The Death Cults of prehistoric Malta.

Malone, C. A. T., Bonanno, A., Gouder, T., Stoddart, S. K. F., and Trump, D.

The Death Cults of prehistoric Malta:Mysteries of the Ancient Ones

reprinted

New light on death in prehistoric Malta: the Brochtorff Circle.

Trump, D., Malone, C and Stoddart, S., ,G. Burenhult, (ed.). 1993, Harper Collins: New York. p. 100-101.

Glycated Hemoglobin and Risk of Death in Diabetic Patients Treated With Hemodialysis: A Meta-analysis

Background: Studies investigating the association between glycated hemoglobin (HbA) level and mortality risk in diabetic patients receiving hemodialysis have shown conflicting results. 
Study Design: We conducted a systematic review and meta-analysis using MEDLINE, EMBASE, Web of Science, and the Cochrane Library. 
Setting & Population: Diabetic patients on maintenance hemodialysis therapy. 
Selection Criteria for Studies: Observational studies or randomized controlled trials investigating the association between HbA values and mortality risk. Study authors were asked to provide anonymized individual patient data or reanalyze results according to a standard template. 
Predictor: Single measurement or mean HbA values. Mean HbA values were calculated using all individual-patient HbA values during the follow-up period of contributing studies. 
Outcome: HR for mortality risk. 
Results: 10 studies (83,684 participants) were included: 9 observational studies and one secondary analysis of a randomized trial. After adjustment for confounders, patients with baseline HbA levels =8.5% (=69 mmol/mol) had increased mortality (7 studies; HR, 1.14; 95% CI, 1.09-1.19) compared with patients with HbA levels of 6.5%-7.4% (48-57 mmol/mol). Likewise, patients with a mean HbA value =8.5% also had a higher adjusted risk of mortality (6 studies; HR,1.29; 95% CI, 1.23-1.35). There was a small but nonsignificant increase in mortality associated with mean HbA levels =5.4% (=36 mmol/mol; 6 studies; HR, 1.09; 95% CI, 0.89-1.34). Sensitivity analyses in incident (=90 days of hemodialysis) and prevalent patients (>90 days of hemodialysis) showed a similar pattern. In incident patients, mean HbA levels =5.4% also were associated with increased mortality risk (4 studies; HR, 1.29; 95% CI, 1.23-1.35). 
Limitations: Observational study data and inability to adjust for diabetes type in all studies. 
Conclusions: Despite concerns about the utility of HbA measurement in hemodialysis patients, high levels (=8.5%) are associated with increased mortality risk. Very low HbA levels (=5.4%) also may be associated with increased mortality risk. 

Substrates modified by advanced glycation end-products cause dysfunction and death in retinal pericytes by reducing survival signals mediated by platelet-derived growth factor

AIMS/HYPOTHESIS: Premature death of retinal pericytes is a pathophysiological hallmark of diabetic retinopathy. Among the mechanisms proposed for pericyte death is exposure to AGE, which accumulate during diabetes. The current study used an in vitro model, whereby retinal pericytes were exposed to AGE-modified substrate and the mechanisms underlying pericyte death explored. METHODS: Pericytes were isolated from bovine retinal capillaries and propagated on AGE-modified basement membrane (BM) extract or non-modified native BM. The extent of AGE modification was analysed. Proliferative responses of retinal pericytes propagated on AGE-modified BM were investigated using a 5-bromo-2-deoxy-uridine-based assay. The effect of extrinsically added platelet-derived growth factor (PDGF) isoforms on these proliferative responses was also analysed alongside mRNA expression of the PDGF receptors. Apoptotic death of retinal pericytes grown on AGE-modified BM was investigated using terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling labelling, mitochondrial membrane depolarisation and by morphological assessment. We also measured both the ability of PDGF to reverse Akt dephosphorylation that was mediated by AGE-modified BM, and increased pericyte apoptosis. RESULTS: Retinal pericytes exposed to AGE-modified BM showed reduced proliferative responses in comparison to controls (p

A morphologic and autoradiographic study of cell death and regeneration in the retinal microvasculature of normal and diabetic rats

Cell loss and regeneration were investigated and compared in the retinal microvasculature of age- and sex-matched normal and streptozotocin diabetic rats. Selective pericyte loss in the diabetic rat was characterized by changes in the pericyte to endothelial cell ratio in retinal capillaries isolated for microscopy by the trypsin digest technique. A comparison of 3- and 9-month-old normal rats showed no significant change in the pericyte to endothelial cell ratio (1:2.7). In diabetic animals the ratio was reduced to 1:4.03, which was statistically significant (P less than .001). Premitotic retinal vascular cells in normal and diabetic rats were labelled with tritiated thymidine and the labelling indices calculated from cell counts of trypsin digest preparations. Methyl H3 thymidine was infused continuously over an eight-day period using osmotic mini pumps. The labelling index of endothelial cells (0.33%) in normal rats increased to 0.91% in diabetic animals (P less than .05). The labelling index of pericyte cells in normal animals (0.16%) did not increase significantly (P greater than .05) in diabetic animals (0.19%). A special stain was used to exclude labelled polymorphonuclear leukocytes from the cell counts.

Worked to Death? A census-based longitudinal study of the relationship between the numbers of hours spent working and mortality risk

Background There has been an increasing interest in the health effects of long
working hours, but little empirical evidence to substantiate early
10 case series suggesting an increased mortality risk. The aim of the
current study is to quantify the mortality risk associated with long
working hours and to see if this varies by employment relations and
conditions of occupation.
Methods A census-based longitudinal study of 414 949 people aged 20-59/64
15 years, working at least 35 h/week, subdivided into four occupational
classes (managerial/professional, intermediate, own account workers,
workers in routine occupations) with linkage to deaths records
over the following 8.7 years. Cox proportional hazards models were
used to examine all-cause and cause-specific mortality risk.
20 Results Overall 9.4% of the cohort worked 55 or more h/week, but this
proportion was greater in the senior management and professional
occupations and in those who were self-employed. Analysis of 4447
male and 1143 female deaths showed that hours worked were
associated with an increased risk of all-cause mortality only for
25 men working for more than 55 or more h/week in routine/semiroutine
occupations [adjusted hazard ratios (adjHR) 1.31: 95%
confidence intervals (CIs) 1.11, 1.55)] compared with their peers
working 35–40 h/week. Their equivalent risk of death from cardiovascular
disease was (adjHR 1.49: 95% CIs 1.10, 2.00).
30 Conclusions These findings substantiate and add to the earlier studies indicating
the deleterious impact of long working hours but also suggest that
the effects are moderated by employment relations or conditions of
occupation. The policy implications of these findings are discussed.

Smoking is a major cause of premature death worldwide

Question. How many deaths were attributable to smoking in 2000 worldwide? Study design. Statistical extrapolation of epidemiological and clinical data. Main results. In the year 2000, about 12% of adults died prematurely from smoking (estimated 4.83 million uncertainty range 3.94-5.93 million). Leading causes of death attributable to smoking were cardiovascular diseases (1.69 million deaths), chronic obstructive pulmonary disease (0.97 million deaths) and lung cancer (0.85 million deaths; 71% of lung cancers were smoking related). Smoking related deaths in men were about 3 times more common than women in industrial countries, and about 7 times more common in developing countries. Authors' conclusions. Smoking was a major cause of death worldwide in 2000. © 2004 Elsevier Ltd. All rights reserved.

Acceleration of ions up to 20MeV/nucleon in the ultrashort, high-intensity regime

The measurements reported here provide scaling laws for the ion acceleration process in the regime of ultrashort (50 fs), ultrahigh contrast (10) and ultrahigh intensity (> 10W/cm ), never investigated previously. The scaling of the accelerated ion energies was studied by varying a number of parameters such as target thickness (down to 10nm), target material (C and Al) and laser light polar- ization (circular and linear) at 35° and normal laser incidence. A twofold increase in proton energy and an order of magnitude enhancement in ion flux have been observed over the investigated thickness range at 35° angle of incidence. Further- more, at normal laser incidence, measured peak proton energies of about 20 MeV are observed almost independently of the target thickness over a wide range (50nm- 10 µm). 1. © 2012 by Società Italiana di Fisica.