Inspiratory-Activated Airway Vagal Preganglionic Neurones Excited by Thyrotropin-Releasing Hormone via Multiple Mechanisms in Neonatal Rats

The airway vagal preganglionic neurons (AVPNs) providing projections to intrinsic tracheobronchial ganglia are considered to be crucial to modulation of airway resistance in physiological and pathological states. AVPNs classified into inspiratory-activated AVPNs (IA-AVPNs) and inspiratory-inhibited AVPNs (II-AVPNs) are regulated by thyrotropin-releasing hormone (TRH)-containing terminals. TRH causes a direct excitatory current and attenuates the phasic inspiratory glycinergic inputs in II-AVPNs, however, whether and how TRH influences IA-AVPNs remains unknown. In current study, TRH regulation of IA-AVPNs and its mechanisms involved were investigated. Using retrogradely fluorescent labeling method and electrophysiology techniques to identify IA-AVPNs in brainstem slices with rhythmic inspiratory hypoglossal bursts recorded by a suction electrode, the modulation of TRH was observed with patch-clamp technique. The findings demonstrate that under voltage clamp configuration, TRH (100 nM) caused a slow excitatory inward current, augmented the excitatory synaptic inputs, progressively suppressed the inhibitory synaptic inputs and elicited a distinctive electrical oscillatory pattern (OP). Such a current and an OP was independent of presynaptic inputs. Carbenoxolone (100 μM), a widely used gap junction inhibitor, fully suppressed the OP with persistence of TRH-induced excitatory slow inward current and augment of the excitatory synaptic inputs. Both tetrodotoxin (1 μM) and riluzole (20 μM) functioned to block the majority of the slow excitatory inward current and prevent the OP, respectively. Under current clamp recording, TRH caused a slowly developing depolarization and continuously progressive oscillatory firing pattern sensitive to TTX. TRH increased the firing frequency in response to injection of a square-wave current. The results suggest that TRH excited IA-AVPNs via the following multiple mechanisms: (1) TRH enhances the excitatory and depresses the inhibitory inputs; (2) TRH induces an excitatory postsynaptic slow inward current; (3) TRH evokes a distinctive OP mediated by gap junction

Receiver operating characteristic curves for predicting mortality in IFD infants by platelet count (PC) and plateletcrit (PCT).

<p>For each indicator, sensitivity (true positive rate) is plotted against 1-specificity (false positive rate). Accuracy is measured by the area under the ROC curve. The AUCs for PC and PCT were 0.775 (95% CI: 0.629–0.920, p = .002) and 0.765 (95% CI: 0.610–0.921, p = .006), respectively.</p

ROC analysis for the prediction of IFD by platelet parameters using the cutoffs with the maximal sum of sensitivity and specificity.

<p>AUC = area under the curve</p><p>ROC analysis for the prediction of IFD by platelet parameters using the cutoffs with the maximal sum of sensitivity and specificity.</p

Birth, clinical characteristics and hematological findings in deceased versus survived IFD at the onset and 14 days after antifungal therapy in survived IFD infants.

<p>Data are presented as the number of subjects in each group, with percentages given in parentheses or mean, with SD given in parentheses.</p><p>^a<i>P</i>1 values compares the deceased IFD with the survived IFD.</p><p>^b<i>P</i>2 values compares hematological parameters at the onset day and at the 14^th day after antifungal treatment in the survived IFD.</p><p>Birth, clinical characteristics and hematological findings in deceased versus survived IFD at the onset and 14 days after antifungal therapy in survived IFD infants.</p

Demographics, clinical characteristics and hematological findings in the study population.

<p>Data are presented as the number of subjects in each group, with percentages given in parentheses or mean, with SD given in parentheses.</p><p>^a Date were collected at the onset of IFD and bacterial sepsis, or about postnatal age of 21 days for preterm control infants.</p><p>^bComparison between IFD vs preterm control <i>p</i><0.05</p><p>^cComparison between IFD vs bacterial sepsis <i>p</i><0.05</p><p>^dComparison between bacterial sepsis vs preterm control <i>p</i><0.05</p><p>Demographics, clinical characteristics and hematological findings in the study population.</p

Receiver operating characteristic curves for the diagnosis of IFD by four platelet parameters.

<p>For each indicator, sensitivity (true positive rate) is plotted against 1-specificity (false positive rate). Accuracy is measured by the area under the ROC curve. Platelet count (PC) and plateletcrit (PCT) showed better accuracy than platelet distribution width (PDW) and hemoglobin (MPV).</p

Clinical Prognosis in Neonatal Bacterial Meningitis: The Role of Cerebrospinal Fluid Protein.

Neonates are at high risk of meningitis and of resulting neurologic complications. Early recognition of neonates at risk of poor prognosis would be helpful in providing timely management. From January 2008 to June 2014, we enrolled 232 term neonates with bacterial meningitis admitted to 3 neonatology departments in Shanghai, China. The clinical status on the day of discharge from these hospitals or at a postnatal age of 2.5 to 3 months was evaluated using the Glasgow Outcome Scale (GOS). Patients were classified into two outcome groups: good (167 cases, 72.0%, GOS = 5) or poor (65 cases, 28.0%, GOS = 1-4). Neonates with good outcome had less frequent apnea, drowsiness, poor feeding, bulging fontanelle, irritability and more severe jaundice compared to neonates with poor outcome. The good outcome group also had less pneumonia than the poor outcome group. Besides, there were statistically significant differences in hemoglobin, mean platelet volume, platelet distribution width, C-reaction protein, procalcitonin, cerebrospinal fluid (CSF) glucose and CSF protein. Multivariate logistic regression analyses suggested that poor feeding, pneumonia and CSF protein were the predictors of poor outcome. CSF protein content was significantly higher in patients with poor outcome. The best cut-offs for predicting poor outcome were 1,880 mg/L in CSF protein concentration (sensitivity 70.8%, specificity 86.2%). After 2 weeks of treatment, CSF protein remained higher in the poor outcome group. High CSF protein concentration may prognosticate poor outcome in neonates with bacterial meningitis

The Effects of Bromocriptine on Preventing Postpartum Flare in Systemic Lupus Erythematosus Patients from South China

Objective. Prolactin plays an important role on the disease flare of postpartum SLE patients. 76 pregnant SLE patients were enrolled in this study to evaluate the efficacy of bromocriptine (an inhibitor of prolactin secretion) on preventing the postpartum disease relapse. Methods. Patients were randomly divided into the treatment group (bromocriptine, 2.5 mg oral, twice a day for 14 days after delivery) and the control group. All the patients were followed up for 12 months. Clinical features were recorded every 4 weeks. Serum prolactin and estradiol levels were measured at the second week and the second month after delivery. The endpoint of the study was disease relapse and defined when SLEDAI score increased by ≥3 points from the antenatal baseline. Results. (1) Serum levels of prolactin and estradiol decreased significantly in bromocriptine treatment group at the second week (P<0.001) and second month (P<0.05) after delivery compared to control group. (2) The relapse rate of the treatment group was lower than the control group (χ2=4.68, P=0.0305). Conclusions. Two weeks of oral bromocriptine treatment in postpartum SLE patients may relieve the disease from hyperprolactinemia and hyperestrogenemia and may be beneficial in preventing the patients from disease relapse