Twelve testable hypotheses on the geobiology of weathering.

Critical Zone (CZ) research investigates the chemical, physical, and biological processes that modulate the Earth's surface. Here, we advance 12 hypotheses that must be tested to improve our understanding of the CZ: (1) Solar-to-chemical conversion of energy by plants regulates flows of carbon, water, and nutrients through plant-microbe soil networks, thereby controlling the location and extent of biological weathering. (2) Biological stoichiometry drives changes in mineral stoichiometry and distribution through weathering. (3) On landscapes experiencing little erosion, biology drives weathering during initial succession, whereas weathering drives biology over the long term. (4) In eroding landscapes, weathering-front advance at depth is coupled to surface denudation via biotic processes. (5) Biology shapes the topography of the Critical Zone. (6) The impact of climate forcing on denudation rates in natural systems can be predicted from models incorporating biogeochemical reaction rates and geomorphological transport laws. (7) Rising global temperatures will increase carbon losses from the Critical Zone. (8) Rising atmospheric P(CO2) will increase rates and extents of mineral weathering in soils. (9) Riverine solute fluxes will respond to changes in climate primarily due to changes in water fluxes and secondarily through changes in biologically mediated weathering. (10) Land use change will impact Critical Zone processes and exports more than climate change. (11) In many severely altered settings, restoration of hydrological processes is possible in decades or less, whereas restoration of biodiversity and biogeochemical processes requires longer timescales. (12) Biogeochemical properties impart thresholds or tipping points beyond which rapid and irreversible losses of ecosystem health, function, and services can occur.

Renal findings in patients with short-term type 2 diabetes.

Under semiambulatory conditions, 85 consecutive patients with the diagnosis of Type 2 diabetes of short duration (excluding patients with islet cell antibodies or maturity onset diabetes of the young) were admitted to a self-control training program and were examined in this study. A comprehensive renal assessment was performed, including evaluation of albumin excretion rate (AER), renal hemodynamics, blood pressure (BP) profile, and indicators of genetic risk. AER > or = 30 mg/24 h was found in 13 (15%) of patients; in two of these patients, AER was > or = 300 mg/24 h. By logistic regression, high HbA1, current smoking, and BP parameters were significantly correlated with an increased risk of microalbuminuria (MA). In a multiple linear regression model, accounting for 57% of total variance, HbA1, ERPF, and current smoking were significantly correlated with AER. Median GFR (Cin(inulin clearance) 136 mL/min per 1.73m2; range, 94 to 194) and ERPF (Cpah(para-aminohippuric acid clearance) 733; range, 451 to 1328) were significantly higher in patients than in control subjects (upper 95th percentile, 131 and 706 mL/min per 1.73m2, respectively). In a multiple linear regression model, explaining 27% of total variance, age, AER, gender, and fasting blood glucose were significantly correlated to GFR. According to the criteria of average daytime BP > or = 135/85 mm Hg or 24-h BP > or = 130/80 mm Hg, 60% of patients were hypertensive (HT). Sixty-one percent of all patients (including 50% of the untreated normotensive patients) were "nondippers", i.e., < 15% nighttime decrease of mean arterial pressure. Either HT or nondipping was found in 79% of all patients, so that only 21% had a completely normal blood pressure profile. Ninety-four percent of untreated hypertensive patients had no MA. First-degree relatives of patients with MA compared with patients without MA had more frequent cardiovascular events (69% versus 31%). The risk of MA in diabetic patients with positive family history was amplified by poor glycemic control. MA, but not hypertension, was marginally related to K(m) of Na+/Li+ countertransport. It was concluded that (1) microalbuminuria is found in 15% of patients newly presenting with Type 2 diabetes; (2) a high proportion of patients exhibit hyperfiltration; (3) according to ambulatory BP only, 21% of patients have a completely normal circadian BP profile; (4) a family history of cardiovascular events interacts with glycemic control to increase the risk of MA.

Increased prevalence of salt sensitivity of blood pressure in IDDM with and without microalbuminuria.

In insulin-dependent diabetes mellitus (IDDM) elevated exchangeable sodium (Na) levels are found even in the absence of hypertension, but it is not known whether this is associated with increased sensitivity of blood pressure to sodium level. To clarify this issue we compared 30 patients with IDDM (19 without and 11 with microalbuminuria, i.e. more than 30 mg albumin/day) and 30 control subjects matched for age, gender and body mass index. The subjects were studied on the 4th day of a low-salt diet (20 mmol/day) under in-patient conditions and were subsequently changed to the same diet with a high-salt supplement, yielding a total daily intake of 220 mmol Na/day. Circadian blood pressure, plasma renin activity (PRA), plasma atrial natriuretic factor (p-ANF), plasma cyclic guanosine 5'-phosphate (p-cGMP) and urinary albumin were measured. The proportion of salt-sensitive subjects, i.e. showing increment of mean arterial pressure > or = 3 mmHg on high-salt diet, was 43% in diabetic patients (50% of diabetic patients with and 37% without microalbuminuria) and 17% in control subjects (p < 0.05). Lying and standing PRA levels on low- or high-salt diet were significantly lower in diabetic patients than in control subjects. Salt-sensitive diabetic patients had significantly higher lying ANF on high-salt (38.7 +/- 4.2 pmol/l vs 20.1 +/- 2.3 pmol/l, p < 0.005) than on low-salt diet. The results suggest that (i) the prevalence of sodium sensitivity is high in IDDM (ii) sodium sensitivity is found even in the absence of nephropathy as indicated by albuminuria.

Renal involvement in type II diabetes.

The incidence and prevalence of renal failure from type II diabetes have been seriously underestimated in the past. Currently, the incidence of uremia in patients with type II diabetes has increased continuously in Europe and the United States, mainly because of better patient survival (ie, they now live until nephropathy develops) and possibly because of a rising prevalence of type II diabetes in the general population (ie, more patients are at risk of developing nephropathy). Generally, renal hemodynamics and glomerular lesions are similar in type I and type II diabetes, but glomerular histology is more diverse in type II diabetes. Given the high prevalence of diabetes and renal failure from various causes in the elderly, coexistence of the two (even in the absence of glomerulosclerosis) occurs in approximately 20% of uremic type II diabetic patients. The development of nephropathy is controlled by strong genetic determinants, but these have not been further characterized.

Postinfectious glomerulonephritis--is there a link to alcoholism?

From January 1984 to May 1993, we observed 30 cases of postinfectious glomerulonephritis (GN)--endocapillary, exudative GN with humps (23 males, 7 females; median age 49 years; range 17-77). They represented 4.5% of all renal biopsies. Crescents were present in 9/26 who had renal biopsies (35%) and there was a mesangioproliferative pattern in 14 (54%). Seventeen of the 30 patients (57%) were alcoholics by history and biochemistry. Cirrhosis was present in 8/17 (47%), but alcoholic hepatitis in none. Nine of the 17 alcoholic (53%) but none of the non-alcoholic patients developed chronic renal failure. Adverse renal prognosis was significantly correlated to alcoholism. We conclude that (i) alcoholism is common in patients with postinfectious GN, and, (ii) alcoholism adversely affects renal prognosis in patients with postinfectious GN.

Analgesic effect of naproxen sodium, codeine, a naproxen-codeine combination and aspirin on the postoperative pain of oral surgery.

In a double-blind study, 198 outpatients with pain after oral surgery were randomly assigned to treatment with a single oral dose of naproxen sodium 550 mg, codeine sulfate 60 mg, a combination of naproxen sodium 550 mg with codeine sulfate 60 mg, aspirin 650 mg or placebo. Using a self-rating record, subjects rated their pain and its relief hourly for 12 hours after medication. Orthogonal contrasts for the four treatments making up the factorial component showed that the naproxen effect was significant for every measurement of total and peak analgesia; the codeine effect was significant for total and peak pain relief and patients' overall evaluation. The naproxen-codeine interaction was not statistically significant for any measure, which suggests that the analgesic effect of the combination represents the additive effect of its constituents. Based on pairwise comparisons, aspirin was significantly superior to placebo for most measures of effect, naproxen was significantly superior to both aspirin and codeine for all measures and the combination was significantly superior to naproxen for patients' overall evaluation. No more patients experienced adverse effects with aspirin or naproxen than with placebo, but significantly more patients receiving the codeine-containing treatments experienced adverse effects than those receiving aspirin and naproxen.