Prognostic significance of programmed ventricular stimulation in patients surviving complicated acute myocardial infarction: a prospective study.

In survivors of complicated myocardial infarction, the inducibility of sustained ventricular tachycardia may help identify a subset that is at increased risk for subsequent sudden cardiac death or spontaneous sustained ventricular tachycardia. We performed prehospital discharge programmed ventricular stimulation in 86 survivors of acute myocardial infarction complicated by heart failure, angina pectoris, or nonsustained ventricular tachycardia. These patients also underwent cardiac catheterization with coronary angiography and 24-hour ambulatory ECG recording. Programmed ventricular stimulation induced sustained ventricular tachycardia in 19 patients (22%) and ventricular fibrillation in six (7%) and did not induce these arrhythmias in 61 patients (71%). During an average follow-up of 18 +/- 13 months, 11 patients had arrhythmic events (seven sudden death and four nonfatal spontaneous sustained ventricular tachycardia) and 10 patients had nonsudden cardiac death. The total cardiac mortality rate was 20%. Arrhythmic events occurred in 32% of the 19 patients with inducible sustained ventricular tachycardia compared with 7% of the remaining 67 patients (p less than 0.003). By multivariate analysis the occurrence of arrhythmic events was independently predicted by both inducible sustained ventricular tachycardia and Killip class III or IV heart failure. The risk of arrhythmic events was 4.4% in the absence of both variables versus 38.4% (p less than 0.001) when both variables were present. The total cardiac mortality rate was best predicted by low left ventricular ejection fraction (less than 30%). Thus programmed ventricular stimulation is useful in risk stratification of survivors of complicated acute myocardial infarction. The prognostic utility appears to be particularly high in patients with infarction complicated by Killip class III or IV heart failure.     

A site-specific single-strand endonuclease from the eukaryote Chlamydomonas.

We have found a unique deoxyribonuclease in extracts of the eukaryotic green alga Chlamydomonas. When incubated with viral DNA from adenovirus-2, this enzyme produces discrete fragments that form bands upon electrophoresis in an agarose gel. Site specificity of the enzymatic cleavage examined by identifying the 5'-terminal nucleotides in cleaved adenovirus-2 DNA and by studies with synthetic polynucleotides of defined sequence, indicates that the initial endonucleolytic cleavage occurs at a site containing a deoxythymidine residue. Electron microscopy of cleaved adenovirus-2 DNA revealed single-strand segments within duplex DNA. We propose that the enzyme acts by making initial site-specific single-strand incisions, followed by subsequent excision on the same strand, producing a gapped duplex molecule; and that double-strand scissions result from limited occurrence of overlapping single-strand gaps on complementary strands.     

Adaptive radiation therapy of breast cancer by repeated imaging during irradiation

Breast cancer is the most frequent cancer among females and also a leading cause of cancer related mortality worldwide. A multimodality treatment approach may be utilized for optimal management of patients with combinations of surgery, radiation therapy (RT) and systemic treatment. RT composes an integral part of breast conserving treatment, and is typically used after breast conserving surgery to improve local control. Recent years have witnessed significant improvements in the discipline of radiation oncology which allow for more focused and precise treatment delivery. Adaptive radiation therapy (ART) is among the most important RT techniques which may be utilized for redesigning of treatment plans to account for dynamic changes in tumor size and anatomy during the course of irradiation. In the context of breast cancer, ART may serve as an excellent tool for patients receiving breast irradiation followed by a sequential boost to the tumor bed. Primary benefits of ART include more precise boost localization and potential for improved normal tissue sparing with adapted boost target volumes particularly in the setting of seroma reduction during the course of irradiation. Herein, we provide a concise review of ART for breast cancer in light of the literature.     

Immunohistochemical characteristics of regenerated bone after surgical therapy of advanced ligature-induced peri-implantitis defects

Objectives

This study seeks to assess and compare immunohistochemical characteristics of regenerated and pristine bone areas following surgical therapy of advanced peri-implantitis.

Methods

At ligature-induced peri-implantitis defects, the intrabony component was filled with a natural bone mineral (NBM), and the supracrestal component was treated by either an equine bone block (EB) or implantoplasty. NBM and EB were soak-loaded with rhBMP-2 or sterile saline. Membrane (i.e., native collagen) protected sites were submerged for 12 weeks. Osteocalcin (OC) and transglutaminase 2 (TG2; angiogenesis) antigen reactivity was assessed within the augmented- (AA) and pristine bone (PB) areas at non-exposed sites (n?=?39 defects).

Results

In all groups investigated, mean OC (AA, 0.5?±?0.4 to 1.9?±?2.9 %/PB, 1.7?±?2.6 to 3.5?±?6.5 %) and TG2 (AA, 0.6?±?0.5 to 1.3?±?1.5 %/PB, 0.5?±?0.5 to 1.6?±?1.9 %) values within AA did not significantly differ from those values assessed within PB (P?>?0.05, respectively).

Conclusions

AA formed in different treatment groups may not be considered as qualitatively (i.e., OC and TG2) compromised bone.     

The nigrostriatal dopaminergic system assessed in vivo by positron emission tomography in healthy volunteer subjects and patients with Parkinson's disease

A group of healthy control subjects and patients with Parkinson's disease were investigated using positron emission tomography and two tracers as indicators of different specific properties of the presynaptic dopaminergic system in caudate nucleus and putamen. The first tracer, 6-L-(18F)-fluorodopa, was used as an analog of levodopa to assess its regional brain uptake, conversion into, and retention as dopamine and further metabolites. The second tracer, (11C)-nomifensine was employed as an indicator of striatal monaminergic reuptake sites that are principally dopaminergic. We have used this tracer to assess dopaminergic nerve terminal density. In patients with Parkinson's disease, striatal uptake of both tracers was decreased, putamen being significantly more affected than caudate. Side-to-side differences of uptake in putamen, but not caudate, correlated with corresponding left-right differences of scored clinical motor performance. Both 6-L(18F)-fluorodopa and (11C)-nomifensine tracer uptake in putamen was decreased on average to 40% of normal values, suggesting that a substantial part of the cellular elements of the dopaminergic nigrostriatal system is still intact in living parkinsonian patients. This is in contrast to the generally extreme depletion of endogenous dopamine in the putamen of patients found at postmortem. Our results lend support to the search for drug treatments that protect against further nigrostriatal cell loss and that could be exhibited as soon as the disease manifests clinically. If successful, a sufficient striatal nerve terminal pool would remain so that the effectiveness of levodopa as a dopamine repletor could persist.     

Animal models for peri‐implant mucositis and peri‐implantitis

The treatment of infectious diseases affecting osseointegrated implants in function has become a demanding issue in implant dentistry. Since the early 1990s, preclinical data from animal studies have provided important insights into the etiology, pathogenesis and therapy of peri‐implant diseases. Established lesions in animals have shown many features in common with those found in human biopsy material. The current review focuses on animal studies, employing different models to induce peri‐implant mucositis and peri‐implantitis.     

Restriction of cell lysis by homologous complement: II. Protection of erythrocytes against lysis by newly activated complement

Our previous work revealed that homologous complement (C) was ineffective in lysing antibody-sensitized erythrocytes (EA) even at high concentrations. It was also shown that activation of complement on homologous EA resulted in the binding of C9 and the formation of EA bearing complement proteins C1 through C9 (EAC1-9), yet few hemolytic sites were formed. Instead, as shown here, the formation of homologous EAC1-9 caused the cells to become resistant to lysis even by heterologous complement during a second incubation. In contrast, when homologous EAC1-8 were produced by incubating EA with C9-depleted serum, such intermediates were not protected against lysis by heterologous complement during a second incubation. Furthermore, homologous C9 on EAC1-9 was able to reduce the hemolytic efficiency of heterologous complement without blocking C activation and the formation of new C5b-9 complexes. Protection was not modified when homologous EAC1-9 were produced in one step, by incubation of EA with serum, or sequentially by adding C9 to EAC1-8. The minimum number of 9-sites required to confer a protective effect on EAC1-9 was less than 200 per cell. Thus, in addition to its known effect in heterologous cell killing, homologous C9 is capable of protecting homologous cells against inadvertent complement lysis.