Dorsal raphe nucleus to basolateral amygdala 5-HTergic neural circuit modulates restoration of consciousness during sevoflurane anesthesia.

The advent of general anesthesia (GA) has significant implications for clinical practice. However, the exact mechanisms underlying GA-induced transitions in consciousness remain elusive. Given some similarities between GA and sleep, the sleep-arousal neural nuclei and circuits involved in sleep-arousal, including the 5-HTergic system, could be implicated in GA. Herein, we utilized pharmacology, optogenetics, chemogenetics, fiber photometry, and retrograde tracing to demonstrate that both endogenous and exogenous activation of the 5-HTergic neural circuit between the dorsal raphe nucleus (DR) and basolateral amygdala (BLA) promotes arousal and facilitates recovery of consciousness from sevoflurane anesthesia. Notably, the 5-HT1A receptor within this pathway holds a pivotal role. Our findings will be conducive to substantially expanding our comprehension of the neural circuit mechanisms underlying sevoflurane anesthesia and provide a potential target for modulating consciousness, ultimately leading to a reduction in anesthetic dose requirements and side effects.

Rapid detection of pathogenic fungi from coastal population with respiratory infections using microfluidic chip technology.

BACKGROUND: Currently, culture methods are commonly used in clinical tests to detect pathogenic fungi including Candida spp. Nonetheless, these methods are cumbersome and time-consuming, thereby leading to considerable difficulties in diagnosis of pathogenic fungal infections, especially in situations that respiratory samples such as alveolar lavage fluid and pleural fluid contain extremely small amounts of microorganisms. The aim of this study was to elucidate the utility and practicality of microfluidic chip technology in quick detection of respiratory pathogenic fungi. METHODS: DNAs of clinical samples (mainly derived from sputa, alveolar lavage fluid, and pleural fluid) from 64 coastal patients were quickly detected using microfluidic chip technology with 20 species of fungal spectrum and then validated by Real-time qPCR, and their clinical baseline data were analyzed. RESULTS: Microfluidic chip results showed that 36 cases infected with Candida spp. and 27 cases tested negative for fungi, which was consistent with Real-time qPCR validation. In contrast, only 16 cases of fungal infections were detected by the culture method; however, one of the culture-positive samples tested negative by microfluidic chip and qPCR validation. Moreover, we found that the patients with Candida infections had significantly higher rates of platelet count reduction than fungi-negative controls. When compared with the patients infected with C. albicans alone, the proportion of males in the patients co-infected with multiple Candidas significantly increased, while their platelet counts significantly decreased. CONCLUSIONS: These findings suggest that constant temperature amplification-based microfluidic chip technology combined with routine blood tests can increase the detection speed and accuracy (including sensitivity and specificity) of identifying respiratory pathogenic fungi.

The States of Different 5-HT Receptors Located in the Dorsal Raphe Nucleus Are Crucial for Regulating the Awakening During General Anesthesia.

General anesthesia is widely used in various clinical practices due to its ability to cause loss of consciousness. However, the exact mechanism of anesthesia-induced unconsciousness remains unclear. It is generally thought that arousal-related brain nuclei are involved. 5-Hydroxytryptamine (5-HT) is closely associated with sleep arousal. Here, we explore the role of the 5-HT system in anesthetic awakening through pharmacological interventions and optogenetic techniques. Our data showed that exogenous administration of 5-hydroxytryptophan (5-HTP) and optogenetic activation of 5-HT neurons in the dorsal raphe nucleus (DR) could significantly shorten the emergence time of sevoflurane anesthesia in mice, suggesting that regulation of the 5-HT system using both endogenous and exogenous approaches could mediate delayed emergence. In addition, we first discovered that the different 5-HT receptors located in the DR, known as 5-HT autoreceptors, are essential for the regulation of general anesthetic awakening, with 5-HT1A and 5-HT2A/C receptors playing a regulatory role. These results can provide a reliable theoretical basis as well as potential targets for clinical intervention to prevent delayed emergence and some postoperative risks.

Protocol for modulating the noradrenergic pathway from locus coeruleus to heart to prevent sudden unexpected death in epilepsy in mouse models.

The locus coeruleus (LC) and noradrenergic neurotransmission are involved in the regulation of sudden unexpected death in epilepsy (SUDEP). Here, we present a protocol for modulating the noradrenergic pathway from LC to heart to prevent SUDEP in acoustic and pentylenetetrazole-induced DBA/1 mouse models of SUDEP. We describe steps for constructing SUDEP models, calcium signal recording, and electrocardiogram monitoring. We then detail measurement of tyrosine hydroxylase content and activity, ß1 and p-ß1-AR content, and destruction of LCNE neurons. For complete details on the use and execution of this protocol, please refer to Lian et al.1.

Optimization of production system of shale oil development in Ordos basin, China.

In this paper, production system (PS) of shale oil is optimized according to production data and indoor experiments, including core and fluid tests. Results showed that: ① Pressure drop rate at wellhead is a reasonable reference for the determination of post-fracture shut-in duration (PFSID). When pressure at a wellhead of horizontal well is relatively stable and the pressure drop less than 0.1 MPa per day for three consecutive days, PFSID ends; ② Flowback intensity of fracturing fluid affects the effectiveness of proppant underground, thus flowback intensity can be determined by the critical flow rate and safety factor of each proppant; ③ Flowback intensity should be varied during different development stages, which could be divided into four according to production gas and oil ratio(GOR) of a shale oil horizontal well: low, medium-high, high and high-low production GOR. During the stage of low production GOR, ratio of flow pressure and saturation pressure should be maintained greater than 1.0, and the initial daily liquid productivity for a hundred-meter oil-bearing lateral length in a horizontal well is 2.4 ~ 2.9 m3/d; and during the medium-high production GOR, high production GOR and high-low production GOR stages, the responding initial daily liquid productivity should be maintained between 0.8 ~ 1.0 or less than 0.8 respectively.

Independent and combined associations of urinary arsenic exposure and serum sex steroid hormones among 6-19-year old children and adolescents in NHANES 2013-2016.

Arsenic exposure may disrupt sex steroid hormones, causing endocrine disruption. However, human evidence is limited and inconsistent, especially for children and adolescents. To evaluate the independent and combined associations between arsenic exposure and serum sex steroid hormones in children and adolescents, we conducted a cross-sectional analysis of data from 1063 participants aged 6 to 19 years from the 2013-2016 National Health and Nutrition Examination Survey (NHANES). Three urine arsenic metabolites were examined, as well as three serum sex steroid hormones, estradiol (E2), total testosterone (TT), and sex hormone-binding globulin (SHBG). The ratio of TT to E2 (TT/E2) and the free androgen index (FAI) generated by TT/SHBG were also assessed. Linear regression, weighted quantile sum (WQS) regression, and Bayesian kernel machine regression (BKMR) were used to evaluate the associations of individual or arsenic metabolite combinations with sex steroid hormones by gender and age stratification. Positive associations were found between total arsenic and arsenic metabolites with TT, E2, and FAI. In contrast, negative associations were found between arsenic metabolites and SHBG. Furthermore, there was an interaction after gender-age stratification between DMA and SHBG in female adolescents. Notably, based on the WQS and BKMR model results, the combined association of arsenic and its metabolites was positively associated with TT, E2, and FAI and negatively associated with SHBG. Moreover, DMA and MMA dominated the highest weights among the arsenic metabolites. Overall, our results indicate that exposure to arsenic, either alone or in mixtures, may alter sex steroid hormone levels in children and adolescents.

TREM-1 induces pyroptosis in cardiomyocytes by activating NLRP3 inflammasome through the SMC4/NEMO pathway.

Sepsis often causes cell death via pyroptosis and hence results in septic cardiomyopathy. Triggering receptors expressed in myeloid cells-1 (TREM-1) may initiate cellular cascade pathways and, in turn, induce cell death and vital organ dysfunction in sepsis, but the evidence is limited. We set to investigate the role of TREM-1 on nucleotide-binding oligomerization domain-like receptors with pyrin domain-3 (NLRP3) inflammasome activation and cardiomyocyte pyroptosis in sepsis models using cardiac cell line (HL-1) and mice. In this study, TREM-1 was found to be significantly increased in HL-1 cells challenged with lipopolysaccharide (LPS). Pyroptosis was also significantly increased in the HL-1 cells challenged with lipopolysaccharide and an NLRP3 inflammasome activator, nigericin. The close interaction between TREM-1 and structural maintenance of chromosome 4 (SMC4) was also identified. Furthermore, inhibition of TREM-1 or SMC4 prevented the upregulation of NLRP3 and decreased Gasdermin-D, IL-1ß and caspase-1 cleavage. In mice subjected to caecal ligation and puncture, the TREM-1 inhibitor LR12 decreased the expression of NLRP3 and attenuated cardiomyocyte pyroptosis, leading to improved cardiac function and prolonged survival of septic mice. Our work demonstrates that, under septic conditions, TREM-1 plays a critical role in cardiomyocyte pyroptosis. Targeting TREM-1 and its associated molecules may therefore lead to novel therapeutic treatments for septic cardiomyopathy.

Impaired V-ATPase leads to increased lysosomal pH, results in disrupted lysosomal degradation and autophagic flux blockage, contributes to fluoride-induced developmental neurotoxicity.

Fluoride is capable of inducing developmental neurotoxicity, yet its mechanisms remain elusive. We aimed to explore the possible role and mechanism of autophagic flux blockage caused by abnormal lysosomal pH in fluoride-induced developmental neurotoxicity, focusing on the role of V-ATPase in regulating the neuronal lysosomal pH. Using Sprague-Dawley rats exposed to sodium fluoride (NaF) from gestation through delivery until the neonatal offspring reached six months of age as an in vivo model. The results showed that NaF impaired the cognitive abilities of the offspring rats. In addition, NaF reduced V-ATPase expression, diminished lysosomal degradation capacity and blocked autophagic flux, and increased apoptosis in the hippocampus of offspring. Consistently, these results were validated in SH-SY5Y cells incubated with NaF. Moreover, NaF increased the SH-SY5Y lysosomal pH. Mechanistically, V-ATPase B2 overexpression and ATP effectively restored V-ATPase expression, reducing NaF-induced lysosomal alkalinization while increasing lysosomal degradation capacity. Notably, those above pharmacological and molecular interventions diminished NaF-induced apoptosis by restoring autophagic flux. Collectively, the present findings suggested that NaF impairs the lysosomal pH raised by V-ATPase. This leads to reduced lysosomal degradation capacity and triggers autophagic flux blockage and apoptosis, thus contributing to neuronal death. Therefore, V-ATPase might be a promising indicator of developmental fluoride neurotoxicity.

Development and validation of MRI-based radiomics signatures models for prediction of disease-free survival and overall survival in patients with esophageal squamous cell carcinoma.

OBJECTIVES: To develop and validate an optimal model based on the 1-mm-isotropic-3D contrast-enhanced StarVIBE MRI sequence combined with clinical risk factors for predicting survival in patients with esophageal squamous cell carcinoma (ESCC). METHODS: Patients with ESCC at our institution from 2015 to 2017 participated in this retrospective study based on prospectively acquired data, and were randomly assigned to training and validation groups at a ratio of 7:3. Random survival forest (RSF) and variable hunting methods were used to screen for radiomics features and LASSO-Cox regression analysis was used to build three models, including clinical only, radiomics only and combined clinical and radiomics models, which were evaluated by concordance index (CI) and calibration curve. Nomograms and decision curve analysis (DCA) were used to display intuitive prediction information. RESULTS: Seven radiomics features were selected from 434 patients, combined with clinical features that were statistically significant to construct the predictive models of disease-free survival (DFS) and overall survival (OS). The combined model showed the highest performance in both training and validation groups for predicting DFS ([CI], 0.714, 0.729) and OS ([CI], 0.730, 0.712). DCA showed that the net benefit of the combined model and of the clinical model is significantly greater than that of the radiomics model alone at different threshold probabilities. CONCLUSIONS: We demonstrated that a combined predictive model based on MR Rad-S and clinical risk factors had better predictive efficacy than the radiomics models alone for patients with ESCC. KEY POINTS: • Magnetic resonance-based radiomics features combined with clinical risk factors can predict survival in patients with ESCC. • The radiomics nomogram can be used clinically to predict patient recurrence, DFS, and OS. • Magnetic resonance imaging is highly reproducible in visualizing lesions and contouring the whole tumor.

Weakened interaction of ATG14 and the SNARE complex blocks autophagosome-lysosome fusion contributes to fluoride-induced developmental neurotoxicity.

Fluoride is capable of inducing developmental neurotoxicity, but the mechanisms involved remain unclear. We aimed to explore the role of autophagosome-lysosome fusion in developmental fluoride neurotoxicity, particularly focusing on the interaction between ATG14 and the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex. We developed in vivo models of Sprague-Dawley rats exposed to sodium fluoride (NaF) from the pregnancy of parental rats until the offspring were two months old and in vitro models of NaF and/or Ad-ATG14-treated SH-SY5Y cells. We assessed neurobehavioral changes in offspring and further investigated the effects of NaF exposure on autophagic flux, apoptosis, autophagosome-lysosome fusion, and the interaction between ATG14 and the SNARE complex. NaF exposure impaired offspring learning and memory capabilities and induced the accumulation of autophagosomes and autophagic flux blockage and apoptosis, as indicated by increased LC3-II, p62, and cleaved-caspase-3 expression in vivo and in vitro. In addition, NaF treatment downregulated the protein expression of ATG14 and the SNARE complex and induced autophagosome-lysosome fusion blockage as evidenced by decreased ATG14, STX17, SNAP29, and VAMP8 expression and diminished colocalization of autophagosomes and lysosomes in vivo and in vitro. Furthermore, ATG14 upregulation enhanced the interaction of ATG14 and the SNARE complex to facilitate autophagosome-lysosome fusion, thereby restoring autophagic flux and alleviating NaF-induced apoptosis. In conclusion, NaF exhibited developmental neurotoxicity by restraining the interaction of ATG14 with the SNARE complex and hindering autophagosome-lysosome fusion, thereby participating in the occurrence and development of fluoride neurotoxicity. Notably, ATG14 upregulation protects against developmental fluoride neurotoxicity, and ATG14 may serve as a promising biomarker for further epidemiological investigation.

3D Printing Experimental Validation of the Finite Element Analysis of the Maxillofacial Model.

Contacts used in finite element (FE) models were considered as the best simulation for interactions in the temporomandibular joint (TMJ). However, the precision of simulations should be validated through experiments. Three-dimensional (3D) printing models with the high geometric and loading similarities of the individuals were used in the validation. This study aimed to validate the FE models of the TMJ using 3D printing models. Five asymptomatic subjects were recruited in this study. 3D models of mandible, disc, and maxilla were reconstructed according to cone-beam CT (CBCT) image data. PLA was chosen for 3D printing models from bottom to top. Five pressure forces corresponding to the central occlusion were applied to the 3D printing models. Ten strain rosettes were distributed on the mandible to record the horizontal and vertical strains. Contact was used in the FE models with the same geometries, material properties, loadings, and boundary conditions as 3D printing models to simulate the interaction of the disc-condyle, disc-temporal bone, and upper-lower dentition. The differences of the simulated and experimental results for each sample were less than 5% (maximum 4.92%) under all five loadings. In conclusion, it was accurate to use contact to simulate the interactions in TMJs and upper-lower dentition.

Course of illness and outcomes in older COVID-19 patients treated with HFNC: a retrospective analysis.

Coronavirus disease-2019 (COVID-19) has rapidly spread worldwide and causes high mortality of elderly patients. High-flow nasal cannula therapy (HFNC) is an oxygen delivery method for severely ill patients. We retrospectively analyzed the course of illness and outcomes in 110 elderly COVID-19 patients (≥65 years) treated with HFNC from 6 hospitals. 38 patients received HFNC (200 mmHg < PaO2/FiO2 ≤ 300 mmHg, early HFNC group), and 72 patients received HFNC (100 mmHg < PaO2/FiO2 ≤ 200 mmHg, late HFNC group). There were no significant differences of sequential organ failure assessment (SOFA) scores and APECH II scores between early and late HFNC group on admission. Compared with the late HFNC group, patients in the early HFNC group had a lower likelihood of developing severe acute respiratory distress syndrome (ARDS), longer time from illness onset to severe ARDS and shorter duration of viral shedding after illness onset, as well as shorter lengths of ICU and hospital stay. 24 patients died during hospitalization, of whom 22 deaths (30.6%) were in the late HFNC group and 2 (5.3%) in the early HFNC group. The present study suggested that the outcomes were better in severely ill elderly patients with COVID-19 receiving early compared to late HFNC.

Singlet Oxygen Generation in Dark-Hypoxia by Catalytic Microenvironment-Tailored Nanoreactors for NIR-II Fluorescence-Monitored Chemodynamic Therapy.

Singlet oxygen (1 O2 ) has a potent anticancer effect, but photosensitized generation of 1 O2 is inhibited by tumor hypoxia and limited light penetration depth. Despite the potential of chemodynamic therapy (CDT) to circumvent these issues by exploration of 1 O2 -producing catalysts, engineering efficient CDT agents is still a formidable challenge since most catalysts require specific pH to function and become inactivated upon chelation by glutathione (GSH). Herein, we present a catalytic microenvironment-tailored nanoreactor (CMTN), constructed by encapsulating MoO42- catalyst and alkaline sodium carbonate within liposomes, which offers a favorable pH condition for MoO42- -catalyzed generation of 1 O2 from H2 O2 and protects MoO42- from GSH chelation owing to the impermeability of liposomal lipid membrane to ions and GSH. H2 O2 and 1 O2 can freely cross the liposomal membrane, allowing CMTN with a built-in NIR-II ratiometric fluorescent 1 O2 sensor to achieve monitored tumor CDT.

Patient-derived non-small cell lung cancer xenograft mirrors complex tumor heterogeneity.

Objective: Patient-derived xenograft (PDX) models have shown great promise in preclinical and translational applications, but their consistency with primary tumors in phenotypic, genetic, and pharmacodynamic heterogeneity has not been well-studied. This study aimed to establish a PDX repository for non-small cell lung cancer (NSCLC) and to further elucidate whether it could preserve the heterogeneity within and between tumors in patients. Methods: A total of 75 surgically resected NSCLC specimens were implanted into immunodeficient NOD/SCID mice. Based on the successful establishment of the NSCLC PDX model, we compared the expressions of vimentin, Ki67, EGFR, and PD-L1 proteins between cancer tissues and PDX models using hematoxylin and eosin staining and immunohistochemical staining. In addition, we detected whole gene expression profiling between primary tumors and PDX generations. We also performed whole exome sequencing (WES) analysis in 17 first generation xenografts to further assess whether PDXs retained the patient heterogeneities. Finally, paclitaxel, cisplatin, doxorubicin, atezolizumab, afatininb, and AZD4547 were used to evaluate the responses of PDX models to the standard-of-care agents. Results: A large collection of serially transplantable PDX models for NSCLC were successfully developed. The histology and pathological immunohistochemistry of PDX xenografts were consistent with the patients' tumor samples. WES and RNA-seq further confirmed that PDX accurately replicated the molecular heterogeneities of primary tumors. Similar to clinical patients, PDX models responded differentially to the standard-of-care treatment, including chemo-, targeted- and immuno-therapeutics. Conclusions: Our established PDX models of NSCLC faithfully reproduced the molecular, histopathological, and therapeutic characteristics, as well as the corresponding tumor heterogeneities, which provides a clinically relevant platform for drug screening, biomarker discovery, and translational research.

Relationship between circulating miRNA-21, atrial fibrosis, and atrial fibrillation in patients with atrial enlargement.

BACKGROUND: Atrial fibrosis is a landmark of cardiac remodeling to perpetuate atrial fibrillation (AF), and recent studies have indicated that microRNAs (miRNAs) are essential regulators of multiple cardiovascular disease processes. Herein, we aimed to investigate the relationship between circulating microRNA-21 (miR-21), atrial fibrosis, and AF in patients with atrial enlargement. METHODS: A total of 60 persistent AF patients and 60 matched sinus rhythm (SR) controls were enrolled in the study. We measured their plasma miR-21 levels by using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Then, each patient underwent transthoracic echocardiography (TTE), while persistent AF patients underwent delayed enhancement magnetic resonance imaging (MRI). RESULTS: The plasma miR-21 concentrations in the AF group were significantly higher than in the controls, and highly correlated [R=0.689, 95% confidence interval (CI): 0.527 to 0.802; P<0.001] with left atrial (LA) fibrosis measured by delayed enhancement MRI. Receiver operating characteristics (ROC) curve analysis showed that the area under the curve (AUC) of plasma miR-21 to identify AF was 0.813 (95% CI: 0.731 to 0.878). The increasing levels of circulating miR-21 were significantly associated with the higher risk of AF by using logistic regression analysis, even after adjustment for known confounding variables. CONCLUSIONS: Circulating miR-21 highly correlates with the quantification of LA fibrosis by using delayed enhancement MRI and is associated with the risk of persistent AF in patients with LA enlargement.

lncRNA LEF1-AS1 Promotes Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Regulating miR-221/PTEN Signaling.

INTRODUCTION: LEF1-AS1 is a characterized oncogenic lncRNA in oral cancer. Analysis of TCGA dataset revealed the upregulation of LEF1-AS1 in non-small-cell lung cancer (NSCLC). This study was therefore carried out to investigate the involvement of LEF1-AS1 in NSCLC. METHODS: A total of 62 NSCLC patients were included to collect paired cancer and non-tumor tissues. RT-qPCR was performed to measure levels of LEF1-AS1 and miR-221 expression. Transient transfections were performed to explore the interactions between LEF1-AS1, miR-221 and PTEN. Cell proliferation and apoptosis were analyzed by cell proliferation assay and cell apoptosis assay, respectively. RESULTS: We found that LEF1-AS1 was upregulated in NSCLC patients. In addition, expression of LEF1-AS1 was negatively correlated with the expression of PTEN but positively correlated with the expression of miR-221 in NSCLC tissue samples. In NSCLC cells, overexpression of LEF1-AS1 led to downregulated expression of PTEN but upregulated expression of miR-221, which can directly target PTEN. Overexpression of LEF1-AS1 and miR-221 promoted cancer cell proliferation and inhibited apoptosis. PTEN played an opposite role and reduced the effects of overexpressing LEF1-AS1 and miR-221. CONCLUSION: LEF1-AS1 may promote the proliferation and induce apoptosis of NSCLC cells by regulating miR-221/PTEN signaling.

Involvement of P450s and nuclear receptors in the hepatoprotective effect of quercetin on liver injury by bacterial lipopolysaccharide.

Objective: Quercetin (Que), a flavonoid, possesses anti-inflammatory and antioxidant properties. It has been shown to protect against liver injury induced by various factors. This study was designed to investigate the underlying mechanism of its protective effect against lipopolysaccharide (LPS)- induced liver damage.Methods: Mice were pretreated with Que for 7 consecutive days and then exposed to LPS. To study the hepatoprotective effect of Que, oxidative stress parameters, inflammatory cytokine levels in liver and serum liver function indexes were examined. Protein and mRNA expression of nuclear orphan receptors and cytochrome P450 enzymes were measured by Western Blotting and qPCR, respectively.Results: Que significantly reduced circulating ALT, AST, ALP, and ameliorated LPS-induced histological alterations. In addition, Que obviously decreased markers of oxidative stress and pro-inflammatory cytokines. Furthermore, Que carried out the hepatoprotective effect via regulation of the expression of nuclear orphan receptors (CAR, PXR) and cytochrome P450 enzymes (CYP1A2, CYP2E1, CYP2D22, CYP3A11).Conclusions: Our findings suggested that Que pretreatment could ameliorate LPS-induced liver injury.

The diagnosis and treatment of adrenocortical carcinoma in pregnancy: a case report.

BACKGROUND: Pregnancy complicated with adrenocortical carcinoma (ACC) is a sporadic syndrome that is characterized by hypertension, uncontrolled hypokalemia, severe heart failure, premature delivery and other adverse effects. The clinical presentation of adrenocortical carcinoma is vague and nonspecific, it is challenging to identify complications of pregnancy with adrenocortical carcinoma. Here we present a case of adrenocortical carcinoma during pregnancy. We describe how to distinguish secondary hypertension from other conditions and the importance of timely detection and treatment of such patients. CASE PRESENTATION: A 22-year-old woman 30 weeks pregnant was hospitalized with uncontrolled hypertension and hypokalemia. An ultrasound examination of the right adrenal gland revealed a large mass. She underwent transabdominal adrenalectomy, and histopathology from the sample removed revealed an adrenocortical carcinoma. Five days after surgery, the patient had a premature rupture of the fetal membranes and gave birth to a newborn girl via vaginal delivery at 32 weeks of gestation. The newborn was transferred to the neonatal pediatrics ward, and the woman started receiving chemotherapy. CONCLUSIONS: Pregnancy with adrenocortical carcinoma is a rare condition. This case alerts the obstetricians that analysis of hypertension, hypokalemia, the plasma level and circadian rhythm of plasma cortisol provides a strategy to diagnose adrenocortical carcinoma during pregnancy.

Effects on loads in temporomandibular joints for patients with mandibular asymmetry before and after orthognathic surgeries under the unilateral molar clenching.

Orthognathic surgery is a useful treatment for the correction of mandibular deformity. Different from other occlusions, unilateral occlusion is frequently used in mastication and influences functions of temporomandibular joints (TMJs). However, stress distributions in TMJ before and after orthognathic surgeries are not under consideration in treatments, crucial to pre- and postoperative temporomandibular disorders (TMDs). The study aims to analyze stress distributions in TMJs for patients with mandibular asymmetry before and after orthognathic surgeries under the unilateral molar clenching. Ten asymptomatic subjects (control group) and 10 patients with mandibular asymmetry were recruited for the study. All patients underwent orthognathic surgeries and were grouped as preoperative and postoperative for the purpose of comparing stress variation in TMJ before and after surgery. Finite element models corresponding to the unilateral molar clenching were constructed. The contact stresses at the ipsilateral side for asymptomatic subjects were significantly greater than those at the contralateral side, while the third principal stresses at the contralateral side were significantly greater than those at the ipsilateral side. No significant difference of stress distribution in TMJ between two sides appeared for the preoperative group. After surgeries, the stress distributions were close to the normal states. The stress of the preoperative group was found to be significantly higher than those of the control and postoperative groups. The variations in stresses before and after the surgery were consistent with the signs and symptoms or recoveries of TMD. Orthognathic surgery could alleviate the high level of stresses caused by mandibular asymmetry and is helpful for the recovery of TMD.