Browse
You are looking at 131 - 140 of 1,472 items for
Search for other papers by Lingjuan Li in
Google Scholar
PubMed
Search for other papers by Jing Qin in
Google Scholar
PubMed
Search for other papers by Lin Ren in
Google Scholar
PubMed
Search for other papers by Shiyuan Xiang in
Google Scholar
PubMed
National Center for Neurological Disorders, Shanghai, China
Shanghai Clinical Medical Center of Neurosurgery, Shanghai, China
Neurosurgical Institute of Fudan University, Shanghai, China
Shanghai Key Laboratory of Medical Brain Function and Restoration and Neural Regeneration, Fudan University, Shanghai, China
Search for other papers by Xiaoyun Cao in
Google Scholar
PubMed
Search for other papers by Xianglan Zheng in
Google Scholar
PubMed
Search for other papers by Zhiwen Yin in
Google Scholar
PubMed
National Center for Neurological Disorders, Shanghai, China
Shanghai Clinical Medical Center of Neurosurgery, Shanghai, China
Neurosurgical Institute of Fudan University, Shanghai, China
Shanghai Key Laboratory of Medical Brain Function and Restoration and Neural Regeneration, Fudan University, Shanghai, China
Search for other papers by Nidan Qiao in
Google Scholar
PubMed
Purpose
We aimed to describe and predict the risk of severe hypernatremia after surgical resection of craniopharyngioma and to identify the association of water intake, urine output, and sodium level change in the patients.
Method
The outcome was postoperative severe hypernatremia. We identified risk factors associated with hypernatremia using multivariable regression. We trained machine learning models to predict the outcome. We compared serum sodium change, intravenous input, oral input, total input, urine output, and net fluid balance according to different nurse shifts.
Results
Among 234 included patients, 125 developed severe hypernatremia after surgery. The peak incidence occurred during day 0 and day 6 after surgery. The risk was increased in patients with gross total resection (odds ratio (OR) 2.41, P < 0.001), high Puget classification (OR 4.44, P = 0.026), preoperative adrenal insufficiency (OR 2.01, P = 0.040), and preoperative hypernatremia (OR 5.55, P < 0.001). The random forest algorithm had the highest area under the receiver operating characteristic curve (0.770, 95% CI, 0.727–0.813) in predicting the outcome and was validated in the prospective validation cohort. Overnight shifts were associated with the highest serum sodium increase (P = 0.010), less intravenous input (P < 0.001), and less desmopressin use (P < 0.001).
Conclusion
The overall incidence of severe hypernatremia after surgical resection of craniopharyngioma was significant, especially in patients with gross total resection, hypothalamus distortion, preoperative adrenal insufficiency, and preoperative severe hypernatremia. Less intravenous input and less desmopressin use were associated with serum sodium increases, especially during overnight shifts.
Search for other papers by Hyunjae Lee in
Google Scholar
PubMed
Search for other papers by Tae-Shin Kim in
Google Scholar
PubMed
Cancer Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea
Search for other papers by Ja-Yoon Gu in
Google Scholar
PubMed
Search for other papers by Mi Ran Yu in
Google Scholar
PubMed
Search for other papers by Seung-Eun Lee in
Google Scholar
PubMed
Search for other papers by Eun Sook Kim in
Google Scholar
PubMed
Cancer Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea
Search for other papers by Hyun Kyung Kim in
Google Scholar
PubMed
Objective
The inflammatory microenvironment has been implicated in differentiated thyroid cancer (DTC). Inflammatory stimuli induce the release of components of neutrophils into extracellular space, leading to formation of neutrophil extracellular trap (NET), which can stimulate growth and progression of cancer. Generation of activated factor XII and thrombin is also involved in cancer progression. This study attempted to determine whether the level of circulating markers of NET, activated factor XII, and endogenous thrombin potential may be useful for detecting the recurrence of DTC.
Methods
A total of 122 patients with DTC were recruited during the postoperative follow-up period. Measurement of the levels of circulating markers of NET (neutrophil elastase, histone–DNA complex, cell-free dsDNA), activated factor XII, and endogenous thrombin potential was performed.
Results
A significantly elevated level of neutrophil elastase was detected in patients with recurrence (n = 12) compared to those without recurrence (n = 110), while significant elevation of the levels of other markers was not observed. The value for area under the curve (0.717, P = 0.018) of neutrophil elastase for detecting recurrence of DTC was superior to that (0.661, P = 0.051) of serum thyroglobulin. An elevated level of neutrophil elastase was significantly associated with recurrence of DTC independent of serum thyroglobulin.
Conclusions
Because an elevated level of neutrophil elastase was detected in patients with recurrence of DTC and showed a significant association with recurrence of DTC, it can be proposed as a novel biomarker for use in detecting recurrence of DTC along with other tests.
Search for other papers by A Bergougnoux in
Google Scholar
PubMed
INSERM Unité 1203 (DEFE), Université de Montpellier, Montpellier, France
Search for other papers by L Gaspari in
Google Scholar
PubMed
Search for other papers by M Soleirol in
Google Scholar
PubMed
Search for other papers by N Servant in
Google Scholar
PubMed
Search for other papers by S Soskin in
Google Scholar
PubMed
Search for other papers by S Rossignol in
Google Scholar
PubMed
Search for other papers by K Wagner-Mahler in
Google Scholar
PubMed
Search for other papers by J Bertherat in
Google Scholar
PubMed
Search for other papers by C Sultan in
Google Scholar
PubMed
Search for other papers by N Kalfa in
Google Scholar
PubMed
Département d'Endocrinologie et de Gynécologie Pédiatrique, Hôpital Arnaud de Villeneuve, Université de Montpellier, Montpellier, France
INSERM Unité 1203 (DEFE), Université de Montpellier, Montpellier, France
Search for other papers by F Paris in
Google Scholar
PubMed
Although hyperandrogenism is a frequent cause of consultation in adolescent girls, more severe forms with virilization must lead to suspicion of an adrenal or ovarian tumor. However, they may also reveal a 46,XY disorder of sexual development (DSD). Here, we describe four adolescent girls referred for pubertal virilization and in whom we diagnosed a 46,XY DSD. We performed gene mutation screening by Sanger sequencing (all patients) and by next-generation sequencing (NGS) in patient #4. We identified new heterozygous NR5A1 gene variants in patients #1 and #2 and a homozygous SRD5A2 gene deletion in patient #3. Patient #4 received a diagnosis of complete androgen insensitivity in childhood; however, due the unusual pubertal virilization, we completed the gene analysis by NGS that revealed two heterozygous HSD17B3 variants. This work underlines the importance of considering the hypothesis of 46,XY DSD in adolescent girls with unexplained virilization at puberty.
Search for other papers by Kathryn Lingen in
Google Scholar
PubMed
Search for other papers by Talia Pikounis in
Google Scholar
PubMed
Search for other papers by Natalie Bellini in
Google Scholar
PubMed
Search for other papers by Diana Isaacs in
Google Scholar
PubMed
Insulin administration remains vital to the treatment of diabetes and although there have been advances in insulin delivery, evidence suggests that many people with diabetes on insulin therapy have suboptimal glycemic management. Recent advancements in insulin administration techniques include connected insulin devices, such as connected insulin pens and pen caps. In this review, we provide an overview of the literature on the use of connected insulin pens and pen caps to further elucidate the clinical benefits and drawbacks of these devices. We discuss the development of these devices, outlining the characteristics of insulin pens and pen caps with regulatory approvals. These devices have different features that can ease the burden of diabetes management, including automatic recording of insulin dose information, tracking of insulin-on-board, bolus calculators, and missed dose alerts. Despite the advantages of connected pens and pen caps, a small percentage of insulin users are currently using these devices, due to many factors, including lack of health-care professional awareness, initial training for prescribers, and setup of the device. Overcoming these barriers and publishing more data demonstrating the glycemic outcomes associated with these systems could improve diabetes management for people living with diabetes. As health-care systems become increasingly digital, connected insulin pens have the potential to allow a data-driven approach to diabetes management for people who are not interested in, cannot afford, or do not have intensive insulin regimens that might warrant use of insulin pumps or automated insulin delivery systems.
Search for other papers by Jelena Stankovic in
Google Scholar
PubMed
Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark
Search for other papers by Kurt Kristensen in
Google Scholar
PubMed
Search for other papers by Niels Birkebæk in
Google Scholar
PubMed
Search for other papers by Jens Otto Lunde Jørgensen in
Google Scholar
PubMed
Steno Diabetes Center Aarhus (SDCA), Aarhus University Hospital, Aarhus, Denmark
Search for other papers by Esben Søndergaard in
Google Scholar
PubMed
Background
The diagnosis of the polyuria–polydipsia syndrome is challenging. Copeptin is a robust biomarker of arginine vasopressin (AVP) secretion. Arginine, which stimulates growth hormone (GH), has been shown also to stimulate copeptin secretion via unknown mechanisms.
Aim
The aim was to investigate copeptin levels in response to three different GH stimulation tests in patients suspected of GH deficiency.
Methods
In this cross-sectional study, we measured plasma copeptin levels at baseline and at 60, 105, and 150 min in patients undergoing a stimulation test for growth hormone deficiency with either arginine (n = 16), clonidine (n = 8) or the insulin tolerance test (ITT) (n = 10).
Results
In patients undergoing the arginine test, the mean age was 9 years, and 10 years for clonidine. The ITT was only performed in adult patients (>18 years) with a mean age of 49 years. Copeptin level increased significantly from baseline to 60 min after arginine (P <0.01) and ITT (P < 0.01). By contrast, copeptin level tended to decrease after clonidine stimulation (P = 0.14).
Conclusion
These data support that infusion of arginine increases plasma copeptin levels and reveal a comparable response after an ITT. We hypothesize that the underlying mechanism is abrogation of somatostatin-induced AVP suppression.
Key Laboratory of Animal Embryo and Development Engineering of Autonomous Region Universities, Inner Mongolia Agricultural University, Hohhot, PR China
Search for other papers by Yufen Zhao in
Google Scholar
PubMed
Key Laboratory of Animal Embryo and Development Engineering of Autonomous Region Universities, Inner Mongolia Agricultural University, Hohhot, PR China
Search for other papers by Erge Namei in
Google Scholar
PubMed
Key Laboratory of Animal Embryo and Development Engineering of Autonomous Region Universities, Inner Mongolia Agricultural University, Hohhot, PR China
Search for other papers by Bingxue Yang in
Google Scholar
PubMed
National Center of Technology Innovation for Dairy Industry, Hohhot, PR China
Search for other papers by Xiangnan Bao in
Google Scholar
PubMed
Search for other papers by Wei Sun in
Google Scholar
PubMed
Key Laboratory of Animal Embryo and Development Engineering of Autonomous Region Universities, Inner Mongolia Agricultural University, Hohhot, PR China
Search for other papers by Gerile Subudeng in
Google Scholar
PubMed
Key Laboratory of Animal Embryo and Development Engineering of Autonomous Region Universities, Inner Mongolia Agricultural University, Hohhot, PR China
Search for other papers by Guifang Cao in
Google Scholar
PubMed
Key Laboratory of Animal Embryo and Development Engineering of Autonomous Region Universities, Inner Mongolia Agricultural University, Hohhot, PR China
Search for other papers by Haijun Li in
Google Scholar
PubMed
Search for other papers by Gui Wang in
Google Scholar
PubMed
Gap junction channels in cumulus–oocyte complexes (COCs) enable the transmission and communication of small molecular signals between adjacent cells, such as cAMP. However, the regulation of gap junction function (GJF) by cAMP and the underlying mechanisms involved are not fully clarified. This study investigated the effect of cAMP on connexin 43 (CX43) expression and GJF in ovine COCs using immunofluorescence, quantitative real-time PCR (qRT-PCR), western blotting, and GJF detection. The CX43 was only found in the cumulus cells (CCs) side of ovine COC. The intra-oocyte cAMP showed a significant increase at 30 min, while the intra-CC cAMP exhibited two peaks at 10 min and 1 h during in vitro maturation (IVM). Phosphorylated CX43 protein exhibited an immediate increase at 10 min, and CX43 protein displayed two peaks at 10 min and 1 h during IVM. The duration of pre-IVM exposure to forskolin and IBMX significantly enhanced phosphorylated and total CX43, as well as Gja1 and Creb genes, for 10 min; these effects were counteracted by Rp-cAMP. Both pre-IVM with forskolin and IBMX for 1 h and the GJF and CX43/p-CX43 ratio were elevated. The closure of gap junction channels caused by phosphorylated CX43 to prevent cAMP outflow from oocytes in early IVM of COC. Cyclic AMP upregulated phosphorylated and total CX43 via genomic and non-genomic pathways, but its functional regulation was dependent on the balance of the two proteins. This study provides a new insight into the regulatory mechanism between cAMP and GJF, which would improve IVM in animal and clinical research.
Search for other papers by Cheryl M Isherwood in
Google Scholar
PubMed
Search for other papers by M Denise Robertson in
Google Scholar
PubMed
Search for other papers by Debra J Skene in
Google Scholar
PubMed
Search for other papers by Jonathan D Johnston in
Google Scholar
PubMed
Obesity is a major cause of type 2 diabetes. Transition from obesity to type 2 diabetes manifests in the dysregulation of hormones controlling glucose homeostasis and inflammation. As metabolism is a dynamic process that changes across 24 h, we assessed diurnal rhythmicity in a panel of 10 diabetes-related hormones. Plasma hormones were analysed every 2 h over 24 h in a controlled laboratory study with hourly isocaloric drinks during wake. To separate effects of body mass from type 2 diabetes, we recruited three groups of middle-aged men: an overweight (OW) group with type 2 diabetes and two control groups (lean and OW). Average daily concentrations of glucose, triacylglycerol and all the hormones except visfatin were significantly higher in the OW group compared to the lean group (P < 0.001). In type 2 diabetes, glucose, insulin, C-peptide, glucose-dependent insulinotropic peptide and glucagon-like peptide-1 increased further (P < 0.05), whereas triacylglycerol, ghrelin and plasminogen activator inhibitor-1 concentrations were significantly lower compared to the OW group (P < 0.001). Insulin, C-peptide, glucose-dependent insulinotropic peptide and leptin exhibited significant diurnal rhythms in all study groups (P < 0.05). Other hormones were only rhythmic in 1 or 2 groups. In every group, hormones associated with glucose regulation (insulin, C-peptide, glucose-dependent insulinotropic peptide, ghrelin and plasminogen activator inhibitor-1), triacylglycerol and glucose peaked in the afternoon, whereas glucagon and hormones associated with appetite and inflammation peaked at night. Thus being OW with or without type 2 diabetes significantly affected hormone concentrations but did not affect the timing of the hormonal rhythms.
Search for other papers by Magdalena Zgliczyńska in
Google Scholar
PubMed
Search for other papers by Magdalena Ostrowska in
Google Scholar
PubMed
Search for other papers by Kinga Żebrowska in
Google Scholar
PubMed
Search for other papers by Iwona Szymusik in
Google Scholar
PubMed
Search for other papers by Konrad Kowalski in
Google Scholar
PubMed
Search for other papers by Dorota Leszczyńska in
Google Scholar
PubMed
Search for other papers by Katarzyna Kosińska-Kaczyńska in
Google Scholar
PubMed
Objective
Vitamin D plays an important role during pregnancy. The aim was to compare vitamin D status in a group of singleton (SP) and twin pregnancies (TP) using two diagnostic methods: chemiluminescence immunoassay (CLIA) and liquid chromatography with tandem mass spectrometry (LC-MS/MS).
Design
This is a cross-sectional study.
Methods
The study was conducted in the population of SP and TP at the gestational age above 20 + 0 at the Bielanski Hospital in Warsaw, Poland, between October 2020 and January 2023. All patients had their venous blood samples collected and were given an original survey containing questions on demography and vitamin D supplementation.
Results
The study group included 53 Caucasian women with SP and 78 with TP aged from 21 to 47. Considering LC-MS/MS, patients with TP had lower concentrations of 25-hydroxyvitamin D (25(OH)D) than patients with SP. However, no significant difference was observed in the frequency of the occurrence of vitamin D deficiency (25(OH)D < 30 ng/mL). In both groups, the levels obtained with CLIA were significantly lower than in case of LC-MS/MS, however, strongly correlated. The intermethod agreement accounted for 52.4% and the Cohen’s kappa coefficient was 0.142.
Conclusions
The concentration of 25(OH)D in pregnant women depends on the type of gestation (SP/TP) and on the diagnostic methods used (CLIA/LC-MS/MS). Based on LC-MS/MS, the incidence of vitamin D deficiency was low in our group and no differences occurred in its frequency between SP and TP. The intermethod agreement between CLIA and LC-MS/MS on the detection of vitamin D deficiency was low.
Significance statement
This is the first study to compare the concentration of 25(OH)D levels between SP and TP using two methods: CLIA and the gold standard – LC-MS/MS. Based on LC-MS/MS, a low incidence of vitamin D deficiency was observed in our group, in which the vast majority of patients took cholecalciferol supplements. Moreover, there were no differences in its frequency between SP and TP. However, the 25(OH)D level was significantly lower in TP. The intermethod agreement between CLIA and LC-MS/MS on the detection of vitamin D deficiency was low, which is associated with substantial clinical implications.
Search for other papers by Souad Daamouch in
Google Scholar
PubMed
Search for other papers by Sylvia Thiele in
Google Scholar
PubMed
Search for other papers by Lorenz Hofbauer in
Google Scholar
PubMed
Search for other papers by Martina Rauner in
Google Scholar
PubMed
The link between obesity and low bone strength has become a significant medical concern. The canonical Wnt signaling pathway is a key regulator of mesenchymal stem cell differentiation into either osteoblasts or adipocytes with active Wnt signaling promoting osteoblastogenesis. Our previous research indicated that Dickkopf-1 (Dkk1), a Wnt inhibitor, is upregulated in bone tissue in obesity and that osteoblast-derived Dkk1 drives obesity-induced bone loss. However, Dkk1 is also produced by adipocytes, but the impact of adipogenic Dkk1 on bone remodeling and its role in obesity-induced bone loss remain unclear. Thus, in this study, we investigated the influence of adipogenic Dkk1 on bone homeostasis and obesity-induced bone loss in mice. To that end, deletion of Dkk1 in adipocytes was induced by tamoxifen administration into 8-week-old male Dkk1fl/fl;AdipoQcreERT2 mice. Bone and fat mass were analyzed at 12 and 20 weeks of age. Obesity was induced in 8-week-old male Dkk1fl/fl;AdipoQcre mice with a high-fat diet (HFD) rich in saturated fats for 12 weeks. We observed that 12-week-old male mice without adipogenic Dkk1 had a significant increase in trabecular bone volume in the vertebrae and femoral bones. While histological and serological bone formation markers were not different, the number of osteoclasts and adipocytes was decreased in the vertebral bones of Dkk1fl/fl;AdipoQcre-positive mice. Despite the increased bone mass in 12-week-old male mice, at 20 weeks of age, there was no difference in the bone volume between the controls and Dkk1fl/fl;AdipoQcre-positive mice. Also, Dkk1fl/fl;AdipoQcre-positive mice were not protected from HFD-induced bone loss. Even though mRNA expression levels of Sost, another important Wnt inhibitor, in bone from Dkk1-deficient mice fed with HFD were decreased compared to Dkk1-sufficient mice on an HFD, this did not prevent the HFD-induced suppression of bone formation. In conclusion, adipogenic Dkk1 may play a transient role in bone mass regulation during adolescence, but it does not contribute to bone homeostasis or obesity-induced bone loss later in life.
Search for other papers by Shenghe Luo in
Google Scholar
PubMed
Department of Cardiology, Yanbian University Hospital, Yanji, China
Search for other papers by Yunhui Zuo in
Google Scholar
PubMed
Search for other papers by Xiaotian Cui in
Google Scholar
PubMed
Search for other papers by Meiping Zhang in
Google Scholar
PubMed
Search for other papers by Honghua Jin in
Google Scholar
PubMed
Search for other papers by Lan Hong in
Google Scholar
PubMed
To observe the effects of liraglutide (analog of glucagon-like peptide 1 (GLP-1)) on atrial natriuretic peptide (ANP) secretion and atrial dynamics, an ex vivo isolated rat atrial perfusion model was used to determine atrial ANP secretion and pulse pressure. DPP-4−/− mice were also established in vivo. ANP levels were determined by radioimmunoassay; GLP-1 content was determined by Elisa. The expression levels of GLP-1 receptor (GLP-1R), PI3K/AKT/mTOR, piezo 1, and cathepsin K were analyzed by Western blot. In the clinical study, patients with acute coronary syndrome (ACS) had low levels of plasma GLP-1 but relatively high levels of plasma ANP. In ex vivo (3.2 nmol/L) and in vivo (30 μg/kg) models, liraglutide significantly decreased ANP levels and atrial pulse pressure. Exendin9–39 alone (GLP-1R antagonist) reversibly significantly increased ANP secretion, and the reduction effect of liraglutide on the secretion of ANP was significantly alleviated by Exendin9–39. Exendin9–39 demonstrated slightly decreased atrial pulse pressure; however, combined liraglutide and Exendin9–39 significantly decreased atrial pulse pressure. Ly294002 (PI3K/AKT inhibitor) inhibited the increase of ANP secretion by liraglutide for a short time, while Ly294002 didn't counteract the decrease in pulse pressure by liraglutide in atrial dynamics studies. Liraglutide increased the expression of GLP-1R and PI3K/AKT/mTOR in isolated rat atria and the hearts of mice in vivo, whereas Exendin9–39 reversibly reduced the expression of GLP-1R and PI3K/AKT/mTOR. Piezo 1 was significantly decreased in wild type and DPP-4−/− mouse heart or isolated rat atria after being treated with liraglutide. Cathepsin K expression was only decreased in in vivo model hearts. Liraglutide can inhibit ANP secretion while decreasing atrial pulse pressure mediated by GLP-1R. Liraglutide probably plays a role in the reduction of ANP secretion via the PI3K/AKT/mTOR signaling pathway. Piezo 1 and cathepsin K may be involved in the liraglutide mechanism of reduction.
