Spontaneous electron emission vs dissociation in internally hot silver dimer anions.

Referring to a recent experiment, we theoretically study the process of a two-channel decay of the diatomic silver anion (Ag2 -), namely, the spontaneous electron ejection giving Ag2 + e- and the dissociation leading to Ag- + Ag. The ground state potential energy curves of the silver molecules of diatomic neutral and negative ions were calculated using proper pseudo-potentials and atomic basis sets. We also estimated the non-adiabatic electronic coupling between the ground state of Ag2 - and the ground state of Ag2 + e-, which, in turn, allowed us to estimate the minimal and mean values of the electron autodetachment lifetimes. The relative energies of the rovibrational levels allow the description of the spontaneous electron emission process, while the description of the rotational dissociation is treated with the quantum dynamics method as well as time-independent methods. The results of our calculations are verified by comparison with the experimental data.

Electronic structure and rovibrational predissociation of the 21Π state in KLi.

Adiabatic potential energy curves of the 31Σ+, 33Σ+, 21Π and 23Π states correlating for large internuclear distance with the K(4s) + Li(2p) atomic asymptote were calculated. Very good agreement between the calculated and the experimental curve of the 21Π state allowed for a reliable description of the dissociation process through a small (∼20 cm-1 for J = 0) potential energy barrier. The barrier supports several rovibrational quasi-bound states and explicit time evolution of these states via the time-dependent nuclear Schrödinger equation, showed that the state populations decay exponentially in time. We were able to precisely describe the time-dependent dissociation process of several rovibrational levels and found that our calculated spectrum match very well with the assigned experimental spectrum. Moreover, our approach is able to predict the positions of previously unassigned lines, particularly in the case of their low intensity.

Electronic structure and time-dependent description of rotational predissociation of LiH.

The adiabatic potential energy curves of the 1Σ+ and 1Π states of the LiH molecule were calculated. They correlate asymptotically to atomic states, such as 2s + 1s, 2p + 1s, 3s + 1s, 3p + 1s, 3d + 1s, 4s + 1s, 4p + 1s and 4d + 1s. A very good agreement was found between our calculated spectroscopic parameters and the experimental ones. The dynamics of the rotational predissociation process of the 11Π state were studied by solving the time-dependent Schrödinger equation. The classical experiment of Velasco [Can. J. Phys., 1957, 35, 1204] on dissociation in the 11Π state is explained for the first time in detail.

Angiotensin-converting enzyme activity and the ACE Alu polymorphism in autosomal dominant polycystic kidney disease.

BACKGROUND: Previous studies concerning Alu I/D polymorphism in the ACE gene and ADPKD severity have used the Alu genotypes as a representative of the true biological variable, namely ACE activity. However, wide individual and ethnic differences in the proportion of variance in ACE activity explained by the I/D genotype may have confounded these studies. This investigation examines the association between ADPKD severity and ACE in terms of plasma enzyme activity and I/D genotypes in individuals from three different countries. METHODS: Blood samples were collected from 307 ADPKD patients (116 Australian, 124 Bulgarian and 67 Polish) for determination of ACE activity levels and I/D genotypes. Chronic renal failure (CRF) was present in 117 patients and end-stage renal failure (ESRF) in 68 patients. RESULTS: ACE activity was related to the I/D genotype, showing a dosage effect of the D allele (P=0.006). The proportion of variance due to the Alu polymorphism was 14%. No difference in ACE activity and I/D genotype distribution was found between patients with CRF versus normal renal function (P=0.494; P=0.576) or between those with ESRF versus those without ESRF (P=0.872; P=0.825). No effect of the I/D genotype on age at development and progression to renal failure (CRF; ESRF) was detected in the overall group, and in subgroups based on ethnic origin, linkage status and sex. CONCLUSION: ACE is not likely to play a role as a determinant of ADPKD phenotype severity.

[Current opinions on the etiology and pathogenesis of autosomal dominant polycystic kidney disease (ADPKD). II. Factors other than genetic factors which have an influence on disease course and selected clinical problems]. / Aktualne poglady na etiologie i patogeneze zwyrodnienia wielotorbielowatego nerek typu doroslych (ADPKD). Czesc II: inne niz genetyczne czynniki wplywajace na przebieg choroby i wybrane problemy kliniczne.

In the first part of this paper achievements in the genetic investigations of ADPKD and pathomechanism of cyst formation have been presented. Majority of authors acknowledge that first type of the disease (ADPKD1) in comparison with the second (ADPKD2) has more severe clinical course. On the basis of clinical analysis of selected affected families the larger and larger emphasis has been put on the influence of such factors like: presence of arterial hypertension, especially role of RAA system, sex, diet, hyperlipoproteinemia, environmental factors, toxic and infectious agents. It seems that genetic analysis of the RAA system and ADPKD will partially explain differences in the clinical course of the disease in different families. Persons with DD genotype in RAA system have statistically significant, more severe clinical course in comparison with their relatives with DI or II genotype. Decidedly worse course of the disease is observed in patients with positive family history of arterial hypertension and in persons with increased blood pressure. Patients sex play a major role. Men have more severe renal manifestations, when in women symptoms and complications associated with liver cysts are more frequent than in men. Frequency of intracranial aneurysms (ICA) in the population of patients with ADPKD have been presented. CT, MRA and classical angiography are in order screening tests for detection of ICA, especially in persons with family history of their prevalence. Prevalence of liver cysts and selected clinical symptoms and complications associated with extrarenal manifestations have been discussed. Problems associated with infections of the urinary tract and cysts, their etiology, pathomechanisms and treatment have been presented. Ultrasonography seems to be the best diagnostic tool because of it's accessibility, high sensitivity and low cost. It is accepted, that presence of 3 cysts in both kidneys in ADPKD kindreds in significant for diagnosis. Modified Ravine's criteria for diagnosis of ADPKD have also been presented. Employment of modern diagnostic methods in combination with genetic analysis (especially linkage analysis) enable early diagnosis in persons who are at risk of ADPKD.

[Current opinions about the etiology and pathogenesis of autosomal dominant polycystic kidney disease (ADPKD). I. Selected genetic aspects and mechanisms of cyst formation]. / Aktualne poglady na etiologie i patogeneze zwyrodnienia wielotorbielowatego nerek typu doroslych (ADPKD). Czesc I: Wybrane aspekty genetyczne i mechanizmy powstawania cyst.

The aim of this study is to present in the chronological order evolution of opinions about the etiopathogenesis of Autosomal Dominant Polycystic Kidney Disease (ADPKD), with the special regard to the newest genetic investigations. Prevalence of this disease is estimated at 1:1000, and patients with ADPKD compose up to 10% patients, who need renal replacement therapy. Since 1957, when inheritance was defined by Daalgard as autosomal dominant, a rapid progression in investigations of genetic aspects of this disease has been done. Actually three genes responsible for the development of the disease are known: PKD1 gene located on the short arm of the chromosome 16 (isolated and described in 1994-1995), PKD2 gene, which is located on the long arm of the chromosome 4 (isolated in 1996) and exceptionally occurs PKD3 gene which is not mapped by linkage analysis neither on the PKD1 nor the PKD2. Loci for PKD3 gene is unknown up to now. Investigations, which have been done indicate dependence between genetic type of ADPKD and clinical picture of the disease. Majority of authors consider ADPKD1 as the severe form of the disease, although it is not a rule. The biggest emphasis has been also lay on the influence of other factors. Pathomechanisms of cyst formation in kidneys, the presence of which is pathognomonic for this disease has been better and better understood. Employment of modern diagnostic methods with combinations of the genetic analysis (especially linkage analysis) afford possibilities for early diagnosis of the disease among persons, who are kindreds of ADPKD family members and are at risk of the disease.