个性化截骨工具辅助下人工全膝关节置换与传统人工全膝关节置换手术精确度及临床疗效比较

目的比较3D打印个性化截骨工具辅助(patient-specific instrumentation,PSI)下人工全膝关节置换术(total knee arthroplasty,TKA)与传统TKA的手术精确度和临床疗效。方法自2017年9月至2018年12月,将40例拟接受初次膝关节置换患者随机分为2组,每组均为20人。一组应用个性化截骨工具辅助TKA手术(PSI组),另一组接受传统TKA(对照组)。比较两组患者的冠状面下肢机械轴线、手术时间、术中出血量、术后引流量以及HSS评分。结果对照组和PSI组的手术时间分别为(103.3±18.7) min和(91.3±15.7) min;术中出血量分别为(372.0±53.0)mL和(332.8±47.0)mL;术后引流量分别为(378.8±97.2)mL和(315.0±89.0)mL。两组手术时间、术中出血量、术后引流量比较差异均有统计学意义(P0.05)。对照组和PSI组术后2周HSS评分分别为(89.3±2.8)分和(88.7±2.9)分,两组比较差异无统计学意义(P0.05)。对照组和PSI组术后全下肢力线差值分别为(1.9±1.1)°和(1.2±1.0)°,冠状面股骨假体角度(frontal femoral component angle,FFC)差值分别为(2.1±1.1)°和(1.1±0.9)°,两组比较差异有统计学意义(P0.05)。冠状面胫骨假体角度(frontal tibia component angle,FTC)差值分别为(1.3±0.8)°和(1.4±0.8)°,两组比较差异无统计学意义(P0.05)。结论PSI辅助TKA较传统TKA手术时间更短、术中出血量更少,并且术后冠状面全下肢力线及股骨力线的改善优于传统TKA手术。     

To die or not to die for neurons in ischemia,traumatic brain injury and epilepsy: a review on the stress-activated signaling pathways and apoptotic pathways

After a severe episode of ischemia, traumatic brain injury (TBI) or epilepsy, it is typical to find necrotic cell death within the injury core. In addition, a substantial number of neurons in regions surrounding the injury core have been observed to die via the programmed cell death (PCD) pathways due to secondary effects derived from the various types of insults. Apart from the cell loss in the injury core, cell death in regions surrounding the injury core may also contribute to significant losses in neurological functions. In fact, it is the injured neurons in these regions around the injury core that treatments are targeting to preserve. In this review, we present our cumulated understanding of stress-activated signaling pathways and apoptotic pathways in the research areas of ischemic injury, TBI and epilepsy and that gathered from concerted research efforts in oncology and other diseases. However, it is obvious that our understanding of these pathways in the context of acute brain injury is at its infancy stage and merits further investigation. Hopefully, this added research effort will provide a more detailed knowledge from which better therapeutic strategies can be developed to treat these acute brain injuries.     

High density of immobilized galactose ligand enhances hepatocyte attachment and function

Galactosylated surface is an attractive substrate for hepatocyte culture because of the specific interaction between the galactose ligand and the asialoglycoprotein receptor on hepatocytes. In this study, we described a scheme to achieve high density of immobilized galactose ligands on polyethylene terephthalate (PET) surface by first surface-grafting polyacrylic acid on plasma-pretreated PET film under UV irradiation, followed by conjugation of a galactose derivative (1-O-(6'-aminohexyl)-D-galactopyranoside) to the grafted polyacrylic acid chains. A high galactose density of 513 nmol/cm(2) on the PET surface was used in this study to investigate the behavior of cultured hepatocyte. This engineered substrate showed high affinity to fluorescein isothiocyanate-lectin binding. Primary rat hepatocytes, when seeded at a density of 2 x 10(5) cells/cm(2), attached to the galactosylated PET substrate at a similar efficiency compared with collagen-coated substrate. The hepatocytes spontaneously formed aggregates 1 day after cell seeding and showed better maintenance of albumin secretion and urea synthesis functions than those cultured on collagen-coated surface.     

小儿肝的年龄解剖学研究

分六个年龄组观察了180个(男98,女82)小儿肝的形态、度量、位置及体表投影.小儿肝相对较大,右叶大于左叶,下界位置较低并逐渐上移.在右锁骨中线的肋弓下一般均可触到.小儿肝重随其年龄(身高)的增长而增长,其增长速度相对较慢,尤以Ⅶ组小儿更明显.     

桡神经及其深支的血供

在25具成人尸体(50例)上,观测了桡神经及其深支的血供。桡神经的营养动脉平均为4.36±0.26支,营养动脉和来源动脉的外径平均为0.38±0.08mm和1.65±0.05mm。桡神经深支的营养动脉平均为1.72±0.16支,营养动脉和来源动脉的外径平均为0.29±0.01mm和1.91±0.07mm。     

Adhesion contact dynamics of HepG2 cells on galactose-immobilized substrates

The specific recognition between asialoglycoprotein receptor and galactose ligand at cell-substrate interfaces has been shown to mediate hepatocyte adhesion and maintain liver specific functions of hepatocytes. Conventionally, the success of hepatocyte attachment on engineered tissue scaffold is inferred from the degree of two-dimensional cell spreading that is measured by transmitted light microscopy. However, the actual contact mechanics and adhesion strength of hepatocytes during two-dimensional cell spreading has not been elucidated due to lack of biophysical probe. In this study, a novel biophysical technique known as confocal reflectance interference contrast microscopy (C-RICM) in conjunction with phase contrast microscopy is utilized to probe the adhesion dynamics, contact mechanics and two-dimensional spreading kinetics of HepG2 cells on galactose immobilized and collagen gel coated substrates. C-RICM demonstrates that HepG2 cells form strong adhesion contacts with both galactose-immobilized surfaces and collagen gel coated substrates. Moreover, HepG2 cells maintain their compact shapes in the presence of asialoglycoprotein receptor-mediated recognition while they become exceedingly spread under integrin-mediated adhesion on collagen gel coated substrate. The initial rate of adhesion contact formation and the steady-state adhesion energy of HepG2 cell population are highest on substrate conjugated with galactose ligand via a longer spacer. The adhesion dynamics and final adhesion energy of HepG2 cells depends both on the type of ligand-receptor interaction and the length of spacer between the ligand and substrate. Most importantly, new biophysical insights into the initial hepatocyte attachment that are critical for hepatocyte culture are provided through the decomposition of two-dimensional spreading and adhesion contact formation on bio-functional substrates.     

Synergistic antimicrobial effect of cefotaxime and minocycline on proinflammatory cytokine levels in a murine model of Vibrio vulnificus infection.

BACKGROUND AND PURPOSE: Vibrio vulnificus causes primary bacteremia and necrotizing wound infection, leading to high morbidity and mortality in humans. This study aimed to evaluate the antimicrobial effect of cefotaxime and minocycline on proinflammatory cytokine levels in a murine model of V. vulnificus infection. METHODS: We investigated the dynamics of proinflammatory cytokines and their modulation by antimicrobial agents using a murine model of V. vulnificus infection. The change in cytokine levels was followed over a time course to identify the antimicrobial activity of the drugs against V. vulnificus. BALB/c female mice were challenged with an intraperitoneal infection using a clinical invasive isolate of Vv05191, and their cytokine levels were assayed over various time points. RESULTS: Serum levels of tumor necrosis factor-alpha, interleukin (IL)-1 beta, and IL-6 post-infection were found to be inoculum dose-dependent and positively correlated to the subsequent fatality rate in the infected mice. With an inoculum of 6.6 x 10(6) colony-forming units and intraperitoneal administration of cefotaxime, minocycline, or both, the serum and peritoneal fluid cytokine levels increased and then declined gradually. Comparison of the 3 antimicrobial regimens revealed that the magnitude of reduction in cytokine levels was greatest in mice treated with cefotaxime-minocycline combination. Moreover, the peritoneal fluid cytokine level in the combination group was significantly lower than that in the groups treated with minocycline or cefotaxime alone. CONCLUSIONS: The current results support the superiority of the combination therapy in treating invasive V. vulnificus infections.     

Association of haplotypes in the beta-chemokine locus with multiple sclerosis

Linkage studies in multiple sclerosis (MS) identified several susceptibility loci. One of these regions includes chromosome 17q11 where a meta-analysis of data from three genome scans suggested linkage. This region encodes a cluster of genes for beta-chemokines or CC chemokine ligands (CCLs), which may be involved in the development of MS lesions. Here we aimed to test if CCL alleles and haplotypes are associated with MS. Using methods of linkage and association, we observed deviations from the expected 50% transmission of haplotypes from unaffected parents to their affected children at CCL2, CCL11-CCL8-CCL13 and CCL3 within the investigated 1.85 MB chromosomal segment. Analyses of the linkage disequilibrium map support that variants with possible relevance to MS can be located within these subregions. Identification of MS associated CCL variants may have direct clinical significance, as it can lead to the design of small competitive antagonists of these molecules with beneficial effects in the treatment of patients with early and active disease.