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Novel application of punch excision therapy in the treatment of keloids: A systematic review

Keloids are fibroproliferative disorders of the skin marked with elevated interleukin-6 and transforming growth factor-beta, causing pain, pruritus, and decreased quality of life.1 Punch excision therapy is emerging as a simple, quick, and accessible treatment option for keloid management. This review summarizes the current evidence on the efficacy and safety of punch excision therapy in keloid management.

People’s sniffing behaviors predict what they are smelling, study shows

Humans and other animals actively sense their surrounding environment. This entails the deliberate adjustment of motor behavior involved in sensory sampling (i.e., movements of the eyes, ears and hands) in line with the stimulus information.

When it comes to the sense of smell, the principal motor behavior that supports active sensing is the sniff, which entails brief inhalations aimed at pulling odor molecules into the nasal cavity. So far, the extent to which sniffing behaviors can be influenced and adapted based on the odors that one is smelling has remained unknown.

Researchers at Northwestern University recently carried out a study aimed at exploring this possibility. Their findings, published in Nature Human Behavior, suggest that people’s sniffing patterns are continuously shaped by what they are smelling and carry detailed information about specific odors.

Footnotes: Claudin-2 deficiency reveals a corticomedullary calcium gradient driving kidney stone formation:

Benjamin D. Humphreys provides an Editor’s Note on Christine V. Behm et al. https://doi.org/10.1172/JCI197807

The figure from Behm et al. shows nephrocalcinosis in older kidney-specific Cldn2-KO mice.


Deposits of hydroxyapatite called Randall’s plaques are found in the renal papilla of calcium oxalate kidney stone formers and likely serve as the nidus for stone formation, but their pathogenesis is unknown. Claudin-2 is a paracellular ion channel that mediates calcium reabsorption in the renal proximal tubule. To investigate the role of renal claudin-2, we generated kidney tubule–specific claudin-2 conditional KO mice (KS-Cldn2 KO). KS-Cldn2 KO mice exhibited transient hypercalciuria in early life. Normalization of urine calcium was accompanied by a compensatory increase in expression and function of renal tubule calcium transporters, including in the thick ascending limb. Despite normocalciuria, KS-Cldn2 KO mice developed papillary hydroxyapatite deposits, beginning at 6 months of age, that resembled Randall’s plaques and tubule plugs.

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