Characteristics of Respiratory Diseases in Older People

Abstract: Pneumonia among old people is the fourth leading cause of death, and its mortality has remained the same for the last 100 years despite development of antibiotics. We have elucidated the onset mechanism of pneumonia among old people and developed methods for its prevention. Its primary cause is considered to be cerebrovascular disorders in the basal ganglia, and absence of substance P causes sub-clinical aspiration, which in turn causes pneumonia. Prevention of pneumonia is now possible without the use of antibiotics by increasing substance P. As old people are immune-compromised by depressed state, measures against depression are important for preventing infections such as pneumonia and common cold. The older the patient is, the more intense the effect of gene appears. It was shown that elderly persons with L polymorphism of heme oxygenase (HO)-1 gene are more susceptible to pulmonary emphysema. Systemic examination of the elderly, particularly their physiological characteristic, is essential for treatment of elderly persons with respiratory diseases

A Study of the Cytological Observations on Thirteen Different Monosmic F\u3csub\u3e1\u3c/sub\u3e Hybrids from Crosses between Two Wheat Varieties

Thirteen different monosomic F1 hybrids between Chinese Spring monosomics and the hard red winter wheat variety Cheyenne, were observed at metaphase I of meiosis with respect to frequencies of extra univalent and lengths of Cheyenne chromosomes. The average number of extra univalent per cell varied from .235 for chromosome 5D (XVIII) to .770 for chromosome 3B (III), with significant differences among different monosomics. A range of from two to six extra univalent per cell was observed. The variation in extra univalent frequency was contributed primarily by the chromosome-to-chromosome variance. The 13 chromosomes of Cheyenne were classified statistically into three distinct groups according to their lengths. The lengths varied from 4.23 microns for chromosome 6D (XIX) to 7.22 microns for chromosome 3B (III). The coefficients of variation ranged from 5.73 percent for chromosome 6A (VI) to 10.09 percent for chromosome 2A (II). The variation in length of specific chromosomes was attributed to the variances due to florets, heads (including sampling dates) and different chromosomes. Advisor: Rosalind Morris

Rhinovirus and airway allergy

Rhinoviruses cause the majority of common colds, which often provoke wheezing in patients with asthma. The precise mechanisms responsible for the rhinovirus infection-induced exacerbations of bronchial asthma remain uncertain. However, several reports have demonstrated airway hyperresponsiveness, increases in chemical mediators in airway secretions, such as kinin and histamine, and airway inflammation in patients with bronchial asthma after rhinovirus infection. Rhinovirus infection induces the accumulation of inflammatory cells in airway mucosa and submucosa, including neutrophils, lymphocytes and eosinophils. Rhinovirus affects the barrier function of airway epithelial cells and activates airway epithelial cells and other cells in the lung to produce proinflammatory cytokines, including various types of interleukins, granulocyte-macrophage colony stimulating factor and RANTES, and histamine. Rhinovirus also stimulates the expression of intercellular adhesion molecule-1 (ICAM-1) and low-density lipoprotein receptors in the airway epithelium, receptors for major and minor rhinoviruses. Rhinovirus infection is inhibited by treatment with soluble ICAM-1 and by the reduction of ICAM-1 expression in airway epithelial cells after treatment with either glucocorticoid or erythromycin. Both soluble ICAM-1 and erythromycin have been reported to reduce the symptoms of common colds. Herein, we review the pathogenesis and management of rhinovirus infection-induced exacerbation of bronchial asthma and the relationship between rhinovirus infection and airway allergy

Effective Induction of Acquired Resistance to Listeria monocytogenes by Immunizing Mice with In Vivo-Infected Dendritic Cells

Splenic dendritic cells (DCs) obtained from mice at 48 h after Listeria monocytogenes infection exhibited up-regulation of CD80 and produced higher titers of gamma interferon (IFN-γ) and interleukin-12 (IL-12) than did DCs obtained from uninfected mice. Mice immunized with DCs obtained from mice that had been infected with L. monocytogenes 48 h before acquired host resistance to lethal infection with L. monocytogenes at 4 and 8 weeks. Immunization with DCs from heat-killed L. monocytogenes failed to induce resistance. Acquired antilisterial resistance is specific, since the immunized mice could not be protected from Salmonella enterica serovar Typhimurium infection. Infected DCs stimulated proliferation of naive CD4(+) and CD8(+) cells in vitro, suggesting that in vivo-infected DCs activate CD8(+) T cells, which are critical in acquired antilisterial resistance, as well as CD4(+) T cells. When wild-type mice were immunized with DCs from IFN-γ-deficient mice, they were protected against a lethal L. monocytogenes challenge. In contrast, when mice were immunized with DCs from anti-IL-12 p40 monoclonal antibody-injected mice, they failed to gain acquired antilisterial resistance. These results suggest that DC-derived IL-12, but not IFN-γ, may play a critical role in induction of acquired antilisterial resistance. Our present results suggest that splenic DCs obtained from mice infected with L. monocytogenes in vivo may be an effective immunogen with which to induce antigen-specific immunity

Decreased postprandial gallbladder emptying in patients with black pigment stones

AIM: To analyze gallbladder contractility in patients with black pigment stones (BPSs) and to compare this with patients with cholesterol stones (CSs) and healthy volunteers

A new strategy with proton pump inhibitors for the prevention of acute exacerbations in COPD

Acute exacerbations of chronic obstructive pulmonary disease (COPD), an acute worsening of respiratory symptoms, generally result in a poor prognosis. Successful prevention and management of such exacerbations is thus important for patient care. Viral infection, primarily with rhinovirus (RV), is the foremost cause of exacerbations in COPD patients. Proton pump inhibitors (PPIs) have been reported to inhibit RV infection in human airway epithelial cells in vitro . Furthermore, clinical trials of PPIs in patients with COPD resulted in a reduction in rates of both common cold and COPD exacerbations. In this review, we discuss the significance of COPD exacerbations, summarize a published trial of the effect of low-dose PPIs on COPD exacerbations, and postulate a mechanism for this effect