Formation of Hyaline Membranes in the Lungs of Albino Rat as a Result of Exposure to Bleomycin During the Neonatal Period

2016 ◽  
Vol 160 (3) ◽  
pp. 390-393 ◽  
Author(s):  
B. Ya. Ryzhavskii ◽  
O. A. Lebed’ko
Keyword(s):  
Neonatal Period ◽  
Albino Rat ◽  
Hyaline Membranes

Immunofluorescence in Group B Streptococcal Infection and Idiopathic Respiratory Distress Syndrome

PEDIATRICS ◽  
1979 ◽  
Vol 63 (4) ◽  
pp. 557-561
Author(s):  
Jacob L. Pinnas ◽  
Robert C. Strunk ◽  
Lawrence J. Fenton
Keyword(s):  
Respiratory Distress ◽  
Distress Syndrome ◽  
Neonatal Period ◽  
Streptococcal Infection ◽  
Newborn Infants ◽  
Mechanical Ventilators ◽  
Factor B ◽  
Hyaline Membranes ◽  
Idiopathic Respiratory Distress Syndrome ◽  
Group B

Immunofluorescence was perfornued on lungtissue obtained at necropsy from 18 newborn infants, including five with group B streptococcal (GBS) sepsis, seven with idiopathic respiratory distress syndrolne (IRDS), and six control infants who died from other causes. Deposits of C3, IgG, and fibrin were found within hyaline membranes of infants who died with GBS sepsis or IRDS within 48 hours after birth. In some cases, C4, factor B, and IgM were also observed. In five infants with IRDS who died more than five days after birth, immunofluorescent lung findings were less common and less intense. Hyaline membranes, attributed to mechanical ventilators and oxygen therapy in two infants who did not have GBS infection or IRDS, were negative for complement and immunoglobulimis although fibrin was detected in one specimen. These data suggest that immunologic processes may contribute to the pathogenesis of certain types of acute lung injury, particularly in infants who die from GBS infection or IRDS during the early neonatal period.

PULMONARY HYALINE MEMBRANES IN NEWBORN INFANTS

PEDIATRICS ◽  
1951 ◽  
Vol 8 (1) ◽  
pp. 5-21
Author(s):  
WILHELM BLYSTAD ◽  
BENJAMIN H. LANDING ◽  
CLEMENT A. SMITH
Keyword(s):  
Amniotic Fluid ◽  
Neonatal Period ◽  
Experimental Studies ◽  
Newborn Infants ◽  
Pulmonary Hemorrhage ◽  
Experimental Production ◽  
Cell Content ◽  
Microscopic Appearance ◽  
Squamous Cells ◽  
Hyaline Membranes

The results of statistical, morphologic and experimental studies on the nature, occurrence and significance of hyaline (asphyxial) membranes seen in the lungs of infants who die in the neonatal period are presented. Analysis of material from 509 consecutive autopsies on newborn infants, together with analysis of the infants' histories, shows that these membranes occur most commonly in premature infants and in more mature infants with a history of a complication of pregnancy, labor or delivery capable of causing fetal anoxia. These hyaline membranes are not seen in stillborn infants nor in infants living less than one hour. They appear to cause atelectasis, by blocking the mouth of alveoli, and to be a major cause of death in the neonatal period. Studies on vernix, meconium and amniotic fluid indicate that these hyaline membranes are not formed of vernix or meconium, but of the concentrated protein of aspirated amniotic fluid. A rise in the squamous cell content of amniotic fluid during the third trimester of pregnancy is demonstrated; this may explain the difference in microscopic appearance between hyaline membranes formed of amniotic fluid which is aspirated before this rise in squamous cells takes place and those containing squamous cells which are seen if the fluid is aspirated after this increase occurs. The membranes are demonstrated to be independent of pulmonary hemorrhage, edema or inflammation and not to be formed of degenerated airway epithelium. Similar membranes were produced experimentally by repeated intratracheal injection of small amounts of amniotic fluid into the excised respiratory tracts of animals while the lungs were alternately expanded and contracted for one hour. The time and volume factors necessary for successful experimental production of these membranes are discussed. The significance of pulmonary hyaline membranes in the production of neonatal atelectasis is indicated. No instances of "congenital alveolar dysplasia" were found in the 509 cases reviewed, and evidence that it may not be a valid clinical and pathologic entity is presented.

The ultrastructure of acinar cells in the external orbital gland of young and old male rats

1978 ◽  
Vol 36 (2) ◽  
pp. 276-277
Author(s):  
R. Carriere
Keyword(s):  
Young Adulthood ◽  
Acinar Cells ◽  
Cell Number ◽  
Male Rats ◽  
Polyploid Cell ◽  
Secretory Cells ◽  
Age Changes ◽  
Albino Rat ◽  
Golgi Membranes ◽  
Diploid Cells

The external orbital gland of the albino rat exhibits both sexual dimorphism and histological age changes. In males, many cells attain a remarkable degree of polyploidy and an increase of polyploid cell number constitutes the major age change until young adulthood. The acini of young adults have a small lumen and are composed of tall serous cells. Subsequently, many acini acquire a larger lumen with an irregular outline while numerous vacuoles accumulate throughout the secretory cells. At the same time, vesicular acini with a large lumen surrounded by pale-staining low cuboidal diploid cells begin to appear and their number increases throughout old age. The fine structure of external orbital glands from both sexes has been explored and in considering acinar cells from males, emphasis was given to the form of the Golgi membranes and to nuclear infoldings of cytoplasmic constituents.

Childhood diaphragmatic hernias presenting after the neonatal period

1988 ◽  
Vol 39 (2) ◽  
pp. 237-244 ◽  
Author(s):  
L BERMAN ◽  
D STRINGER ◽  
S EIN ◽  
B SHANDLING
Keyword(s):  
Neonatal Period ◽  
Diaphragmatic Hernias

Sensory Restriction in the Albino Rat: Electrocortical Correlates

1969 ◽  
Author(s):  
Leland E. Rhodes ◽  
Donovan E. Fleming
Keyword(s):  
Albino Rat

A Case of Congenital Glucose Galactose Malabsorption with a New Mutation in the SLC5A1 Gene

2020 ◽  
Author(s):  
Hasan Akduman ◽  
Dilek Dilli ◽  
Serdar Ceylaner
Keyword(s):  
Mutation Analysis ◽  
Autosomal Recessive ◽  
Glucose Transporter ◽  
Neonatal Period ◽  
Autosomal Recessive Disorder ◽  
Homozygous Mutation ◽  
New Mutation ◽  
Early Neonatal Period ◽  
Sodium Dependent ◽  
Hypernatremic Dehydration

AbstractCongenital glucose-galactose malabsorption (CGGM) is an autosomal recessive disorder originating from an abnormal transporter mechanism in the intestines. It was sourced from a mutation in the SLC5A1 gene, which encodes a sodium-dependent glucose transporter. Here we report a 2-day-old girl with CGGM who presented with severe hypernatremic dehydration due to diarrhea beginning in the first hours of life. Mutation analysis revealed a novel homozygous mutation NM_000343.3 c.127G > A (p.Gly43Arg) in the SLC5A1 gene. Since CGGM can cause fatal diarrhea in the early neonatal period, timely diagnosis of the disease seems to be essential.

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