Objective:To compare the clinical effect of femoral neck system (FNS) and cannulated compression screw internal fixation in the treatment of femoral neck fractures in young and middle-aged patients.Methods:The databases of CNKI, Wanfang Data Knowledge Service Platform, VIP, Chinese Medical Journal Full-text Database, PubMed, Embase, Web of Science and Cochrane Library were searched. The intraoperative blood loss, intraoperative fluoroscopy times, hospital stay, fracture healing time, Harris hip function score, partial weight-bearing time and complication rate were extracted to compare the clinical efficacy of the two surgical methods. Stata18.0 statistical software was used for meta-analysis.Results:A total of 699 patients from 11 studies were included in this study. Compared with cannulated compression screw internal fixation, the FNS had a shorter operation time [ WMD= -8.54, 95% CI(-14.87, -2.21), P=0.008], fewer intraoperative fluoroscopy times[ WMD= -8.29, 95% CI(-11.45, -5.12), P< 0.001], a shorter fracture healing time [ WMD=-1.59, 95% CI(-2.49, -0.68), P=0.001], a shorter partial weight-bearing time[ WMD=-3.45, 95% CI(-4.43, -2.46), P<0.001], a lower incidence of postoperative complications [ RR=0.41, 95% CI(0.22, 0.76), P= 0.004], and a lower incidence of postoperative nonunion [ RR=0.40, 95% CI(0.18, 0.88), P=0.022]. Meanwhile, the FNS group had more intraoperative blood loss [ WMD=9.53, 95% CI(2.70, 16.35), P=0.006] and a higher Harris hip function score at the last follow-up [ WMD=3.50, 95% CI(2.11, 4.89), P<0.001] than the cannulated compression screw internal fixation group. There were no statistically significant differences in the length of hospital stay [ WMD=-0.48, 95% CI(-0.82, -0.13), P=0.092] or the incidence of femoral head necrosis [ RR=0.57, 95% CI(0.26, 1.24), P=0.159] between the two groups. Conclusion:Compared with cannulated compression screw internal fixation in the treatment of femoral neck fracture in young and middle-aged patients, FNS has more intraoperative blood loss, but it has more advantages in operation time, intraoperative blood loss, intraoperative fluoroscopy times, postoperative fracture healing time, Harris hip function score, partial weight-bearing time, postoperative nonunion rate and postoperative complications rate.

Objective:To compare the clinical effect of femoral neck system (FNS) and cannulated compression screw internal fixation in the treatment of femoral neck fractures in young and middle-aged patients.Methods:The databases of CNKI, Wanfang Data Knowledge Service Platform, VIP, Chinese Medical Journal Full-text Database, PubMed, Embase, Web of Science and Cochrane Library were searched. The intraoperative blood loss, intraoperative fluoroscopy times, hospital stay, fracture healing time, Harris hip function score, partial weight-bearing time and complication rate were extracted to compare the clinical efficacy of the two surgical methods. Stata18.0 statistical software was used for meta-analysis.Results:A total of 699 patients from 11 studies were included in this study. Compared with cannulated compression screw internal fixation, the FNS had a shorter operation time [ WMD= -8.54, 95% CI(-14.87, -2.21), P=0.008], fewer intraoperative fluoroscopy times[ WMD= -8.29, 95% CI(-11.45, -5.12), P< 0.001], a shorter fracture healing time [ WMD=-1.59, 95% CI(-2.49, -0.68), P=0.001], a shorter partial weight-bearing time[ WMD=-3.45, 95% CI(-4.43, -2.46), P<0.001], a lower incidence of postoperative complications [ RR=0.41, 95% CI(0.22, 0.76), P= 0.004], and a lower incidence of postoperative nonunion [ RR=0.40, 95% CI(0.18, 0.88), P=0.022]. Meanwhile, the FNS group had more intraoperative blood loss [ WMD=9.53, 95% CI(2.70, 16.35), P=0.006] and a higher Harris hip function score at the last follow-up [ WMD=3.50, 95% CI(2.11, 4.89), P<0.001] than the cannulated compression screw internal fixation group. There were no statistically significant differences in the length of hospital stay [ WMD=-0.48, 95% CI(-0.82, -0.13), P=0.092] or the incidence of femoral head necrosis [ RR=0.57, 95% CI(0.26, 1.24), P=0.159] between the two groups. Conclusion:Compared with cannulated compression screw internal fixation in the treatment of femoral neck fracture in young and middle-aged patients, FNS has more intraoperative blood loss, but it has more advantages in operation time, intraoperative blood loss, intraoperative fluoroscopy times, postoperative fracture healing time, Harris hip function score, partial weight-bearing time, postoperative nonunion rate and postoperative complications rate.

Norepinephrine (NE) modulates synaptic transmission and long-term plasticity through distinct subtype adrenergic receptor (AR)-mediated-intracellular signaling cascades. However, the role of NE modulates glutamatergic long-term potentiation (LTP) in the hypothalamic paraventricular nucleus (PVN) magnocellular neuroendocrine cells (MNCs) is unclear. We here investigate the effect of NE on high frequency stimulation (HFS)-induced glutamatergic LTP in rat hypothalamic PVN MNCs in vitro, by whole-cell patch-clamp recording, biocytin staining and pharmacological methods. Delivery of HFS induced glutamatergic LTP with a decrease in N2/N1 ratio in the PVN MNCs, which was enhanced by application of NE (100 nM).HFS-induced LTP was abolished by the blockade of N-methyl-D-aspartate receptors (NMDAR) with D-APV, but it was rescued by the application of NE. NE failed to rescue HFS-induced LTP of MNCs in the presence of a selective β1-AR antagonist, CGP 20712. However, application of β1-AR agonist, dobutamine HCl rescued HFS-induced LTP of MNCs in the absence of NMDAR activity. In the absence of NMDAR activity, NE failed to rescue HFS-induced MNC LTP when protein kinase A (PKA) was inhibited by extracellular applying KT5720 or intracellular administration of PKI. These results indicate that NE activates β1-AR and triggers HFS to induce a novel glutamatergic LTP of hypothalamic PVN NMCs via the postsynaptic PKA signaling pathway in vitro in rats.

Norepinephrine (NE) modulates synaptic transmission and long-term plasticity through distinct subtype adrenergic receptor (AR)-mediated-intracellular signaling cascades. However, the role of NE modulates glutamatergic long-term potentiation (LTP) in the hypothalamic paraventricular nucleus (PVN) magnocellular neuroendocrine cells (MNCs) is unclear. We here investigate the effect of NE on high frequency stimulation (HFS)-induced glutamatergic LTP in rat hypothalamic PVN MNCs in vitro, by whole-cell patch-clamp recording, biocytin staining and pharmacological methods. Delivery of HFS induced glutamatergic LTP with a decrease in N2/N1 ratio in the PVN MNCs, which was enhanced by application of NE (100 nM).HFS-induced LTP was abolished by the blockade of N-methyl-D-aspartate receptors (NMDAR) with D-APV, but it was rescued by the application of NE. NE failed to rescue HFS-induced LTP of MNCs in the presence of a selective β1-AR antagonist, CGP 20712. However, application of β1-AR agonist, dobutamine HCl rescued HFS-induced LTP of MNCs in the absence of NMDAR activity. In the absence of NMDAR activity, NE failed to rescue HFS-induced MNC LTP when protein kinase A (PKA) was inhibited by extracellular applying KT5720 or intracellular administration of PKI. These results indicate that NE activates β1-AR and triggers HFS to induce a novel glutamatergic LTP of hypothalamic PVN NMCs via the postsynaptic PKA signaling pathway in vitro in rats.

Norepinephrine (NE) modulates synaptic transmission and long-term plasticity through distinct subtype adrenergic receptor (AR)-mediated-intracellular signaling cascades. However, the role of NE modulates glutamatergic long-term potentiation (LTP) in the hypothalamic paraventricular nucleus (PVN) magnocellular neuroendocrine cells (MNCs) is unclear. We here investigate the effect of NE on high frequency stimulation (HFS)-induced glutamatergic LTP in rat hypothalamic PVN MNCs in vitro, by whole-cell patch-clamp recording, biocytin staining and pharmacological methods. Delivery of HFS induced glutamatergic LTP with a decrease in N2/N1 ratio in the PVN MNCs, which was enhanced by application of NE (100 nM).HFS-induced LTP was abolished by the blockade of N-methyl-D-aspartate receptors (NMDAR) with D-APV, but it was rescued by the application of NE. NE failed to rescue HFS-induced LTP of MNCs in the presence of a selective β1-AR antagonist, CGP 20712. However, application of β1-AR agonist, dobutamine HCl rescued HFS-induced LTP of MNCs in the absence of NMDAR activity. In the absence of NMDAR activity, NE failed to rescue HFS-induced MNC LTP when protein kinase A (PKA) was inhibited by extracellular applying KT5720 or intracellular administration of PKI. These results indicate that NE activates β1-AR and triggers HFS to induce a novel glutamatergic LTP of hypothalamic PVN NMCs via the postsynaptic PKA signaling pathway in vitro in rats.

Norepinephrine (NE) modulates synaptic transmission and long-term plasticity through distinct subtype adrenergic receptor (AR)-mediated-intracellular signaling cascades. However, the role of NE modulates glutamatergic long-term potentiation (LTP) in the hypothalamic paraventricular nucleus (PVN) magnocellular neuroendocrine cells (MNCs) is unclear. We here investigate the effect of NE on high frequency stimulation (HFS)-induced glutamatergic LTP in rat hypothalamic PVN MNCs in vitro, by whole-cell patch-clamp recording, biocytin staining and pharmacological methods. Delivery of HFS induced glutamatergic LTP with a decrease in N2/N1 ratio in the PVN MNCs, which was enhanced by application of NE (100 nM).HFS-induced LTP was abolished by the blockade of N-methyl-D-aspartate receptors (NMDAR) with D-APV, but it was rescued by the application of NE. NE failed to rescue HFS-induced LTP of MNCs in the presence of a selective β1-AR antagonist, CGP 20712. However, application of β1-AR agonist, dobutamine HCl rescued HFS-induced LTP of MNCs in the absence of NMDAR activity. In the absence of NMDAR activity, NE failed to rescue HFS-induced MNC LTP when protein kinase A (PKA) was inhibited by extracellular applying KT5720 or intracellular administration of PKI. These results indicate that NE activates β1-AR and triggers HFS to induce a novel glutamatergic LTP of hypothalamic PVN NMCs via the postsynaptic PKA signaling pathway in vitro in rats.

Norepinephrine (NE) modulates synaptic transmission and long-term plasticity through distinct subtype adrenergic receptor (AR)-mediated-intracellular signaling cascades. However, the role of NE modulates glutamatergic long-term potentiation (LTP) in the hypothalamic paraventricular nucleus (PVN) magnocellular neuroendocrine cells (MNCs) is unclear. We here investigate the effect of NE on high frequency stimulation (HFS)-induced glutamatergic LTP in rat hypothalamic PVN MNCs in vitro, by whole-cell patch-clamp recording, biocytin staining and pharmacological methods. Delivery of HFS induced glutamatergic LTP with a decrease in N2/N1 ratio in the PVN MNCs, which was enhanced by application of NE (100 nM).HFS-induced LTP was abolished by the blockade of N-methyl-D-aspartate receptors (NMDAR) with D-APV, but it was rescued by the application of NE. NE failed to rescue HFS-induced LTP of MNCs in the presence of a selective β1-AR antagonist, CGP 20712. However, application of β1-AR agonist, dobutamine HCl rescued HFS-induced LTP of MNCs in the absence of NMDAR activity. In the absence of NMDAR activity, NE failed to rescue HFS-induced MNC LTP when protein kinase A (PKA) was inhibited by extracellular applying KT5720 or intracellular administration of PKI. These results indicate that NE activates β1-AR and triggers HFS to induce a novel glutamatergic LTP of hypothalamic PVN NMCs via the postsynaptic PKA signaling pathway in vitro in rats.

AIM: To study the correlation between meibomian gland dysfunction(MGD)patients and their sleep quality.METHODS: Retrospective case-control study. A total of 150 MGD patients treated in our hospital from January 2021 to October 2022 were selected and divided into sleep disorder group(75 cases, PSQI>10 points)and control group(75 cases, PSQI≤10 points)according to the Pittsburgh sleep quality index(PSQI). Both groups were scored using the ocular surface disease index(OSDI), underwent meibomian gland-related examinations(eyelid margin morphology, meibomian gland secretion ability, meibomian gland secretion quality score), corneal fluorescein staining(FL)score, Schirmer Ⅰ test(SⅠt), tear film break-up time(BUT)was measured, and sleep indicators(sleep quality, sleep latency, subjective sleep quality, sleep time)were evaluated.RESULTS: There were significant differences in OSDI score, FL score, SⅠt, BUT, eyelid margin morphology score, meibomian gland secretion ability score, and meibomian gland secretion quality score between the two groups(P<0.05). In the sleep disorder group, PSQI score, sleep latency score, subjective sleep quality score, and sleep time score were significantly positively correlated with OSDI score, FL score, meibomian gland secretion ability score, and meibomian gland secretion quality score(P<0.05); PSQI score, subjective sleep quality score, and sleep time score were significantly positively correlated with eyelid margin morphology score(P<0.05); PSQI score, sleep latency score, and subjective sleep quality score were significantly negatively correlated with BUT and SⅠt(P<0.05); sleep time score was significantly negatively correlated with BUT(P<0.05); sleep latency score was not significantly correlated with eyelid margin morphology score(P>0.05); sleep time score was not significantly correlated with SⅠt(P>0.05).CONCLUSION:The ocular surface condition of MGD patients is correlated with multiple sleep quality indicators, and a decline in sleep quality may increase the risk of MGD.

Atherosclerosis ; Humans ; Polysomnography ; Sleep Apnea, Obstructive/complications*