Indications and limitations of locked plating

The goal of fracture fixation is to achieve bone healing and restore the function of the injured limb in the shortest possible time without compromising safety. Newer technologies such as the locking compression plate (LCP) and its derivatives are valuable additions to the orthopaedic traumatologist's armamentarium. As with any emerging technology, the indications will be extended until a threshold is reached and the limitations of the technology are seen. It is vital that surgeons involved in fracture care are aware of when locked plating is superior to other methods and also when they should use another treatment modality.This paper reviews the use of locked plating as a fixation method. Five topics covered in this review are: a historical perspective on locked plating, general indications, specific modes and techniques, patterns of failure, and an anatomical overview of current indications for locked plating.     

新型纳米根管充填材料对成骨细胞生长的影响

通过体外培养的成骨细胞,采用二甲基噻唑二苯基四唑溴盐比色法和流式细胞术对新型纳米根管充填材料(nHA-PA66)作用下的成骨细胞生长情况的变化进行研究,评价其对成骨细胞生长的影响。以该材料的细胞培养基浸提液作用于实验组细胞,对照组采用培养基本身。实验组和对照组成骨细胞的生长情况和细胞周期无显著性差异,表明该新型纳米材料对成骨细胞的生长和细胞周期无不良影响。提示新型纳米根管充填材料的成骨细胞相容性较好,具有用作根充材料的基础。     

甲氧苄氨嘧啶—PVP共沉淀物的研究

本工作用差示扫描量热法(DSC)研究甲氧苄氨嘧啶与PVP溶剂法制备的共沉淀物,表明已不存在甲氧苄氨嘧啶晶体。用x射线衍射法研究了1:12共沉淀物,证明无甲氧苄氨嘧啶的晶体衍射峰。经分光光度法测定结果,1:12共沉淀物比原药的溶解度大28.3倍。     

Predicting outcome in severe heart failure. Who will benefit from device therapy (CRT)?

Dyssynchronous ventricular contraction in severe heart failurecontributes to low cardiac output, worsening symptoms, and poorprognosis. Recognition of the effect of dyssynchrony in heartfailure, and the possibility of manipulating the sequence ofelectrical cardiac activation to improve the efficiency of mechanicalevents, led Cazeau et al. to attempt four-chamber pacing in1994.¹ This early system could stimulate both atria and bothventricles extrinsically, and could dictate the temporal relationshipbetween atrial systole and ventricular systole, and the ventriculo-ventricularrelationship. Modern cardiac resynchronization therapy (CRT),involving pacing of the right and left ventricles, with rightatrial pacing to optimize atrio-ventricular delay, has evolvedrapidly from this beginning. Left bundle branch block (LBBB) on the surface electrocardiogram(ECG) has been considered a marker of mechanical dyssynchronyas it represents a delay in conduction of depolarization tothe left ventricle, with the greatest delay usually being in     

Global transcriptional profiling demonstrates the combination of type I and type II interferon enhances antiviral and immune responses at clinically relevant doses.

A role for type II interferon (IFN-gamma) in resolving viral infection is suggested by the correlation of hepatitis C virus (HCV) clearance with enhancement of IFN-gamma-producing activated T cells in the resolution of acute HCV infection. Using vesicular stomatitis virus (VSV), a synergistic direct antiviral effect was documented using IFN-gamma1b and a potent, consensus type I IFN (IFN alfacon-1). Global expression profiling following EC50 exposure to IFN alfacon-1, IFN-gamma1b, or a cocktail of the two allowed the antiviral state to be correlated with induction of a subset of IFN-stimulated genes (ISGs). Genes identified through this analysis corresponded to classic antiviral components, ISGs more recently associated with direct antiviral functions, as well as expressed sequence tags (ESTs) and hypothetical proteins. The magnitude of these antiviral EC50-correlated expression events in human hepatoma (Huh7) cells exposed to clinically relevant doses of IFN alfacon-1, IFN-gamma1b, or a cocktail of the two was also probed because the standard of care for patients with chronic hepatitis C is type I IFN-containing regimens. Relative to type I IFNs used alone, the addition of type II IFN caused enhanced expression not only of many of the genes correlated with the direct antiviral state but also of genes involved in (1) antigen presentation to cytotoxic T lymphocytes (CTLs), (2) macrophage, natural killer (NK), and T helper 1 (Th1) cell recruitment and activation, (3) complement system function, (4) apoptosis, and (5) ISGs with unknown functions. As many of these processes are correlated clinically with resolution of chronic HCV infection, the combined use of these IFNs could display a beneficial effect on viral clearance in patients infected with HCV and other viruses through enhancement of one of these processes or of the direct antiviral state.     

Inhibition of the ubiquitin-proteasome system: a new avenue for atherosclerosis.

BACKGROUND: The ubiquitin-proteasome system (UPS) is thought to be functionally active in atherosclerosis (AS) lesions. Aspirin was found to be a potent inhibitor of the UPS in some tumour studies; however, its effect on AS remains to be demonstrated in vivo. METHODS: New Zealand rabbits were placed on a normal diet (N) or on a normal diet with aspirin (NI) or on an atherogenic diet without (H) or with aspirin (HI) for 12 weeks. Proteasome activity, concentrations of plasma lipids and levels of peroxidation were determined. Ubiquitin/ubiquitin-conjugates (Ub), IkappaBalpha, phosphorylated IkappaB (pIkappaBalpha) and p65 were investigated by Western blotting or immunochemistry. RESULTS: Concentrations of plasma lipids and peroxidation levels were higher in H or HI vs. N or NI. Histological analysis showed that atheroma was increased in H. Ub and IkappaBalpha were mainly localised in subendothelium and media vascular smooth muscle cells. Western blots revealed that Ub, IkappaBalpha, and pIkappaBalpha were increased, whereas p65 was lower in HI vs. H. The activity of the 20S proteasome was functionally active in H vs. N, NI or HI, while the 26S proteasome was not affected in any of the groups. CONCLUSIONS: Aspirin can attenuate the pathogenesis of atheroma formation, the degradation of IkappaBalpha and pIkappaBalpha, and lower the expression of p65, indicating that its therapeutic effects on AS may be via inhibition of the UPS.     

PR35THE INCIDENCE OF NON‐MELANOMA SKIN CANCER IN NEW ZEALAND

Background It is estimated that skin cancers cost $33 million per annum to the New Zealand healthcare system. Basal cell carcinoma and squamous cell carcinoma are the commonest types of non melanoma skin cancers (NMSCs). Anecdotal evidence indicates that there has been a doubling in the incidence of NMSCs in New Zealand over the last decade. Because of the high incidence mandatory reporting of NMSCs to the National Cancer Registry is not required. This lack of accurate data has led to poor health care policies and strategies including funding and workforce planning. Aims The aims of this study are to (1) present the latest statistics on NMSCs in New Zealand, including the incidence across different regions over the last decade, patient demographics, anatomic distribution of NMSCs, incidence and sites of metastasis, and disease‐specific survival; to (2) the histopathology of NMSCs, including surgical margins, histologic grade, and perineural, lymphatic, and vascular invasion; and (3) the relative role of different faculties treating NMSCs. Method This project has been approved by the multi‐centre ethics committee. A retrospective review was conducted from patients’ histology records from public and private pathology laboratories within defined catchment areas. Criterion for analysis is a confirmed diagnosis of NMSC treated surgically. A Microsoft Access database is created that will facilitate subsequent data retrieval and analysis. Results and Conclusion It is hoped that this up‐to‐date data will form the framework for the development of sound and sustainable healthcare policies of management of NMSCs including management strategies and workforce planning, and research direction on this common disease.