Observations of increased tropical rainfall preceded by air passage over forests.

Vegetation affects precipitation patterns by mediating moisture, energy and trace-gas fluxes between the surface and atmosphere. When forests are replaced by pasture or crops, evapotranspiration of moisture from soil and vegetation is often diminished, leading to reduced atmospheric humidity and potentially suppressing precipitation. Climate models predict that large-scale tropical deforestation causes reduced regional precipitation, although the magnitude of the effect is model and resolution dependent. In contrast, observational studies have linked deforestation to increased precipitation locally but have been unable to explore the impact of large-scale deforestation. Here we use satellite remote-sensing data of tropical precipitation and vegetation, combined with simulated atmospheric transport patterns, to assess the pan-tropical effect of forests on tropical rainfall. We find that for more than 60 per cent of the tropical land surface (latitudes 30 degrees south to 30 degrees north), air that has passed over extensive vegetation in the preceding few days produces at least twice as much rain as air that has passed over little vegetation. We demonstrate that this empirical correlation is consistent with evapotranspiration maintaining atmospheric moisture in air that passes over extensive vegetation. We combine these empirical relationships with current trends of Amazonian deforestation to estimate reductions of 12 and 21 per cent in wet-season and dry-season precipitation respectively across the Amazon basin by 2050, due to less-efficient moisture recycling. Our observation-based results complement similar estimates from climate models, in which the physical mechanisms and feedbacks at work could be explored in more detail.

Hemolytic uremic syndrome associated with invasive pneumococcal disease: the United kingdom experience.

OBJECTIVE: To describe the presentation, management, and outcome of 43 cases of pneumococcal-associated hemolytic uremic syndrome (P-HUS). An increased incidence of P-HUS has been noted in the United Kingdom between January 1998 and May 2005. STUDY DESIGN: Cases with microangiopathic hemolytic anemia (Hb <10 g/dL with fragmented RBCs), thrombocytopenia (platelet count < 130 x 10(9)/L), acute renal impairment with oliguria and elevated plasma creatinine for age, confirmed or suspected pneumococcal infection and/or T-activation were included. RESULTS: The median age at presentation was 13 months (range, 5-39 months). Pneumococcus was identified in 34 of 43 cases; T-activation was identified in 36 of 37 cases. Twelve strains were serotyped: serotypes 3 (n = 2), 6A (n = 2), 12F (n = 1), 14 (n = 1), 19A (n = 6). Empyema was present in 23 of 35 pneumonia cases; 13 cases had confirmed (9) or suspected (4) pneumococcal meningitis; 36 cases required dialysis (median, 10 days; range, 2-240 days). The mortality rate was 11%, comprising 3 cases of meningitis, 1 case of sepsis and 1 case of pulmonary embolism at 8 months follow up while on dialysis. Follow-up data were available for 35 of 38 patients who survived (median follow-up period, 9 months; range, 1-63 months); of these, 10 patients had renal dysfunction, 1 patient was dialysis-dependent, 5 patients had hypertension and 8 patients had at least 1+ proteinuria on urinalysis. CONCLUSION: P-HUS has increased compared with historic surveys (0/288 in 1985-1988; 8/413 in 1997-2001, 43/315 in 1998-May 2005). Early mortality remains high (8-fold that of VTEC-induced HUS). Ten of 12 strains identified would not be covered by the PCV7 vaccine.

The late histologic findings in diarrhea-associated hemolytic uremic syndrome.

Kidney biopsies were undertaken for persisting proteinuria 3.3 to 7 years (mean 5.4 years) from the onset of diarrhea-associated hemolytic uremic syndrome (D + HUS) in 5 boys and 2 girls (age at presentation mean 3.2 years, range 1.0 to 9.7 years). At 1 year the mean early morning urine protein/creatinine ratio was 100 mg/mmol, and the mean glomerular filtration rate was 65 mL/min/1.73 m2. At 5 years the mean early morning urine protein/creatinine ratio was 81 mg/mmol, and the mean glomerular filtration rate was 73 mL/min/1.73 m2. The biopsy specimens were compared with those of 7 age- and sex-matched children who were investigated for isolated persistent microscopic hematuria but in whom no abnormality was detected. Global glomerulosclerosis was noted in 6 patients with D + HUS, and 2 of these had segmental sclerosing lesions. Tubular atrophy and interstitial scarring were seen in all but 1 patients. The glomeruli in the D + HUS group were significantly larger than in the control group (P < .01). These findings are typically found in kidneys with reduced nephron numbers and are compatible with changes of hyperperfusion and hyperfiltration in surviving nephrons. Long-term follow-up of patients with D + HUS and proteinuria is advisable.

Prognostic significance of proteinuria one year after onset of diarrhea-associated hemolytic-uremic syndrome.

We examined the prognostic value of changes in the amount of proteinuria, measured as protein/creatinine ratios in early-morning urine samples, in 40 children who had had diarrhea-associated hemolytic-uremic syndrome. One year after diagnosis, 87% of those who seemed to have fully recovered had normal urinary protein/creatinine ratios, compared with none of those with poor outcomes (p less than 0.001). None of those with poor outcomes achieved normal protein/creatinine ratios during follow-up to a maximum of 5 1/2 years, but 93% of those who made a full clinical recovery no longer had proteinuria. Measurement of the protein/creatinine ratio in an early-morning sample of urine is a simple, cost-effective, and noninvasive means of monitoring the progress of patients with diarrhea-associated hemolytic-uremic syndrome, provided that a technique sensitive at low protein concentrations is employed.

Growth in the international physician supply. 1950 through 1979.

The recent growth in domestic physician supply prompted an investigation of international trends. Using data from the World Health Organization, it was determined that the number of physicians in the world grew from 4.8 per 10,000 population to 10.1 per 10,000 during the period 1950 through 1979. There was a 96% increase in industrialized nations, 223% in nations with centrally planned economies, 164% in middle-income nations, and 29% in low-income nations. Relationships in growth in physician supply and production of medical graduates are discussed. Implications of the inequities between the various groupings of countries are discussed.