Spontaneous uterine venous rupture combined with ovarian rupture in late pregnancy is extremely rare. It often has an insidious onset and atypical symptoms, develops rapidly, and is easily ...misdiagnosed. Wewould like to discuss and share this case of spontaneous uterine venous plexus combined with ovarian rupture in the third trimester of pregnancy with colleagues.
A pregnant woman, G1P0 at 33
weeks of gestation,was admitted to the hospital due to threatened preterm labour on March 3, 2022. After admission, she was treated with tocolytic inhibitors and foetal lung maturation agents. The patient's symptoms did not improve during the treatment. After many examinations, tests, discussions, a diagnosis, and a caesarean section, the patient was finally diagnosed with atypical pregnancy complicated by spontaneous uterine venous plexus and ovarian rupture.
Spontaneous rupture of the uterine venous plexus combined with ovarian rupture in late pregnancy is an occult and easily misdiagnosed condition, and the consequences are serious. Clinical attention should be given to the disease and prevention attempted to avoid adverse pregnancy outcomes.
Most of follicles undergo a degenerative process called follicular atresia. This process directly affects the egg production of laying hens and is regulated by external and internal factors. External ...factors primarily include nutrition and environmental factors. In follicular atresia, internal factors are predominantly regulated at 3 levels; organic, cellular and molecular levels. At the organic level, the hypothalamic-pituitary-ovary (HPO) axis plays an essential role in controlling follicular development. At the cellular level, gonadotropins and cytokines, as well as estrogens, bind to their receptors and activate different signaling pathways, thereby suppressing follicular atresia. By contrast, oxidative stress induces follicular atresia by increasing ROS levels. At the molecular level, granulosa cell (GC) apoptosis is not the only factor triggering follicular atresia. Autophagy is also known to give rise to atresia. Epigenetics also plays a pivotal role in regulating gene expression in processes that seem to be related to follicular atresia, such as apoptosis, autophagy, proliferation, and steroidogenesis. Among these processes, the miRNA regulation mechanism is well-studied. The current review focuses on factors that regulate follicular atresia at organic, cellular and molecular levels and evaluates the interaction network among these levels. Additionally, this review summarizes atretic follicle characteristics, in vitro modeling methods, and factors preventing follicular atresia in laying hens.
The objective of this study was to investigate the effects of difloxacin (DIF) and avermectin (AVM) on glutamate decarboxylase (GAD) and GABA-transaminase (GABA-T) in different tissues of crucian ...carp (
Carassius auratus gibelio
). After the treatments of DIF and AVM, the mRNA expressions of GAD and GABA-T in different tissues were detected by quantitative real-time PCR (qPCR). The results showed that the mRNA expressions of GAD
65
, GAD
67
, and GABA-T in the telencephalon (Tel), mesencephalon (Mes), cerebella (Cer), and medulla oblongata (Med) were downregulated significantly with the safe dose (SD, 20 mg/kg) of DIF (
P
< 0.05 or
P
< 0.01). While the expressions of GAD
65
and GAD
67
in the kidney at 12 h had strikingly upregulated to 13.81 ± 1.06** and 150.67 ± 12.85** times. Treated with the lethal dose of 50% (LD
50
, 2840 mg/kg b. W.) of DIF, the mRNA expressions of GAD
65
, GAD
67
, and GABA-T in all tissues were increased significantly (
P
< 0.01). The results of AVM group showed that the mRNA expressions of GAD
65
, GAD
67
, and GABA-T both in the central and peripheral tissues were all remarkably downregulated at the safe concentration (SC, 0.0039 mg/L) and the lethal concentration of 50% (LC
50
, 0.039 mg/L), except for the mRNA inhibitions of GAD
65
, GAD
67
, and GABA-T in the muscle at 2 h which sharply downregulated to 0.20 ± 0.02
ΔΔ
× 10
−2
, 0.57 ± 0.06
ΔΔ
× 10
−1
and 0.44 ± 0.02
ΔΔ
× 10
−1
, respectively (
P
< 0.01).
Microcystin-LR (MC-LR) is a well-known hepatotoxin; however, increasing evidence suggests that it might induce kidney injury. Grass carp (
Ctenopharyngodon idella
) is one of the most important ...farmed species and may be affected by MC-LR releasing into waterbody during cyanobacterial bloom. Here, this present study aimed to explore the nephrotoxicity of grass carp by MC-LR. The grass carp received a single intraperitoneal injection of different doses of MC-LR (0, 25, 75, and 100 μg/kg body weight (BW)), and the kidneys were isolated at 24 and 96 h post-injection (hpi). Histopathological examination revealed kidney lesions, with severe hemorrhage, necrosis of the interstitium, and dilation of Bowman’s capsule in the 75 and 100 μg MC-LR/kg BW groups. Under transmission electron microscopy, a larger number of swelling and vacuolated degeneration of mitochondria were observed; moreover, apoptotic features, such as condensed chromatin and shrinkage of cells, were observed in the 75 and 100 μg MC-LR/kg BW groups at 96 hpi. MC-LR significantly upregulated the number of apoptotic cells in the 75 and 100 μg/kg BW groups at 96 hpi as indicated by terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) assay (
P
< 0. 05). The results of quantitative assays showed that the mRNA expression of Bax, caspase-9, and caspase-3 in grass carp kidney were significantly increased at 96 hpi in the 75 and 100 μg MC-LR/kg BW groups compared with that in the control group, but Bcl-2 mRNA expression was significantly decreased in all the treatment groups at 24 and 96 hpi. Taken together, these results indicated that MC-LR damaged the kidney structure and resulted in renal apoptosis which may occur via the mitochondrial pathway.
To explore the molecular mechanisms of fatty liver hemorrhagic syndrome (FLHS) in laying hens, an experiment was conducted to reveal the differences in histopathological observation and gene ...expression between FLHS group and normal group.
We compared the histopathological difference using hematoxylin and eosin staining and proceeded with RNA sequencing of adipose tissue to search differentially expressed genes and enriched biological processes and pathways. Then we validated the mRNA expression levels by real-time polymerase chain reaction and quantified protein levels in the circulation by enzyme-linked immunosorbent assay.
We identified 100 differentially expressed transcripts corresponding to 66 genes (DEGs) were identified between FLHS-affected group and normal group. Seven DEGs were significantly enriched in the immune response process and lipid metabolic process, including phospholipase A2 group V, WAP kunitz and netrin domain containing 2, delta 4-desaturase sphingolipid 2, perilipin 3, interleukin-6 (IL-6), ciliary neurotrophic factor (CNTF), and suppressor of cytokine signaling 3 (SOCS3). And these genes could be the targets of immune response and be involved in metabolic homeostasis during the process of FLHS in laying hens. Based on functional categories of the DEGs, we further proposed a model to explain the etiology and pathogenesis of FLHS. IL-6 and SOCS3 mediate inflammatory responses and the satiety hormone of leptin, induce dysfunction of Jak-STAT signaling pathway, leading to insulin resistance and lipid metabolic disorders. Conversely, CNTF may reduce tissue destruction during inflammatory attacks and confer protection from inflammation-induced insulin resistance in FLHS chickens.
These findings highlight the therapeutic implications of targeting the JAK-STAT pathway. Inhibition of IL6 and SOCS3 and facilitation of CNTF could serve as a favorable strategy to enhance insulin action and improve glucose homoeostasis, which are of importance for treating obesity-related disorders for chickens.
Epigenetic regulation of gene expression has been reported in the pathogenesis of metabolic disorders such as diabetes and liver steatosis in humans. However, the molecular mechanisms of fatty liver ...hemorrhagic syndrome (FLHS) in chickens have been rarely studied. H3K27ac chromatin immunoprecipitation coupled with high-throughput sequencing and high-throughput RNA sequencing was performed to compare genome-wide H3K27ac profiles and transcriptomes of liver tissue between healthy and FLHS chickens. In total, 1,321 differential H3K27ac regions and 443 differentially expressed genes were identified (| log2Fold change| ≥ 1 and
-value ≤ 0.05) between the two groups. Binding motifs for transcription factors involved in immune processes and metabolic homeostasis were enriched among those differential H3K27ac regions. Differential H3K27ac peaks were associated with multiple known FLHS risk genes, involved in lipid and energy metabolism (
,
,
, and
) and the immune system (
,
, and
). Previous studies and our current results suggested that the high-energy, low-protein (HELP) diet might have an impact on histone modification and chromatin structure, leading to the dysregulation of candidate genes and the peroxisome proliferator-activated receptor (PPAR) signaling pathway, which causes excessive accumulation of fat in the liver tissue and induces the development of FLHS. These findings highlight that epigenetic modifications contribute to the regulation of gene expression and play a central regulatory role in FLHS. The PPAR signaling pathway and other genes implicated in FLHS are of great importance for the development of novel and specific therapies for FLHS-susceptible commercial laying hens.
Background
Enrofloxacin (ENR) is a kind of quinolone antibiotic that is most widely used antimicrobials in veterinary practice, and possesses both a broad spectrum antimicrobial activity against a ...range of bacteria and adverse effects towards plants and animals.
Objectives
This study was conducted to explore the permeability of blood–brain barrier (BBB) to ENR and brain injury based on crucian carp orally administrated with high dose of ENR.
Methods
Juvenile Pengze crucian carp were treated with half lethal dose (LD50) or safe dose (SD50) of ENR. BBB permeability was determined by evaluating ENR contents detected by HPLC and evens blue contents estimated by confocal laser scanning microscope. Brain damage was evaluated by measuring protein and mRNA contents of related molecules with western blotting and qPCR.
Results
Data indicated that ENR destroyed BBB structure of crucian carp and enhanced permeability of the biological barrier, resulting in more ENR crossed BBB and induced brain damage of crucian carp.
Conclusions
This data indicated that ENR can induce brain damage of crucian carp through destroying BBB structure and enhancing permeability.
(1) High dose of ENR damages BBB structure of crucian carp and increases BBB permeability.
(2) ENR induces brain damage of crucian carp that can be indicated by S100B and GFAP protein contents in serum.
Cidea and Cidec are two members of Cell death‐inducing DNA fragmentation factor‐alpha‐like effector family proteins, which could be involved in lipid or fat metabolism. To better understand the roles ...of Cidea and Cidec in fatty liver hemorrhagic syndrome (FLHS), 150 healthy 155‐day‐old Hyline Brown laying hens were randomly divided into control group (fed with basic diet) and experimental group (fed with high‐energy low‐protein HELP diet). Analysis of the liver by tissue sectioning and hematoxylin and eosin staining showed that the HELP diet induced micro‐vesicular steatosis in laying hens. Subsequently, based on the liver color scores and the range of lipid accumulation observed in histological examination, we classified livers with <50% vacuolization as mild FLHS and >50% as severe FLHS. The results showed that the levels of Cidea and Cidec mRNA expression were markedly elevated in the liver and adipose tissues with FLHS and the levels of Cidea and Cidec mRNA expression in the liver with severe FLHS were significantly higher than that in the liver with mild FLHS. Thus, the present study revealed that the Cidea and Cidec genes may be involved in pathways of FLHS formation.
In order to investigate the effect of dietary soybean phospholipid supplement on hepatic and serum indexes relevant to fatty liver hemorrhagic syndrome (FLHS) in layers, 135 300‐day‐old Hyline Brown ...layers were randomly divided into three groups (control, pathology and prevention), and each group had 45 layers with three replicates. Birds in the three groups were respectively fed the control diet, high‐energy low‐protein diet and high‐energy high‐protein diet affixed with 3% soybean phospholipid instead of maize. Results showed in the 30th day, birds’ livers in the pathology group became yellowish, enlarged in size and had hemorrhagic spots, while the prevention and control groups’ layers did not have such pathological changes. Contents of triglyceride, total cholesterol, low‐density lipoprotein – cholesterol, non‐esterified fatty acid and malondialdehyde in serum or liver homogenate in prevention and control groups were remarkably lower than those in the pathology group (P < 0.05 or P < 0.01), as with the activities of glutamic oxalacetic transaminase and glutamic‐pyruvic transaminase (P < 0.01); high‐density lipoprotein – cholesterol value was strikingly higher than that of the pathology group (P < 0.01). It is suggested dietary soybean phospholipids supplement may effectively improve hepatic and blood indexes relevant to FLHS, which provides a new point for preventing FLHS occurrence rate in laying flocks and treating human non‐alcohol fatty liver disease.
Objective: To explore the molecular mechanisms of fatty liver hemorrhagic syndrome (FLHS) in laying hens, an experiment was conducted to reveal the differences in histopathological observation and ...gene expression between FLHS group and normal group. Methods: We compared the histopathological difference using hematoxylin and eosin staining and proceeded with RNA sequencing of adipose tissue to search differentially expressed genes and enriched biological processes and pathways. Then we validated the mRNA expression levels by real-time polymerase chain reaction and quantified protein levels in the circulation by enzyme-linked immunosorbent assay. Results: We identified 100 differentially expressed transcripts corresponding to 66 genes (DEGs) were identified between FLHS-affected group and normal group. Seven DEGs were significantly enriched in the immune response process and lipid metabolic process, including phospholipase A2 group V, WAP kunitz and netrin domain containing 2, delta 4-desaturase sphingolipid 2, perilipin 3, interleukin-6 (IL-6), ciliary neurotrophic factor (CNTF), and suppressor of cytokine signaling 3 (SOCS3). And these genes could be the targets of immune response and be involved in metabolic homeostasis during the process of FLHS in laying hens. Based on functional categories of the DEGs, we further proposed a model to explain the etiology and pathogenesis of FLHS. IL-6 and SOCS3 mediate inflammatory responses and the satiety hormone of leptin, induce dysfunction of Jak-STAT signaling pathway, leading to insulin resistance and lipid metabolic disorders. Conversely, CNTF may reduce tissue destruction during inflammatory attacks and confer protection from inflammation-induced insulin resistance in FLHS chickens. Conclusion: These findings highlight the therapeutic implications of targeting the JAK-STAT pathway. Inhibition of IL6 and SOCS3 and facilitation of CNTF could serve as a favorable strategy to enhance insulin action and improve glucose homoeostasis, which are of importance for treating obesity-related disorders for chickens.
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