Objective To observe the distribution of atypical memory B cells in peripheral blood of children with frequently relapsing nephrotic syndrome(FRNS).Methods A total of 60 children with primary ne-phrotic syndrome(PNS)admitted to the hospital from October 2020 to March 2023 were selected as the re-search objects.According to the response to glucocorticoid(GC),they were divided into non-frequently relap-sing nephrotic syndrome(NFRNS)group(25 cases)and FRNS group(35 cases).A total of 20 age-and gen-der-matched healthy children were enrolled as the control group.The changes of atypical memory B cells in each group before and after GC treatment were compared,and the correlation between the changes and clinical data was analyzed.Results Before GC treatment,The percentages of total B cells(CD19+CD20+),total memory B cells(CD19+CD20+CD27+),resting memory B cells(CD19+CD20+CD21+CD27+)and atypical memory B cells(CD19+CD20+CD21-CD27-)in FRNS group and NFRNS group were significantly higher than those in control group.And the FRNS group was significantly higher than the NFRNS group(P＜0.05).After GC treatment,the percentages of total B cells,total memory B cells,resting memory B cells,acti-vated memory B cells(CD19+CD20+CD21-CD27+)and atypical memory B cells in FRNS group and NFRNS group were lower than those before GC treatment(P＜0.05).The FRNS group had a significantly higher pro-portion of atypical memory B cells than the NFRNS group and the control group(P＜0.05).Before GC treat-ment,the 24 h urinary protein in FRNS group and NFRNS group were higher than those in control group,and the levels of immunoglobulin G and albumin were lower than those in control group.The 24 h urinary protein in FRNS group was significantly higher than that in NFRNS group(P＜0.05).Before GC treatment,there was a positive correlation between 24 h urinary protein and the proportion of atypical memory B cells in FRNS group(P＜0.05).Conclusion There is abnormal distribution of atypical memory B cells in peripheral blood of FRNS children.The increase of atypical memory B cells can be used as a marker of recurrence of FRNS af-ter GC treatment.

Rapid turnover of the intestinal epithelium is a critical strategy to balance the uptake of nutrients and defend against environmental insults, whereas inappropriate death promotes the spread of inflammation. PPARα is highly expressed in the small intestine and regulates the absorption of dietary lipids. However, as a key mediator of inflammation, the impact of intestinal PPARα signaling on cell death pathways is unknown. Here, we show that Pparα deficiency of intestinal epithelium up-regulates necroptosis signals, disrupts the gut vascular barrier, and promotes LPS translocation into the liver. Intestinal Pparα deficiency drives age-related hepatic steatosis and aggravates hepatic fibrosis induced by a high-fat plus high-sucrose diet (HFHS). PPARα levels correlate with TRIM38 and MLKL in the human ileum. Inhibition of PPARα up-regulates necroptosis signals in the intestinal organoids triggered by TNF-α and LPS stimuli via TRIM38/TRIF and CREB3L3/MLKL pathways. Butyric acid ameliorates hepatic steatosis induced by intestinal Pparα deficiency through the inhibition of necroptosis. Our data suggest that intestinal PPARα is essential for the maintenance of microenvironmental homeostasis and the spread of inflammation via the gut-liver axis.

Objective To study the expression of hypoxia inducible factor-1 (HIF-1 ) and Notch signaling pathway downstream gene HES 1 in the hippocampus of pubertal rats with status epilepsy (SE), and to explore the regulation site of HIF-1αin Notch signaling pathway. Methods One hundred and seventy-six 21-day-old SD rats were randomly divided into control group (NS group), pentetrazole (PTZ)-induced SE group (PTZ group), and Notch signaling pathway speciifc inhibitor (DAPT) intervention group (DAPT group). In PTZ group PTZ was intraperitoneally injected to build SE model and in NS group normal saline was injected as control. The intraperitoneal injection of diazepam was used to terminate SE seizures. After successful modeling, the bilateral hippocampuses were isolated after the rats were sacriifced at 0.5, 1, 2, 4 and 8 h, respectively, and RT-PCR was performed to detect the mRNA expression of HES 1 and HIF-1α. The Western Blot was performed to detect protein expression in hippocampuses which were collected at 2 , 4 , 8 , 12 , and 24 h after successful modeling. DAPT group received intraperitoneal injection of DAPT 30 min before the start of molding, then the hippocampuses were isolated at 2 and 8 h after successful modeling. RT-PCR was performed to detect the mRNA expression of HES 1 and HIF-1αat 2 h, and Western blot was performed to detect protein expression at 8 h. Results At each time point after SE, the expression of mRNA of HES 1 and HIF-1αand the expression of protein were higher than the same time point of NS group (P