Optical probes operating in the second near-infrared window (NIR-II, 1,000-1,700 nm), where tissues are highly transparent, have expanded the applicability of fluorescence in the biomedical field. NIR-II fluorescence enables deep-tissue imaging with micrometric resolution in animal models, but is limited by the low brightness of NIR-II probes, which prevents imaging at low excitation intensities and fluorophore concentrations. Here, we present a new generation of probes (Ag₂S superdots) derived from chemically synthesized Ag₂S dots, on which a protective shell is grown by femtosecond laser irradiation. This shell reduces the structural defects, causing an 80-fold enhancement of the quantum yield. PEGylated Ag₂S superdots enable deep-tissue in vivo imaging at low excitation intensities (<10 mW cm⁻²) and doses (<0.5 mg kg⁻¹), emerging as unrivaled contrast agents for NIR-II preclinical bioimaging. These results establish an approach for developing superbright NIR-II contrast agents based on the synergy between chemical synthesis and ultrafast laser processing.

Despite attracting increased attention from clinicians, brain temperature distribution, fluctuations, and changes in response to external stimuli are still largely unknown and refractory to conventional temperature‐probing approaches. Fluorescence nanothermometry in the second near‐infrared window (NIR‐II, 1000–1700 nm), as shown here, can provide contactless brain thermal sensing through the scalp and skull in real time with a subdegree resolution. As a proof of concept, Ag₂S nanothermometers have been used to monitor brain thermoregulation in a cooling/heating process and temperature changes associated to a barbiturate coma.

. The isometric response to arginine‐vasopressin (10⁻¹⁰‐10⁻⁷m) was studied in 2 mm long rabbit arterial segments isolated from several vascular beds (cutaneous, pial, renal, coronary, muscular, mesenteric and pulmonary). . Vasopressin induced contraction in central ear (cutaneous), basilar (pial), renal, coronary and saphenous (muscular) arteries, but had no effect in mesenteric and pulmonary arteries; the order of potency for the contraction was: ear > basilar > renal > coronary > saphenous arteries. . Treatment with the blocker of nitric oxide synthesis N^G‐nitro‐L‐arginine methyl ester (L‐NAME; 10⁻⁶‐10⁻⁴m) increased significantly (P< 0.05) the contraction to vasopressin in ear (148% of control), basilar (150% of control), renal (304% of control), coronary (437% of control) and saphenous (235% of control) arteries. Removal of the endothelium increased significantly (P< 0.05) the contraction to vasopressin in basilar (138% of control), renal (253% of control), coronary (637% of control) and saphenous (662% of control) arteries, but not in ear artery. Mesenteric and pulmonary arteries in the presence of L‐NAME or after endothelium removal did not respond to vasopressin, as occurred in control conditions. . The specific antagonist for V₁vasopressin receptors d(CH₂)₅Tyr(Me)AVP (3 × 10⁻⁹‐10⁻⁷m) was more potent (pA₂= 9.3–10.1) than the antagonist for both V₁and V₂vasopressin receptors desGly‐d(CH₂)₅‐D‐Tyr(Et)ValAVP (10⁻⁷‐10⁻⁶m) (pA₂= 7.4–8.4) to block the contraction to vasopressin of ear, basilar, renal and coronary arteries. . The specific V₂vasopressin agonist [deamino‐Cys¹, D‐Arg⁸]‐ vasopressin (desmopressin) (10⁻¹⁰‐10⁻⁷m) did not produce any effect in any of the arteries studied, with or without endothelium. . In arteries precontracted with endothelin‐1, vasopressin or desmopressin did not produce relaxation. . These results suggest: (a) most arterial beds studied (5 of 7) exhibit contraction to vasopressin with different intensity; (b) the vasoconstriction to this peptide is mediated mainly by stimulation of V₁vasopressin receptors, and (c) endothelial nitric oxide may inhibit the vasoconstriction to this peptide, especially in coronary and renal vasculatures.