ABSTRACT
To explore the diagnostic specificity and clinical application of neonatal umbilical cord blood gas analysis in the prognosis of fetal distress, and to provide theoretical basis for neonatal rescue. Clinical data of a total of 240 singleton pregnant women and their neonates who delivered in the Obstetrics Department of our hospital from January 2021 to December 2021 were retrospectively analyzed. The pregnant women and their newborns were divided into an acute group (acute fetal distress), a chronic group (chronic fetal distress) and a control group (no fetus distress), with 80 cases in each. The umbilical artery blood gas analysis values including power of hydrogen (PH), partial pressure of carbon dioxide (PCO2), partial pressure of oxygen (PO2), bicarbonate radical (HCO3 -), buffer excess (BE) and the Apgar score, as well as the neonatal asphyxia outcome after birth were recorded. There were statistically significant differences in fetal condition, PH and BE between newborns with asphyxia and normal newborns (P<0.05). The incidence of neonatal distress was 1.25% in the control group and 19.38% in the fetal distress group (including acute and chronic groups). Logistic regression analysis found that fetal distress was a risk factor for neonatal asphyxia (Odds Ratio (OR)=11.064, P=0.012). The specificity and sensitivity of neonatal cord blood gas analysis in diagnosing neonatal asphyxia were 95.69% and 80.65%, respectively. The specificity of Apgar score in the diagnosis of neonatal asphyxia was 94.74%, and the sensitivity was 70.97%. The rate of neonatal asphyxia in the chronic fetal distress group (26.25%) was higher than that in the acute fetal distress group (12.5%). The proportion of neonatal severe asphyxia in the chronic fetal distress group (66.67%) was higher than that in the acute group (20%). The PH and BE levels in the chronic fetal distress group were lower than those in the control group and acute fetal distress group (P<0.05). Cord blood gas analysis can help to improve the accuracy of fetal distress diagnosis. Cord blood gas is closely related to neonatal prognosis. Compared with acute fetal distress, chronic fetal distress is more likely to lead to neonatal acidosis and asphyxia.
ABSTRACT
OBJECTIVES: The objective of this study was to develop and validate a model, based on the blood biochemical (BBC) indexes, to predict the recurrence of acute pancreatitis patients. METHODS: We retrospectively enrolled 923 acute pancreatitis patients (586 in the primary cohort and 337 in the validation cohort) from January 2014 to December 2016. Aiming for an extreme imbalance between recurrent acute pancreatitis (RAP) and non-RAP patients (about 1:4), we designed BBC index selection using least absolute shrinkage and selection operator regression, along with an ensemble-learning strategy to obtain a BBC signature. Multivariable logistic regression was used to build the RAP predictive model. RESULTS: The BBC signature, consisting of 35 selected BBC indexes, was significantly higher in patients with RAP (P < 0.001). The area under the curve of the receiver operating characteristic curve of BBC signature model was 0.6534 in the primary cohort and 0.7173 in the validation cohort. The RAP predictive nomogram incorporating the BBC signature, age, hypertension, and diabetes showed better discrimination, with an area under the curve of 0.6538 in the primary cohort and 0.7212 in the validation cohort. CONCLUSIONS: Our study developed a RAP predictive nomogram with good performance, which could be conveniently and efficiently used to optimize individualized prediction of RAP.
Subject(s)
Nomograms , Pancreas/pathology , Pancreatitis/diagnosis , Precision Medicine/methods , Acute Disease , Adult , Aged , Female , Humans , Logistic Models , Male , Middle Aged , Multivariate Analysis , Prognosis , Recurrence , Reproducibility of Results , Sensitivity and SpecificityABSTRACT
AIM: Early diagnosis and treatment are crucial for the survival of severe Coronavirus Disease 2019 (COVID-19) patients, but data with regard to risk factors for disease progression from milder COVID-19 to severe COVID-19 remain scarce. METHODS: We conducted a retrospective analysis on 116 patients. RESULTS: Three factors were observed to be independently associated with progression to severe COVID-19 during 14 days after admission: (a) age 65 years or older (hazard ratio [HR] = 8.456; 95% CI: 2.706-26.426); (b) creatine kinase (CK) ≥ 180 U/L (HR = 3.667; 95% CI: 1.253-10.733); and (c) CD4+ T-cell counts <300 cells/µL (HR = 4.695; 95% CI: 1.483-14.856). The difference in rates of severe COVID-19 development was found to be statistically significant between patients aged 65 years or older (46.2%) and those younger than 65 years (90.2%), between patients with CK ≥ 180 U/L (55.6%) and those with CK < 180 U/L (91.5%), and between patients with CD4+ T-cell counts <300 cells/µL (53.8%) and those with CD4+ cell counts ≥300 cells/µL (83.2%). CONCLUSIONS: Age ≥ 65 years, CK ≥ 180 U/L, and CD4+ T-cell counts <300 cells/µL at admission were risk factors independently associated with disease progression to severe COVID-19 during 14 days after admission and are therefore potential markers for disease progression in patients with milder COVID-19.
ABSTRACT
BACKGROUND: Cerebral air embolism (CAE) is a rare but potentially devastating complication of endoscopic procedures. Only 3 cases, to our knowledge, have been reported. CASE PRESENTATION: A 50-year-old female patient presented with hepatitis C virus-related hepatic cirrhosis, emergency endoscopy and endoscopic variceal ligation was performed in an awakened state. CAE occurred during procedure, the patient passed away the next day in the intensive care unit. CONCLUSIONS: CAE is a rare but potentially devastating complication in endoscopic procedures. We need more preventive tools and treatments.
Subject(s)
Embolism, Air/etiology , Endoscopy/adverse effects , Esophageal and Gastric Varices/surgery , Intracranial Embolism/etiology , Ligation/adverse effects , Endoscopy/methods , Fatal Outcome , Female , Humans , Ligation/methods , Middle AgedABSTRACT
The synthetic dipeptides alanyl-glutamine (Ala-Gln) and glycyl-glutamine (Gly-Gln) are used as Gln substitution to provide energy source in the gastrointestinal tract due to their high solubility and stability. This study aimed to investigate the effects of Gln, Ala-Gln and Gly-Gln on mitochondrial respiration and protein turnover of enterocytes. Intestinal porcine epithelial cells (IPEC-J2) were cultured for 2 days in Dulbecco's modified Eagle's-F12 Ham medium (DMEM-F12) containing 2.5 mM Gln, Ala-Gln or Gly-Gln. Results from 5-ethynyl-2'-deoxyuridine incorporation and flow cytometry analysis indicated that there were no differences in proliferation between free Gln and Ala-Gln-treated cells, whereas Gly-Gln treatment inhibited the cell growth compared with Gln treatment. Significantly lower mRNA expressions of Sp1 and PepT1 were also observed in Gly-Gln-treated cells than that of Ala-Gln treatment. Ala-Gln treatment increased the basal respiration and ATP production, compared with free Gln and Gly-Gln treatments. There were no differences in protein turnover between free Gln and Ala-Gln-treated cells, but Gly-Gln treatment reduced protein synthesis and increased protein degradation. Ala-Gln treatment stimulated mTOR activation whereas Gly-Gln decreased mTOR phosphorylation and increased the UB protein expression compared with free Gln treatment. These results indicate that Ala-Gln has the very similar functional profile to free Gln in porcine enterocytes in vitro and can be substituted Gln as energy and protein sources in the gastrointestinal tract.
Subject(s)
Dipeptides/pharmacology , Enterocytes/drug effects , Animals , Cell Line , Cell Proliferation/drug effects , Cell Survival/drug effects , Enterocytes/cytology , Enterocytes/metabolism , Glutamine/analogs & derivatives , Glutamine/pharmacology , In Vitro Techniques , SwineABSTRACT
The present study aimed to examine the association between hypoxia-inducible factor (HIF)-1α and the Wnt/ß-catenin signaling pathway in a hypoxic environment. The study also aimed to explore the possible mechanisms underlying the invasion of hypoxic gastric cancer cells in vitro and in vivo. The pcDNA™ 6.2GW/EmGFPmiRßcatenin plasmid was transfected into SGC7901 gastric cancer cells, resulting in cells with stable suppression of ßcatenin expression. The biological characteristics of the control, liposome, negative control, ßcatenin knockdown, hypoxia and hypoxia ßcatenin knockdown groups were tested using an invasion assay. The differences in the invasive capacity of the control, negative control and liposome groups were not statistically significant. However, the hypoxia group demonstrated a significantly enhanced invasive capacity, as compared with that in the control group (P<0.05). In the hypoxia ßcatenin knockdown group, reduced cell penetration and diminished invasive behavior was observed (P<0.05). In the hypoxia and double (chemical + physical) hypoxia groups, HIF1α, ßcatenin, urokinasetype plasminogen activator (uPA) and matrix metalloproteinase (MMP7) protein and mRNA expression levels were elevated. In response to knockdown of ßcatenin expression, HIF1α, ßcatenin, uPA and MMP7 protein as well as mRNA expression levels were significantly reduced in the hypoxia ßcatenin knockdown and the double hypoxia ßcatenin knockdown groups. In an in vivo experiment, the growth rate of xenograft tumors of hypoxic and control cells was high alongside increased HIF1α, ßcatenin, uPA and MMP7 levels according to western blot and immunohistochemical analyses, while growth and protein levels of tumors from hypoxic ßcatenin knockdown cells were significantly lower and those of ßcatenin knockdown cells were lowest. In conclusion, these results suggested that HIF1α activation was able to regulate the Wnt/ßcatenin pathway, and that HIF1α may be controlled by the Wnt/ßcatenin pathway. A potential mechanism underlying SGC7901 tumorigenicity is the activation of the Wnt/ßcatenin signaling pathway, which activates uPA and MMP7 expression and contributes to the enhanced invasion of hypoxic cancer cells.