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Disease Domain	Count

Neoplasms	1

Top 5 Drug Type	Count

ASO	1

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NEGF2(Midkine)	1

Author: Robertson, Graham R. ; Xie, Hao ; Hoefler, Gerald ; Schweiger, Martina ; Wagner, Erwin F. ; Schabbauer, Gernot ; Bakiri, Latifa ; Wolinski, Heimo ; Heier, Christoph ; Grabner, Gernot F. ; Pototschnig, Isabella ; Meng, Xia ; Schauer, Silvia ; Tang, Zhiyuan ; Zechner, Rudolf ; Baumgartner, Vanessa J. ; Zeng, Wenwen

Cancer-associated cachexia (CAC) is a hypermetabolic syndrome characterized by unintended weight loss due to the atrophy of adipose tissue and skeletal muscle. A phenotypic switch from white to beige adipocytes, a phenomenon called browning, accelerates CAC by increasing the dissipation of energy as heat. Addressing the mechanisms of white adipose tissue (WAT) browning in CAC, we now show that cachexigenic tumors activate type 2 immunity in cachectic WAT, generating a neuroprotective environment that increases peripheral sympathetic activity. Increased sympathetic activation, in turn, results in increased neuronal catecholamine synthesis and secretion, β-adrenergic activation of adipocytes, and induction of WAT browning. Two genetic mouse models validated this progression of events. 1) Interleukin-4 receptor deficiency impeded the alternative activation of macrophages, reduced sympathetic activity, and restrained WAT browning, and 2) reduced catecholamine synthesis in peripheral dopamine β-hydroxylase (DBH)–deficient mice prevented cancer-induced WAT browning and adipose atrophy. Targeting the intraadipose macrophage-sympathetic neuron cross-talk represents a promising therapeutic approach to ameliorate cachexia in cancer patients.

Scientific ReportsQ3 · CROSS-FIELD

Serum Midkine, estimated glomerular filtration rate and chronic kidney disease-related events in elderly women: Perth Longitudinal Study of Aging Women

Q3 · CROSS-FIELD

ArticleOA

Author: Zhu, Kun ; Raymond, Warren D ; Robertson, Graham R ; Lim, Wai H ; Lewis, Joshua R ; Cao, Qi ; Lee, Vincent W ; Wang, Jeffrey ; Byrnes, Elizabeth ; Prince, Richard L ; Wong, Germaine

AbstractMidkine (MDK), a heparin-binding growth factor cytokine, is involved in the pathogenesis of kidney diseases by augmenting leukocyte trafficking and activation. Animal models and small case control studies have implicated MDK as a pathological biomarker in chronic kidney diseases (CKD), however this is yet to be confirmed in prospective human studies. In a prospective study of 499 elderly, predominantly Caucasian women aged over 70 years the association between serum MDK collected in 1998, and renal function change and the risk of CKD-related hospitalisations and deaths at 5 and 14.5 years, respectively, was examined. Baseline serum MDK was not associated with 5-year change in estimated glomerular filtration rate using the CKD Epidemiology Collaboration creatinine and cystatin C equation (Standardised β = − 0.09, 95% confidence interval − 3.76–0.48, p = 0.129), 5-year rapid decline in renal function (odds ratio = 0.97, 95% confidence interval 0.46–2.02, p = 0.927) or the risk of 14.5-year CKD-related hospitalisations and deaths (hazard ratio = 1.27, 95% confidence interval .66–2.46, p = 0.470) before or after adjusting for major risk factors. In conclusion, in this cohort of elderly women with normal or mildly impaired renal function, serum MDK was not associated with renal function change or future CKD-related hospitalisations and deaths, suggesting that MDK may not be an early biomarker for progression of CKD.

100 Deals associated with Lyramid Ltd.

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100 Translational Medicine associated with Lyramid Ltd.

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Pipeline

Pipeline Snapshot as of 25 Dec 2024

The statistics for drugs in the Pipeline is the current organization and its subsidiaries are counted as organizations,Early Phase 1 is incorporated into Phase 1, Phase 1/2 is incorporated into phase 2, and phase 2/3 is incorporated into phase 3

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