RESUMO
UNLABELLED: In 23 subjects with chronic obstructive pulmonary disease (COPD) who wheezed when changing their position from sitting to dorsal decubitus (DD), we recorded lung volumes and flow volume loops in sitting (S1), DD and immediately after resuming sitting (S2). We found three main patterns of ventilatory changes associated with wheezing in DD: (1) acute obstruction (AO) in 14 subjects characterized by FEV1 > or = -10% and %FEV1/FVC > or = -3%; functional residual capacity or residual volume was increased, decreased or unchanged; (2) acute restriction (AR) in 7 subjects characterized by absence of obstruction spirographically and FVC and/or FRC > -10%; (3) indeterminate response (IR) in 2 subjects. Except for 3 subjects, the changes recorded in DD returned to baseline in S2. Both AO and AR responses in DD and their rapid resolution in S2 were reproducible (11 subjects). IN CONCLUSION: (1) in COPD, DD may trigger wheezing; (2) the physiologic changes during DD wheezing are reproducible, rapidly reversible when the sitting position is resumed and unlike those recorded during bronchoprovocation, heterogeneous.
Assuntos
Pulmão/fisiopatologia , Postura/fisiologia , Sons Respiratórios/etiologia , Volume Expiratório Forçado , Capacidade Residual Funcional , Humanos , Pneumopatias Obstrutivas/fisiopatologia , Masculino , Pessoa de Meia-IdadeRESUMO
Insulin-like growth factor I (IGF I) regulates the expression of a select few genes in quiescent BALB/c-3T3 cells. This was demonstrated by gel electrophoresis of radiolabeled proteins and by molecular cloning of twelve distinct IGF I-regulated cDNAs. Together, the electrophoretic and cloning data show that IGF I stimulates the expression of about 0.15% of the genes expressed by 3T3 cells, perhaps 30 genes in total. The genes encode both cytoplasmic and nuclear proteins. At the regulatory level the IGF I-controlled genes segregate into two categories. Category I genes (the minority) respond preferentially to IGF I. Their induction is prevented by actinomycin D, and they are superinduced by the combination of IGF I and anisomycin. Category II genes (the majority) respond to platelet-derived growth factor as well as to IGF I. The response of category II genes to IGF I is insensitive to actinomycin D. The data indicate that category II genes are constitutively transcribed and that IGF I regulates stability of the transcripts. The expression of category II genes correlates well with the ability of 3T3 cells to survive in serum-free culture medium.
Assuntos
Clonagem Molecular , Regulação da Expressão Gênica , Fator de Crescimento Insulin-Like I/farmacologia , Somatomedinas/farmacologia , Animais , Anisomicina/farmacologia , Linhagem Celular , Sobrevivência Celular , DNA/genética , Dactinomicina/farmacologia , Eletroforese em Gel de Poliacrilamida , Humanos , Camundongos , Camundongos Endogâmicos BALB C , Peso Molecular , Fator de Crescimento Derivado de Plaquetas/farmacologia , RNA Mensageiro/biossíntese , RNA Mensageiro/genética , Transcrição GênicaRESUMO
Human serum contains, in addition to the "classical" 7.5-kDa insulin-like growth factors (IGFs) I and II, small amounts of larger IGF-II. A 10-kDa IGF-II was isolated by gel filtration, immunoaffinity chromatography, and reversed-phase HPLC. Upon amino acid sequence determination, a substitution of Cys-Gly-Asp for Ser-33 was found as well as a COOH-terminal extension of 21 residues (E peptide). These sequence differences suggest that 10-kDa IGF-II is a precursor of a variant IGF-II. Since the substitution is not located at a known intron/exon hinge region, the finding of this variant IGF-II is evidence for the presence of more than one gene for IGF-II.
