Search

Abstract Background Fetal growth restriction (FGR) in utero leads to failure of fetus to reach the genetically normal growth potential. Currently available means of treating FGR are limited. And it remains unknown how pregnant women who give birth to FGR fetus differ in gut microbiota composition from normal pregnant women. Methods In this case-control study, fecal samples were obtained from maternal rectum in the operation room by an obstetrician under strict aseptic conditions. We compared gut microbiota of 14 pregnant women with FGR and 18 normal controls by performing 16S rDNA amplicon sequencing. Results We identified significant differences in β-diversity between the FGR and control groups (P

Objective To explore the potential relationship between different connexins and mitochondrial dynamic imbalance and mitochondrial injury in early acute kidney injury after liver transplantation. Methods 24 healthy specific pathogen-free （SPF） SD male rats were randomly divided into the sham operation group （sham group， n = 6）， and 2-， 4- and 8-h reperfusion liver transplantation groups （M2， M4 and M8 groups， n = 6 each）. In the sham group， open surgery alone was performed for vessel separation. In the M2， M4 and M8 groups， orthotopic liver transplantation was conducted. Renal function and renal pathological examination were determined. The expression levels of connexin 32 （Cx32）， Cx43， dynamin-related protein 1 （Drp1）， mitofusin-1 （Mfn1）， Mfn2， optic atrophy 1 （Opa1） and C/EBP homologous protein （CHOP）， an endoplasmic reticulum stress-related protein， were detected in each group. The morphological changes of mitochondria were observed under electron microscope. Results Compared with the sham group， the pathological score of kidney tissue injury in the M2 group was increased （P < 0.01）， and gradually increased over reperfusion time， and reached the peak in the M8 group （P < 0.001）. However， serum creatinine （SCr） and blood urea nitrogen （BUN） levels were up-regulated only in the M8 group （P < 0.001， P < 0.05）. Compared with the sham group， Cx32 level was increased in the M2 group （P < 0.01）， Cx43 level was increased in the M4 group （P < 0.001）， and reached the peak in the M8 group （both P < 0.001）. Compared with the sham group， the expression levels of Drp1， Mfn1， Mfn2 and OPA1 were up-regulated in the M2 group （all P < 0.001）. Under electron microscope， mitochondrial injury， mitochondrial autophagy， lysosomal autophagy and slightly swollen rough endoplasmic reticulum were observed in the M2 group. The degree of mitochondrial injury was aggravated over reperfusion time during liver transplantation. Mitochondrial autophagy and endoplasmic reticulum - mitochondria contact sites were observed in the M2， M4 and M8 groups. Conclusions Kidney pathological injury and mitochondrial injury occur early after autogenous orthotopic liver transplantation in SD rats. The diagnosis of kidney injury by SCr and BUN levels can be delayed. The expression level of Cx32 in the renal tissues is up-regulated early after liver transplantation. Active mitochondrial division and fusion can be seen， suggesting that the transmission of injury signals by Cx32 is associated with mitochondrial injury and mitochondrial dynamic imbalance， which may be an important mechanism of early acute kidney injury after liver transplantation.

AimThis study aimed to evaluate the association between serum calcium level and the risk of acute kidney injury (AKI) in patients with subarachnoid hemorrhage (SAH).MethodsIn this retrospective cohort study, data on adults from the Medical Information Mart for Intensive Care (MIMIC-III and MIMIC-IV) databases, spanning from 2008 to 2019, were extracted. In the logistic regression models, confounding variables, including age, white blood cell (WBC), systolic blood pressure (SBP), heart rate, blood urea nitrogen (BUN), glucose, international normalized ratio (INR), and the Charlson Comorbidity Index (CCI), were finally adjusted by stepwise regression. The outcome event was the occurrence of AKI after intensive care unit (ICU) admission. The univariate and multivariate logistic regression models were utilized to assess the association between serum calcium level and the risk of AKI in SAH patients, with odds ratios (ORs) and 95% confidence intervals (CIs). To further explore the association, subgroup analyses were performed, stratified by age, Glasgow Coma Scale (GCS) scores, drugs, and surgical methods.ResultsA total of 1,128 patients with SAH were included in the study, of which 457 patients developed AKI. Low levels of serum calcium were significantly associated with a high risk of AKI in patients with SAH, with an OR (95%CI) of 1.38 (1.01–1.89). Further subgroup analyses showed that low levels of calcium were significantly associated with a high risk of AKI in SAH patients aged ≥60 years (OR = 0.27, 95%CI: 0.09–0.83), who had GCS score ≥13 (OR = 1.57, 95%CI: 1.08–2.30), who did not use calcium channel blockers (CCB) (OR = 2.22, 95%CI: 1.16–4.25) and angiotensin-converting enzyme (ACE) inhibitors (OR = 1.51, 95%CI: 1.06–2.14), and who did not undergo aneurysm embolization (OR = 1.48, 95%CI: 1.01–2.17) and aneurysm clipping (OR = 1.45, 95%CI: 1.04–2.01).ConclusionThe results of our study indicated that low levels of serum calcium were significantly associated with the risk of AKI in patients with SAH.