gov identifier, NCT02982161; EudraCT number, 2016-000592-24.
MeSH term(s)	Adult ; Humans ; Tramadol/adverse effects ; Celecoxib/therapeutic use ; Celecoxib/adverse effects ; Acute Pain/drug therapy ; Analgesics, Opioid/adverse effects ; Tooth Extraction/adverse effects ; Double-Blind Method ; Pain, Postoperative/drug therapy
Chemical Substances	Tramadol (39J1LGJ30J) ; Celecoxib (JCX84Q7J1L) ; Analgesics, Opioid
Language	English
Publishing date	2024-01-06
Publishing country	United States
Document type	Randomized Controlled Trial ; Clinical Trial, Phase III ; Multicenter Study ; Journal Article
ZDB-ID	632651-1
ISSN	1865-8652 ; 0741-238X
ISSN (online)	1865-8652
ISSN	0741-238X
DOI	10.1007/s12325-023-02744-2
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Zs.A 2101: Show issues

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Article: A New Pharmacophore Model for the Design of Sigma-1 Ligands Validated on a Large Experimental Dataset.

Pascual, Rosalia / Almansa, Carmen / Plata-Salamán, Carlos / Vela, José Miguel

Frontiers in pharmacology

2019 Volume 10, Page(s) 519

Abstract: The recent publication of the σ1R crystal structure is an important cornerstone for the derivation of more accurate activity prediction models. We report here a comparative study involving a set of more than 25,000 structures from our internal database ... ...

Abstract	The recent publication of the σ1R crystal structure is an important cornerstone for the derivation of more accurate activity prediction models. We report here a comparative study involving a set of more than 25,000 structures from our internal database that had been screened for σ1R affinity. Using the recently published crystal structure, 5HK1, two new pharmacophore models were generated. The first one,
Language	English
Publishing date	2019-05-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2019.00519
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Article: Co-crystals as a new approach to multimodal analgesia and the treatment of pain.

Almansa, Carmen / Frampton, Christopher S / Vela, José Miguel / Whitelock, Steve / Plata-Salamán, Carlos R

Journal of pain research

2019 Volume 12, Page(s) 2679–2689

Abstract: Pain is highly prevalent, but frequently untreated or under-treated, and health care professionals are faced with a range of treatment challenges. Multimodal therapy is recommended and can be achieved using open combinations (ie, concomitant ... ...

Abstract	Pain is highly prevalent, but frequently untreated or under-treated, and health care professionals are faced with a range of treatment challenges. Multimodal therapy is recommended and can be achieved using open combinations (ie, concomitant administration) of individual agents, fixed-dose combinations (FDCs), or multimodal agents (ie, single agents with multiple mechanisms of action). Co-crystallization of active pharmaceutical ingredients (APIs) offers another approach, with the potential to provide drugs with unique properties and advantages for therapeutic applications compared to combinations. API-API co-crystals are single-entity forms that offer a unique possibility of improving the physicochemical properties of both constituent APIs, as well as permitting their synchronous release. Consequently, this may positively impact on their pharmacokinetic (PK) properties and profiles, providing a potential advantage over FDCs and translating into improved clinical efficacy and safety profiles. We report here a revision of the literature concerning API-API co-crystals for the treatment of pain. It becomes apparent that identifying APIs with complementary mechanisms of action that can be adequately co-crystallized in an appropriate molecular ratio applicable for therapeutic use is challenging. In addition, API-API co-crystals normally result in a mere increased exposure of an API without defined clinical benefits (since, to maintain the benefit-risk, the dose needs to be proportionally reduced to adjust for the increased exposure). An exception to this is the co-crystal of tramadol-celecoxib (CTC), that represents a unique concept in co-crystal technology. In CTC neither of its three active components that have complementary mechanisms of action (ie, the two enantiomers of tramadol and celecoxib) show increased exposure levels versus commercially available single-entity reference products, but rather show a change in their PK profile with potential clinical advantages. CTC is in Phase III clinical development for the treatment of pain.
Language	English
Publishing date	2019-09-04
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2495284-9
ISSN	1178-7090
ISSN	1178-7090
DOI	10.2147/JPR.S208082
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Article ; Online: Efficacy and safety of co-crystal of tramadol-celecoxib (CTC) in acute moderate-to-severe pain after abdominal hysterectomy: A randomized, double-blind, phase 3 trial (STARDOM2).

Langford, Richard / Morte, Adelaida / Sust, Mariano / Cebrecos, Jesús / Vaqué, Anna / Ortiz, Esther / Fettiplace, James / Adeyemi, Shola / Raba, Grzegorz / But-Husaim, Liudmila / Gascón, Neus / Plata-Salamán, Carlos

European journal of pain (London, England)

2022 Volume 26, Issue 10, Page(s) 2083–2096

Abstract: Background: STARDOM2 is a randomized, double-blind, phase 3 trial evaluating the efficacy and safety of co-crystal of tramadol-celecoxib (CTC)-a first-in-class analgesic co-crystal comprising racemic tramadol hydrochloride and celecoxib in a ... ...

Abstract	Background: STARDOM2 is a randomized, double-blind, phase 3 trial evaluating the efficacy and safety of co-crystal of tramadol-celecoxib (CTC)-a first-in-class analgesic co-crystal comprising racemic tramadol hydrochloride and celecoxib in a supramolecular network that modifies their pharmacokinetic properties-for the management of acute postoperative pain (NCT03062644; EudraCT:2016-000593-38). Methods: Patients with moderate-to-severe pain following abdominal hysterectomy were randomized 2:2:2:2:2:1 to oral CTC 100 mg (rac-tramadol hydrochloride 44 mg/celecoxib 56 mg) twice daily (BID); CTC 150 mg (66/84 mg) BID; CTC 200 mg (88/112 mg) BID; immediate-release tramadol 100 mg four times daily (QID); celecoxib 100 mg BID; or placebo, for 5 days. The primary endpoint was the sum of pain intensity differences over 0-4 h (SPID<sub>0-4</sub> ). Key secondary endpoints were rescue medication use within 4 h, 50% response rate at 4 h, and safety/tolerability. Results: Of 1355 patients enrolled, 1138 were randomized (full analysis set) and 1136 treated (safety analysis set). In the prespecified gatekeeping analysis of SPID<sub>0-4</sub> , CTC 200 mg was not superior to tramadol but showed non-inferior efficacy (p < 0.001) that was sustained throughout the 120-h period, despite a 5-day cumulative tramadol administration of 880 mg with CTC 200 mg BID versus 2000 mg with tramadol 100 mg QID. Treatment-emergent adverse events (TEAEs) and severe TEAEs were less common with CTC 200 mg versus tramadol. Treatment-related TEAEs were 14.4% with CTC 200 mg and 23.6% with tramadol. Conclusions: Although the study did not meet its primary endpoint, CTC 200 mg showed a clinically relevant improvement in overall benefit/risk profile versus tramadol alone, with considerably lower cumulative opioid exposure. Significance: In the randomized, double-blind, phase 3 STARDOM2 trial-in acute moderate-to-severe pain after abdominal hysterectomy-the novel co-crystal of tramadol-celecoxib (CTC) 200 mg BID was superior to placebo and non-inferior to tramadol 100 mg QID. Although superiority to tramadol was not reached, CTC 200 mg BID exposed patients to lower cumulative opioid (tramadol) doses than tramadol (100 mg QID) alone, with fewer treatment-emergent adverse events. CTC 200 mg thus has a clinically relevant improved benefit/risk profile compared with tramadol alone.
MeSH term(s)	Acute Pain/drug therapy ; Analgesics, Opioid/adverse effects ; Celecoxib/chemistry ; Celecoxib/therapeutic use ; Cyclooxygenase 2 Inhibitors/adverse effects ; Double-Blind Method ; Drug Combinations ; Female ; Humans ; Hysterectomy/adverse effects ; Pain, Postoperative/drug therapy ; Tramadol/therapeutic use
Chemical Substances	Analgesics, Opioid ; Cyclooxygenase 2 Inhibitors ; Drug Combinations ; Tramadol (39J1LGJ30J) ; Celecoxib (JCX84Q7J1L)
Language	English
Publishing date	2022-09-24
Publishing country	England
Document type	Clinical Trial, Phase III ; Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	1390424-3
ISSN	1532-2149 ; 1090-3801
ISSN (online)	1532-2149
ISSN	1090-3801
DOI	10.1002/ejp.2021
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Zs.A 5194: Show issues

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Article ; Online: Celecoxib-tramadol co-crystal in patients with moderate-to-severe pain following bunionectomy with osteotomy: A phase 3, randomized, double-blind, factorial, active- and placebo-controlled trial.

Viscusi, Eugene R / de Leon-Casasola, Oscar / Cebrecos, Jesús / Jacobs, Adam / Morte, Adelaida / Ortiz, Esther / Sust, Mariano / Vaqué, Anna / Gottlieb, Ira / Daniels, Stephen / Gimbel, Joseph S / Muse, Derek / Winkle, Peter / Kuss, Michael E / Videla, Sebastián / Gascón, Neus / Plata-Salamán, Carlos

Pain practice : the official journal of World Institute of Pain

2022 Volume 23, Issue 1, Page(s) 8–22

Abstract: Background: Celecoxib-tramadol co-crystal (CTC) is a first-in-class analgesic co-crystal of celecoxib and racemic tramadol with an improved pharmacologic profile, conferred by the co-crystal structure, compared with its active constituents administered ... ...

Abstract	Background: Celecoxib-tramadol co-crystal (CTC) is a first-in-class analgesic co-crystal of celecoxib and racemic tramadol with an improved pharmacologic profile, conferred by the co-crystal structure, compared with its active constituents administered alone/concomitantly. Aim: We evaluated CTC in moderate-to-severe acute postoperative pain. Materials and methods: This randomized, double-blind, factorial, active- and placebo-controlled phase 3 trial (NCT03108482) was conducted at 6 US clinical research centers. Adults with moderate-to-severe acute pain following bunionectomy with osteotomy were randomized to oral CTC (200 mg [112 mg celecoxib/88 mg rac-tramadol hydrochloride] every 12 h), tramadol (50 mg every 6 h), celecoxib (100 mg every 12 h), or placebo for 48 h. Patients, investigators, and personnel were blinded to assignment. The primary endpoint was the 0-48 h sum of pain intensity differences (SPID0-48) in all randomized patients. Pain intensity was assessed on a 0-10 numerical rating scale (NRS). Safety was analyzed in patients who received study medication. Funded by ESTEVE Pharmaceuticals. Results: In 2017 (March to November), 1323 patients were screened and 637 randomized to CTC (n = 184), tramadol (n = 183), celecoxib (n = 181), or placebo (n = 89). Mean baseline NRS was 6.7 in all active groups. CTC had a significantly greater effect on SPID0-48 (least-squares mean: -139.1 [95% confidence interval: -151.8, -126.5]) than tramadol (-109.1 [-121.7, -96.4]; p < 0.001), celecoxib (-103.7 [-116.4, -91.0]; p < 0.001), or placebo (-74.6 [-92.5, -56.6]; p < 0.001). Total treatment-emergent adverse events (TEAEs) were 358 for CTC and 394 for tramadol. Drug-related TEAEs occurred in 37.7% patients in the CTC group, compared with 48.6% in the tramadol group. There were no serious TEAEs/deaths. Conclusion: CTC provided greater analgesia than comparable daily doses of tramadol and celecoxib, with similar tolerability to tramadol. CTC is approved in the United States.
MeSH term(s)	Adult ; Humans ; Celecoxib/therapeutic use ; Celecoxib/chemistry ; Tramadol/therapeutic use ; Cyclooxygenase 2 Inhibitors/therapeutic use ; Analgesics, Opioid ; Drug Combinations ; Pain, Postoperative/drug therapy ; Pain, Postoperative/etiology ; Osteotomy ; Double-Blind Method
Chemical Substances	Celecoxib (JCX84Q7J1L) ; Tramadol (39J1LGJ30J) ; Cyclooxygenase 2 Inhibitors ; Analgesics, Opioid ; Drug Combinations
Language	English
Publishing date	2022-07-08
Publishing country	United States
Document type	Randomized Controlled Trial ; Clinical Trial, Phase III ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2151272-3
ISSN	1533-2500 ; 1530-7085
ISSN (online)	1533-2500
ISSN	1530-7085
DOI	10.1111/papr.13136
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Zs.A 5928: Show issues

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Article: Cytokines and feeding.

Plata-Salamán, C R

International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity

2001 Volume 25 Suppl 5, Page(s) S48–52

Abstract: Various categories of cytokines participate in the control of feeding, including interleukin-1 and -6 and other activators of gp 130, leptin (ob protein), interleukin-8 and other chemokines, tumor necrosis factor-alpha, and interferon-alpha. These ... ...

Abstract	Various categories of cytokines participate in the control of feeding, including interleukin-1 and -6 and other activators of gp 130, leptin (ob protein), interleukin-8 and other chemokines, tumor necrosis factor-alpha, and interferon-alpha. These feeding-inhibitory cytokines may play a role in the regulation of food intake during physiological (eg a role proposed for leptin) and pathophysiological (eg proinflammatory cytokines) conditions. Data show that various cytokines participate in acute and chronic disease-associated anorexia such as during infection, inflammation or malignancy. Food intake suppression (reported as anorexia) is also a common central manifestation observed during cytokine immunotherapy in humans. The concept of local production of various cytokines within specific brain regions in response to peripheral challenges and pathophysiological processes has broad implications for the interpretation of brain cytokines as mediators or participants in CNS modulation of feeding and anorexia.
MeSH term(s)	Anorexia ; Brain/physiology ; Cytokines/physiology ; Eating/physiology ; Food ; Humans ; Inflammation ; Neurons/physiology
Chemical Substances	Cytokines
Language	English
Publishing date	2001-12
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1103255-8
ISSN	0307-0565
ISSN	0307-0565
DOI	10.1038/sj.ijo.0801911
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Zs.A 1325: Show issues

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Article: Ingestive behavior and obesity.

Plata-Salamán, C R

Nutrition (Burbank, Los Angeles County, Calif.)

2000 Volume 16, Issue 10, Page(s) 797–799

MeSH term(s)	Feeding Behavior/psychology ; Humans ; Obesity/etiology ; Obesity/physiopathology ; Obesity/therapy
Language	English
Publishing date	2000-10-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	639259-3
ISSN	1873-1244 ; 0899-9007
ISSN (online)	1873-1244
ISSN	0899-9007
DOI	10.1016/s0899-9007(00)00461-5
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Zs.A 2290: Show issues

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Article: Central nervous system mechanisms contributing to the cachexia-anorexia syndrome.

Plata-Salamán, C R

Nutrition (Burbank, Los Angeles County, Calif.)

2000 Volume 16, Issue 10, Page(s) 1009–1012

Abstract: The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, ... ...

Abstract	The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, cardiovascular disease, and rheumatoid arthritis. Cachexia makes an organism susceptible to secondary pathologies and can result in death. Cachexia-anorexia may result from pain, depression or anxiety, hypogeusia and hyposmia, taste and food aversions, chronic nausea, vomiting, early satiety, malfunction of the gastrointestinal system (delayed digestion, malabsorption, gastric stasis and associated delayed emptying, and/or atrophic changes of the mucosa), metabolic shifts, cytokine action, production of substances by tumor cells, and/or iatrogenic causes such as chemotherapy and radiotherapy. The cachexia-anorexia syndrome also involves metabolic and immune changes (mediated by either the pathophysiologic process, i.e., tumor, or host-derived chemical factors, e.g., peptides, neurotransmitters, cytokines, and lipid-mobilizing factors) and is associated with hypertriacylglycerolemia, lipolysis, and acceleration of protein turnover. These changes result in the loss of fat mass and body protein. Increased resting energy expenditure in weight-losing cachectic patients can occur despite the reduced dietary intake, indicating a systemic dysregulation of host metabolism. During cachexia, the organism is maintained in a constant negative energy balance. This can rarely be explained by the actual energy and substrate demands by tumors in patients with cancer. Overall, the cachectic profile is significantly different than that observed during starvation. Cachexia may result not only from anorexia and a decreased caloric intake but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions). In any case, the major deficit of a cachectic organism is a negative energy balance. Cytokines are proposed to participate in the development and/or progression of cachexia-anorexia; interleukin-1, interleukin-6 (and its subfamily members such as ciliary neurotrophic factor and leukemia inhibitory factor), interferon-gamma, tumor necrosis factor-alpha, and brain-derived neurotrophic factor have been associated with various cachectic conditions. Controversy has focused on the requirement of increased cytokine concentrations in the circulation or other body fluids (e.g., cerebrospinal fluid) to demonstrate cytokine involvement in cachexia-anorexia. Cytokines, however, also act in paracrine, autocrine, and intracrine manners, activities that cannot be detected in the circulation. In fact, paracrine interactions represent a predominant cytokine mode of action within organs, including the brain. Data show that cytokines may be involved in cachectic-anorectic processes by being produced and by acting locally in specific brain regions. Brain synthesis of cytokines has been shown in peripheral models of cancer, peripheral inflammation, and during peripheral cytokine administration; these data support a role for brain cytokines as mediators of neurologic and neuropsychiatric manifestations of disease and in the brain-to-peripheral communication (e.g., through the autonomic nervous system). Brain mechanisms that merit significant attention in the cachexia-anorexia syndrome are those that result from interactions among cytokines, peptides/neuropeptides, and neurotransmitters. These interactions could result in additive, synergistic, or antagonistic activities and can involve modifications of transducing molecules and intracellular mediators. Thus, the data show that the cachexia-anorexia syndrome is multifactorial, and understanding the interactions between peripheral and brain mechanisms is pivotal to characterizing the underlying integrative pathophysiology of this disorder.
MeSH term(s)	Anorexia/etiology ; Anorexia/physiopathology ; Brain/physiopathology ; Cachexia/etiology ; Cachexia/physiopathology ; Chronic Disease ; Cytokines/physiology ; Humans ; Time Factors
Chemical Substances	Cytokines
Language	English
Publishing date	2000-10-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	639259-3
ISSN	1873-1244 ; 0899-9007
ISSN (online)	1873-1244
ISSN	0899-9007
DOI	10.1016/s0899-9007(00)00413-5
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Zs.A 2290: Show issues

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Article: 1998 Curt P. Richter Award. Brain mechanisms in cytokine-induced anorexia.

Plata-Salamán, C R

Psychoneuroendocrinology

1999 Volume 24, Issue 1, Page(s) 25–41

Abstract: Our research focuses on the mechanisms underlying cytokine action in the central nervous system (CNS) using an integrative and multidisciplinary strategy organized through supracellular (behavioral analysis by computerized monitoring systems), cellular ( ... ...

Abstract	Our research focuses on the mechanisms underlying cytokine action in the central nervous system (CNS) using an integrative and multidisciplinary strategy organized through supracellular (behavioral analysis by computerized monitoring systems), cellular (extracellular and intracellular neurophysiological recording), and molecular (patch-clamp recording, and DNA, RNA and protein analyses) approaches. An integrative strategy that combines computerized meal pattern analyses with cellular and molecular biology approaches allows the study of underlying brain mechanisms in cytokine- and disease-associated anorexia. This paper presents a comprehensive discussion of our laboratory's previously published data on brain mechanisms involved in cytokine-induced anorexia including the relevance of meal pattern analysis (meal size, meal duration, meal frequency, intermeal intervals), modulation of hypothalamic neuronal activity, molecular processes involving ionic conductances, cytokine-cytokine and cytokine-peptide interactions, and modulation of cytokine and peptide/neuropeptide system components (ligands, endogenous inhibitors, receptor subtypes, signal transduction molecules, intracellular mediators) and cytokine feedback systems.
MeSH term(s)	Acetylmuramyl-Alanyl-Isoglutamine/pharmacology ; Acetylmuramyl-Alanyl-Isoglutamine/toxicity ; Animals ; Anorexia/chemically induced ; Anorexia/physiopathology ; Appetite/drug effects ; Awards and Prizes ; Brain/drug effects ; Brain/physiopathology ; Calcium Channels/drug effects ; Calcium Channels/physiology ; Cytokines/administration & dosage ; Cytokines/physiology ; Cytokines/toxicity ; Feeding Behavior/drug effects ; GTP-Binding Proteins/physiology ; Gene Expression Regulation/drug effects ; Humans ; Hypothalamus/drug effects ; Hypothalamus/physiopathology ; Injections, Intraventricular ; Interleukin-1/pharmacology ; Interleukin-1/physiology ; Interleukin-1/toxicity ; Lipopolysaccharides/pharmacology ; Lipopolysaccharides/toxicity ; Molecular Biology ; Nerve Tissue Proteins/physiology ; Rats
Chemical Substances	Calcium Channels ; Cytokines ; Interleukin-1 ; Lipopolysaccharides ; Nerve Tissue Proteins ; Acetylmuramyl-Alanyl-Isoglutamine (53678-77-6) ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	1999-01
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	197636-9
ISSN	1873-3360 ; 0306-4530
ISSN (online)	1873-3360
ISSN	0306-4530
DOI	10.1016/s0306-4530(98)00045-6
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Zs.A 1235: Show issues

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Article: Hypothalamus and the control of feeding: fifteen decades of direct association.

Plata-Salamán, C R

Nutrition (Burbank, Los Angeles County, Calif.)

1998 Volume 14, Issue 1, Page(s) 67–70

MeSH term(s)	Animals ; Eating/physiology ; History, 20th Century ; Hypothalamic Diseases/complications ; Hypothalamic Diseases/history ; Hypothalamus/physiology ; Obesity/etiology ; Obesity/history
Language	English
Publishing date	1998-01
Publishing country	United States
Document type	Biography ; Historical Article ; Journal Article
ZDB-ID	639259-3
ISSN	1873-1244 ; 0899-9007
ISSN (online)	1873-1244
ISSN	0899-9007
DOI	10.1016/s0899-9007(97)00400-0
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