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The risk factors for sentinel lymph node metastasis in our study were consistent with those in the Memorial Sloan-Kettering Cancer Center nomogram. The Memorial Sloan-Kettering Cancer Center nomogram is a useful tool that could accurately predict the probability of sentinel lymph node metastasis in our breast cancer patients. Axillary surgical staging might be avoided in patients with a predictive value of <16% and axillary lymph node dissection might be done directly in those with a predictive value >70%, while other patients should still accept sentinel lymph node biopsy.

The hippocampal CA3 contributes to spatial working memory (SWM), but which stage of SWM the CA3 neurons act on and whether the lateralization of CA3 function occurs in SWM is also unknown. Here, we reveal increased neural activity in both sample and choice phases of SWM. Left CA3 (LCA3) neurons show higher sensitivity in the choice phase during the correct versus error trials compared with right CA3 (RCA3) neurons. LCA3 initiates firing prior to RCA3 in the choice phase. Optogenetic suppression of pyramidal neurons in LCA3 disrupts SWM only in the choice phase. Furthermore, we discover that parvalbumin (PV) neurons, rather than cholinergic neurons in the medial septum (DB were cholinergic neurons), can project directly to unilateral CA3. Selective suppression of PV neurons in the MS projecting to LCA3 impairs SWM. The findings suggest that MS PV-LCA3 projection plays a crucial role in manipulating the lateralization of LCA3 in the retrieval of SWM.

Background Asthma is a prevailing respiratory disease among children, characterized by allergic airway inflammation, airway remodeling, and airway hyperresponsiveness. Although it is well‐known that long non‐coding RNAs (lncRNAs) are linked to a variety of human diseases and well‐documented, very few studies explore its role in asthma. In this study, we investigate the effects of lncRNA PVT1 on the promotion of airway inflammation and its associated mechanisms. Methods and Materials Human small airway epithelial cells (HSAECs) with PVT1 overexpressed or knocked down were constructed, and platelet activating factor (PAF) was used to treat HSAECs to mimic the pathological process of asthma in vitro. The expressions of prostaglandin E2 (PGE2), interleukin‐1β (IL‐1β), IL‐6, and tumor necrosis factor‐α (TNF‐α) were measured by enzyme‐linked immunosorbent assay (ELISA). The expressions of PKC, MyD88, and NF‐ĸB were measured by Western blot. Monolayer permeability of HSAECs was also compared within different groups. Luciferase reporter gene assay was employed to detect the targeting relationship between PVT1 and miR‐149. Results The knockdown of PVT1 attenuated the levels of inflammatory factors induced by PAF and destruction of cell‐barrier function. The overexpression of PVT1 facilitated the pathological development. Additionally, miR‐149 was identified as a target microRNA of PVT1, and the overexpression of miR‐149 could reverse the effects of PVT1 on PAF‐induced HSAECs. Conclusion These findings suggest that PVT1 may represent a novel potential target for treatment of asthma.