Bleeding is largely unavoidable following syringe needle puncture of biological tissues and, while inconvenient, this typically causes little or no harm in healthy individuals. However, there are certain circumstances where syringe injections can have more significant side effects, such as uncontrolled bleeding in those with haemophilia, coagulopathy, or the transmission of infectious diseases through contaminated blood. Herein, we present a haemostatic hypodermic needle able to prevent bleeding following tissue puncture. The surface of the needle is coated with partially crosslinked catechol-functionalized chitosan that undergoes a solid-to-gel phase transition in situ to seal punctured tissues. Testing the capabilities of these haemostatic needles, we report complete prevention of blood loss following intravenous and intramuscular injections in animal models, and 100% survival in haemophiliac mice following syringe puncture of the jugular vein. Such self-sealing haemostatic needles and adhesive coatings may therefore help to prevent complications associated with bleeding in more clinical settings.

Nanofiber‐based hydrocolloid scaffold is prepared by colloid electrospinning of thermoplastic polyurethane (TPU)/sodium carboxymethyl cellulose (S.CMC) in tetrahydrofuran (THF)/dimethylformamide (DMF). The most suitable process of electrospinning for successful formation of fibers is investigated by controlling the concentration of polymeric solution and co‐solvent ratio. In order to accomplish high wettability, the amount of colloid (S.CMC) and the co‐solvent ratio (THF/DMF), which affects the morphology of fibers, are adjusted. Finally, the open wound healing effect is confirmed using nanofiber‐hydrocolloid from in vivo animal studies. A detailed study of the wound healing process is also demonstrated for the first time.

Lapatinib is one of several tyrosine kinase inhibitors used against solid tumour cancers such as breast and lung cancer. Although lapatinib is associated with a risk of QT prolongation, the effects of the drug on cellular cardiac electrical properties and on action potential duration (APD) have not been studied. To evaluate the potential effects of lapatinib on cardiac repolarization, we investigated its electrophysiological effects using a whole-cell patch-clamp technique in transiently transfected HEK293 cells expressing human ether-à-go-go (hERG; to examine the rapidly activating delayed rectifier K + current, I Kr ), KCNQ1 ⁄ KCNE1 (to examine the slowly activating delayed rectifier K + current, I Ks ), KCNJ2 (to examine the inwardly rectifying K + current, I K1 ), or SCN5A (to examine the inward Na + current, I Na ) and in rat cardiac myocytes (to examine the inward Ca 2+ current, I Ca ). We also examined its effects on the APD at 90% (APD 90 ) in isolated rabbit Purkinje fibres. In ion channel studies, lapatinib inhibited the hERG current in a concentration-dependent manner, with a half-maximum inhibition concentration (IC 50 ) of 0.8 € 0.09 lM. In contrast, at concentrations up to 3 lM, lapatinib did not significantly reduce the I Na , I K1 or I Ca amplitudes; at 3 lM, it did slightly inhibit the I Ks amplitude (by 19.4 € 4.7%; p < 0.05). At 5 lM, lapatinib induced prolongation of APD 90 by 16.1% (p < 0.05). These results suggest that the APD 90 -prolonging effect of lapatinib on rabbit Purkinje fibres is primarily a result of inhibition of the hERG current and I Ks , but not I Na , I K1 or I Ca .