Lymphangioleiomyomatosis and pregnancy: a mini-review.

Lymphangioleiomyomatosis(LAM) is a slow progressive, rare cystic lung disease in women of reproductive age, associated with infiltration of the lung by atypical smooth muscle like cells, leading to the cystic destruction of the lung parenchyma. As LAM exclusively affects women of childbearing age, it can arise or exacerbate during pregnancy. Many patients with LAM are discouraged from pregnancy, although there is not much objective evidence effect on fertility. Patients diagnosed with LAM during pregnancy experience worse outcomes, so the safety of pregnancy is a vexing problem. What was worse, treatment strategies are limited on the effects of LAM on pregnancy outcomes. Pregnancy could be considered in LAM patients. Successful delivery in women with LAM depends on the condition of the LAM, which is in turn dependent on obstetricians and respiratory physicians. In this review, we describe the epidemiology, pathogenesis, diagnosis, clinical features and the treatment strategies of LAM during pregnancy.

In situ copper faceting enables efficient CO2/CO electrolysis.

The copper (Cu)-catalyzed electrochemical CO2 reduction provides a route for the synthesis of multicarbon (C2+) products. However, the thermodynamically favorable Cu surface (i.e. Cu(111)) energetically favors single-carbon production, leading to low energy efficiency and low production rates for C2+ products. Here we introduce in situ copper faceting from electrochemical reduction to enable preferential exposure of Cu(100) facets. During the precatalyst evolution, a phosphate ligand slows the reduction of Cu and assists the generation and co-adsorption of CO and hydroxide ions, steering the surface reconstruction to Cu (100). The resulting Cu catalyst enables current densities of > 500 mA cm-2 and Faradaic efficiencies of >83% towards C2+ products from both CO2 reduction and CO reduction. When run at 500 mA cm-2 for 150 hours, the catalyst maintains a 37% full-cell energy efficiency and a 95% single-pass carbon efficiency throughout.

Inhibition of spinal Rac1 attenuates chronic inflammatory pain by regulating the activation of astrocytes.

BACKGROUND: Spinal astrocyte-mediated neuroinflammation is an important mechanism for the maintenance of chronic inflammatory pain. Previous studies have investigated that Ras-related C3 botulinum toxin substrate 1 (Rac1) is closely related to astrocyte activation after central nervous system injury. However, the role of Rac1 in astrocyte activation in chronic inflammatory pain has not been reported. METHODS: Complete Freund's adjuvant (CFA)-induced chronic inflammatory pain model and LPS-stimulated astrocytes were used to investigate the role of Rac1 in astrocyte activation and the underlying mechanism. Rac1-interfering adeno-associated virus (AAV) targeting astrocytes was delivered to spinal astrocytes by intrathecal administration and a Rac1 specific inhibitor, NSC23766, was used to block cultured astrocytes. The glial fibrillary acidic protein (GFAP), proinflammatory cytokines, p-NF-κB, and nod-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome were detected by RT-qPCR, Western blotting, and immunofluorescence to investigate the activation of astrocytes. RESULTS: CFA induced spinal astrocyte activation and increased the expression of active Rac1 in spinal astrocytes. Knockdown of astrocyte Rac1 alleviated chronic inflammatory pain and inhibited astrocyte activation. Inhibition of Rac1 activation in cultured astrocytes decreased the expression of GFAP and proinflammatory cytokines. Knockdown of Rac1 inhibited the increase of expression of NLRP3 inflammasome and phosphorylation of NF-κB in the spinal lumbar enlargement after CFA injection. Similarly, the inhibition of Rac1 suppressed the increase of NLRP3 inflammasome and p-NF-κB protein level after LPS stimulation. CONCLUSION: Knockdown of astrocyte Rac1 attenuated CFA-induced hyperalgesia and astrocyte activation possibly by blocking the expression of NLRP3 inflammasome and phosphorylation of NF-κB.

Effects of different fractions of inspired oxygen on gas embolization during hysteroscopic surgery: A double-blind, randomized, controlled trial.

OBJECTIVE: Gas embolism is a common complication of hysteroscopic surgery that causes serious concern among gynecologists and anesthesiologists due to the potential risk to patients. The factors influencing gas embolism in hysteroscopic surgery have been extensively studied. However, the effect of the oxygen concentration inhaled by patients on gas embolism during hysteroscopic surgery remains elusive. Therefore, we designed a double-blind, randomized, controlled trial to determine whether different inhaled oxygen concentrations influence the occurrence of gas embolism during hysteroscopic surgery. METHODS: This trial enrolled 162 adult patients undergoing elective hysteroscopic surgery who were randomly divided into three groups with inspired oxygen fractions of 30%, 50%, and 100%. Transthoracic echocardiography (four-chamber view) was used to evaluate whether gas embolism occurred. Before the start of surgery, the four-chamber view was continuously monitored. RESULTS: The number of gas embolisms in the 30%, 50%, and 100% groups was 36 (69.2%), 30 (55.6%), and 24 (44.4%), respectively. The incidence of gas embolism gradually decreased with increasing inhaled oxygen concentration (P = 0.031). CONCLUSION: In hysteroscopic surgery, a higher oxygen concentration inhaled by patients may reduce the incidence of gas embolism, indicating that a higher inhaled oxygen concentration, especially 100%, could be recommended for patients during hysteroscopic surgery. TRIAL REGISTRATION: Chinese Clinical Trial Registry (https://www.chictr.org.cn/showproj.html?proj=53779, Registration number: ChiCTR2000033202).

Airway Management of Esophageal Atresia and Tracheoesophageal Fistula Combined with Anal Atresia.

Esophageal atresia (EA) associated with tracheoesophageal fistula (TEF) is a common congenital airway anomaly and may be associated with other gastrointestinal abnormalities. Neonates with EA/TEF are at high risk of gastrointestinal distension due to the shunting of air via the fistula, leading to progressive diaphragmatic elevation and regurgitation of the gastrointestinal contents. EA/TEF associated with anal atresia in a neonate makes airway management even more challenging particularly when managed for the repair of TEF through thoracotomy. Here, we report a case where we succeeded in conducting the flexible bronchoscopy insertion through a laryngeal mask to block the fistula by bronchial blocker under spontaneous breathing.

Norepinephrine versus phenylephrine infusion for preventing postspinal hypotension during cesarean section for twin pregnancy: a double-blinded randomized controlled clinical trial.

BACKGROUND: Compared with singleton pregnancy, twin gestation is featured by a greater increase in cardiac output. Therefore, norepinephrine might be more suitable than phenylephrine for maintaining blood pressure during cesarean section for twins, as phenylephrine causes reflex bradycardia and a resultant decrease in cardiac output. This study was to determine whether norepinephrine was superior to phenylephrine in maintaining maternal hemodynamics during cesarean section for twins. METHODS: Informed consent was obtained from all the patients before enrollment. In this double-blinded, randomized clinical trial, 100 parturients with twin gestation undergoing cesarean section with spinal anesthesia were randomized to receive prophylactic norepinephrine (3.2 µg/min) or phenylephrine infusion (40 µg/min). The primary outcome was the change of heart rate and blood pressure during the study period. The secondary outcomes were to compare maternal complications, neonatal outcomes, Apgar scores and umbilical blood acid-base status between the two vasopressors. RESULTS: There was no significant difference observed for the change of heart rate between two vasopressors. The mean standardized area under the curve of heart rate was 78 ± 12 with norepinephrine vs. 74 ± 11 beats/min with phenylephrine (mean difference 4.4, 95%CI - 0.1 to 9.0; P = .0567). The mean standardized area under the curve of systolic blood pressure (SBP) was significantly lower in parturients with norepinephrine, as the mean of differences in standardized AUC of SBP was 6 mmHg, with a 95% CI from 2 to 9 mmHg (P = .0013). However, requirements of physician interventions for correcting maternal hemodynamical abnormalities (temporary cessation of vasopressor infusion for reactive hypertension, rescuing vasopressor bolus for hypotension and atropine for heart rate less < 50 beats/min) and neonatal outcomes were also not significantly different between two vasopressors. CONCLUSION: Infusion of norepinephrine was not associated with less overall decrease in heart rate during cesarean section for twins, compared with phenylephrine. TRIAL REGISTRATION: Chinese Clinical Trial Registry ( ChiCTR1900021281 ).

Interaction between astrocytic colony stimulating factor and its receptor on microglia mediates central sensitization and behavioral hypersensitivity in chronic post ischemic pain model.

Accumulation of microglia occurs in the dorsal horn in the rodent model of chronic post ischemic pain (CPIP), while the mechanism how microglia affects the development of persistent pain largely remains unknown. Here, using a rodent model of CPIP induced by ischemia-reperfusion (IR) injury in the hindpaw, we observed that microglial accumulation occurred in the ipsilateral dorsal horn after ischemia 3h, and in ipsilateral and contralateral dorsal horn in the rats with ischemia 6h. The accumulated microglia released BDNF, increased neuronal excitability in dorsal horn, and produced pain behaviors in the modeled rodents. We also found significantly increased signaling mediated by astrocytic colony-stimulating factor-1 (CSF1) and microglial CSF1 receptor (CSF1R) in dorsal horn in the ischemia 6h modeled rats. While exogenous M-CSF induced microglial activation and proliferation, BDNF production, neuronal hyperactivity in dorsal horn and behavioral hypersensitivity in the naïve rats, inhibition of astrocytic CSF1/microglial CSF1R signaling by fluorocitric or PLX3397 significantly suppressed microglial activation and proliferation, BDNF upregulation, and neuronal activity in dorsal horn, as well as the mechanical allodynia and thermal hyperalgesia, in the rats with ischemia 6h. Collectively, these results demonstrated that glial CSF1/CSF1R pathway mediated the microglial activation and proliferation, which facilitated the nociceptive output and contributed to the chronic pain induced by IR injury.

Inhibition of interleukin-6 function attenuates the central sensitization and pain behavior induced by osteoarthritis.

Chronic pain is the most prominent and disabling symptom in the patients with osteoarthritis (OA), and the underlying mechanism largely remains unclear. Interleukin-6 (IL-6), a proinflammatory cytokine, is critically involved in the development and maintenance of central sensitization in several rodent models of chronic pain. The present study aims to elucidate the IL-6 mediated neurological adaptation in dorsal horn in the rat with monosodium iodoacetate (MIA) - induced OA. Significant upregulation of IL-6 expression was detected in the dorsal horn in the modeled rats. Blockade of IL-6 function by tocilizumab markedly suppressed the activation of astrocytes and microglia in the ipsilateral dorsal horn, reduced c-Fos immunoreactivity in dorsal horn neurons, and attenuated the upregulation of glutamate receptor subunits GluR1 and NR2B in dorsal horn in the rats with MIA-induced OA. It was further reported that administration of tocilizumab significantly improved the performance in weight-bearing test and mitigated the mechanical allodynia in the modeled rats. These data illustrated spinal IL-6 mediated mechanism underlying the chronic pain, and proposed the potential therapeutic effect of tocilizumab on the chronic pain in the setting of OA.

[Cariporide Pretreatment Attenuates Lung Ischemia-Reperfusion Injury in Rabbits].

OBJECTIVE: To explore the effects of selective Na+/H+ exchanger antagonist Cariporide on ischemia-reperfusion induced lung injury. METHODS: Twenty four New Zealand White rabbits with lung ischemia-reperfusion model were established and randomly divided into four groups (n=6 per group) including sham group (S group), ischemia-reperfusion group (IR group), low potassium dextran group (LPD group) and Cariporide group (HOE group). Blood and lung tissue samples were obtained for blood gas, biochemical analyses and histologic examination. RESULTS: Systemic administration of HOE increased oxygenation index (arterial oxygen tension/fraction of inspire oxygen, PaO2/FiO2) and superoxide dismutase (SOD) activities, while decreased malondialdehyde (MDA) contents, proinflammatory cytokines and natrium hydrogen exchanger-1 (NHEI) expressions, along with the reduction of lung water content (LWC) except for histologic evaluation scores (P< 0. 05, versus IR group and LPD group). CONCLUSION: Systemic administration of Cariporide before ischemia could protects the lung from ischemia-reperfusion injury via decreasing NHE1 expression. The protective effect seems to be closely related to regulating intracellular calcium overload, oxidative damage and antioxidant enzyme activities and neutrophil infiltration.