Results 161 to 170 of about 2,954,568 (313)

ACR lung-RADS: updates and future directions. [PDF]

Cancer Imaging
Petranović M, Prosper AE, Hunsaker AR, Lam S, Christensen JD.   +4 more
europepmc   +1 more source

The C‐terminal truncated splicing variant of NK1R negatively modulates substance P‐stimulated NK1R signaling

FEBS Open Bio, EarlyView.
The neurokinin 1 receptor exists as full‐length (NK1L) and C‐terminally truncated (NK1S) splice variants. We show that NK1S heterodimerizes with NK1L, impairing Gαq coupling and Ca2+ mobilization while enhancing β‐arrestin1 recruitment. NK1S suppresses substance P‐driven gene expression and cell migration, revealing NK1S as an endogenous biased ...
Lan Phuong Nguyen, Duc Trung Nguyen, Minyoung Cho, Jihun Kim, Soyeon In, Thai Uy Nguyen, Sunghoon Hurh, Beom Jin Park, Jong‐Ik Hwang   +8 more
wiley   +1 more source

Lung Metastases of Pancreatic Adenocarcinoma Masquerading as Temporary Improvement of Bilateral Diffuse Lung Opacities Following Treatment for Interstitial Lung Disease. [PDF]

Respirol Case Rep
Kusunoki S, Tasato M, Sokai A, Iwata T, Hayashi Y, Yasuda N, Kashiwagi I, Nishimura T.   +7 more
europepmc   +1 more source

Selective elimination of quiescent cancer cells by dequalinium chloride via ROS‐mediated ferroptosis

FEBS Open Bio, EarlyView.
Dequalinium chloride (DQ) selectively eliminates quiescent cancer cells (QCCs) by amplifying mitochondrial ROS. QCCs exhibit elevated basal ROS and limited redox‐buffering capacity, making them vulnerable to further ROS increases. DQ‐induced ROS exceeds the tolerance threshold, triggering lipid peroxidation and ferroptosis, whereas proliferating cells ...
Kotaro Miyamoto, Shiori Sakai, Minori Endo, Terigele, Mizuho Niibori, Taiki Morita, Yu Goto, Arisa Yoshida, Tomohiro Tanaka, Ning Lin, Takahiro Kuchimaru, Hiroyuki Nakamura, Masahiro Inoue, Shinae Kizaka‐Kondoh, Tetsuya Kadonosono   +14 more
wiley   +1 more source

Cellular Senescence Dysregulates Antiviral Interferon Responses in Idiopathic Pulmonary Fibrosis. [PDF]

Aging Cell
Hughes JB, Reisser Y, Hornung F, Hilsabeck TAU, Senchyna F, Coelho AL, Ho TC, Schneider K, Furman D, Hogaboam CM, Le Saux CJ, Desprez PY, Deinhardt-Emmer S.   +12 more
europepmc   +1 more source

TRPML1 agonist ML‐SA5 attenuates pulmonary fibroblast activation by suppressing mTOR and restoring autophagic flux

FEBS Open Bio, EarlyView.
TGF‐β1 stimulation downregulates lysosomal channel TRPML1 in pulmonary fibroblasts. The TRPML1 agonist ML‐SA5 suppressed fibroblast‐to‐myofibroblast activation and collagen production. Mechanistically, ML‐SA5 inhibited mTOR phosphorylation, restored autophagic flux, and its effects were enhanced by rapamycin (mTOR inhibitor) and reversed by MHY1485 ...
Jiatong Yao, Xiaoting Kang, Lulu Meng, Shaoxuan Zhang, Qiujie Li, Jinyu Zhou, Mengyue Xue, Chu Li, Hua Zhu, Pengzhou Hang, Jing Zhao   +10 more
wiley   +1 more source

Cytokine Expression Profiling in Idiopathic Pulmonary Fibrosis: Insights From Integrative Proteomic Analysis

Canadian Respiratory Journal
Chenyou Shen, Wei Wang, Guirong Li, Dong Wei, Xusheng Yang, Cheng Jiang, Yating Sheng, Yuan Chen, Jingjing Xu, Shugao Ye, Jingyu Chen   +10 more
doaj   +1 more source

Transcatheter Aortic Valve Implantation Followed by Lung Cancer Resection in an Older Patient: A Case Report. [PDF]

Cureus
Khan L, Qadri SS.
europepmc   +1 more source

Fluorination: A strategy to tune the interactions of molecules and nanoscale systems with biological matter

FEBS Open Bio, EarlyView.
This minireview explores fluorination as a key strategy to optimize therapeutic molecules and nanocarriers. By incorporating different fluorinated motifs—from single atoms to linear and branched chains—drug delivery, cellular uptake, and colloidal stability can be improved and fine‐tuned.
Martina Beccalli, Beatrice Lucia Bona, Francesca Baldelli Bombelli   +2 more
wiley   +1 more source

Chronobiology of Cancer: How Aging Fuels Oncogenesis at the Molecular Level

Aging and Cancer, EarlyView.
This graphical abstract illustrates the key biological pathways linking aging with cancer development and progression. In the upper left, cumulative exposure to ultraviolet radiation, toxins, and reactive oxygen species (ROS) causes DNA damage and genomic instability, whereas age‐related decline in repair mechanisms, such as ATM/ATR, BER, and NER ...
Anu Singh, Aroonima Misra, Sufian Zaheer
wiley   +1 more source