Objective: This research aimed to evaluate the effects of age on growth, tibia development, and intestinal calcium (Ca) and phosphorus (P) transporter gene expressions in broiler chickens.Methods: A total of 224 male Arbor Acres broilers were fed with nutrient-adequate diets and reared in eight cages (28 broilers per cage). Eight broilers (one broiler per cage) were selected and killed at 5, 10, 15, 20, 25, 30, 35, and 40 days of age, respectively.Results: Body weight continuously increased with age of broiler chickens from 5 to 40 days. The bone weight, ash weight, diameter, and length of the tibia also increased with broiler age. By contrast, the tibia ash, Ca, and P percentages quadratically changed with age (p<0.001), and the highest values of mineral contents were observed at 20, 25, and 25 days of age, respectively. The mRNA abundances of calcium-binding protein 28-kDa (CaBP-D28k), sodium-calcium exchanger 1 (NCX1), and plasma membrane ATPase 1b (PMCA1b) increased from 5 to 25 days and then decreased up to 40 days. Similar results were noted in the mRNA abundances of IIb sodium-phosphate cotransporter (NaPi-IIb), inorganic phosphate transporter 1 (PiT-1), inorganic phosphate transporter 2 (PiT-2), nuclear vitamin D receptor (nVDR), and membrane vitamin D receptor (mVDR). The mRNA abundances of Ca and P transporters and VDRs were the highest at 25 days of age.Conclusion: These data indicate that age quadratically affects intestinal Ca and P transporter gene expression and mineral absorption capacity in broiler chickens.

Breast cancer is one of the most common malignant tumors among women, which seriously threatens women’s health. Human epidermal growth factor receptor 2 (HER2)-positive breast cancer, characterized by poor prognosis, is an aggressive phenotype accounting for 15–20% of all kinds of breast cancers. Therefore, it has attracted great interest among researchers in discovering targeted therapy drugs countering HER2, and they have been considered as the pivotal therapeutic regimen for HER2-positive breast cancer patients. Nowadays, large progress has been achieved in HER2-targeted drugs, and this review categorizes them into four types according to the drug action mode, including monoclonal antibodies (mAbs), tyrosine kinase inhibitors (TKIs), antibody-drug conjugates (ADCs), and bispecific antibodies (bsAbs). The progress of HER2-targeted drugs reflects the discovery of drug targets, the screening of drug compounds, and the modification of antibodies, which offer diverse medical options and better therapeutic benefits for individual patients. In detail, we focus on the indication, administration, efficacy, strengths, and challenges of HER2-targeted drugs, concerning approved drugs and clinical trials. This review aims to provide significant references for the targeted therapeutic regimen and a more precise treatment strategy for HER2-positive breast cancer.

The objective of this study is investigating the effects of Lonicerae flos extract (LFE) on antioxidant status, intestinal development, and jejunum barrier function in heat-stressed broilers. Two hundred and forty male broilers (28-day-old) were assigned to normal control group (NOR, 22°C, basal diet), heat stress group (HS, 32°C, basal diet) and Lonicerae flos extract supplementation group (LFE, 32°C, basal diet with 400 mg/kg, 800 mg/kg, 1200 mg/kg LFE). Results indicated that Heat stress significantly impaired growth performance, increased serum aspartate aminotransferase (AST) and d-lactate levels, decreased jejunal mucosal total antioxidant capacity (T-AOC) and jejunal villus height (P < 0.05) throughout the entire experimental period. Although not statistically significant for growth performance, Lonicerae flos extract numerically reduced the feed-to-gain ratio by 8.5 % after 14 days. Lonicerae flos extract, particularly at 800 mg/kg, significantly mitigated the heat stress-induced elevation in serum AST and d-lactate levels and enhanced jejunal T-AOC and superoxide dismutase (SOD) activity and jejunal villus height (P < 0.05). Lonicerae flos extract activated Nrf-2 pathway, downregulated the mRNA expressions of endoplasmic reticulum stress (ERS) and apoptosis-related genes, and enhanced the mRNA expressions of tight junction proteins in jejunum mucosa of heat stressed-broilers. The 800 mg/kg dose was identified as the most effective. In conclusion, dietary LFE effectively improved intestinal integrity and antioxidant capacity in heat-stressed broiler through activating Nrf-2 pathway, alleviating ERS-dependent apoptosis and improving jejunum barrier function.

Perinatal antibiotic exposure poses a significant risk to maternal-offspring immune programming and infant gut microbiota development. This study investigated the time-specific effects of maternal cefoperazone sodium (CPZ) administration on IgG transfer and offspring gut microbiota in a murine model. Pregnant C57BL/6J mice were assigned to control (CON), gestational (G-CPZ), lactational (L-CPZ), and combined gestational/lactational (GL-CPZ) treatment groups. Results showed that all CPZ treatments significantly reduced IgG and its subtype levels in maternal serum, colostrum, and offspring serum (p < 0.05). Concurrently, mRNA expression of the neonatal Fc receptor (FcRn), critical for IgG transport, was downregulated in both maternal breast and offspring intestinal tissues (p < 0.05). Furthermore, 16S rRNA sequencing revealed that CPZ exposure altered offspring gut microbiota diversity and composition. Alpha diversity was reduced, particularly in the G-CPZ group, while beta diversity showed significant separation in L-CPZ and GL-CPZ groups (p < 0.05). Taxonomic shifts included decreased Bacteroidetes and Lactobacillus, and in the GL-CPZ group, a marked increase in Firmicutes and potential pathobionts like Enterococcus and Hungatella (p < 0.05). These findings demonstrate that perinatal antibiotic exposure, depending on its timing, impairs maternal-offspring IgG transfer via the FcRn pathway and induces distinct, persistent alterations in the offspring’s gut microbiota, which may have implications for neonatal immunity and long-term health.