Ecological feedbacks following deforestation create the potential for a catastrophic ecosystem shift in tropical dry forest

The long-term ecological response to recurrent deforestation associated with shifting cultivation remains poorly investigated, especially in the dry tropics. We present a study of phosphorus (P) dynamics in the southern Yucatán, highlighting the possibility of abrupt shifts in biogeochemical cycling resulting from positive feedbacks between vegetation and its limiting resources. After three cultivation–fallow cycles, available soil P declines by 44%, and one-time P inputs from biomass burning decline by 76% from mature forest levels. Interception of dust-borne P (“canopy trapping”) declines with lower plant biomass and leaf area, limiting deposition in secondary forest. Potential leaching losses are greater in secondary than in mature forest, but the difference is very small compared with the difference in P inputs. The decline in new P from atmospheric deposition creates a long-term negative ecosystem balance for phosphorus. The reduction in soil P availability will feed back to further limit biomass recovery and may induce a shift to sparser vegetation. Degradation induced by hydrological and biogeochemical feedbacks on P cycling under shifting cultivation will affect farmers in the near future. Without financial support to encourage the use of fertilizer, farmers could increase the fallow period, clear new land, or abandon agriculture for off-farm employment. Their response will determine the regional balance between forest loss and forest regrowth, as well as the frequency of use and rate of recovery at a local scale, further feeding back on ecological processes at multiple scales.     

Application of sensitive enzymeimmunoassay for determination of cortisol in blood plasma of yaks (Poephagus grunniens L.)

As an alternative to radioimmunoassays, a simple, highly sensitive and quick enzymeimmunoassay (EIA) for determination of cortisol in blood plasma of yaks on microtiterplates using second antibody coating technique and cortisol-horseradish peroxidase as a label has been developed. The wells of the microtiterplate were coated with affinity-purified goat IgG (antirabbit IgG) that binds the hormone specific antibody. The EIA was carried out directly in 20 microl of heat treated plasma after 1:5 dilution with PBS. The cortisol standard curve, with doses ranged from 0.4 to 100 pg/well. The sensitivity of the assay was 20 pg/ml. Cortisol standard curve in buffer showed parallelism with serially diluted yak plasma containing high endogenous cortisol. Intra- and inter-assay coefficients of variation (CV) determined using pooled plasma was found 6.58 and 11.35%, respectively. Recovery of known concentrations of added cortisol in charcoal stripped plasma was linear (r = 0.98). For biological validation of cortisol enzymeimmunoassay, the blood samples were collected from yak cows at -48 and -24h before and 0, 12, 24, 36, 48, 60, 72, 84 and 96 h after dexamethasone administration. The plasma cortisol before dexamethasone administration was significantly (P < 0.05) higher than after dexamethasone administration. The developed EIA was further validated biologically by estimating cortisol in peri-parturient cows beginning day 10 prior to calving till day 10 post-calving; the concentrations were along with the expected lines as reported in bovine. In conclusion, the EIA developed in this study is simple, highly sensitive, valid and sufficiently reliable method for estimation of cortisol directly in bovine plasma.     

Pulmonary embolism: computer-aided detection at multidetector row spiral computed tomography

BACKGROUND: We aimed to evaluate the feasibility and performance of a computer-aided detection (CAD) tool for automated detection of segmental and subsegmental pulmonary emboli. METHODS: A CAD tool (ImageChecker CT, R2 Technology, Inc) for automated detection of pulmonary emboli was evaluated on multidetector-row CT studies of varying diagnostic quality in 23 patients (13 female, mean age 52 y) with pulmonary embolism (PE) and of 13 patients (all female, mean age 49 y) without PE. A collimation of 16 x 1 mm and a reconstructed section width of 1.25 mm had been used in each patient. The performance of the CAD tool for the detection of emboli in the segmental and subsegmental pulmonary arterial tree was assessed. Consensus reading of the same studies by 2 radiologists, with a third for adjudication, for the identification of segmental and subsegmental pulmonary emboli was used as the standard of reference. RESULTS: Consensus reading revealed 130 segmental pulmonary emboli and 107 subsegmental pulmonary emboli in the 23 patients with PE. All 23 patients with PE were correctly identified as having PE by the CAD system. In a vessel-by-vessel analysis, the sensitivity of the CAD algorithm was 92% (119/130) for the detection of segmental pulmonary emboli and 90% (92/107) for subsegmental pulmonary emboli. The overall specificity, positive predictive value (95% confidence interval) and negative predictive value (95% confidence interval) of the algorithm were 89.9%, 63.2% (57.9%-68.2%) and 97.7% (96.7%-98.4%), respectively. The average false positive rate of the CAD algorithm was 4.8 (range 1 to 9) false positive detection marks per case. CONCLUSION: CAD of segmental and subsegmental pulmonary emboli based on 1-mm multidetector-row CT studies is feasible. Application of CAD tools may improve the diagnostic accuracy and decrease the interpretation time of computed tomographic angiography for the detection of pulmonary emboli in the peripheral arterial tree and further enhance the acceptance of this test as the first line diagnostic modality for suspected PE.     

The clinical significance of the spectrum of interactions of CAP+1 (A-->C), a silent beta-globin gene mutation, with other beta-thalassemia mutations and globin gene modifiers in north Indians

OBJECTIVES: To assess the clinical significance of the interactions of CAP+1 (A-->C), a silent beta-globin gene mutation, with other beta-thalassemia mutations and globin gene modifiers in north Indians. METHODS: The clinical phenotypes associated with compound heterozygosity for the CAP+1 (A-->C) mutation with other beta-thalassemia mutations, together with the potential effect of the genetic modifiers alpha-thalassemia and the Xmn-1(G)gamma C-->T polymorphism were studied in 30 patients. The frequency of the CAP+1 (A-->C) polymorphism was determined and an analysis of the red cell indices, HbA(2) levels, iron status, and alpha-globin genes was carried out in 35 heterozygotes. RESULTS: Based on an analysis of 1075 beta-thalassemia alleles the CAP+1 (A-->C) mutation constituted 3.2% of north Indians. There was a wide spectrum of phenotypic severity in compound heterozygotes; 18 of 30 were transfusion dependent. There was a very high frequency of the -/- genotype of the Xmn-1(G)gamma polymorphism in compound heterozygotes. Analysis of 35 heterozygotes indicated that approximately half were hematologically normal and therefore genuine 'silent' carriers. CONCLUSIONS: Compound heterozygotes for CAP+1 (A-->C) and other severe beta-thalassemia alleles are phenotypically severe enough to necessitate appropriate therapy and counseling. The unexpected severity of these interactions may be due, in part, to the high frequency of beta-thalassemia alleles associated with the Xmn-1(G)gamma- allele in Indian populations. It is concluded that the CAP+1 (A-->C) mutation can pose serious difficulties in screening and counseling programs in populations in which it occurs at a significant frequency.     

Low levels of plasma soluble complement receptor type 1 in patients receiving thrombolytic therapy for acute myocardial infarction

Background Administration of recombinant soluble CR1 (sCR1) has been shown to attenuate complement mediated myocardial injury in animal models of acute MI. The plasma level of sCR1 in humans with acute MI is not known. We determined the levels of the complement regulatory protein, complement receptor type-1 (CR1) in plasma and its expression on the surface of leukocytes of patients receiving thrombolysis for acute myocardial infarction (AMI). Methods Plasma sCR1 was measured by a sandwich ELISA. The levels in patients with AMI were compared with those in normal controls. Leukocyte surface expression of CR1 was measured by flowcytometry. We correlated these parameters with clinical outcome and left ventricular ejection fraction. Results Patients had very low plasma sCR1 levels. Mean plasma sCR1 levels were significantly less than in controls (6 ± 3.6 ng/mL vs. 44.6 ± 12.2 ng/mL, P < 0.00001). Patients who had an adverse in-hospital outcome had significantly lower sCR1 levels when compared to those who had an uneventful course (3.8 ± 2.0 ng/mL and 7.1 ± 3.8 ng/mL respectively, P = 0.01). The low plasma sCR1 was despite significantly greater lymphocyte and monocyte surface CR1 (which is a potential source of plasma sCR1). Conclusion Plasma sCR1 levels are reduced in patients receiving thrombolysis for AMI. Replenishing plasma sCR1 might limit complement-mediated injury in this setting.     

Metformin is effective in achieving biochemical response in patients with nonalcoholic fatty liver disease (NAFLD) not responding to lifestyle interventions

Background: Insulin resistance plays an important role in the pathogenesis of NAFLD. Pharmacological treatment of patients with NAFLD is still evolving. Insulin sensitizing drugs like metformin may be effective in these patients. Twenty five adult patients with NAFLD who did not achieve normalization of alanine transaminases (ALT) after 6 months of lifestyle interventions and UDCA were treated with metformin 500mg tid for 6 months. Insulin resistance was determined by HOMA-IR. Liver function tests were done monthly and patients were defined having no response, partial response or complete biochemical response depending on the change in ALT. Results were compared with 25 patients with NAFLD from the same cohort treated only with lifestyle interventions (disease controls). Results: Thirteen (52%) patients had class III (n = 5) or class IV (n = 8) disease amounting to histological NASH. Of these 13 patients none had severe inflammation and none had stage 4 fibrosis (cirrhosis). All 25 patients with NAFLD had insulin resistance in comparison to healthy controls. In comparison to disease controls (127.5 ± 41.8 vs. 118 ± 21.6 p = NS), all patients treated with metformin had partial biochemical response (mean ALT 122.2 ± 26.8 vs 74.3 ± 4.2 p < 0.01) and 14 (56%) of them achieved complete normalization of ALT. Conclusions: Metformin is effective to achieve biochemical response in patients with NAFLD who do not respond to lifestyle interventions and UDCA.     

Neuropsychological deficits in human immunodeficiency virus type 1 clade C-seropositive adults from South India

Most studies of cognitive functioning in human immunodeficiency virus type 1 (HIV-1)-seropositive (HIV-1+) subjects have been done in the United States and Europe, where clade B infections predominate. However, in other parts of the world such as South India, where clade C HIV is most common, the prevalence of HIV-1 is increasing. Standardized neuropsychological tests were used to assess cognitive functioning in a sample of 119 adults infected with clade C HIV-1 who were not on antiretroviral medications. The subjects did not have neurological or psychiatric illness and were functioning adequately. Neuropsychological test performance was compared with gender-, age-, and education-matched normative data derived from a sample of 540 healthy volunteers and a matched cohort of 126 healthy, HIV-1-seronegative individuals. Among the seropositive subjects, 60.5% had mild to moderate cognitive deficits characterized by deficits in the domains of fluency, working memory, and learning and memory. None of the subjects had severe cognitive deficits. The HIV-1+ sample was classified into groups according to the level of immune suppression as defined by CD4 count (<200, 201–499, and >500 cells/mm³) and viral load (<5000, 5001–30,000, 30,001–99,999, 100,000–1,000,000, and >1,000,001 copies). Although the most immunosuppressed group (CD4 count <200 cells/mm³ or viral load >1,000,001 copies) was small, their rate of impairment in visual working memory was greater when compared to groups with better immune functioning. Mild to moderate cognitive deficits can be identified on standardized neuropsychological tests in clade C-infected HIV-1+ adults who do not have any clinically identifiable functional impairment. The prevalence of cognitive deficits is similar to that reported in antiretroviral treatment-naïve individuals infected with clade B virus in the western world.