Midgut abnormalities.
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Diagnostic Techniques, Digestive System↗
Biomedical subjects
John R Gosche
Publications and source records attributed to John R Gosche.
Acute, subacute, and chronic cervical lymphadenitis in children.
Lymphadenopathy refers to any disease process involving lymph nodes that are abnormal in size and consistency. Lymphadenitis specifically refers to lymphadenopathies that are caused by inflammatory processes. Cervical lymphadenopathy is a common problem in the pediatric age group and is largely inflammatory and infectious in etiology. Although most patients are treated successfully by their primary care physician, surgical consultation is frequently required for patients who fail to respond to initial therapy or for those in whom there is an index of suspicion for a neoplastic process. This article addresses current approaches to the diagnosis and management of cervical lymphadenitis in children.
Acute Disease↗
Congenital diaphragmatic hernia: searching for answers.
BACKGROUND: Pulmonary hypoplasia and hypertension are the primary causes of morbidity and mortality in infants with congenital diaphragmatic hernia (CDH). At present, the origin of CDH and the causes of pulmonary hypoplasia and hypertension are unknown. DATA SOURCES: This article reviews the available published data regarding the origin of CDH and the pathogenesis of the associated pulmonary hypertension and hypoplasia. These investigations have employed human tissues as well as two types of CDH animal models. CONCLUSIONS: Investigations performed to date have not yet provided definitive answers regarding the pathogenesis of CDH. However, they have yielded many new and exciting discoveries and several opportunities for intervention. Ongoing research should open new possibilities to improve the outcome for these unfortunate babies with CDH.
Animals↗
Nitrovasodilator responses in pulmonary arterioles from rats with nitrofen-induced congenital diaphragmatic hernia.
BACKGROUND/PURPOSE: Many infants with congenital diaphragmatic hernias (CDHs) experience persistent pulmonary hypertension that is refractory to treatment with inhaled nitric oxide (NO). We have examined the responses of isolated pulmonary arterioles from prenatal and postnatal rats with and without nitrofen (2,4-dichlorophenyl-p-nitrophenyl ether)-induced CDH to a variety of activators of the NO-cyclic guanosine monophosphate (cGMP) pathway. METHODS: Right-sided CDH was induced in fetal rats by feeding nitrofen to pregnant rats on day 12 of gestation. Control rats were fed olive oil (vehicle). Third-generation pulmonary arterioles were isolated from the right lung of prenatal rats at term and from newborn rats within 8 hours after birth. Responses to increasing concentrations of sodium nitroprusside (SNP), atrial natriuretic peptide, or 8-bromo-cGMP were measured in pulmonary arterioles from control rats and from rats with nitrofen-induced CDH. Postnatal responses to 8-bromo-cGMP were also recorded in the presence of zaprinast, a type V phosphodiesterase inhibitor. RESULTS: Pulmonary arterioles from prenatal rats did not dilate in response to SNP, atrial natriuretic peptide, or 8-bromo-cGMP. Vasodilatory responses of postnatal pulmonary arterioles from control rats to SNP and 8-bromo-cGMP were significantly greater than for arterioles from rats with CDH. Zaprinast pretreatment resulted in similar responses for postnatal CDH and control arterioles to 8-bromo-cGMP. CONCLUSIONS: Postnatal pulmonary arterioles from CDH rats exhibit altered nitrovasodilator responsiveness, which may be due to rapid degradation of cGMP.
Animals↗