Israel Medical Association Journal

Background: Alteration of innate and acquired immunity can play a role in the mechanism involved in the development of dementia. Epidemiologic studies indicate that the use of non-steroidal anti-inflammatory drugs can delay the onset or slow progression of Alzheimer disease.

Objectives: To determine whether the use of NSAIDs[1] is associated with natural killer activity alteration in AD[2] and multi-infarct vascular dementia patients, as compared with non-demented elderly and healthy young people.

Methods: In this prospective open study four groups of subjects (AD, VD[3], non-demented elderly, and healthy young people) were treated with an NSAID drug (rofecoxib 12.5 mg/day or ibuprofen 400 mg twice daily) for 7 days. Natural killer cell cytotoxicity was measured after flow cytometry analysis before and after treatment.

Results: Of the 49 subjects studied, 15 had a diagnosis of AD (3 men, 12 women; mean age 83.5 ± 8.1 years), 15 had a diagnosis of multi-infarct VD (7 men, 8 women; mean age 75.5 ± 8.4), 13 were non-demented elderly (1 man, 12 women; mean age 80.2 ± 7.2), and 6 were healthy young volunteers (3 men, 3 women; mean age 36.8 ± 4.4). While all examined subjects showed decreased NK[4] cell cytotoxicity after treatment, this decrease was most prominent and statistically significant in elderly patients suffering from vascular dementia –  from an average of 30.5 ± 11.8% before treatment to 22.5 ± 16% after treatment (P = 0.04). The decrease in NK cell cytotoxicity was only moderate and not statistically significant in all other elderly and young subjects. Young healthy volunteers exhibited a significantly higher total NK cytotoxicity before and after treatment compared to all age groups (P < 0.001).

Conclusion: These findings suggest that NSAIDs decrease NK activity in vascular dementia patients. Our findings also suggest that natural killer activity alteration cannot explain the ability of anti-inflammatory drugs to delay the onset or slow the progression of AD.

Background: Alteration of innate and acquired immunity can play a role in the mechanism involved in the development of dementia. Epidemiologic studies indicate that the use of non-steroidal anti-inflammatory drugs can delay the onset or slow progression of Alzheimer disease.

Objectives: To determine whether the use of NSAIDs[1] is associated with natural killer activity alteration in AD[2] and multi-infarct vascular dementia patients, as compared with non-demented elderly and healthy young people.

Methods: In this prospective open study four groups of subjects (AD, VD[3], non-demented elderly, and healthy young people) were treated with an NSAID drug (rofecoxib 12.5 mg/day or ibuprofen 400 mg twice daily) for 7 days. Natural killer cell cytotoxicity was measured after flow cytometry analysis before and after treatment.

Results: Of the 49 subjects studied, 15 had a diagnosis of AD (3 men, 12 women; mean age 83.5 ± 8.1 years), 15 had a diagnosis of multi-infarct VD (7 men, 8 women; mean age 75.5 ± 8.4), 13 were non-demented elderly (1 man, 12 women; mean age 80.2 ± 7.2), and 6 were healthy young volunteers (3 men, 3 women; mean age 36.8 ± 4.4). While all examined subjects showed decreased NK[4] cell cytotoxicity after treatment, this decrease was most prominent and statistically significant in elderly patients suffering from vascular dementia –  from an average of 30.5 ± 11.8% before treatment to 22.5 ± 16% after treatment (P = 0.04). The decrease in NK cell cytotoxicity was only moderate and not statistically significant in all other elderly and young subjects. Young healthy volunteers exhibited a significantly higher total NK cytotoxicity before and after treatment compared to all age groups (P < 0.001).

Conclusion: These findings suggest that NSAIDs decrease NK activity in vascular dementia patients. Our findings also suggest that natural killer activity alteration cannot explain the ability of anti-inflammatory drugs to delay the onset or slow the progression of AD.

The prevalence of obesity worldwide has risen sharply during the last four decades. The etiology of obesity is complex and includes a host of genetic influences in addition to the overconsumption of energy coupled with a sedentary lifestyle. Obesity is known to cause or exacerbate many co-morbid conditions such as diabetes, hypertension, dyslipidemia, coronary heart disease, stroke, certain cancers, arthritis and obstructive sleep apnea. Modest weight losses of 5–10% of actual weight are related to significant improvements in co-morbid conditions, but unfortunately the rate of recidivism with short-term therapy for obesity is high. The recent recognition of obesity as a chronic disease that should be treated with long-term programs and possibly with polypharmacy, and the alarming increase in its prevalence, have prompted extensive research and the development of new pharmacotherapy.

While some claim that germ-line engineering is a definite possibility, the law in Israel and in most countries states that it should be avoided. This paper suggests that using GLE[1] in order to ‘self-evolve’ (when it becomes safe) is not only inevitable but also morally justified. This paper argues that,  

• The great achievements of healthcare during the last century, enabling longer life, have made almost everyone prey to late-onset diseases.


• The conundrum of healthcare allocation is worsening, partly due to late-onset dysfunctional genes that have escaped the barriers of natural selection.


• Trying to free future generations from late-onset diseases (such as Alzheimer’s for instance) may be considered as ‘eugenics’ but, if pursued freely and justly, is a noble goal.


• We will be affecting future generations whether or not we use GLE.


• By definition, GLE might be reversible; it follows therefore that GLE may not necessarily represent the dramatic change inserted in the germ line forever – as is usually suggested.


• Reproductive freedom and justice are paramount in this scenario. These values are not necessarily incompatible if the right policies are in place.

Background: Left main coronary artery disease is considered a surgical indication in most centers. However, in some cases prohibited from surgery or in patients with prior bypass grafting, there is a need for percutaneous coronary intervention in LMCA[1] disease scenarios.

Objectives: To assess the clinical outcomes among patients undergoing stent-based LMCA angioplasty.

Methods: We identified 34 consecutive patients who underwent PCI[2] in LMCA at our institution. Procedural data and clinical outcomes were obtained for all patients.

Results: The mean age was 71 ± 12 years. There were 27 elective and 7 emergent procedures performed on 23 “protected” LMCA and 11 “unprotected” LMCA. In emergent procedures, the prevalence of cardiogenic shock (29% vs. 0%, P = 0.04) in patients with prior coronary bypass (29% vs. 8.5%, P = 0.007) was significantly higher compared to elective cases. Procedural success in emergent procedures was significantly lower than in elective procedures (71 vs. 100%, P = 0.04). In emergent versus elective procedures, the in-hospital mortality rate was higher (43 vs. 0%, P = 0.006). The rate of cumulative major adverse cardiac events at 1 and 6 months was 43% and 71% in emergent cases versus 0% and 33% in elective cases (P < 0.05 for both comparisons). In patients with “unprotected” LMCA the overall major cardiac events at 1 month was higher compared to “protected” LMCA patients (27 vs. 0%, P = 0.02). Multivariate analysis revealed emergent procedure as an independent predictor for mortality and adverse cardiac events (odds ratio 6.7; 95% confidence interval 1.2–36; P = 0.02).

Conclusions: Percutaneous interventions in LMCA are feasible and relatively safe in carefully selected cases. Procedural outcomes and clinical prognosis is highly dependent on the nature of disease prior to angioplasty (e.g., elective vs. emergent procedure) as well as on protection of the LMCA by patent grafts.

Background: Pulmonary disease is the most frequent cause of morbidity and mortality in cystc fibrosis patients. New techniques such as non-invasive positive pressure ventilation have resulted in prolongation of life expectancy in CF[1] patients with end-stage lung disease.

Objectives: To determine the role of NIPPV[2] in CF patients awaiting lung transplantation.

Methods: Between 1996 and 2001 nine CF patients (5 females) with end-stage lung disease were treated with bi-level positive airway pressure ventilation in the "spontaneous" mode.

Results: The patients' mean age at initiation of BiPAP[3] was 15 years (range 13–40 years) and the mean duration of BiPAP usage was 8 months (range 3–16 months). Four patients underwent successful lung transplantation, three patients died while awaiting transplantation, and the remaining two are still on NIPPV while waiting for transplantation. Patients' body mass index increased significantly (P < 0.05) during BiPAP therapy (from 16.1 to 17.2 kg/m²). Blood pH, p_aCO₂, and bicarbonate improved significantly (from 7.31 to 7.38, 90.8 to 67.2 mmHg, and 48.9 to 40.3 mEq/L, respectively). Pulmonary function tests were not affected by BiPAP usage. The patients experienced a significant alleviation in morning headaches and improvement in quality of sleep (P < 0.003). There were no major complications during BiPAP usage.

Conclusions: We demonstrated that long-term NIPPV can stabilize and improve physiologic parameters such as ventilation, arterial blood gases and body mass index, as well as subjective symptoms such as sleep pattern, daily activity level, and morning headaches in CF patients with end-stage lung disease. Further prospectively controlled studies are needed to evaluate the potential of BiPAP therapy and its influence on morbidity and mortality in the post-lung transplantation period.