CLINICO-DIAGNOSТIC STUDIES OF SELLEK-FRADE'S ТЕSТ IN PAТIENTS WIТH EPIDEMIC HEPATIТIS

In recent years, due to its mass spread, epidemic hepatitis became а medical рroblem of world-wide importance. Оnе of the still unsatisfactorily solved prblems in connection with this infectious disease is the question related to its diagnosis. Extensive efforts are made to introduce appropriate and reliable clinico-laboratory test particularly having in mind the lack of trustworthy аnd practical applicble specific microbiological tests for etiological diagnosis.Informed from the literature about а new test - that of Sellek-Frade, we set ourselves the task to prove the diagnootic value of this test in оur patients, suffering from epidemic hepatitis.The test is introduced bу Sellek and Fгade in 1957 in Наbапа. The author recommend this test as а very easily performed flocculation test with а considerble diagпostic importance in hepatic disorders. The test is examined later in the clinic of А. Lemaire in Paris.Тhe test of Sellek and Frade is а colloid-stability test, in which cuprum acetate being used as а substance, which disturbs the colloid stability of blооd serum. Similar to most other colloid-stability tests this best becomes positive when the relation between albumins and globulins is disturbed

Structure of the germline genome of Tetrahymena thermophila and relationship to the massively rearranged somatic genome

The germline genome of the binucleated ciliate Tetrahymena thermophila undergoes programmed chromosome breakage and massive DNA elimination to generate the somatic genome. Here, we present a complete sequence assembly of the germline genome and analyze multiple features of its structure and its relationship to the somatic genome, shedding light on the mechanisms of genome rearrangement as well as the evolutionary history of this remarkable germline/soma differentiation. Our results strengthen the notion that a complex, dynamic, and ongoing interplay between mobile DNA elements and the host genome have shaped Tetrahymena chromosome structure, locally and globally. Non-standard outcomes of rearrangement events, including the generation of short-lived somatic chromosomes and excision of DNA interrupting protein-coding regions, may represent novel forms of developmental gene regulation. We also compare Tetrahymenas germline/soma differentiation to that of other characterized ciliates, illustrating the wide diversity of adaptations that have occurred within this phylum.</p

Free Energy Simulations of a GTPase: GTP and GDP Binding to Archaeal Initiation Factor 2

International audienceArchaeal initiation factor 2 (aIF2) is a protein involved in the initiation of protein biosynthesis. In its GTP-bound, "ON" conformation, aIF2 binds an initiator tRNA and carries it to the ribosome. In its GDP-bound, "OFF" conformation, it dissociates from tRNA. To understand the specific binding of GTP and GDP and its dependence on the ON or OFF conformational state of aIF2, molecular dynamics free energy simulations (MDFE) are a tool of choice. However, the validity of the computed free energies depends on the simulation model, including the force field and the boundary conditions, and on the extent of conformational sampling in the simulations. aIF2 and other GTPases present specific difficulties; in particular, the nucleotide ligand coordinates a divalent Mg(2+) ion, which can polarize the electronic distribution of its environment. Thus, a force field with an explicit treatment of electronic polarizability could be necessary, rather than a simpler, fixed charge force field. Here, we begin by comparing a fixed charge force field to quantum chemical calculations and experiment for Mg(2+):phosphate binding in solution, with the force field giving large errors. Next, we consider GTP and GDP bound to aIF2 and we compare two fixed charge force fields to the recent, polarizable, AMOEBA force field, extended here in a simple, approximate manner to include GTP. We focus on a quantity that approximates the free energy to change GTP into GDP. Despite the errors seen for Mg(2+):phosphate binding in solution, we observe a substantial cancellation of errors when we compare the free energy change in the protein to that in solution, or when we compare the protein ON and OFF states. Finally, we have used the fixed charge force field to perform MDFE simulations and alchemically transform GTP into GDP in the protein and in solution. With a total of about 200 ns of molecular dynamics, we obtain good convergence and a reasonable statistical uncertainty, comparable to the force field uncertainty, and somewhat lower than the predicted GTP/GDP binding free energy differences. The sign and magnitudes of the differences can thus be interpreted at a semiquantitative level, and are found to be consistent with the experimental binding preferences of ON- and OFF-aIF2

Naa12 compensates for Naa10 in mice in the amino-terminal acetylation pathway

Amino-terminal acetylation is catalyzed by a set of N-terminal acetyltransferases (NATs). The NatA complex (including X-linked Naa10 and Naa15) is the major acetyltransferase, with 40-50% of all mammalian proteins being potential substrates. However, the overall role of amino-terminal acetylation on a whole-organism level is poorly understood, particularly in mammals. Male mice lacking Naa10 show no globally apparent in vivo amino-terminal acetylation impairment and do not exhibit complete embryonic lethality. Rather Naa10 nulls display increased neonatal lethality, and the majority of surviving undersized mutants exhibit a combination of hydrocephaly, cardiac defects, homeotic anterior transformation, piebaldism, and urogenital anomalies. Naa12 is a previously unannotated Naa10-like paralog with NAT activity that genetically compensates for Naa10. Mice deficient for Naa12 have no apparent phenotype, whereas mice deficient for Naa10 and Naa12 display embryonic lethality. The discovery of Naa12 adds to the currently known machinery involved in amino-terminal acetylation in mice

Naa12 compensates for Naa10 in mice in the amino-terminal acetylation pathway.

Amino-terminal acetylation is catalyzed by a set of N-terminal acetyltransferases (NATs). The NatA complex (including X-linked Naa10 and Naa15) is the major acetyltransferase, with 40-50% of all mammalian proteins being potential substrates. However, the overall role of amino-terminal acetylation on a whole-organism level is poorly understood, particularly in mammals. Male mice lacking Naa10 show no globally apparent in vivo amino-terminal acetylation impairment and do not exhibit complete embryonic lethality. Rather Naa10 nulls display increased neonatal lethality, and the majority of surviving undersized mutants exhibit a combination of hydrocephaly, cardiac defects, homeotic anterior transformation, piebaldism and urogenital anomalies. Naa12 is a previously unannotated Naa10-like paralogue with NAT activity that genetically compensates for Naa10. Mice deficient for Naa12 have no apparent phenotype, whereas mice deficient for Naa10 and Naa12 display embryonic lethality. The discovery of Naa12 adds to the currently known machinery involved in amino-terminal acetylation in mice

Impact of vesicoureteral reflux on the size of renal lesions after an episode of acute pyelonephritis

PURPOSE: We determined the impact of vesicoureteral reflux (VUR) on the size of renal lesions in children after an episode of acute pyelonephritis. MATERIALS AND METHODS: A total of 161 children (mean age 2.44 years) with acute pyelonephritis were studied. All had renal lesions on dimercapto-succinic acid scintigraphy done at admission to the hospital. A second dimercapto-succinic acid scan was performed at 3 months. Voiding cystourethrography was done at 6 weeks and VUR was graded I to V. For each renal unit layouts of renal lesions were drawn, and the damage surface was calculated and reported for the total surface of the kidney. RESULTS: Mean size of acute lesions and scars increased with severity of reflux (p &lt;0.0001), with an important overlap of individual values. Mean size of renal scars in the group of renal units with acute lesions was 5.8% +/- 8.5% in patients without VUR, 9.9% +/- 7.3% in those with grade I reflux, 7.7% +/- 11.0% in those with grade II reflux, 17.7% +/- 14.7% in those with grade III reflux and 17.4% +/- 27.7% in those with grade IV reflux (p &lt;0.001). The size of renal lesions decreased significantly with time. The rate of regression of lesions decreased with increasing reflux. When analyzed according to 3 age groups sizes of scars increased significantly with age. CONCLUSIONS: VUR has an impact on the size of renal lesions after an episode of pyelonephritis. Children with a grade III or IV reflux are more likely to have larger renal scars. On the other hand, acute lesions of important size may develop even in the absence of VUR

SPECT in periodic lateralized epileptiform discharges (PLEDs): a form of partial status epilepticus?

Periodic lateralized epileptiform discharges (PLEDs) are a well defined electroencephalographic entity but whether PLEDs represent an ictal condition or not remains debated. Much work has been done using electroencephalography (EEG) but new approaches using cerebral perfusion imaging may give more information about this question. We aimed to evaluate if PLEDs were associated with high regional cerebral blood flow (rCBF). We studied 18 patients with PLEDs and different pathologies, and performed brain single-photon-emission computed tomography (SPECT) during and, for three cases, after the disappearance of PLEDs. Qualitative variations and locations of rCBF were compared with PLEDs. Association with seizures and type of seizures were also assessed. SPECT showed high rCBF in 18/18 patients (100%). The location of PLEDs and high rCBF matched in 17/18 cases (94%). In the three cases where SPECT was performed after PLEDs disappeared, the high rCBF had cleared (100%). Eighteen cases (100%) presented seizures before recording of PLEDs, mainly motor (partial motor or generalized tonic-clonic). Where there was a decreased rCBF (related to a lesion) there was little relationship to PLEDs and all patients with decreased rCBF had an adjacent increased rCBF. These results confirm preliminary case reports. Hyperperfusion adds further to the argument that PLEDs may be related to a form of partial status epilepticus