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Weaning is considered to be one of the most critical periods in pig production, which is related to the economic benefits of pig farms. However, in actual production, many piglets are often subjected to weaning stress due to the sudden separation from the sow, the changes in diet and living environment, and other social challenges. Weaning stress often causes changes in the morphology and function of the small intestine of piglets, disrupts digestion and absorption capacity, destroys intestinal barrier function, and ultimately leads to reduced feed intake, increased diarrhea rate, and growth retardation. Therefore, correctly understanding the effects of weaning stress on intestinal health have important guiding significance for nutritional regulation of intestinal injury caused by weaning stress. In this review, we mainly reviewed the effects of weaning stress on the intestinal health of piglets, from the aspects of intestinal development, and intestinal barrier function, thereby providing a theoretical basis for nutritional strategies to alleviate weaning stress in mammals in future studies.

In clinical practice, ovarian pregnancy is extremely rare and is always found to be ruptured. A definitive diagnosis for ruptured ovarian pregnancy is difficult to obtain. We present two cases of unruptured ovarian pregnancies detected during laparoscopy and review existing literature to better understand the clinical characteristics of ectopic pregnancies in this rare site. Intrauterine devices, assisted reproductive technology, and intrauterine operations are all high-risk factors in ovarian pregnancy. Moreover, menopause, abdominal pain, and vaginal bleeding are clinical manifestations. Ovarian pregnancy can be diagnosed using serum hCG, transvaginal ultrasound, and magnetic resonance imaging. Laparoscopy is the treatment of choice for ovarian pregnancy. It is recommended that the intact gestational sac be excised and the ovarian function be protected to the greatest extent possible during the operation. More definitive diagnosis of ovarian pregnancy must be reported in order to gain a better understanding of ovarian pregnancy.

This study was conducted to evaluate the effects of dietary supplementation of different recommended levels of Cu and Zn on antioxidant capacity, tissue mineral status, minerals excretion, meat quality, digestive enzyme activity, and metal transporters in finishing pigs. A total of 120 pigs (with an average initial body weight (BW) of 70.0 ± 2.1 kg) were randomly divided into four treatments: (1) basal diet without added Cu or Zn (control), (2) basal diet+35 mg cupreous N-carbamylglutamate chelate (NCG-Cu) +150 mg zinc-methionine chelate (Zn-Met) (AC), (3) basal diet + 3.0 mg of NCG-Cu + 43 mg Zn-Met (CN), and (4) basal diet + 3.5 mg NCG-Cu + 50 mg Zn-Met (NRC100). Pig growth performance was not affected by the level of Cu or Zn. Among the four treatments, the AC treatment had the highest concentration (P < 0.05) of glutathione peroxidase (GSH-Px). Pigs fed the AC diet had the highest (P < 0.05) liver Zn, fecal Cu, and fecal Zn among the four treatments. The protein levels of trypsin and aminopeptidase N (APN) in the intestinal mucosa showed their highest levels (P < 0.05) in the NRC100 and AC treatments. The mRNA levels of trypsinogen and APN were significantly up-regulated (P < 0.05) in the AC, CN, and NRC100 treatments compared with the control. The mRNA levels for the Zn transporter genes SLC30A1 (ZnT1) and SLC30A2 (ZnT2) were significantly up-regulated (P < 0.05) in the AC treatment, and the mRNA levels for SLC39A4 (ZIP4) and metallothionein 1 (MT) in the AC, CN, and NRC100 treatments were significantly up-regulated (P < 0.05) compared with the control. Meat quality were not affected (P > 0.05) by the different recommended levels of Cu and Zn. These results indicated that the supplemental Cu and Zn levels routinely used in AC diets in Chinese commercial feed enterprises should be reduced.

Hepatocellular carcinoma (HCC) is one of the most frequent malignancies and the third leading cause of cancer-related deaths worldwide. Besides, it has been revealed that long non-coding RNA (LncRNA) cancer susceptibility candidate 11 (CASC11) is involved in cancer progression. However, the functional role and underlying mechanism of CASC11 in HCC remains largely unknown. In this context, here, it was found that CASC11 was upregulated in HCC tissues and associated with tumor grades, metastasis, and prognosis of HCC patients. Functionally, CASC11 facilitated HCC cell proliferation, migration, and invasion in vitro, and enhanced tumor growth and metastasis in vivo. Mechanistically, CASC11 associated with and stabilized Ubiquitin-conjugating enzyme E2T (UBE2T) mRNA. To be specific, it decreased UBE2T N6-methyladenosine (m6A) level via recruiting ALKBH5. Moreover, CASC11 inhibited the association between UBE2T mRNA and m6A reader protein YTHDF2. Taken together, our findings demonstrate the epigenetic mechanism of CASC11 in the regulation of UBE2T expression and possibly provide a novel therapeutic target for HCC treatment.

Background: A recent study disclosed that ferroptosis was an important myocyte death style in myocardial infarction (MI). However, the diagnostic value of ferroptosis regulators and correlated underlying mechanisms in acute myocardial infarction (AMI) remain unknown.Methods: Bioinformatical analyses were conducted to identify the candidate biomarkers for AMI, and the collected local samples were used to validate the findings via real-time quantitative PCR. Bioinformatical analysis and luciferase reporter assay were implemented to identify the transcriptional factor. Transient transfection and ferroptosis characteristic measurement, including glutathione peroxidase 4, malondialdehyde, iron, and glutathione, was performed to verify the ability of the candidate gene to regulate the ferroptosis of cardiomyocytes. A meta-analysis was conducted in multiple independent cohorts to clarify the diagnostic value.Results: A total of 121 ferroptosis regulators were extracted from previous studies, and aldo-keto reductase family 1 member C3 (AKR1C3) was significantly downregulated in the peripheral blood samples of AMI cases from the analysis of GSE48060 and GSE97320. HOXB4 served as a transcriptional activator for AKR1C3 and could suppress the ferroptosis of the H9C2 cells treated with erastin. Besides this, peripheral blood samples from 16 AMI patients and 16 patients without coronary atherosclerotic disease were collected, where AKR1C3 and HOXB4 both showed a high diagnostic ability. Furthermore, a nomogram including HOXB4 and AKR1C3 was established and successfully validated in six independent datasets. A clinical correlation analysis displayed that AKR1C3 and HOXB4 were correlated with smoking, CK, CK-MB, and N-terminal-pro-B-type natriuretic peptide.Conclusion: Taken together, this study demonstrates that AKR1C3 and HOXB4 are promising diagnostic biomarkers, providing novel insights into the ferroptosis mechanisms of AMI.

IntroductionKetamine, which is widely used in anesthesia, can induce cortical neurotoxicity in patients. This study aims to investigate the effects of long non-coding RNA LINC00641 on the ketamine-induced neural injury.Materials and MethodsIn this study, rat pheochromocytoma cells (PC12 cells) were used as a cell model and Sprague–Dawley postnatal day 7 rats were used for experiments in vivo. Ketamine-induced aberrant expression levels of LINC00641, miR-497-5p and brain-derived neurotrophic factor (BDNF) were examined by qRT-PCR. The effects of LINC00641 and miR-497-5p on ketamine-induced neural injury were then examined by MTT assays and TUNEL analysis. In addition, the activity of ROS and caspase-3 was measured. The regulatory relationships between LINC00641 and miR-497-5p, miR-497-5p and BDNF were detected by dual-luciferase reporter assay, respectively.ResultsKetamine induced the apoptosis of PC12 cells, accompanied by down-regulation of LINC00641 and BDNF, and up-regulation of miR-497-5p. LINC00641 overexpression enhanced the resistance to the apoptosis of PC12 cells, while transfection of miR-497-5p had opposite effects. Furthermore, LINC00641 could bind to miR-497-5p and reduce its expression, but indirectly increase the BDNF expression, which was considered as a protective factor in neural injury and activated TrkB/PI3K/Akt pathway.ConclusionCollectively, LINC00641/miR-497-5p/BDNF axis was validated to be an important signaling pathway in modulating ketamine-induced neural injury.