Application of preoperative 3D printing in the internal fixation of posterior rib fractures with embracing device: a cohort study.

BACKGROUND: To explore the impact of preoperative 3D printing on the fixation of posterior rib fractures utilizing a memory alloy embracing device of rib under thoracoscopy. METHODS: The enrolled patients were divided into the 3D printing (11 patients) and the non-3D printing (18 patients) groups, based on whether a 3D model of ribs was prepared prior to surgery. Analysis was conducted comparing the average fixation time per fracture, postoperative fixation loss, and poor reduction of fractured end between the two groups. RESULTS: The average fixation time of each fracture was 27.2 ± 7.7 min in the 3D printing group and 29.3 ± 8.2 min in the non-3D printing group, with no statistically significant difference observed between the two groups (P > 0.05). The incidence of poor fracture fixation in the 3D printing group was statistically lower than that in the non-3D printing group (12.9% vs. 44.7%, P < 0.05). Further stratified analysis revealed that the off-plate rate in the 3D printing group and the non-3D group was (3.2% vs. 12.8%, P > 0.05), and the dislocation rate of the fractured end was (9.7% vs. 31.9%, P < 0.05). CONCLUSIONS: The application of 3D printing technology to prepare the rib model before surgery is proves beneficial in reducing the occurrence of poor fixation of fractures and achieving precise and individualized treatment.

Diagnostic value of D-dimer for lower extremity deep venous thrombosis caused by rib fracture: a retrospective study.

OBJECTIVE: This study aimed to investigate the role of D-dimer in the diagnosis of lower extremity deep venous thrombosis (DVT) in patients with rib fractures. METHOD: Retrospective analysis was conducted on the clinical data of 499 patients with rib fractures who were admitted to the Third Hospital of Shijiazhuang between October 2020 and September 2021. These patients were divided into the DVT and the non-DVT groups. D-dimer levels were compared between the two groups at 24, 48, and 72 h after the injury. Receiver operating characteristic curves were utilized to evaluate the diagnostic efficacy of dynamically monitoring changes in D-dimer for DVT. RESULTS: The D-dimer levels in the DVT group were significantly higher than those in the non-DVT group at 24, 48, and 72 h after the injury. The area under the curve values for predicting DVT based on D-dimer level at 24, 48, and 72 h after injury in patients with rib fractures were 0.788, 0.605, and 0.568, respectively. CONCLUSION: Detecting D-dimer levels 24 h after the injury can enhance diagnostic efficacy and sensitivity for DVT, thereby reducing the rate of missed diagnoses, which is of great clinical value.

Environmental Enrichment Protects Offspring of a Rat Model of Preeclampsia from Cognitive Decline.

Preeclampsia affects 5-7% of all pregnancies and contributes to adverse pregnancy and birth outcomes. In addition to the short-term effects of preeclampsia, preeclampsia can exert long-term adverse effects on offspring. Numerous studies have demonstrated that offspring of preeclamptic women exhibit cognitive deficits from childhood to old age. However, effective ways to improve the cognitive abilities of these offspring remain to be investigated. The aim of this study was to explore whether environmental enrichment in early life could restore the cognitive ability of the offspring of a rat model of preeclampsia and to investigate the cellular and molecular mechanisms by which EE improves cognitive ability. L-NAME was used to establish a rat model of preeclampsia. The spatial learning and memory abilities and recognition memory of 56-day-old offspring were evaluated by the Morris water maze and Novel object recognition (NOR) task. Immunofluorescence was performed to evaluate cell proliferation and apoptosis in the DG region of the hippocampus. qRT-PCR was performed to examine the expression levels of neurogenesis-associated genes, pre- and postsynaptic proteins and inflammatory cytokines. An enzyme-linked immune absorbent assay was performed to evaluate the concentration of vascular endothelial growth factor (VEGF) and inflammatory cytokines in the hippocampus. The administration of L-NAME led to increased systolic blood pressure and urine protein levels in pregnant rats. Offspring in the L-NAME group exhibited impaired spatial learning ability and memory as well as NOR memory. Hippocampal neurogenesis and synaptic plasticity were impaired in offspring from the L-NAME group. Furthermore, cell apoptosis in the hippocampus was increased in the L-NAME group. The hippocampus was skewed to a proinflammatory profile, as shown by increased inflammatory cytokine levels. EE improved the cognitive ability of offspring in the L-NAME group and resulted in increased hippocampal neurogenesis and synaptic protein expression levels and decreased apoptosis and inflammatory cytokine levels. Environmental enrichment resolves cognitive impairment in the offspring of a rat model of preeclampsia by improving hippocampal neurogenesis and synaptic plasticity and normalizing the apoptosis level and the inflammatory balance.

Perfluorooctane sulfonate exposure induces preeclampsia-like syndromes by damaging trophoblast mitochondria in pregnant mice.

Preeclampsia, defined as a hypertensive disorder during pregnancy, is a major cause of maternal and fetal mortality. Observational studies have shown that the exposure of per- and polyfluoroalkyl substances, such as perfluorooctane sulfonate (PFOS), is emerging as a significant environmental factor associated with preeclampsia risk. However, epidemiologic evidence is of correlative in nature, and unable to establish a causal relationship. Here, we established an animal model of PFOS-induced preeclampsia to explore the molecular mechanism of PFOS in placental trophoblast. In the mouse model, PFOS exposure by gavage at a dose of 10 mg/kg/d from embryonic day 7.5-16.5 was sufficient to induce preeclampsia-like symptoms such as hypertension, proteinuria, and renal glomerular endotheliosis, accompanied with placental abnormal stromal collagen deposition. In-vitro experiments of JEG-3 cells, PFOS exposure impaired trophoblast motility including the compromised abilities of migration, invasion and vascularization. Mechanistically, these pathological effects on cells resulted from SLC25A5-mediated mitochondrial damages, characterized by excessive ROS generation, decreased ATP production and mitochondrial membrane potential loss, and accompanied by the activation of p38 MAPK and JNK signaling pathways. This pioneering study provided biological plausibility to the causality verified by the animal model and the in vitro experiments, which indicates that PFOS exposure may cause preeclampsia during pregnancy via impairing trophoblast mitochondria.

Plasmonic Bi nanoparticles encapsulated by N-Carbon for dual-imaging and photothermal/photodynamic/chemo-therapy.

In this work, the plasmonic Bi@N-Carbon@PEG-DOX nanocomposites were constructed to integrate the imaging and synergistic therapy in one nanoplatform. Here, Bi nanoparticles were encapsulated into the N-doped carbon nanomaterials via a simple solvothermal method. The accumulated adjacent semimetal Bi nanoparticles in Bi@N­carbon enhanced the local surface plasmon resonance (LSPR) to make the great NIR harvest and high photothermal converting efficiency (52.3%, Bi@C-2). And that also was confirmed by the Finite Difference Time Domain (FDTD) calculation. Moreover, the LSPR would induce the hot charges (polarization charges), which were captured by O2 and H2O molecules to form ROS for photodynamic therapy (PDT). And the heterostructure of Bi and N­carbon further improved the effective segregation of the hot charges, making the 6.9 times ROS production (Bi@C-2) in comparing with pure Bi sample. In view of the ultrahigh X-ray attenuation coefficient of Bi and great photothermal effect, Bi@N-Carbon@PEG possessed the outstanding computerized tomography (CT) and photothermal imaging capacity. Meanwhile, they also exhibited the favourable biodegradation ability, inducing the elimination via urine and feces within 14 day. The integration of the multi-model (CT and Thermal) imaging and the PTT/PDT/chemotherapy makes Bi@N­carbon@PEG-DOX to be a potential candidate for cancer treatment.

The Inhibition of Protein Kinase C ß Contributes to the Pathogenesis of Preeclampsia by Activating Autophagy.

BACKGROUND: Preeclampsia is a devastating hypertensive disorder of pregnancy with unknown mechanism. Recent studies have considered abnormal autophagy as a new cellular mechanism for this disorder, while little is known about how autophagy is specifically involved and what factors are implicated. Here, we report a previously unrecognized preeclampsia-associated autophagic regulator, PKCß, that is involved in placental angiogenesis. METHODS: PKCß levels were evaluated by quantitative real-time PCR, western blotting, immunofluorescence and by the analysis of public data. The autophagy-regulating role of PKCß inhibition in preeclampsia pathogenesis was studied in a mouse model, and in human umbilical vein endothelial cells (HUVECs) and human choriocarcinoma cells (JEG-3). FINDINGS: PKCß was significantly downregulated in human preeclamptic placentas. In a mouse model, the selective inhibition of PKCß by Ruboxistaurin was sufficient to induce preeclampsia-like symptoms, accompanied by excessive autophagic flux and a disruption in the balance of pro- and anti-angiogenic factors in mouse placentas. In contrast, autophagic inhibition by 3-methyladenine partially normalized hypertension, proteinuria and placental angiogenic imbalance in PKCß-inhibited mice. Our in vitro experiments demonstrated that PKCß inhibition activated autophagy, thus blocking VEGFA-induced HUVEC tube formation and resulting in the significant upregulation of sFLT1 and downregulation of VEGFA in JEG-3 cells. INTERPRETATION: These data support a novel model in which autophagic activation due to PKCß inhibition leads to the impairment of angiogenesis and eventually results in preeclampsia. FUNDING: Shanghai Key Program of Clinical Science and Technology Innovation, National Natural Science Foundation of China and Shanghai Medical Center of Key Programs for Female Reproductive Diseases.