Results 101 to 110 of about 37,908 (274)

Mitigating Cancer Therapy–Related Cognitive Impairment by Targeted Activation of Undruggable Phosphatase

open access: yesAdvanced Science, EarlyView.
An RVG‑engineered exosomal saRNA delivery system (RVG‑EVs‑saPtpro) effectively targets and activates hippocampal PTPRO, functioning as a “molecular brake” to alleviate cancer therapy‑related cognitive impairment (CTRCI) by enhancing neuronal survival, neurogenesis, and synaptic plasticity.
Zhimeng Yao   +18 more
wiley   +1 more source

Doctor of Pharmacy [PDF]

open access: yes, 1983
dissertationThe preliminary purpose of this study was to document the incidence of clinical and subclinical spontaneous abortion in women who have no reproductive capability impairment.
Joy, Martha E.
core  

FGF13 Deficiency Ameliorates Paclitaxel‐Induced Neuropathic Pain by Inhibiting VASH1‐Mediated Microtubule Detyrosination to Promote Mitophagy

open access: yesAdvanced Science, EarlyView.
FGF13 is upregulated in DRG neurons of PIPNP model mice. DRG neuron‐specific knockout of FGF13 ameliorates PIPNP symptoms. Mechanistically, FGF13 potentiates microtubule detyrosination by promoting VASH1 binding to microtubules. FGF13 knockout suppresses VASH1‐mediated microtubule detyrosination and promotes α‐tubulin tyrosination.
Yiming Dong   +10 more
wiley   +1 more source

Doctor of Pharmacy [PDF]

open access: yes, 1987
dissertationVerapamil was first introduced in the early 1960\u27s as a smooth muscle relaxant with potent vasodilator properties. Antiarrhythmic effects were demonstrated in the mid-1960\u27s, but it V83 not until August, 1981 that the Food awl Drug ...
McCormick, Mary Alice
core  

Unveiling Lactylation: A Novel Frontier in Cancer Stemness and Therapy

open access: yesAdvanced Science, EarlyView.
Tumor metabolism and epigenetic regulation are intrinsically linked. This review highlights lactylation as a pivotal bridge connecting these processes, acting as an active epigenetic effector in cancer stemness. We delineate how lactylation orchestrates the cancer stem cell landscape and evaluate its regulatory networks.
Ting Li   +9 more
wiley   +1 more source

Engineering Approaches to Modify Immunomodulatory Functions of Mesenchymal Stromal Cells (MSCs): Tissue Regeneration and Clinical Application

open access: yesAdvanced Science, EarlyView.
Mesenchymal stromal cells (MSCs) show promise for treating immune‐related disorders through immunomodulation and tissue regeneration. This review gives a brief overview of current clinical approval of MSC therapies. It also discussed how bioengineering, including genetic modification, biomaterial delivery, extracellular vesicles, and iPSC‐derived MSCs,
Sichen Yang   +6 more
wiley   +1 more source

Nanomaterials in pharmacology / edited by Zheng-Rong Lu, Shinji Sakuma. [PDF]

open access: yes, 2016
pharmacy bookfair2016Includes bibliographical references and index.xii, 485 p
Sakuma, Shinji, Lu, Zheng-Rong
core  

ANKS1B in the Nucleus Accumbens Controls Escalated Cocaine Self‐Administration via Regulating CBP‐FoxO3 Complex

open access: yesAdvanced Science, EarlyView.
ANKS1B in the nucleus accumbens plays a critical role in the transition from controlled to escalated cocaine intake. Mechanistically, ANKS1B interacts with CBP to epigenetically suppress FoxO3 through H3K27 acetylation. The ANKS1B‐CBP‐FoxO3 signaling cascade presents a novel theraputic target for the treatment of cocaine addiction.
Liping Yang   +15 more
wiley   +1 more source

VDAC1 Upregulation Induces Hyperexcitability of Nociceptive Sensory Neurons Via Enhanced Mitochondrial Atp Efflux in Neuropathic Pain

open access: yesAdvanced Science, EarlyView.
The mechanism diagram of VDAC1 mediating neuronal excitability and neuropathic pain. Briefly, VDAC1 is expressed in DRG neurons and is upregulated following CCI‐induced neuropathic pain. This upregulation enhances ATP transport from mitochondria to the cytoplasm in sensory neurons, leading to increased neuronal excitability and pain behavior.
Fengrun Sun   +7 more
wiley   +1 more source

TOLLIP Inhibits Psoriasis Progression via Suppressing PKM2‐Mediated Glycolysis in Keratinocytes

open access: yesAdvanced Science, EarlyView.
In this study, we identify TOLLIP as a critical regulator of psoriasis pathogenesis through its modulation of glycolytic metabolism. Our findings establish the TOLLIP‐PKM2‐glycolysis axis as a key mechanism linking metabolic reprogramming to psoriasis pathogenesis, and propose TOLLIP as a promising therapeutic target.
Xiuhuan Jiang   +11 more
wiley   +1 more source

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