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Vaginal breech delivery (VBD) has been widely discouraged over the last two decades due to associated neonatal risks. However, many gynaecologists are still challenging this approach, at least in selected settings.To study short-term neonatal outcomes in singleton pregnancies undergoing VBD.Retrospective cohort study conducted on singleton pregnancies who delivered in breech presentation between 2012 and 2019. Neonatal complications in terms of mortality, umbilical artery (UA) pH, 5-min Apgar score, and postnatal admission to neonatal intensive care unit (NICU) were evaluated.Overall, 804 breech deliveries were considered. Of these, 53.86 % had VBD, 26.62 % had emergency caesarean sections (CS) and 19.53 % had elective CS. No perinatal deaths were reported. After multivariate adjustment, VBD was associated with higher incidence of UA pH 7.10 compared with both elective and emergency CS. No significant associations were found between VBD and UA pH 7.00 or 5-min Apgar score 3 or 7. No significant differences in NICU hospitalization were observed for different modes of delivery. Gestational age was inversely correlated with UA pH 7.00, 5-min Apgar score 3 and 7, and NICU hospitalization.VBD in an experienced setting does not increase the risk of negative short-term perinatal outcomes significantly. Gestational age was the most important risk factor for low UA pH or 5-min Apgar score and NICU hospitalization, independent of mode of delivery.

An increasing number of patients have refractory angina despite optimal medical therapy and are without further revascularization options. Preclinical studies indicate that human CD34 + stem cells can stimulate new blood vessel formation in ischemic myocardium, improving perfusion and function. In ACT34-CMI ( N = 167), patients treated with autologous CD34 + stem cells had improvements in angina and exercise time at 6 and 12 months compared to placebo; however, the longer-term effects of this treatment are unknown. ACT34 was a phase II randomized, double-blind, placebo-controlled clinical trial comparing placebo, low dose (1 × 10 5 CD34/kg body weight), and high dose (5 × 10 5 CD34/kg) using intramyocardial delivery into the ischemic zone following NOGA ® mapping. To obtain longer-term safety and efficacy in these patients, we compiled data of major adverse cardiac events (MACE; death, myocardial infarction, acute coronary syndrome, or heart failure hospitalization) up to 24 months as well as angina and quality of life assessments in patients who consented for 24-month follow-up. A total of 167 patients with class III–IV refractory angina were randomized and completed the injection procedure. The low-dose-treated patients had a significant reduction in angina frequency ( p = 0.02, 0.035) and improvements in exercise tolerance testing (ETT) time ( p = 0.014, 0.017) compared to the placebo group at 6 and 12 months. At 24 months, patients treated with both low-and high-dose CD34 + cells had significant reduction in angina frequency ( p = 0.03). At 24 months, there were a total of seven deaths (12.5%) in the control group versus one (1.8%) in the low-dose and two (3.6%) in the high-dose ( p = 0.08) groups. At 2 years, MACE occurred at a rate of 33.9%, 21.8%, and 16.2% in control, low-, and high-dose patients, respectively ( p = 0.08). Autologous CD34 + cell therapy was associated with persistent improvement in angina at 2 years and a trend for reduction in mortality in no-option patients with refractory angina.

An increasing number of patients have refractory angina despite optimal medical therapy and are without further revascularization options. Preclinical studies indicate that human CD34

Rationale: A growing number of patients with coronary disease have refractory angina. Preclinical and early-phase clinical data suggest that intramyocardial injection of autologous CD34+ cells can improve myocardial perfusion and function. Objective: Evaluate the safety and bioactivity of intramyocardial injections of autologous CD34+ cells in patients with refractory angina who have exhausted all other treatment options. Methods and Results: In this prospective, double-blind, randomized, phase II study (ClinicalTrials.gov identifier: NCT00300053), 167 patients with refractory angina received 1 of 2 doses (1×10 5 or 5×10 5 cells/kg) of mobilized autologous CD34+ cells or an equal volume of diluent (placebo). Treatment was distributed into 10 sites of ischemic, viable myocardium with a NOGA mapping injection catheter. The primary outcome measure was weekly angina frequency 6 months after treatment. Weekly angina frequency was significantly lower in the low-dose group than in placebo-treated patients at both 6 months (6.8±1.1 versus 10.9±1.2, P =0.020) and 12 months (6.3±1.2 versus 11.0±1.2, P =0.035); measurements in the high-dose group were also lower, but not significantly. Similarly, improvement in exercise tolerance was significantly greater in low-dose patients than in placebo-treated patients (6 months: 139±151 versus 69±122 seconds, P =0.014; 12 months: 140±171 versus 58±146 seconds, P =0.017) and greater, but not significantly, in the high-dose group. During cell mobilization and collection, 4.6% of patients had cardiac enzyme elevations consistent with non-ST segment elevation myocardial infarction. Mortality at 12 months was 5.4% in the placebo-treatment group with no deaths among cell-treated patients. Conclusions: Patients with refractory angina who received intramyocardial injections of autologous CD34+ cells (10 5 cells/kg) experienced significant improvements in angina frequency and exercise tolerance. The cell-mobilization and -collection procedures were associated with cardiac enzyme elevations, which will be addressed in future studies.

From late December 2007 to February 2008, the number of adverse responses to heparin infusions rose noticeably above baseline levels in North America, ultimately resulting in a widespread recall of all heparin vial products made by Baxter Healthcare. Using various analytical techniques and the de novo synthesis of a fully sulfated chondroitin sulfate (FSCS) derivative, the authors have confirmed the identity of the contaminant as an oversulfated chondroitin sulfate (OSCS) and have also defined the heterogeneity and concentration of this contaminant in various lots of heparin. Using both contaminated heparin products and the synthetically produced derivative, the authors have shown that the OSCS produces a dose-dependent hypotension in both pigs and rats and that the response in rats can be abrogated with bradyzide, a rodent-selective B(2) bradykinin receptor antagonist. The no observed effect level (NOEL) for this contaminant appears to be approximately 1 mg/kg, corresponding to a contamination level in finished lots of heparin of approximately 3%. Using human plasma, the OSCS derivative was shown to activate kallikrein. These data provide insight into the etiology of the adverse events, particularly refractory hypotension, observed in patients who were exposed to heparin contaminated with OSCS.

For certain one-dimensional Schroedinger-type difference operators with a complex potential, a "complete" set of exponentially decaying eigenvectors is shown to exist. "Completeness" entails that the parameters involved are obtained through evaluation of analytic functions on a Riemann surface.

It is shown that the logarithmic potential associated with the integrated density of states is constant on the spectrum of the almost Mathieu operator in case the irrational frequency is sufficiently well approximable by rationals in terms of a diophantine condition.

It is shown that for any irrational rotation number and any admissible gap labelling number the almost Mathieu operator (also known as Harper's operator) has a gap in its spectrum with that labelling number. This answers the strong version of the so-called "Ten Martini Problem". When specialized to the particular case where the coupling constant is equal to one, it follows that the "Hofstadter butterfly" has for any quantum Hall conductance the exact number of components prescribed by the recursive scheme to build this fractal structure., Comment: 17 pages. Corrected a misstatement in Remark 2) following the proof of Theorem 1.4, and changed the wording in the discussion of the system (2.1) in the second paragraph of Section 2

To study the regulation of proliferation of lung alveolar epithelial type 2 cells, we have established a cell line derived from neonatal type 2 cells by transfection with the SV40 large T antigen gene. We find that this cell line, designated SV40-T2, displays the same post-transcriptional control of expression of proliferation-related genes, including c-myc, ornithine decarboxylase, thymidine kinase, and histone, that we have previously described in primary isolates of type 2 cells (Clement et al., Proc. Natl. Acad. Sci. USA 87, 318–322, 1990). Both proliferating and nonproliferating SV40-T2 cells express these genes at high levels, but their translation products are only detected in proliferating cells. Using the histone gene as an example, we have found that regulation of expression occurs at the level of transcription and of mRNA turnover, as previously described in other mammalian systems. However, in addition, regulation of expression also occurs at the level of translation of the histone mRNA, because its protein product is not detectable in nonproliferating SV40-T2 cells. We have analyzed the steps which are potentially involved in this translational regulation of histone gene expression in SV40-T2 cells. In both proliferating and nonproliferating cells, histone mRNA was found to be efficiently transported from the nucleus to the cytoplasm and to associate with the translationally active heavy polysomal fractions. These results indicate that control of histone gene expression (and perhaps that of other proliferation-related genes) in lung epithelial cells may involve either rapid and selective degradation of histone protein or binding factor(s) which modulate translational efficiency of histone mRNA.

Linear discriminant analysis (LDA) as a dimension reduction method is widely used in classification such as face recognition. However, it suffers from the small sample size (SSS) problem when data dimensionality is greater than the sample size, as in images where features are high dimensional and correlated. In this paper, we propose to address the SSS problem in the framework of statistical learning theory. We compute linear discriminants by regularized least squares regression, where the singularity problem is resolved. The resulting discriminants are complete in that they include both regular and irregular information. We show that our proposal and its nonlinear extension belong to the same framework where powerful classifiers such as support vector machines are formulated. In addition, our approach allows us to establish an error bound for LDA. Finally, our experiments validate our theoretical analysis results.

Nuclear transport as well as reassembly of the nuclear envelope (NE) after completion of mitosis are processes that have been shown to require GTP and ATP. To study the presence and localization of GTP-binding proteins in the NE, we have combined complementary techniques of [alpha-32P]GTP binding to Western-blotted proteins and UV crosslinking of [alpha-32P]GTP with well-established procedures for NE subfractionation. GTP binding to blotted NE proteins revealed five low molecular mass GTP-binding proteins of 26, 25, 24.5, 24, and 23 kDa, and [alpha-32P]GTP photoaffinity labeling revealed major proteins with apparent molecular masses of 140, 53, 47, 33, and 31 kDa. All GTP-binding proteins appear to localize preferentially to the inner nuclear membrane, possibly to the interface between inner nuclear membrane and lamina. Despite the evolutionary conservation between the NE and the rough endoplasmic reticulum, the GTP-binding proteins identified differed between these two compartments. Most notably, the 68- and 30-kDa GTP-binding subunits of the signal recognition particle receptor, which photolabeled with [alpha-32P]GTP in the rough endoplasmic reticulum fraction, were totally excluded from the NE fraction. Conversely, a major 53-kDa photolabeled protein in the NE was absent from rough endoplasmic reticulum. Whereas Western-blotted NE proteins bound GTP specifically, all [alpha-32P]GTP photolabeled proteins could be blocked by competition with ATP, although with a competition profile that differed from that obtained with GTP. In comparative crosslinking studies with [alpha-32P]ATP, we have identified three specific ATP-binding proteins with molecular masses of 160, 78, and 74 kDa. The localization of GTP- and ATP-binding proteins within the NE appears appropriate for their involvement in nuclear transport and in the GTP-dependent fusion of nuclear membrane vesicles required for reassembly of the nucleus after mitosis.

Quantitative measurement of [3H]thymidine [( 3H]TdR) incorporation into cultured cells is widely used as an indicator of cell proliferation. The observation that adult type II cells are able to incorporate large amounts of [3H]TdR despite the fact that they are not proliferating raised the question of the meaning of [3H]TdR incorporation in these cells. Comparing different systems of proliferating and nonproliferating type II cells and lung fibroblasts, we show that nonproliferating type II cells are able to synthesize some thymidine nucleotides used as immediate precursors for DNA synthesis and that most of the radioactivity incorporated into acid-insoluble material in these cells is actually in DNA. We found that hydroxyurea inhibited [3H]TdR incorporation into DNA, suggesting that nonreplicating type II cells use thymidine for scheduled, i.e., replicative, rather than unscheduled, or repair, DNA synthesis. However, newly synthesized DNA does not appear to be in a stable form, available for replication. These studies demonstrate that, in culture, adult type II cells initiate but are unable to complete scheduled DNA synthesis. They also establish that [3H]TdR incorporation cannot be used as an indicator of cell proliferation in cultured type II cells.

Linear discriminant analysis (LDA) as a dimension reduction method is widely used in data mining and machine learning. It however suffers from the small sample size (SSS) problem when data dimensionality is greater than the sample size. Many modified methods have been proposed to address some aspect of this difficulty from a particular viewpoint. A comprehensive framework that provides a complete solution to the SSS problem is still missing. In this paper, we provide a unified approach to LDA, and investigate the SSS problem in the framework of statistical learning theory. In such a unified approach, our analysis results in a deeper understanding of LDA. We demonstrate that LDA (and its nonlinear extension) belongs to the same framework where powerful classifiers such as support vector machines (SVMs) are formulated. In addition, this approach allows us to establish an error bound for LDA. Finally our experiments validate our theoretical analysis results.

Linear discriminant analysis (LDA) is a very important approach to selecting features in classification such as facial recognition. However it suffers from the small sample size (SSS) problem where LDA cannot be solved numerically. The SSS problem occurs when the number of training samples is less than the number of dimensions, which is often the case in practice. Researchers have proposed several modified versions of LDA to deal with this problem. However, a solid theoretical analysis is missing. In this paper, we analyze LDA and the SSS problem based on learning theory. LDA is derived from Fisher’s criterion. However, when formulated as a least square approximation problem, LDA has a direct connection to regularization network (RN) algorithms. Many learning algorithms such as support vector machines (SVMs) can be viewed as regularization networks. LDA turns out to be an RN without the regularization term, which is in general an ill-posed problem. This explains why LDA suffers from the SSS problem. In order to transform the ill-posed problem into a well-posed one, the regularization term is necessary. Thus, based on statistical learning theory, we derive a new approach to discriminant analysis. We call it discriminant learning analysis (DLA). DLA is wellposed and behaves well in the SSS situation. Experimental results are presented to validate our proposal.

It is shown that the complete localization of eigenvectors for the almost Mathieu operator entails the absence of Cantor spectrum for this operator.

suggest that all three proteins have evolved at different rates and have acquired unique functions in their respective spe­ cies and organs. A comparative fine structure analysis would greatly facilitate our understanding of the regulation of tis­ sue-specificity and hormonal control of these three homolo­ gous genes, as well as the ligand binding and other properties of their corresponding proteins. It is likely that such research would yield insight into the rather poorly understood physio­ logic role of these proteins. Uteroglobin (also called blastokinin) is encoded by a sin­ gle copy gene of 3 kb (8) and is composed of three exons and two introns. The protein is a dimer of two identical subunits of 70 amino acids each (after cleavage of a 21-amino acid leader peptide), which are joined by two disulfide bonds. In the rabbit uterus, uteroglobin is induced during the preim­

Our laboratory is studying mechanisms of growth control in alveolar type 2 cells. This highly differentiated cell is induced to proliferate in lungs of animals of all ages during various forms of growth and during the repair process after lung injury. Using type 2 (T2) cells isolated from adult and neonatal rat lungs and an SV40-T transfected T2 cell line, we have shown tha growth-arrested T2 cells constitutively express genes associated with G1 and S phase of the cell cycle, yet they do not efficiently translate the proteins encoded by these genes. This block of growth-related gene expression is post-transcriptional and appears to involve mechanisms that control translation, perhaps at the level of initiation. Furthermore, growth-arrested T2 cells initiate DNA synthesis; however, the cells do not complete the cell cycle, suggesting that they are arrested in a late stage, perhaps the G1/S border. Differential screening of a cDNA library of growth-arrested T2 cells with DNA from growing and growth-arrested T2 cells has identified four families of genes preferentially expressed in the growth-arrested cells. These genes, which are in the process of being characterized, may be responsible for the unusual type of growth arrest demonstrated by T2 cells.

We have used the yeast two-hybrid system to isolate cDNAs encoding proteins that specifically interact with the 42-aa β-amyloid peptide (Aβ), a major constituent of senile plaques in Alzheimer’s disease. The carboxy terminus of α 2 -macroglobulin (α2M), a proteinase inhibitor released in response to inflammatory stimuli, was identified as a strong and specific interactor of Aβ, utilizing this system. Direct evidence for this interaction was obtained by co-immunoprecipitation of α2M with Aβ from the yeast cell, and by formation of SDS-resistant Aβ complexes in polyacrylamide gels by using synthetic Aβ and purified α2M. The association of Aβ with α2M and various purified amyloid binding proteins was assessed by employing a method measuring protein–protein interactions in liquid phase. The dissociation constant by this technique for the α2M–Aβ association using labeled purified proteins was measured ( K d = 350 nM). Electron microscopy showed that a 1:8 ratio of α2M to Aβ prevented fibril formation in solution; the same ratio to Aβ of another acute phase protein, α 1 -antichymotrypsin, was not active in preventing fibril formation in vitro . These results were corroborated by data obtained from an in vitro aggregation assay employing Thioflavine T. The interaction of α2M with Aβ suggests new pathway(s) for the clearance of the soluble amyloid peptide.

We have used a photoreactive cross-linking reagent, poly(A/8-N3-A) (a poly(A) of average molecular mass of 100 kDa in which 5-10% of the A residues are replaced by 8-N3-A), to label poly(A) binding proteins of rat liver nuclear envelopes. This reagent was prepared by polymerizing a mixture of ADP and 8-N3-ADP with polynucleotide phosphorylase. The purified poly(A) was labeled in the 5'-position with a 32P group. In nuclear envelopes prepared by a low salt DNase I procedure, the poly(A/8-N3-A) labeled a protein-nucleic acid complex of approximately 270 kDa, which on degradation with RNase U2 or NaOH at pH 10 yielded two polypeptides of approximately 50 and 30 kDa. These photoreaction products were markedly decreased when resealed nuclear envelopes or non-nuclear envelope proteins were irradiated in the presence of poly(A/8-N3-A). The affinity labeling was intensified when resealed vesicles were made leaky by freezing or ultrasonication, suggesting that the poly(A) binding proteins are accessible from the nucleoplasmic but not the cytoplasmic face of the envelope. Moreover binding was specific for poly(A). Alternative reagents, random poly(A/8-N3-A,C,G,U) of about 100 kDa and poly(dA) (molecular mass between 350 and 515 kDa), showed a very low affinity for poly(A) recognition proteins in the low salt DNase I-treated nuclear envelopes; the 270-kDa band was labeled only weakly. The binding site was not protected by poly(A,C,G,U), weakly by poly(dA), and distinctly by poly(A).

The authors present the case of a 60-year old woman who developed acquired immunedeficiency syndrome (AIDS) 43 months after a blood transfusion. The blood donor was identified as a sexually active homosexual man who frequently used intravenous drugs. Although he was asymptomatic, physical examination revealed generalized lymphadenopathy of cervical, axillary, and inguinal areas. 47 months after his blood donation, the donor underwent lymph node biopsy which revealed follicular hyperplasia. He was seropositive for antibodies to human T-lymphotropic virus type III (HTLV-III) and had serologic evidence of prior infection with cytomegalovirus, Epstein-Barr virus, and hepatitis B virus. On the other hand, he had a normal total lymphocyte count and normal T-cell subsets. Striking was the difference between the seropositivity of the high-risk donor and the seronegativity of the patient with transfusion-associated AIDS with respect to cytomegalovirus, Epstein-Barr virus, and hepatitis B virus. The demonstration of apparent transmission of HTLV-III by blood transfusion and the inability to detect evidence of infection with other viruses strongly indicate a primary etiologic role for this virus in the pathogenesis of AIDS. The high-risk blood donor continues to be an asymptomatic carrier of HTLV-III. The authors are currently comparing the HTLV-III isolates obtained from the blood donor with the HTLV-III-related RNA sequences detected in the spleen of the patient in order to determine whether molecular changes occurred after transmission of the virus that might be related to the development of AIDS.

The following matrices are considered $$A_k = \left( {\begin{array}{*{20}c} k \\ 1 \\ \end{array} \begin{array}{*{20}c} 2 \\ k \\ \end{array} } \right), B_k \left( {\begin{array}{*{20}c} {k - 1} \\ 1 \\ \end{array} \begin{array}{*{20}c} 1 \\ {k + 1} \\ \end{array} } \right),k \in \mathbb{N},$$ which are strong shift equivalent in the sense ofWilliams [7]. In case\(k + \sqrt 2 \) is a prime number of the algebraic field\(\mathbb{Q}(\sqrt 2 )\) matrices are defined which determine the possible choices of rank two matrices connectingAk andBk in the sense of strong shift equivalence. A complete list of all these matrices is given.

Simian T-lymphotropic retroviruses with structural, antigenic, and cytopathic features similar to the etiologic agent of human acquired immunodeficiency syndrome, human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV), have been isolated from a variety of primate species including African green monkeys (STLV-IIIAGM). This report describes nucleic acid cross-reactivity between STLV-IIIAGM and HTLV-III/LAV, molecular cloning of the STLV-IIIAGM genome, and evaluation of its structure and genetic relationship to other retroviruses. Overlapping clones from a cell line infected with virus from a single animal were found to encompass the entire STLV-IIIAGM genome and exhibit a limited degree of restriction-site variability. Specific hybridizing fragments were detected in DNA from this and other STLV-IIIAGM-infected cell lines. A fraction of viral DNA present in at least two STLV-IIIAGM lines persists as unintegrated viral DNA, a characteristic of infection with cytopathic retroviruses. Strongest cross-reactivity was detected between HTLV-III/LAV pol- and gag- genes and STLV-IIIAGM, whereas no cross-reactivity was detected between STLV-IIIAGM and molecular clones of human T-lymphotropic virus types I and II (HTLV-I and -II), visna virus, bovine leukemia virus, or feline leukemia virus.

A concept of eigenstates is discussed for almost Mathieu operators, relating these operators to the rotation C*-algebras they are associated with and to the integrated density of states. For irrational rotations the eigenstates give rise to a notion of multiplicity for all points in the spectrum of an almost Mathieu operator, an integer which is either 1 or 2. It is shown how the occurrence of point spectrum relates to the multiplicity of the corresponding eigenvalues.

Closed nuclear envelope ghosts in the physiological orientation were prepared from rat liver and nuclei as previously described. Here we report transport measurements of various proteins and ribonucleic acids across the envelope of these vesicles. Histones were accumulated rapidly in the ghosts, in contrast to other, nonnuclear, proteins. Triton X-100 removal of the external nuclear membrane from loaded vesicles, as well as comparative studies with open vesicles, excluded the effects of external adsorption. The exchange rate of histones across the nuclear envelope is strongly depressed in the presence of GTP and GDP. The vesicles contain the translocation mechanism for poly(A)-containing RNA. The translocation of poly(A), messenger RNA, and ribosomal RNA was investigated after entrapment of these nucleic acids during the preparation of vesicles. Our data show that the complete export of only poly(A)-containing RNA from the vesicles is enhanced in the presence of 2 mM ATP. This RNA, as well as poly(A), is transported unidirectionally.

A unital C*-algebra is said to satisfy the Dixmier property if for each element x in the closed convex hull of all elements of the form u*xu, u being a unitary in , intersects the centre of ((2), 2·7). The von Neumann algebras and also some other classes of C*-algebras are known to satisfy the Dixmier property (cf. (2), (3), (4), (6)). If is a simple C*-algebra which satisfies the Dixmier property then has at most one tracial state. In (3) Archbold raised the question whether there exists a unital simple C*-algebra which has at most one tracial state without satisfying the Dixmier property. In the present note we characterize the unital simple C*-algebras with at most one tracial state in terms of a condition which is similar to the Dixmier property, but is in fact formally weaker in the framework of simple C*-algebras. This characterization relies on the method used by Pedersen in (5) in order to show that for a unital simple C*-algebra which has at most one tracial state and at least one non-trivial projection the linear span of all projections in is dense in As an application we characterize those unital simple C*-algebras with a unique tracial state which satisfy the Dixmier property.

Although much is now known of the strain variation among the type-1 human immunodeficiency virus (HIV-1), which is the cause of AIDS (acquired immune deficiency syndrome) in the United States, Europe, and Central Africa, much less is yet known about a second group of viruses that have been found in West Africans. One member of this group, named human T-cell lymphotropic virus type 4 (HTLV-4), has been isolated from healthy Senegalese. Another is the virus isolated from West Africans with AIDS-like illness and originally called LAV-2 but now renamed HIV-2. Both these viruses seem to be less closely related to HIV-1 than they are to a virus of healthy African green monkeys, known variously as simian T-cell lymphotropic virus type 3 (STLV-3) or simian immunodeficiency virus (SIV), which in turn is related to viruses isolated from healthy sooty mangabeys and captive macaques with a form of immunodeficiency (to distinguish these viruses they are referred to as STLV-3 (or SIV)agm, STLV-3mac, or STLV-3smm). To clarify the relationship between the various HIVs, STLV-3s and HTLV-4 we are determining and comparing the molecular and biological characteristics of several of them. Following our recent publication of a restriction-site map of STLV-3agm, we now report that the equivalent map of three isolates of HTLV-4 is remarkably similar to it. In addition we present comparative sequence data on the long terminal repeats (LTR) of HTLV-4, STLV-3agm, HIV-1 and HIV-2, together with evidence that cloned HTLV-4 uses the same receptor as HIV-1 and induces some, but not all, of the cytopathic effects attributed to most isolates of HIV-1 and HIV-2.

The notion of strong decomposable operators on topological direct integrals will be introduced and without any countability assumption fundamental properties are proved.

Feline leukaemia viruses (FeLV) are exogenous retroviruses that can be detected in most cats with leukaemia, aplastic anaemia, myeloproliferative diseases and fatal immunosuppression. FeLV isolates have been divided into three subgroups, based on the viral envelope-determined properties of interference and host range in vitro. FeLV-A is present in all natural isolates and is generally minimally pathogenic. FeLV-B is found with FeLV-A in isolates from approximately 40% of natural infections and in a higher percentage of cats with lymphoma. Following the fundamental observations of genetic reassortment of avian retroviruses with endogenous viral genes and the origination of lymphomagenic viruses during the ontogeny of AKR mice, we show here that transfection of feline cells with FeLV-A DNA results in its recombination with endogenous FeLV-related sequences to produce viruses with the structural and host range properties of FeLV-B. Thus in vitro propagation of a retrovirus may result in the generation of variants with very different properties.

The nuclear envelope (NE) separates the two major compartments of eukaryotic cells, the nucleus and the cytoplasm. Recent studies suggest that the uptake of nuclear proteins into the nucleus is initiated by binding of nuclear location signals (NLSs) contained within these proteins to receptors in the NE, followed by translocation through the nuclear pore complex. To examine the binding step without interference from intranuclear events, we have used a system consisting of (i) purified rat liver NEs fixed onto glass slides and (ii) the prototype simian virus 40 large T antigen (SV40 T) NLS conjugated to nonnuclear carrier proteins, and we have visualized the receptor-ligand interaction by indirect immunofluorescence. In this system, incubation of isolated NEs with the wild-type SV40 T NLS conjugate with carrier proteins resulted in binding that was signal sequence-dependent, could be competitively blocked with excess conjugated and unconjugated wild-type peptide, did not require ATP, and was not affected by the transport-inhibiting lectin wheat germ agglutinin. In contrast, only minimal binding was observed with a mutant SV40 T NLS conjugate. These results are consistent with those obtained in other, more complex in vitro systems and suggest that binding of the SV40 T NLS is receptor-mediated. Binding is largely abolished by extraction of the NE with the nonionic detergent Triton X-100, suggesting that the receptor is soluble in detergent. We find in the Triton X-100 supernatant four major NLS-binding proteins with apparent molecular masses of 76, 67, 59, and 58 kDa by photoaffinity labeling with a highly specific crosslinker, azido-NLS. The reduced complexity of the system described here should be useful for the functional study of other potential NLSs for the identification and isolation of their binding sites and for the screening of antibodies raised against these binding sites.

Feline leukemia virus (FeLV) C-Sarma (or FSC) is a prototype of subgroup C FeLVs, which induce fatal aplastic anemia in outbred specific-pathogen-free (SPF) cats. FeLV C isolates also possess an extended host range in vitro, including an ability, unique among FeLVs, to replicate in guinea pig cells. To identify the viral determinants responsible for the pathogenicity and host range of FSC we constructed a series of proviral DNAs by exchanging gene fragments between FSC and FeLV-61E (or F6A), the latter of which is minimally pathogenic and whose host range in vitro is restricted to feline cells. Transfer of an 886-base-pair (bp) fragment of FSC, encompassing the codons for 73 amino acids at the 3' end of pol (the integrase/endonuclease gene) and the codons for 241 amino acids of the N-terminal portion of env [the extracellular glycoprotein (gp70) gene], into the F6A genome was sufficient to confer onto chimeric viruses the ability to induce fatal aplastic anemia in SPF cats. In contrast, no chimera lacking this sequence induced disease. When assayed in vitro, all chimeric viruses containing the 886-bp fragment of FSC acquired the ability to replicate in heterologous cells, including dog and guinea pig cells. Thus, the pathogenic and the host range determinants of the feline aplastic anemia retrovirus colocalize to a 3' pol-5' env region of the FSC genome and likely reside within a region encoding 241 amino acid residues of the N terminus of the extracellular glycoprotein.

On montre que toute algebre de Von Neumann #7B-M avec un vecteur cyclique et separant peut decomposer en facteurs de facon que le type de #7B-M soit preserve sous cette decomposition

Nuclear envelope membranes from rat liver cells contain ATPases, one of which can be inhibited and irreversibly labeled by (S-dinitrophenyl)-6-mercaptopurine riboside triphosphate. Inhibition and covalent substitution of the ATPase are achieved only after disruption of the nuclei, the ATP analogue is inactive on the ATPase activity of whole nuclei or on vesicles of the membrane prepared after a modified heparin method of Bornens and Courvalin. Electron micrographs and scanning micrographs helped to establish the characterization of closed vesicles and intact nuclei. With the aid of (alpha-32P)-labeled, and of the (beta, gamma-32P)-labeled analogue, it was possible to demonstrate the incorporation of the nucleotide into a few protein regions of the nuclear membrane disc electrophoresis pattern.

Nucleotide sequence analysis of the 3′ portion of the genome of simian T-lymphotropic virus type 3 from African green monkeys (STLV-3agm) reveals that it has the same general genome structure as the human immunodeficiency virus (HIV-1), the etiologic agent of AIDS. Short segments of strong amino acid homology and similar predicted protein structure characterize the tat and art/trs open reading frames (orf) of both viruses. Strong conservation of 3′ orf and of another, cs-orf, for which no protein product has been identified suggests that they both encode proteins important to the life cycle of these viruses. The extracellular glycoproteins of STLV-3 and HIV-1 share a similar backbone structure and 50%–55% amino acid homology in constant domains of the HIV-1 protein. The most evident departure in structural organization is truncation of the transmembrane glycoproteins in two STLV-3agm clones and a biologically active, noncytopathic clone of HTLV-4.

The purpose of these notes is twofold. First we bring together the mathematical structure underlying quantum logics, namely orthomodular lattices on the one side, and a notion of abstract "projections" in ordered vector spaces we introduced in [5], and which we called fundamental units on the other side. Second we present an extension theorem for states on an orthomodular lattice satisfying the chain condition.

We report the first complete nucleotide sequence (8,440 base pairs) of a biologically active feline leukemia virus (FeLV), designated FeLV-61E (or F6A), and the molecular cloning, biological activity, and env-long terminal repeat (LTR) sequence of another FeLV isolate, FeLV-3281 (or F3A). F6A corresponds to the non-disease-specific common-form component of the immunodeficiency disease-inducing strain of FeLV, FeLV-FAIDS, and was isolated from tissue DNA of a cat following experimental transmission of naturally occurring feline acquired immunodeficiency syndrome. F3A clones were derived from a subgroup-A-virus-producing feline tumor cell line. Both are unusual relative to other molecularly cloned FeLVs studied to date in their ability to induce viremia in weanling (8-week-old) cats and in their failure to induce acute disease. The F6A provirus is organized into 5'-LTR-gag-pol-env-LTR-3' regions; the gag and pol open reading frames are separated by an amber codon, and env is in a different reading frame. The deduced extracellular glycoproteins of F6A, F3A, and the Glasgow-1 subgroup A isolate of FeLV (M. Stewart, M. Warnock, A. Wheeler, N. Wilkie, J. Mullins, D. Onions, and J. Neil, J. Virol. 58:825-834, 1986) are 98% homologous, despite having been isolated from naturally infected cats 6 to 13 years apart and from widely different geographic locations. As a group, their envelope gene sequences differ markedly from those of the disease-associated subgroup B and acutely pathogenic subgroup C viruses. Thus, F6A and F3A correspond to members of a highly conserved family and represent prototypes of the horizontally transmitted, minimally pathogenic FeLV present in all naturally occurring infections.