老年妇科手术围手术期临床特点分析

目的探索老年妇科手术围手术期的临床特点。方法2001年1月至2004年3月老年妇女(年龄≥60岁)妇科手术病人50例为研究组,同期中年妇女(40～59岁)50例为对照组。监测麻醉前、达到完全阻滞平面时以及手术结束时病人的收缩压(SBP)、舒张压(DBP)、平均动脉压(MAP)、心率(HR)、血氧饱和度(SPO2)值,及术后最高体温、发热持续时间和其它并发症情况。结果两组病人达到完全阻滞平面时、手术结束时的SBP、DBP、MAP均较麻醉前显著降低(P<0.05),老年组下降幅度更大(P<0.001),而HR、SPO2及术后发热情况无明显差异。老年组术后并发症率16%,其中一例死于急性肺栓塞。中年组术后并发症率10%。结论老年妇女对妇科手术的耐受性较好,加强围手术期监护有助于提高手术的安全性。     

Operando unraveling photothermal-promoted dynamic active-sites generation in NiFe2O4 for markedly enhanced oxygen evolution

The ability to develop highly active and low-cost electrocatalysts represents an important endeavor toward accelerating sluggish water-oxidation kinetics. Herein, we report the implementation and unraveling of the photothermal effect of spinel nanoparticles (NPs) on promoting dynamic active-sites generation to markedly enhance their oxygen evolution reaction (OER) activity via an integrated operando Raman and density functional theory (DFT) study. Specifically, NiFe₂O₄ (NFO) NPs are first synthesized by capitalizing on amphiphilic star-like diblock copolymers as nanoreactors. Upon the near-infrared light irradiation, the photothermal heating of the NFO-based electrode progressively raises the temperature, accompanied by a marked decrease of overpotential. Accordingly, only an overpotential of 309 mV is required to yield a high current density of 100 mA cm⁻², greatly lower than recently reported earth-abundant electrocatalysts. More importantly, the photothermal effect of NFO NPs facilitates surface reconstruction into high-active oxyhydroxides at lower potential (1.36 V) under OER conditions, as revealed by operando Raman spectroelectrochemistry. The DFT calculation corroborates that these reconstructed (Ni,Fe)oxyhydroxides are electrocatalytically active sites as the kinetics barrier is largely reduced over pure NFO without surface reconstruction. Given the diversity of materials (metal oxides, sulfides, phosphides, etc.) possessing the photo-to-thermal conversion, this effect may thus provide a unique and robust platform to boost highly active surface species in nanomaterials for a fundamental understanding of enhanced performance that may underpin future advances in electrocatalysis, photocatalysis, solar-energy conversion, and renewable-energy production.

Motivated by the need for accelerating sluggish reaction kinetics at the anode (1, 2), the focus of water electrolysis has been centered heavily on oxygen evolution reaction (OER) toward sustainable hydrogen fuel production. To date, there has been much effort in developing low-cost yet high-performance earth-abundant transition-metal alternatives to commonly used noble metals for OER. Intriguingly, many Ni-, Co-, Fe-, and Mn-based oxides experience a dynamic surface-reconstruction process to form more active oxyhydroxides, which are recognized as true catalytically active species for OER in alkaline media (3, 4). Among various transition metal-based OER catalysts, bimetal spinel-structured oxides in the form of AB₂O₄ (A and B are different metal ions) have garnered much attention due to their rich compositions, electron configurations, and valence states (5). Interestingly, inverse spinel NiFe₂O₄ (NFO), in principle, exhibits enhanced catalytic activity toward OER because of the presence of multivalent elements (i.e., Ni³⁺/Ni²⁺ and Fe³⁺/Fe²⁺) (6). It is important to note that studies on facilitating the surface reconstruction of NFO to achieve high-performance OER are relatively few, and a fundamental understanding as to what makes the derived OER catalysts perform well remains elusive.Recently, introducing thermal energy to promote electrocatalytic conversion has attracted significant interest (7–10). The thermal energy could accelerate the motion of reactant molecules, promote their effective collisions during the reaction, and thus make it easier to overcome the activation barrier (11, 12). Moreover, the use of thermal energy could also promote the surface reconstruction of catalysts into highly active species and accelerate the electrocatalytic kinetics, thereby leading to improved efficiency (13). Electrocatalysts with photothermal effect (referred to as photothermal electrocatalysts) enable in situ heating due to photo-to-thermal conversion under illumination with visible or near-infrared (NIR) light, thereby dispensing with the need for extra devices required to provide thermal energy. More importantly, in sharp contrast to common approaches where the entire solution is heated (14), the photothermal effect is localized on electrocatalysts themselves (15), thus effectively enabling heat modulation to a defined region (i.e., the working electrode). Despite recent impressive advances in transition metal oxides (e.g., Fe₃O₄ and Co₃O₄) as photothermal agents for cancer therapy (15), their implementations for photothermal-assisted OER, in particular spinel oxides, are comparatively few and limited in scope. Moreover, it has been reported that Ni- and Co-based OER catalysts are prone to surface reconstruction into highly active oxyhydroxides (16, 17). Surprisingly, the photothermal effect on promoting surface reconstruction in spinel oxide catalysts has yet to be explored.Herein, we report an integrated operando Raman and density functional theory (DFT) plus Hubbard U (DFT + U) study to exercise and unveil the photo-to-thermal conversion of inverse spinel oxide nanoparticles (NPs) in promoting the generation of dynamic active sites via surface reconstruction into oxyhydroxides and thus greatly enhancing their OER activity. First, a series of amphiphilic star-like poly(acrylic acid)-block-poly(styrene-co-acrylonitrile) (denoted PAA-b-PSAN) diblock copolymers with a well-defined molecular weight (MW) and low polydispersity index (PDI) are exploited as nanoreactors to synthesize a set of PSAN-ligated NFO NPs with different sizes and PSAN chain lengths. The effects of the NFO NP sizes and the outer PSAN chain lengths on catalytic activity of NFO NPs are then scrutinized. Interestingly, NFO NPs of the largest size (∼12 nm) ligated with the shortest PSAN chains (M_n = 7K) display the best OER reactivity on a glassy carbon (GC) electrode in alkaline media as a result of the high fraction of the exposed electrochemically active surface area and the fastest electrocatalytic kinetics. Subsequently, the photothermal effect of PSAN-ligated NFO NPs is exploited to promote their surface reconstruction and thus boost OER. More importantly, an operando Raman spectroelectrochemistry study is performed to unveil the mechanism of photothermal-assisted enhancement in OER reaction, revealing the emergence of electrocatalytically active γ-NiOOH at a lower potential (1.36 V) during the surface-reconstruction process with a photothermal effect. Finally, the first-principle calculations substantiate that the reconstructed surface, i.e., (Ni,Fe)oxyhydroxides, plays a pivotal role as the active site for electrocatalytic reaction. As such, photothermal electrocatalysts (e.g., metal oxides, sulfides, phosphides, etc.) may render significantly low overpotential and fast OER kinetics, representing an array of important materials that couple the localized heating with electrochemistry for effective renewable-energy production.     

Developmental synaptic regulator,TWEAK/Fn14 signaling,is a determinant of synaptic function in models of stroke and neurodegeneration

Identifying molecular mediators of neural circuit development and/or function that contribute to circuit dysfunction when aberrantly reengaged in neurological disorders is of high importance. The role of the TWEAK/Fn14 pathway, which was recently reported to be a microglial/neuronal axis mediating synaptic refinement in experience-dependent visual development, has not been explored in synaptic function within the mature central nervous system. By combining electrophysiological and phosphoproteomic approaches, we show that TWEAK acutely dampens basal synaptic transmission and plasticity through neuronal Fn14 and impacts the phosphorylation state of pre- and postsynaptic proteins in adult mouse hippocampal slices. Importantly, this is relevant in two models featuring synaptic deficits. Blocking TWEAK/Fn14 signaling augments synaptic function in hippocampal slices from amyloid-beta–overexpressing mice. After stroke, genetic or pharmacological inhibition of TWEAK/Fn14 signaling augments basal synaptic transmission and normalizes plasticity. Our data support a glial/neuronal axis that critically modifies synaptic physiology and pathophysiology in different contexts in the mature brain and may be a therapeutic target for improving neurophysiological outcomes.

Neural circuit patterning, refinement, and plasticity are enabled by the dynamic strengthening, weakening, and pruning of chemical synapses in response to circuit activity. However, synapse loss and reduced plasticity are early hallmarks of chronic neurological disorders such as autism, schizophrenia and Alzheimer’s disease (AD) (1–3). It is therefore hypothesized that the underlying molecular mechanisms of pruning, although normally balanced in health, are dysregulated in disease. Particularly interesting is the notion that the mechanisms responsible for the reduction in functional synapses in disease reflect the aberrant reactivation of pathways important for synapse elimination in development. For example, in an AD model, synapse elimination was shown to be mediated by the complement pathway in the hippocampus (HC), reflecting aberrant reactivation of complement-dependent synapse elimination that occurs in the dorsal lateral geniculate nucleus (dLGN) of the thalamus during visual development (4). In such a paradigm, the reactivation of developmental mechanisms enables pathways that can act universally across different ages, circuits, and brain regions. Thus, the mechanisms underlying normal circuit development and their potential reactivation as key contributors to neurological diseases are areas of deep interest.In addition to chronic neurological disorders, circuitry changes also occur in acute ischemic stroke, the second leading cause of death worldwide and a cause of debilitating long-term disability. Interruptions in blood flow that deprive neurons of oxygen and nutrients result in significant cell death, followed by deficits in neurophysiological activity that are associated with poor motor recovery (5). Remarkably, the adult brain can undergo some degree of spontaneous poststroke recovery, apparently by engaging neuroplasticity mechanisms including remapping, synaptogenesis, and synaptic strengthening (5, 6). Despite these adaptations, over half of ischemic stroke patients fail to recover completely and continue to experience persistent long-term disability (7). The underlying signaling pathways that regulate synaptic physiology after stroke are an active topic of investigation.TNF-like weak inducer of apoptosis (TWEAK) protein, originally discovered as a cytokine produced by macrophages (8), signals through its injury-inducible transmembrane receptor, FGF-inducible molecule-14 (Fn14) (9). Consequently, the function of TWEAK/Fn14 signaling was elucidated as a driver of tissue remodeling in contexts of injury and disease in a variety of organ systems (10). Recently, findings have suggested a role for the TWEAK/Fn14 pathway in the central nervous system (CNS). Namely, several compelling observations indicate that TWEAK signaling through Fn14 might be a key molecular modulator of synaptic function in contexts of neurological challenge. TWEAK and Fn14 are up-regulated in the CNS in AD (11, 12, 13 and SI Appendix, Fig. S6A) and after ischemic stroke in humans and mice (14–16). Importantly, TWEAK/Fn14 signaling was also recently shown to be a pathway necessary for synapse maturation during experience-dependent visual development. Light-induced up-regulation of Fn14 in thalamocortical excitatory neurons and corresponding up-regulation of TWEAK in microglia mediate the elimination of weak synapses and strengthening of remaining synapses in the dLGN (17, 18). Indeed, the communication between neurons and supporting microglia has emerged as a key mechanism regulating neuronal circuitry, with microglia deploying their ramified processes to continuously survey and refine synapses in response to neural activity. Interestingly, TWEAK expression has also been shown to be microglia-enriched in the mouse cortex (19), suggesting that it may play a role in multiple brain regions. Thus, like the complement pathway, the TWEAK/Fn14 pathway could be an important regulator of synapse biology in visual development which is re-engaged and acts generally in different ages and brain regions to contribute to pathology.The involvement of TWEAK/Fn14 signaling in synapse physiology or pathophysiology outside of the developing visual system is unknown. We considered it to be a strong candidate modifier of synaptic function in adults given that Fn14 is up-regulated and required for synaptic refinement in experience-dependent visual development, and TWEAK and Fn14 are up-regulated in contexts of neurological injury/disease, suggesting that the TWEAK/Fn14 system is tuned to periods of substantial change in neuronal activity levels or environment (e.g., eye opening, ischemic stroke). We employed HC slices to test the hypothesis that the TWEAK/Fn14 pathway regulates synaptic function in adult mice and in different disease contexts and delineate its mechanism of action. Herein, we reveal that TWEAK, through neuronal Fn14, mediates acute dampening of basal synaptic transmission and synaptic plasticity in hippocampal slices from mature mice. Furthermore, we demonstrate that TWEAK/Fn14 signaling broadly impacts the phosphorylation state of critical synaptic proteins, suggesting a general role in synapse modulation. Finally, we show that pathway deficiency or pharmacological inhibition of TWEAK/Fn14 signaling augments synaptic transmission and plasticity in amyloid-beta (Aβ)–overexpressing mice and post ischemic stroke animals, two model systems featuring synaptic functional deficits. Thus, our results support that TWEAK/Fn14 constitutes a synaptic regulatory pathway with therapeutic potential for CNS disorders in the adult brain.     

Role of medical thoracoscopy in the treatment of tuberculous pleural effusion

Background

Fibrous tuberculous pleural effusion (TPE) represents common disease in tuberculous clinic. Medical thoracoscopy has been used to treat pleural empyema and shown promising outcomes, but data of its use in multiloculated and organized TPE remains limited to know.

Methods

The study was performed on 430 cases with TPE. The cases were divided into free-flowing, multiloculated effusion and organized effusion group. Each group was subdivided into two or three types of therapeutic approaches: ultrasound guided pigtail catheter, large-bore tube chest drainage and medical thoracoscopy. Patients with multiloculated or organized effusions received streptokinase, introduced into the pleural cavity via chest tubes. The successful effectiveness of the study was defined as duration of chest drainage, time from treatment to discharge days and no further managements.

Results

Patients with organized effusion were older than those with free-flowing effusion and incidence of organized effusion combined with pulmonary tuberculosis (PTB) was higher than those of multiloculated effusion and free-flowing effusion respectively. Positive tuberculosis of pleural fluid culture was higher in organized effusion than that in free-flowing effusion. Sputum positive for acid-fast bacillus (AFB) in organized effusion was higher than that in multiloculated effusion and free-flowing effusion. Medical thoracoscopy showed significant efficacy in the group of multiloculated effusion and organized effusion but free-flowing effusion. No chronic morbidity and mortality related to complications was observed.

Conclusions

Medical thoracoscopy was a safe and successful method in treating multiloculated and organized TPE.     

止血镇痛冰块的研制及临床应用效果观察

目的 寻找扁桃体摘除术后局部止血镇痛的有效方法。方法 自行研制了止血镇痛冰块(下称药冰)。100例扁桃体摘除术后患者(观察组)术后2小时起含化药冰,每1～2小时1次,每日8～12次;对照组(50例同期行扁桃体摘除术的患者)术后2小时舌根部含化冰淇淋或雪糕。观察两组术后出血疼痛、伤口愈合等情况。结果 观察组术后疼痛明显减轻,24小时出血量少,进食情况较好,与对照组相关指标比较,P均<0.01。结论药冰制作简单、价格低廉、无异味,止血、镇痛、促伤口愈合效果可靠,优于传统方法。     

Peer environment mediates parental history and individual risk in the etiology of cannabis use disorder in boys: a 10-year prospective study

Previous research has shown that a trait termed neurobehavior disinhibition (ND) measured in childhood predicts substance use disorder by young adulthood. The present investigation extends these findings by determining the degree to which peer environment mediates the association between ND and development of cannabis use disorder (CUD). ND was measured in a sample of 216 boys 10-12 years of age. The peer environment was assessed at age 16. Current CUD was determined at age 22. Paternal and maternal SUD predicted son's ND which, in turn, predicted son's peer environment and, subsequently, son's cannabis use frequency and CUD. Peer environment mediated the association between ND and cannabis use and ND and CUD. Maternal and paternal SUD predicted the peer environment. Parental SUD, son's ND, and son's peer environment predicted CUD at age 22 with 84% accuracy.     

Distinct architecture and composition of mouse axonemal radial spoke head revealed by cryo-EM

The radial spoke (RS) heads of motile cilia and flagella contact projections of the central pair (CP) apparatus to coordinate motility, but the morphology is distinct for protozoa and metazoa. Here we show the murine RS head is compositionally distinct from that of Chlamydomonas. Our reconstituted murine RS head core complex consists of Rsph1, Rsph3b, Rsph4a, and Rsph9, lacking Rsph6a and Rsph10b, whose orthologs exist in the protozoan RS head. We resolve its cryo-electron microscopy (cryo-EM) structure at 3.2-Å resolution. Our atomic model further reveals a twofold symmetric brake pad-shaped structure, in which Rsph4a and Rsph9 form a compact body extended laterally with two long arms of twisted Rsph1 β-sheets and potentially connected dorsally via Rsph3b to the RS stalk. Furthermore, our modeling suggests that the core complex contacts the periodic CP projections either rigidly through its tooth-shaped Rsph4a regions or elastically through both arms for optimized RS–CP interactions and mechanosignal transduction.

The majority of motile cilia and flagella are composed of nine dynein arm-containing peripheral doublet microtubules (DMTs) surrounding a central pair (CP) of MTs (the “9+2” axoneme). The radial spoke (RS) is a T-shaped protein complex with an orthogonal head pointing toward the CP and a stalk anchored on each A-tubule of the DMTs (1–5). It acts as the mechanochemical transducer between the CP and axonemal dynein arms to regulate flagellar/ciliary motility (6–11). The flagella of Chlamydomonas reinhardtii, a widely used model organism, contain two full-size RSs (RS1 and RS2) in each 96-nm repeat unit of the axoneme. In contrast, motile cilia/flagella of Tetrahymena thermophila and metazoa possess triplet RSs (RS1 to RS3) (2–4, 11). The Chlamydomonas RS is composed of at least 23 subunit proteins (RSP1 to RSP23) (2, 12, 13). Seventeen of them have mammalian homologs (14). Mutations leading to the loss of the entire RS or RS head result in immotile flagella in Chlamydomonas (6–8) but in rotatory ciliary beat in mammals, causing primary ciliary dyskinesia (PCD), a genetic syndrome characterized by recurrent respiratory infections, situs inversus, infertility, and hydrocephalus (4, 15–21).The most striking morphological differences in the RS lie in the RS head, the key structural domain that mediates the mechanosignaling by directly contacting projections of the CP (9–11). The heads of RS1 and RS2 consist of two structurally identical, rotationally symmetric halves that differ largely from that of RS3 (3, 4). Furthermore, their morphologies differ dramatically between protozoa and metazoa. In Chlamydomonas and Tetrahymena, for instance, the heads of RS1 and RS2 are rich in lateral branches that also form a connection between the two heads (2, 4). In contrast, in sea urchin (Strongylocentrotus purpuratus) and human, the heads of RS1 and RS2 resemble a pair of ice skate blades with many fewer interfaces toward the CP (3, 4). Despite the importance of the RS and RS head in cilia/flagella motility, the structural details of the RS and the RS–CP interactions remain poorly understood, especially in mammals.The RS heads have probably been remodeled to comply with both structural and functional alterations of the axoneme during evolution. How the morphological changes occurred, however, remains unclear. The Chlamydomonas RS head is composed of RSP1, -4, -6, -9, and -10 and part (the C terminus) of the stalk component, RSP3. Each of the symmetrical halves of the head contains one copy of these components (2, 10, 22). All the head components have mammalian orthologs (Rsph1, -4a, -6a, -9, -10b, and -3b) (11, 14). In sharp contrast to the markedly reduced surface area of metazoan RS heads, the peptides of human RSPH4A, -6A, and -10B are longer than their Chlamydomonas orthologs by 1.5-, 1.3-, and 4-fold, respectively (11). Only RSPH1 (309 amino acids [aa]) is shorter than RSP1 (814 aa) (11). The lengths of mouse RS head proteins are also similarly changed as their human counterparts (SI Appendix, Fig. S1A). Furthermore, while murine Rsph4a is essential for the head formation of RS1 to RS3 in motile multicilia of the trachea, ependyma, and oviduct (15), Rsph6a is specifically expressed in sperm for their normal flagellar formation (23). RSP4/Rsph4a and RSP6/Rsph6a are paralogs: RSP4 and RSP6 share 48% sequence identity (24), whereas murine Rsph4a is 63% identical to Rsph6a (SI Appendix, Fig. S1B). Sea urchin and Ciona, however, have only one ortholog (11, 25). These results suggest that, unlike the protozoan RS heads, the metazoan ones may not simultaneously contain Rsph4a and Rsph6a. The general shapes of the RS structure in axonemes have been determined by conventional electron microscopy (EM) (26–28) and cryo-electron tomography (cryo-ET) (2–5). Recently, a 15-Å-resolution RS structure of Chlamydomonas was resolved by cryo-EM single-particle analysis (29). The resolutions, however, do not suffice for the delineation of the locations of individual RS subunits.In the present study, by biochemical and structural analyses, we show the murine RS head is both compositionally and morphologically distinct from that of Chlamydomonas. Our study suggests that the RS head has experienced profound remodeling to probably comply with both structural and functional alterations of the axoneme during evolution for coordinated ciliary or flagellar motility.     

单克隆抗体ELISA检测班氏丝虫病人血清循环抗原

应用抗马来微丝蚴抗原4B_1株单克隆抗体(McAb)和抗马来成虫代谢抗原4B_7株McAb酶联免疫吸附试验(ELISA)检测班氏微丝蚴血症者血清中循环抗原,阳性率分别为78.46％(102/130)和87.13％(88/101);检测51例晚期丝虫病人血清,阳性率分别为3.92％和1.96％;36例经治疗后微丝蚴血症阴转者血清,阳性率分别为13.89％和8.33％。丝虫病非流行区99例肠道蠕虫感染者阳性率分别为16.16％和5.05％。结果表明抗马来成虫代谢抗原4B_7株McAb应用于诊断班氏丝虫感染的效果优于抗马来微丝螺4B_1株McAb。     

Sugar-sweetened soft drinks, diet soft drinks, and serum uric acid level: the Third National Health and Nutrition Examination Survey

OBJECTIVE: Sugar-sweetened soft drinks contain large amounts of fructose, which may significantly increase serum uric acid levels and the risk of gout. Our objective was to evaluate the relationship between sugar-sweetened soft drink intake, diet soft drink intake, and serum uric acid levels in a nationally representative sample of men and women. METHODS: Using data from 14,761 participants age>or=20 years from the Third National Health and Nutrition Examination Survey (1988-1994), we examined the relationship between soft drink consumption and serum uric acid levels using linear regression. Additionally, we examined the relationship between soft drink consumption and hyperuricemia (serum uric acid level>7.0 mg/dl for men and >5.7 mg/dl for women) using logistic regression. Intake was assessed by a food-frequency questionnaire. RESULTS: Serum uric acid levels increased with increasing sugar-sweetened soft drink intake. After adjusting for covariates, serum uric acid levels associated with sugar-sweetened soft drink consumption categories (<0.5, 0.5-0.9, 1-3.9, and >or=4 servings/day) were greater than those associated with no intake by 0.08, 0.15, 0.33, and 0.42 mg/dl, respectively (95% confidence interval 0.11, 0.73; P<0.001 for trend). The multivariate odds ratios for hyperuricemia according to the corresponding sweetened soft drink consumption levels were 1.01, 1.34, 1.51, and 1.82, respectively (P=0.003 for trend). Diet soft drink consumption was not associated with serum uric acid levels or hyperuricemia (multivariate P>0.13 for trend). CONCLUSION: These findings from a nationally representative sample of US adults suggest that sugar-sweetened soft drink consumption is associated with serum uric acid levels and frequency of hyperuricemia, but diet soft drink consumption is not.