Hantavirus pulmonary syndrome (HPS) is characterized by the rapid onset of pulmonary edema and a high case-fatality rate. Hantavirus antigens have been demonstrated in pulmonary capillary endothelial cells, but the mechanisms causing capillary leakage remain unclear. Immunohistochemical staining was used to enumerate cytokine-producing cells (monokines: interleukin [IL]-1alpha, IL-1beta, IL-6, and tumor necrosis factor [TNF]-alpha; lymphokines: interferon-gamma, IL-2, IL-4, and TNF-beta) in tissues obtained at autopsy from subjects with HPS. High numbers of cytokine-producing cells were seen in the lung and spleen tissues of HPS patients, but only low numbers in the livers and kidneys. A modest increase in the numbers of cytokine-producing cells was detected in the lungs of patients who died with non-HPS acute respiratory distress syndrome (ARDS), and very few (or no) cytokine-producing cells were detected in the lungs of patients who died of causes other than ARDS. These results suggest that local cytokine production may play an important role in the pathogenesis of HPS.

Analysis of mitotic and meiotic recombination in mammalian cells has been hampered by the complexity of the reactions involved as well as lack of mutants. Furthermore, none of the genes involved in the process has yet been identified. In budding yeast, Saccharomyces cerevisiae, the RADSI gene is essential along with other genes of the RAD52 epistasis group for mitotic and meiotic recombination and DNA repair. The Rad5l protein is structurally similar toEscherichia coi RecA protein, which is required in homologous recombination and SOS responses in bacteria. Here we report the isolation of a mouse homolog of the yeast RADSI gene. The amino acid sequence predicted from the gene shows 83% and 55% homology with those of the yeast RADSI and the E. coli recA product, respectively. The mouse gene complemented a rdSl mutation of S. cerevisiae with sensitivity to methylmethanesulfonate, which produces double-strand breaks of DNA. This gene is expressed in the thymus, testis, ovary, spleen, and intestine, suggesting that its product is involved in mitotic and meiotic recombination in addition to DNA repair. MATERIALS AND METHODSIsolation of Mouse Rad5l cDNA Clone and DNA Sequencing Analysis. Two oligonucleotides (5'-AGTTGGATCCGAA/ GTTC/TA/CGIACIGGIAAA/G-3' and 5'-AAGGAAGCT-TGCIAA/GA/GTGCATT/CTGICT/GA/G/C/TGC-3', where I refers to inosine) were designed to code for two peptides in the conserved regions of Saccharomyces cerevisiae, RAD51, and its Schizosaccharomyces pombe homolog. The amino acid sequences used were EFRTGKS, corresponding to residues 186-192, and ARQMHLA, corresponding to residues 298-304 of the RAD51 gene of S. cerevisiae (6), encompassing the two ATP binding motifs. The oligonucleotides were used in a reverse transcriptase polymerase chain reaction with total RNA from mouse testis as a template. The 360-bp fragment generated was subcloned and used as a probe to screen a AZAP cDNA library from 129/Sv mouse testes. A clone, pMR51, was isolated and both strands were sequenced.Complementation

An increasingly large body of work suggests that atypical adenomatous hyperplasia (AAH) of the lung may be a forerunner of pulmonary adenocarcinoma. Recognizing this fact, the World Health Organization now acknowledges the existence of AAH while noting difficulties that may be encountered in distinguishing AAH from the nonmucinous variant of bronchioloalveolar carcinoma. Regrettably, a universally acceptable definition of morphologic criteria for the diagnosis of AAH has not been achieved. This review of the literature examines the epidemiology, gross appearance, light microscopic findings, morphometry, immunohistochemistry, and molecular features of AAH and suggests a set of histopathologic features that may help the practicing pathologist identify this intriguing lesion. These features include the following: irregularly bordered focal proliferations of atypical cells spreading along the preexisting alveolar framework; prominent cuboidal to low columnar alveolar epithelial cells with variable degree of atypia but less than that seen in adenocarcinoma; increased cell size and nuclearcytoplasmic ratio with hyperchromasia and prominent nucleoli, generally intact intercellular attachment of atypical cells with occasional empty-looking spaces between them without high cellularity and without tufting or papillary structures; and slight thickening of the alveolar walls on which the AAH cells have spread, with some fibrosis but without scar formation or significant chronic inflammation of the surrounding lung tissue. Several lines of evidence indicate that AAH is a lesion closely associated with adenocarcinoma of the lung, suggesting AAH may be involved in the early stage of a complex multistep carcinogenesis of pulmonary adenocarcinoma.

The phonon Hall effect has been observed in the paramagnetic insulator, Tb3Gd5O12. A magnetic field applied perpendicularly to a heat current induces a temperature gradient that is perpendicular to both the field and the current. We show that this effect is due to resonant skew scattering of phonons from the crystal field states of superstoichiometric Tb 3+ ions. This scattering originates from the coupling between the quadrupole moment of Tb 3+ ions and the lattice strain. The estimated magnitude of the effect is consistent with experimental observations at T ∼ 5 K, and can be significantly enhanced by increasing temperature.PACS numbers: 72.20.Pa, 72.15.Gd When a linear magnetic field is applied perpendicularly to a heat current in a sample of terbium gallium garnet (TGG), Tb 3 Ga 5 O 12 , a transverse temperature gradient is induced in the third perpendicular direction 1,2 . This is the "phonon Hall effect (PHE)". The effect was observed in this insulator at low temperature (T ∼ 5 K), a situation in which there are no mobile charges such as electrons or holes 3 . The Neel temperature of TGG is 0.24 K 4 , so it is a paramagnet at T ∼ 5 K. Hence magnons do not contribute to the heat current and one does not expect a contribution from the magnon Hall effect 5-8 . Phonons are not charged and hence cannot be affected by the Lorentz force which gives rise to the usual classical Hall effect. Therefore the mechanism for the PHE must be related to the spin-orbit interaction. However, the spin-orbit interaction for phonons is not at all obvious, unlike in the anomalous Hall effect and spin Hall effect for electrons [9][10][11] . Thus, an understanding of the origin of the observed PHE is a fundamental problem.So far, there have been a few theoretical attempts to explain the PHE 12-15 . Refs. 12 and 13 assumed a Ramantype interaction between the spin of stoichiometric Tb 3+ ions and the phonon. This interaction results in "elliptically polarized" phonons. According to 12,13, the "elliptic polarization", in combination with scattering from impurities, leads to the PHE. In this scenario the type of impurity is unimportant and hence phonon -impurity scattering is considered in the leading Born approximation. This is an intrinsic-extrinsic scenario, i.e., the "elliptic polarization" is an intrinsic effect and the scattering from impurities is an extrinsic effect. The major problem with this scenario was realized in Ref. 14 -in spite of the "elliptic polarization" the Born approximation does not result in the PHE. Ref. 14 attempted to go beyond the leading Born approximation in impurity scattering. However, the problem has not been resolved yet. An intrinsic mechanism for the PHE, based on the Berry curvature of phonon bands, was suggested in Ref. 15. This is similar to the Berry curvature mechanism in the Hall effect for light 16 . The Berry curvature mechanism is certainly valid for materials with specially structured phonon bands, however, it is hard to see how the mechanism can be realized in TGG which has the simple...