Ceftriaxone-induced severe hemolytic anemia, renal calculi, and cholecystolithiasis in a 3-year-old child: a case report and literature review.

Ceftriaxone is widely used in pediatric outpatient care for its efficacy against respiratory and digestive system infections, yet its increasing association with severe immune hemolytic reactions requires heightened vigilance from pediatricians. This report details a rare and severe case of ceftriaxone-induced severe immune hemolytic anemia (IHA), hemolytic crisis, myocardial injury, liver injury, renal calculi, and cholecystolithiasis in a previously healthy 3-year-old child. The child, treated for bronchitis, experienced sudden pallor, limb stiffness, and altered consciousness following the fifth day of ceftriaxone infusion, with hemoglobin (Hb) levels precipitously dropping to 21 g/L. Immediate cessation of ceftriaxone and the administration of oxygen therapy, blood transfusion, intravenous immunoglobulin (IVIG), and corticosteroids led to a gradual recovery. Despite initial improvements, the patient's condition necessitated extensive hospital care due to complications including myocardial injury, liver injury, renal calculi, and cholecystolithiasis. After a 12-day hospital stay and a 3-month follow-up, the child showed complete normalization of Hb and liver function and resolution of calculi. In children, ceftriaxone infusion may trigger severe, potentially fatal, hemolytic reactions. Pediatricians must promptly recognize symptoms such as pallor, limb stiffness, and unresponsiveness, indicative of ceftriaxone-induced severe IHA, and immediately discontinue the drug. Effective management includes timely blood transfusion, respiratory support, IVIG administration, and corticosteroids when necessary, along with rigorous vital signs monitoring. Continued vigilance is imperative, even after cessation of ceftriaxone, to promptly address any residual adverse effects.

Case report: unprecedented case of infantile cerebral infarction following COVID-19 and favorable outcome.

The 2019 novel coronavirus, SARS-CoV-2, was highly prevalent in China as of December 2022, causing a range of symptoms, predominantly affecting the respiratory tract. While SARS-CoV-2 infection in children is generally mild, severe cases, especially in infants, are rare. We present a case of a previously healthy 7-month-old infant who developed cerebral infarction and coagulation dysfunction three days after COVID-19 onset. Clinically, the infant had weakness in the left limbs and pinpoint bleeding spots. A cranial magnetic resonance imaging showed ischemic strokes in the right basal ganglia and thalamus. Laboratory tests indicated thrombocytopenia and coagulation dysfunction. Inflammatory cytokines like interleukin-10 were elevated, with increased CD3+, CD4+, and CD8+ T lymphocytes but decreased CD3- CD16+ CD56+ natural killer cells. Treatment included mannitol, dexamethasone, oral aspirin, and vitamins B1 and B6 for reducing intracranial pressure, antiinflammation, anticoagulation, and nerve support, respectively. During the recovery phase, rehabilitation therapy focused on strength training, fine motor skills, and massage therapy. The infant gradually improved and successfully recovered. While rare, such cases can lead to severe complications. These combined efforts were instrumental in achieving significant functional recovery in the patient, demonstrating that even in severe instances of pediatric cerebral infarction due to COVID-19, positive outcomes are attainable with early and comprehensive medical response.

Early life stress induces irritable bowel syndrome from childhood to adulthood in mice.

Background: Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorder. Traditionally, early life stress (ELS) is predisposed to IBS in adult. However, whether ELS induces IBS in early life remains unclear. Methods: Separated cohort studies were conducted in neonatal male pups of C57BL/6 mice by maternal separation (MS) model. MS and non-separation mice were scheduled to be evaluated for prime IBS-phenotypes, including visceral hypersensitivity, intestinal motility, intestinal permeability, and anxiety-like behavior. Ileal contents and fecal samples were collected and analyzed by 16S rRNA gene sequencing and bacterial community analyses. Subcellular structures of intestinal epithelial, such as epithelial tight junctions and mitochondria, were observed under transmission electron microscopy. Results: MS induced visceral hypersensitivity and decreased total intestinal transit time from childhood to adulthood. In addition, MS induced intestinal hyperpermeability and anxiety-like behavior from adolescence to adulthood. Besides, MS affected intestinal microbial composition from childhood to adulthood. Moreover, MS disrupted intestinal mitochondrial structure from childhood to adulthood. Conclusion: The study showed for the first time that MS induced IBS from early life to adulthood in mice. The disrupted intestinal mitochondrial structure and the significant dysbiosis of intestinal microbiota in early life may contribute to the initiation and progress of IBS from early life to adulthood.

Case report: Catastrophic event: neonatal gastric perforation and complication of capillary leak syndrome.

Neonatal gastric perforation (NGP) is a rare, but life-threatening condition that can lead to serious conditions, such as capillary leak syndrome (CLS). Here, we present the case of a preterm male infant with NGP complicated by CLS after stomach repair. The patient was born at 33 2/7 weeks, weighed 1,770 g, and was diagnosed with respiratory distress syndrome. On the fourth day of life, the patient presented with distention and an unstable cardiovascular system. Routine blood tests revealed a white blood cell count of 2.4 × 109/L. Chest and abdominal radiography revealed a pneumoperitoneum, suggesting a gastrointestinal perforation. The patient was urgently transferred to a tertiary hospital for exploratory laparotomy, where a 2 cm diameter perforation was discovered in the stomach wall and subsequently repaired. Pathological findings indicated the absence of a muscular layer in the stomach wall. The patient unexpectedly developed CLS postoperatively, leading to multiorgan dysfunction and eventual death. The underlying pathological mechanism of NGP-induced CLS may be related to severe chemical peritonitis, sepsis, endothelial glycocalyx dysfunction, enhanced systemic inflammation, and translocation of the gut microbiota, causing endothelial hyperpermeability. Notablely, abdominal surgery itself can be a significant triggering factor for CLS occurrence. Complications of NGP and CLS are extremely dangerous. Investigating the mechanism by which NGP triggers CLS could potentially improve the prognosis. Conservative treatment for pneumoperitoneum secondary to gastric perforation may be a reasonable option, especially when the condition of the patient is unstable.

Alterations in the Fecal Microbiota Composition in Pediatric Acute Diarrhea: A Cross-Sectional and Comparative Study of Viral and Bacterial Enteritis.

Objective: To examine the association between the fecal microbiota of acute diarrhea in children and provide gut microbiota information related the acute diarrhea with rotavirus. Patients and Methods: Children with acute diarrhea aged 3-60 months were selected for the study. Routine stool examination was performed, and stool samples were collected and stored at -80 °C until further analysis. Fecal microbial DNA was extracted, and DNA concentration and quality were detected. PCR amplification and 16S rDNA high-throughput sequencing analysis using the Illumina MiSeq platform were performed, and intestinal flora was statistically analyzed. Results: Children with acute diarrhea exhibited gut microbial dysbiosis. Lower microbial diversity and richness were observed in the viral enteritis and bacterial enteritis groups than in the control group. Composition of the microbiota in acute diarrhea differed from that in the control group. The Bacteroidetes/Firmicutes dramatically decreased in the viral enteritis and bacterial enteritis groups. However, the relative abundance of Proteobacteria and Fusobacteria increased, especially in the bacterial enteritis group. In addition, the relative abundance of Actinobacteria had dramatically increased in the viral enteritis group. According to the Kyoto Encyclopedia of Genes and Genomes map analysis, the membrane transport dysfunction was caused by rotavirus infection, while the membrane transport dysfunction was more evident in bacterial infection. Conclusion: Acute diarrhea infections cause fecal microbiota dysbiosis in children. Changes in fecal microflora in children suggest that the regulation of intestinal flora in children with acute diarrhea should be strengthened.

Maternal separation leads to dynamic changes of visceral hypersensitivity and fecal metabolomics from childhood to adulthood.

We assessed dynamic changes in visceral hypersensitivity and fecal metabolomics through a mouse model of irritable bowel syndrome (IBS) from childhood to adulthood. A mouse model of IBS was constructed with maternal separation (MS) in early life. Male mice aged 25, 40, and 70 days were used. Visceral sensitivity was assessed by recording the reaction between the abdominal withdrawal reflex and colorectal distension. Metabolomics was identified and quantified by liquid chromatography-tandem mass spectrometry. The visceral sensitivity of the MS group was significantly higher than that of the non-separation (NS) group in the three age groups. The top four fecal differential metabolites in the different age groups were lipids, lipid molecules, organic heterocyclic compounds, organic acids and derivatives, and benzenoids. Five identical differential metabolites were detected in the feces and ileal contents of the MS and NS groups at different ages, namely, benzamide, taurine, acetyl-L-carnitine, indole, and ethylbenzene. Taurine and hypotaurine metabolism were the most relevant pathways at P25, whereas histidine metabolism was the most relevant pathway at P40 and P70. Visceral hypersensitivity in the MS group lasted from childhood to adulthood. The different metabolites and metabolic pathways detected in MS groups of different ages provide a theoretical basis for IBS pathogenesis.

Low FODMAP Diet Relieves Visceral Hypersensitivity and Is Associated with Changes in Colonic Microcirculation in Water Avoidance Mice Model.

(1) Background: Irritable bowel syndrome (IBS) is a global public health problem, the pathogenesis of which has not been fully explored. Limiting fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAP) can relieve symptoms in some patients with IBS. Studies have shown that normal microcirculation perfusion is necessary to maintain the primary function of the gastrointestinal system. Here, we hypothesized that IBS pathogenesis might be related to abnormalities in colonic microcirculation. A low-FODMAP diet could alleviate visceral hypersensitivity (VH) by improving colonic microcirculation; (2) Methods: C57BL/6 mice were raised to establish an IBS-like rodent model using water avoidance (WA) stress or SHAM-WA as a control, one hour per day for ten days. The mice in the WA group were administered different levels of the FODMAP diet: 2.1% regular FODMAP (WA-RF), 10% high FODMAP diet (WA-HF), 5% medium FODMAP diet (WA-MF), and 0% low FODMAP diet (WA-LF) for the following 14 days. The body weight and food consumption of the mice were recorded. Visceral sensitivity was measured as colorectal distention (CRD) using the abdominal withdrawal reflex (AWR) score. Colonic microcirculation was assessed using laser speckle contrast imaging (LCSI). Vascular endothelial-derived growth factor (VEGF) was detected using immunofluorescence staining; (3) Results: The threshold values of CRD pressure in the WA-RF, WA-HF, and WA-MF groups were significantly lower than those in the SHAM-WA group. Moreover, we observed that colonic microcirculation perfusion decreased, and the expression of VEGF protein increased in these three groups of mice. Interestingly, a low-FODMAP dietary intervention could reverse this situation. Specifically, a low-FODMAP diet increased colonic microcirculation perfusion, reduced VEGF protein expression in mice, and increased the threshold of VH. There was a significant positive correlation between colonic microcirculation and threshold for VH; (4) Conclusions: These results demonstrate that a low-FODMAP diet can alter VH by affecting colonic microcirculation. Changes in intestinal microcirculation may be related to VEGF expression.

Profound Hypothermia Concomitant With Severe Coagulation Dysfunction and Leukopenia in a Preterm Infant: A Case Report and Literature Review.

BACKGROUND: Neonatal hypothermia is common around the world; however, profound hypothermia is a very rare-but life-threatening-event. CLINICAL FINDINGS: This was a very rare case involving a 15-day old preterm infant diagnosed with profound hypothermia (rectal temperature, 27°C) concomitant with severe coagulation dysfunction and leukopenia on admission. PRIMARY DIAGNOSIS: Profound hypothermia together with severe coagulopathy, leukopenia, late-onset sepsis, and pneumonia. INTERVENTIONS: The patient was rewarmed slowly, with a rectal temperature rising at a rate of 0.5°C/h < R < 1°C/h. Vital signs were closely monitored. Coagulation factors were supplemented by intravenous infusion of fresh frozen plasma. Supportive treatment with intravenous infusion of immunoglobulin was provided, and antibiotics were used empirically. Nil per os and intravenous rehydration were also implemented. OUTCOMES: The condition of the preterm infant gradually improved and was successfully discharged. PRACTICE RECOMMENDATIONS: Profound hypothermia is very rare in preterm infants. However, once it occurs, it may be concomitant with severe coagulopathy and leukopenia. Successful management involves slow rewarming, prompt supplementation of coagulation factors, empirical antibiotics, and supportive treatment.

Potential Roles of Enterochromaffin Cells in Early Life Stress-Induced Irritable Bowel Syndrome.

Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders, also known as disorders of the gut-brain interaction; however, the pathophysiology of IBS remains unclear. Early life stress (ELS) is one of the most common risk factors for IBS development. However, the molecular mechanisms by which ELS induces IBS remain unclear. Enterochromaffin cells (ECs), as a prime source of peripheral serotonin (5-HT), play a pivotal role in intestinal motility, secretion, proinflammatory and anti-inflammatory effects, and visceral sensation. ECs can sense various stimuli and microbiota metabolites such as short-chain fatty acids (SCFAs) and secondary bile acids. ECs can sense the luminal environment and transmit signals to the brain via exogenous vagal and spinal nerve afferents. Increasing evidence suggests that an ECs-5-HT signaling imbalance plays a crucial role in the pathogenesis of ELS-induced IBS. A recent study using a maternal separation (MS) animal model mimicking ELS showed that MS induced expansion of intestinal stem cells and their differentiation toward secretory lineages, including ECs, leading to ECs hyperplasia, increased 5-HT production, and visceral hyperalgesia. This suggests that ELS-induced IBS may be associated with increased ECs-5-HT signaling. Furthermore, ECs are closely related to corticotropin-releasing hormone, mast cells, neuron growth factor, bile acids, and SCFAs, all of which contribute to the pathogenesis of IBS. Collectively, ECs may play a role in the pathogenesis of ELS-induced IBS. Therefore, this review summarizes the physiological function of ECs and focuses on their potential role in the pathogenesis of IBS based on clinical and pre-clinical evidence.

Severe neonatal anemia affected by massive fetomaternal hemorrhage: a single-center retrospective observational study.

OBJECTIVES: Massive fetomaternal hemorrhage (FMH) is a rare but sometimes life-threatening event, and surviving neonates may suffer major neurological complications. Severe neonatal anemia (SNA) affected by massive FMH is less reported in the literature. This study aims to explore the clinical characteristics, laboratory diagnoses, treatments and outcomes of SNA affected by massive FMH. METHODS: Data were collected retrospectively from the hospital's electronic medical record system. All neonates born in the hospital and admitted to the neonatal unit diagnosed as SNA affected by massive FMH from 1 January 2013 to 31 June 2017 were included. RESULTS: A total of 8 cases of SNA affected by FMH were identified among 6825 neonates admitted to the neonatal unit. They all presented with pallor but without hydrops at birth. Median gestational age and birthweight were 375/7 (360/7‒401/7) weeks and 2,625 (2300‒3050) g, respectively. Median hemoglobin level was 39.5 (25‒53) g/L at birth and 109.5 (94-127) g/L at discharge. Median maternal serum alpha-fetoprotein (AFP) was 3958.5 (1606‒14,330) ng/mL, which was significantly increased. Three out of eight cases manifested as antenatal decreased fetal movement. Only 1 with the lowest initial hemoglobin 25 g/L manifested as characteristic sinusoidal fetal heart rate tracing and suffered severe neonatal asphyxia and hypovolemic shock. Having experienced resuscitation, he was admitted to the neonatal unit and received twice transfusion of cross-matched red blood cells there. Another case with the initial hemoglobin 45 g/L received positive pressure ventilation and once transfusion. All cases were successfully discharged with a median hospital stay of 8 (5-12) days. Follow-up was available for 6 (75%) of 8 neonates (age range 13 months to 50 months), and all infants were observed to be in good condition with normal neurological status. In our series of eight cases, there were no neonatal deaths. CONCLUSION: This study strengthens the idea that maternal AFP testing is valuable to confirm massive fetomaternal hemorrhage. Surviving neonates of massive FMH might have a good outcome despite severe anemia at birth.

The Influence of Cesarean Section on the Composition and Development of Gut Microbiota During the First 3 Months of Life.

The intestinal microbiota has emerged as a critical regulator of growth and development in the early postnatal period of life. Cesarean section (CS) delivery is one of the strongest disrupting factors of the normal colonization process and has been reported as a risk factor for disorders in later life. In this study, we dynamically and longitudinally evaluated the impact of CS on the initial colonization pattern and development of gut microbiota by 16 healthy Chinese infants with fecal samples collected at 9 time points (day 5, day 8, day 11, week 2, week 4, week 6, week 7, month 2, and month 3) during the first 3 months of life. The V3-V4 regions of 16S rRNA gene were analyzed by Illumina sequencing. In comparison with vaginally delivered (VD) infants, infants born by CS showed decreased relative abundance of Bacteroides and Parabacteroides and enrichment of Clostridium_sensu_stricto_1, Enterococcus, Klebsiella, Clostridioides, and Veillonella. Most interestingly, Firmicutes/Bacteroidetes ratio was found to be significantly higher in the CS group than in the VD group from day 5 until month 3. Besides, the results of microbial functions showed that the VD group harbored significantly higher levels of functional genes in vitamin B6 metabolism at day 5, day 8, week 2, week 4, week 6, week 7, month 2, and month 3 and taurine and hypotaurine metabolism at day 5, while the phosphotransferase system and starch and sucrose metabolism involved functional genes were plentiful in the CS group at day 11, week 2, week 4, week 6, week 7, and month 2 and at week 2, week 7, and month 2, respectively. Our results establish a new evidence that CS affected the composition and development of gut microbiota in the first 3 months and provide a novel insight into strategies for CS-related disorders in later life.

Exploratory Investigation of Intestinal Structure and Function after Stroke in Mice.

Stroke is the second leading cause of death worldwide. Patients who have a stroke are susceptible to many gastrointestinal (GI) complications, such as dysphagia, GI bleeding, and fecal incontinence. However, there are few studies focusing on the GI tract after stroke. The current study is to investigate the changes of intestinal structure and function in mice after ischemic stroke. Ischemic stroke was made as a disease model in mice, in which brain and ileal tissues were collected for experiments on the 1st and 7th day after stroke. Intestinal motility of mice was inhibited, and intestinal permeability was increased after stroke. Hematoxylin-eosin (HE) staining showed the accumulation of leucocytes in the intestinal mucosa. Myeloperoxidase (MPO) activity and inflammatory proteins (nuclear factor kappa-B (NF-κB), inducible nitric oxide synthase (iNOS)) in the small intestine were significantly increased in mice after stroke. The expression of tight junction (TJ) proteins (zonula occludens-1 (ZO-1), occludin, and claudin-1) was downregulated, and transmission electron microscopy (TEM) showed broken TJ of the intestinal mucosa after stroke. Glial fibrillary acidic protein (GFAP) and the apoptosis-associated proteins (tumor necrosis factor (TNF-α), caspase-3, and cleaved caspase-3) were notably upregulated as well. Ischemic stroke led to negative changes on intestinal structure and function. Inflammatory mediators and TNF-α-induced death receptor signaling pathways may be involved and disrupt the small intestinal barrier function. These results suggest that stroke patients should pay attention to GI protection.

Maternal Separation Induced Visceral Hypersensitivity Evaluated via Novel and Small Size Distention Balloon in Post-weaning Mice.

Early life stress (ELS) disposes to functional gastrointestinal diseases in adult, such as irritable bowel syndrome (IBS). Maternal separation (MS) is a well-known animal model of IBS and has been shown to induce visceral hypersensitivity in adult rats and mice. However, to the best of our knowledge, it has not been reported whether MS induces visceral hypersensitivity in young mice, such as the post-weaning mice. Moreover, the method for evaluation of visceral sensitivity also has not been described. Accordingly, the present study aims to evaluate the visceral sensitivity caused by MS in post-weaning mice and develop a novel and small size distention balloon for assessment of visceral sensitivity of such mice. Male pups of C57BL/6 mice were randomly divided into two groups, MS (n = 12) and non-separation (NS) (n = 10). MS pups were separated from the dams through postnatal days (PND) 2 to 14, while NS pups were undisturbed. After, all pups stayed with respective dams and were weaned at PND 22. Visceral sensitivity was evaluated by colorectal distention (CRD) with a novel and small size distention balloon at PND 25. The threshold of abdominal withdrawal reflex (AWR) scores were significantly lower in MS than NS. In addition, AWR scores at different pressures of CRD were significantly higher in MS than NS. The results demonstrate that MS induced visceral hypersensitivity in post-weaning mice. The designed small size distention balloon for evaluation of visceral sensitivity is of significance to further study the pathophysiology of IBS from early life to adulthood.

Perinatal Risk Factors Influencing Neonatal Hypoxic Ischemic Encephalopathy in Southern China: A Case-Control Study.

OBJECTIVE: In this study, our objective was to explore the relevant influencing factors of neonatal hypoxic-ischemic encephalopathy (HIE) in Southern China and provide scientific basis for improving the quality of life for neonates. STUDY DESIGN: A retrospective analysis of 306 cases with HIE neonates who were admitted during April 2015 to October 2017 was conducted. A total of 306 non-HIE patients admitted to the same hospital during the same period were also included as controls. The basic clinical characteristics were analyzed, and the risk factors for HIE were assessed by logistic regression analysis. RESULTS: Univariate analysis showed that the differences in medicals during pregnancy, placenta previa, fetal distress during labor, cesarean section, amniotic fluid contamination, abnormal labor stage, and Apgar showed significantly different in the case group and the control group (p < 0.05). The multivariate logistic regression analysis revealed that the placenta previa, medicals during pregnancy, fetal distress, abnormal labor stage, Apgar's score, amniotic fluid contamination, and cesarean section were independent risk factors for HIE. CONCLUSION: The placenta previa, medicals during pregnancy, fetal distress, and abnormal labor stage can increase the risk of HIE. Early detection, early diagnosis, and treatment might make great achievement in improving the life quality of HIE neonates.

The relationship between umbilical cord blood vitamin A levels and late preterm infant morbidities: a prospective cohort study.

The aim of this study is to explore the association between umbilical cord blood (UCB) vitamin A levels and late preterm infants morbidities. We conducted a prospective cohort study of 208 late-preterm infants(from 34 0/7 to 36 6/7 weeks gestational age) between January 1, 2014 and June 30, 2015. UCB specimens were collected shortly after birth, and vitamin A levels were determined by enzyme-linked immunosorbent assay. Prevalence of low UCB vitamin A level < 0.7 µmol/L was 37.5% in late preterm infants. In comparison to vaginal delivery, cesarean section was associated with UCB vitamin A level < 0.7 µmol/L (P < 0.001). Nevertheless, UCB vitamin A levels did not correlate with gestational age, birth weight, and gender. UCB vitamin A level < 0.7 µmol/L was not an independent risk factor for hospitalization, oxygen supplementation, hyperbilirubinemia, sepsis, and respiratory distress syndrome.Conclusions: Low umbilical cord blood vitamin A levels are common among late-preterm infants. Cesarean section delivery is associated with low umbilical cord blood vitamin A level. Low umbilical cord blood vitamin A levels at birth do not increase morbidity of late-preterm infants, including hyperbilirubinemia, sepsis, and respiratory distress syndrome. What is Known: • Late preterm infants have a higher morbidity and mortality rates when compared to term infants. • Low plasma vitamin A levels increase the risk of preterm infants' morbidity. What is New: • Late preterm infants commonly have low level of umbilical cord blood vitamin A. • Low umbilical cord blood vitamin A level at birth appears to be not associated with the morbidity of late-preterm infants. • Cesarean section is associated with low umbilical cord blood vitamin A level < 0.7 µmol/L compared with vaginal delivery.

Long non-coding RNA RHPN1-AS1 promotes tumorigenesis and metastasis of ovarian cancer by acting as a ceRNA against miR-596 and upregulating LETM1.

BACKGROUND: In recent decades, long non-coding RNAs (lncRNAs) have been reported as crucial functional regulators involved in ovarian cancer. In the present study, we explored how lncRNA RHPN1-AS1 influences the progression of epithelial ovarian cancer (EOC) through tumor cell-dependent mechanisms. RESULTS: The expression of RHPN1-AS1 in EOC tissues was higher than that in para-cancerous control tissues. High expression of RHPN1-AS1 was closely associated with poor prognosis in EOC patients. N6-methyladenosine (m6A) improved the stability of RHPN1-AS1 methylation transcript by reducing RNA degradation, which resulted in upregulation of RHPN1-AS1 in EOC. In vitro and in vivo functional experiments showed that RHPN1-AS1 promoted EOC cell proliferation and metastasis. RHPN1-AS1 acted as a ceRNA to sponge miR-596, consequently increasing LETM1 expression and activating the FAK/PI3K/Akt signaling pathway. CONCLUSION: RHPN1-AS1-miR-596-LETM1 axis plays a crucial role in EOC progression. Our findings may provide promising drug targets for EOC treatment. METHODS: We determined the aberrantly expressed lncRNAs in EOC via microarray analysis and validated RHPN1-AS1 expression by qRT-PCR. The RHPN1-AS1-miR-596-LETM1 axis was examined by dual-luciferase reporter assay and RIP assay. The mechanism of RHPN1-AS1 was investigated through gain- and loss-of-function studies both in vivo and in vitro.

[Vitamin A level and diseases of premature infants].

Vitamin A is a fat-soluble vitamin, and it is not only necessary for the normal growth and development of epithelial cells, but also plays a very important role in the normal growth and development of the retina, lungs, gastrointestinal tract, brain, and immune system. Studies have confirmed that the low level of vitamin A in premature infants at birth can last through the entire infancy. Recently, there have been particular concerns about the level of vitamin A and development of diseases in premature infants, with major focuses on the related mechanisms of action of vitamin A in respiratory distress syndrome, chronic lung disease, retinopathy of prematurity, necrotizing enterocolitis, patent ductus arteriosus, and infections in premature infants, which still awaits further investigation.This paper summarizes and analyzes the current status of research on vitamin A level and diseases of premature infants at home and abroad. In addition, although enough evidence suggests that vitamin A supplementation is beneficial to preterm infants, evidence is still lacking for recommended methods for supplementation and dose of vitamin A, and further studies are needed.