金属对金属大头径微创全髋关节置换术治疗青中年股骨头坏死的临床研究

目的探讨金属对金属（金对金）大头径假体微创全髋关节置换术（THA）治疗青中年股骨头坏死Ⅲ、Ⅳ期的临床疗效。方法本组32例（35髋）青中年股骨头缺血性坏死Ⅲ、Ⅳ期患者,年龄24～59岁,平均45岁,术前髋关节Harris评分平均（37．9±7．5）分;以改良后外侧小切口、肌间隙人路、充分保留关节动力性组织结构为特征的金对金大头径微创THA治疗。术中严格采取正确的假体植入技术,术中保留完整的软骨下骨和髋臼横韧带,击入臼杯时一次性安装成功,正确运用万古霉素预防感染。术后口服利伐沙班片抗凝,术后12h开放负压引流及卧床行功能锻炼,术后第2天拔除引流管后扶拐下地部分负重行走,术后2—3周患者即可弃拐完全负重行走。结果本组32例35髋患者均获随访,随访时间为12个月～6年,平均为4年。所有患者切口均一期愈合,无深静脉血栓形成、关节脱位、坐骨神经损伤、髋臼及股骨疲劳骨折、关节疼痛等严重并发症,X线片示髋关节假体位置均良好,无松动、移位、股骨柄下沉、假体周围骨折等表现。末次随访Harris评分由术前平均（37．9±7．5）分,提高至术后平均（92．2±4．6）分,前后比较有统计学意义（t=44．341,P〈0．05）。所有患者末次随访时髋关节功能明显优于术前,均对治疗效果满意,完全恢复正常生活及工作。结论采用金对金大头径微创THA治疗青中年股骨头坏死Ⅲ、Ⅳ期患者,能够明显降低手术风险,缩短卧床时问,迅速恢复髋关节功能,减少手术并发症,取得了满意的近期临床疗效。随着基础和临床研究的不断深入,金对金大头径髋关节假体的长期疗效还需要进一步探讨。     

In vitro evaluation of residual procoagulants in human intravenous immunoglobulins from 11 Chinese blood fractionation companies

Introduction

Residual procoagulants has been suggested to play an important role in the occurrence of thromboembolic events with intravenous immunoglobulin.

Objective

This study investigated the predominant plasma proteases in 81 intravenous immunoglobulin lots from 11 Chinese manufacturers to examine the procoagulants of these human therapeutic intravenous immunoglobulin products.

Methods

In one-stage clotting assays, the procoagulant activities of factors II, VII, IX, X, XI, and XII were quantified. Non-activated partial thromboplastin time and a modified thrombin generation test served as global and activated coagulation factor XI specific clotting assays, respectively.

Results

The coagulation factor clotting activities of the 78 intravenous immunoglobulin lots were below the detection limit of the assays. The time to peak of thrombin generation using a thrombin generation test was longer than 35 min. The relevant amount of activated coagulation factor XI was below 0.37 nM. Non-activated partial thromboplastin time was greater than 203 s, except for the three pilot samples of manufacturer B in which we observed 0.48 to 0.09 IU/mL factor XI lever, 20 to 26 min for the time to peak of thrombin generation, 0.54 to 37.99 nM activated coagulation factor XI, and 155 to 182 s for non-activated partial thromboplastin time.

Conclusions

The three intravenous immunoglobulin lots from manufacturer B showed significant procoagulant potential. Further study is required to determine whether a program for activated coagulation factor XI determination in intravenous immunoglobulin products should be launched in China.     

Functional neuroimaging studies of bipolar disorder: Examining the wide clinical spectrum in the search for disease endophenotypes

Bipolar disorder (BP) is among the top ten most disabling illnesses worldwide. This review includes findings from recent studies employing functional neuroimaging to examine functional abnormalities in neural systems underlying core domains of the psychopathology in BP: emotion processing, emotion regulation and executive control, and common comorbid features of BP, that are relevant to the wide spectrum of BP rather than focused on the more traditional BPI subtype, and that may facilitate future identification of diagnostically-relevant biomarkers of the disorder. In addition, an emerging number of studies are reviewed that demonstrate the use of neuroimaging to elucidate biomarkers whose identification may help to (1) identify at-risk individuals who will subsequently develop the illness to facilitate early intervention, (2) identify targets for treatment and markers of treatment response. The use of newer neuroimaging techniques and potential confounds of psychotropic medication upon neuroimaging findings in BP are also examined. These approaches will help to improve diagnosis and the mental well-being of all individuals with BP.     

Genetic association study of glucocerebrosidase gene L444P mutation in essential tremor and multiple system atrophy in mainland China

The glucocerebrosidase (GBA) gene mutation is emerging as an important risk factor for Parkinson’s disease. We previously reported that the GBA gene L444P mutation is an important risk factor for PD in the Chinese population. The prevalence of this mutation in other neurodegenerative diseases and movement disorders remains completely unexplored in mainland China. In the present study, we extended the screening of GBA gene L444P mutation to Chinese patients with essential tremor (ET) and multiple system atrophy (MSA). We searched for the GBA gene L444P mutation in 109 patients with ET, 54 patients with MSA, and 657 controls from mainland China. None of the 109 patients with ET or 54 patients with MSA carried the GBA gene L444P mutation. Among the 657 controls, we found one L444P heterozygote. The difference in mutation frequencies between patients with ET or MSA and the control group was not statistically significant (chi-squared test, p = 1, respectively). The results suggest that the GBA gene L444P mutation may be not responsible for ET in mainland China. Whether the GBA gene L444P mutation modifies the risk for MSA deserves further study in larger samples.     

Resection or multi-lobe disconnection for intractable epilepsy with open-lip schizencephaly

The surgical treatment of medication-resistant epilepsy with schizencephaly is difficult. A standardized method of surgical treatment for schizencephalic patients has not yet been established. We present two patients with poorly controlled epilepsy with schizencephaly. The first patient underwent a resection of the right temporal lobe and part of the posterior lip of the schizencephaly, while the other patient underwent a multi-lobe disconnection. Based on the study of these two patients, we conclude that the location of the epileptic zone, reorganization of eloquent areas and anatomical characteristics of the schizencephaly do not allow a universal surgical approach for treating epilepsy with schizencephaly. Every patient has individual characteristics.     

Saturable Leptin Transport Across the BBB Persists in EAE Mice

We have shown that mice with experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, have upregulated leptin receptor expression in reactive astrocytes of the hippocampus, a region involved in sickness behavior. Leptin can exacerbate EAE when its serum concentration is high. Although leptin receptors in astrocytes modulate leptin transport across cultured endothelial cell monolayers, it is not known how leptin transport in EAE mice is regulated. Here, we determined brain and cervical spinal cord uptake of leptin in early and recovery stages of EAE, after either intravenous delivery or in situ brain perfusion of ¹²⁵I-leptin and the vascular marker ¹³¹I-albumin. While increased vascular space and general blood–brain barrier (BBB) permeability after EAE were expected, the specific saturable transport system for leptin crossing the BBB also persisted. Moreover, there was upregulation of leptin transport in hippocampus and cervical spinal cord in the early stage of EAE, shown by higher leptin uptake in these regions and by competitive inhibition with coadministered excess unlabeled leptin. We conclude that EAE induced a time- and region-specific increase of leptin transport. The results provide a link between circulating leptin and enhanced leptin signaling that may play a crucial role in disease progression.     

Hypersomnolence and Reduced Activity in Pan-Leptin Receptor Knockout Mice

Excessive obesity correlates with hypersomnolence and impaired cognitive function, presumably induced by metabolic factors and cytokines. Production of the adipokine leptin correlates with the amount of adiposity, and leptin has been shown to promote sleep. To determine whether leptin plays a major role in the hypersomnolence of obesity, we measured sleep architecture in pan-leptin receptor knockout (POKO) mice that do not respond to leptin because of the production of a mutant, non-signaling receptor. The obese POKO mice had more non-rapid eye movement (NREM) sleep and less waking time than their littermate controls. This was mainly seen during the light span, although increased bouts of rapid eye movement sleep were also seen in the dark span. The increase of NREM sleep correlated with the extent of obesity. The POKO mice also had decreased locomotor activity and more immobility in the open field test, but there was no increase of forced immobility nor reduction of sucrose intake as would be seen in depression. The increased NREM sleep and reduced locomotor activity in the POKO mice suggest that it was obesity, rather than leptin signaling, that played a predominant role in altering sleep architecture and activity.     

The Expression Changes of Cystathionine-β-synthase in Brain Cortex After Traumatic Brain Injury

Cystathionine-β-synthase (CBS) catalyzes the condensation of serine with homocysteine to form cystathionine and occupies a crucial regulatory position between the methionine cycle and the biosynthesis of cysteine by transsulfuration. It was reported that CBS was a novel marker of both differentiation and proliferation for certain cell types, suggesting that CBS represents a survival-promoting protein. However, its expression and function in the central nervous system lesion are not well understood. To investigate changes of CBS after traumatic brain injury (TBI) and its possible role, mice TBI model was established by controlled cortical impact system, and the expression and cellular localization of CBS after TBI was investigated in the present study. Western blot analysis revealed that CBS was present in normal mice brain cortex. It gradually decreased, reached a valley at the third day after TBI, and then restored to basal level. Importantly, more CBS was colocalized with neuron. In addition, Western blot detection showed that the third day postinjury was also the apoptosis peak indicated by the elevated expression of caspase-3. Importantly, immunohistochemistry analysis revealed that injury-induced expression of CBS was colabeled by Bcl-2 and had no co-localization with caspase-3. These data suggested that CBS may be implicated in the apoptosis of neuron and involved in the pathophysiology of brain after TBI.     

Extensive removal of thallium by graphene oxide functionalized with aza-crown ether

Thallium (Tl) is a highly toxic heavy metal, and its pollution and remediation in aquatic environments has attracted considerable attention. To reduce or remove Tl pollution in the environment, various strategies have been applied. Graphene oxide (GO) has abundant oxygen-containing functional groups, indicating its high application potential for pollution remediation via methods involving binding to metal ions or positively charged organic molecules or electrostatic interaction and coordination. However, the adsorption of Tl to GO occurs via physical adsorption, for which the adsorption efficiency is low. Therefore, herein, we report a new method to effectively remove Tl pollution in water. We combined GO with aza-crown ether, which enhanced the electronegativity and ability to bind metal ions. The functionalized graphene oxide (FGO) demonstrated high efficiency through a wide pH gradient of 5–10, with a dominant Tl(i) adsorption capacity (112.21 mg g⁻¹) based on the Langmuir model (pH 9.0, adsorbent concentration of 0.8 g L⁻¹). The adsorption of Tl(i) during removal fit a pseudo-second-order kinetic model well. The mechanisms of Tl removal involve physical and chemical adsorption. In summary, our study provides a new method for the detection and treatment of Tl-containing wastewater by using FGO.

Thallium (Tl) is a highly toxic heavy metal, and its pollution and remediation in aquatic environments has attracted considerable attention.