A Survey on the Factors of Breast Feeding Failure Related to the Role of Medical Personnels

PURPOSE: The reasons for breast feeding failure within the first month of birth were related to inappropriate handling of problems in breast feeding. We investigated common reasons for the failure during the neonatal period and assessed medical personnels' attempts to solve them. METHODS: We conducted a survey with a prepared questionnaire on one-hundred-twenty mothers who failed in breast feeding within the first month after delivery. They were selected among those who brought their infants to local private clinics or general hospitals in Taegu from July to August 1999. RESULTS: The breast feeding rate at the starting time of feeding after delivery was significantly higher in the infants who were born at local clinics than general hospitals(52.7% vs 31.8%, P< 0.05), and higher with rooming-in service than routine nursery care(62.1% vs 31.8%, P<0.05). Most with routine nursery care(79.7%) had to feed breast milk at the appointed time. As a consequence, hospital policy was inconvenient for breast feeding. 51.7 per cent of the responders did not even try breast feeding until discharge from hospitals. Information about breast feeding were obtained mainly from their mothers' advice(39.3%). And it was only 7.7 per cent of the responders who obtained information from physicians. The common reasons for breast feeding failure within the first month were insufficient secretion of milk(36.7%), looser stool(16.7%), and inverted nipple(15%), which could have been solved with adequate support and advice from medical personnel. CONCLUSION: To increase the breast feeding rate, medical personnel should actively recommend breast feeding as early as possible after delivery, should educate mothers on the problems that may arise during breast feeding, and should make the hospital environment more convenient for breast feeding.

A Case of Rheumatic Fever Associated with Acute Poststreptococcal Glomerulonephritis

It is well known that both acute glomerulonephritis and rheumatic fever are a common sequelae of group A streptococcal infection. However, their simultaneous occurrence is uncommon. Only a few cases have been reported because they are different in epidemiologic, clinical, serologic and immunopathogenic characteristics. We experienced a 10-year-old boy who presented the manifestation of acute rheumatic fever and acute poststreptococcal glomerulonephritis. We report this case with brief review of literature.

Effects of FK224, a NK1 and NK2 Receptor Antagonist, on Plasma Extravasation of Neurogenic Inflammation in Rat Airways / 결핵

BACKGROUND: Asthma is an inflammatory disease because there are many inflammatory changes in the asthmatic airways. Axon reflex mechanisms may be involved in the pathogenesis of asthma. Sensory neuropeptides are involved in this inflammation, which is defined as neurogenic inflammation. Substance p, neurokinin A, and neurokinin B may be main neuropeptides of neurogenic inflammation in airways. These tachykinins act on neurokinin recptors. Three types of neurokinin receptors, such as NK1, NK2, and NK3, are currently recognized, at which substance p,neurokinin A, and neurokinin B may be the most relvant natural agonist of neurogenic inflammation in airways. The receptor subtypes present in several tissues have been characterized on the basis of differential sensitivity to substance p, neurokinin A, and neurokinin B. Plasma extravasation and vasodilation are induced by substance p more potently than by neurokinin A, indicating NK1 receptors on endothelial cells mediate the response. But airway contraction is induced by neurokinin A more potently than by substance P, indicating the NK2 receptors in airway smooth muscles. These receptors are used to evaulate the pathogenesis of brochial asthma. FK224 was identified from the fermentation products of Streptomyces violaceoniger. FK224 is a dual antagonist of both NK1 and NK2 recptors. PURPOSE: For a study of pathogenesis of bronchial asthma, the effect of FK224 on plasma extravasation induced by vagal NANC electrical stimulation was evaluated in rat airway. METHOD: Male Sprague-Dawley rats weighing 180~450gm were anesthetized by i.p. injection of urethane. Plasma extravasation was induced by electrical stimulation of cervical vagus NANC nerves with 5Hz, 1mA, and 5V for 2 minutes(NANC2 group) and for sham operation without nerve stimulation(control group). To evaluate the effect of FK224 on plasma extravasation in neurogenic inflammation, FK224(lmg/kg, Fujisawa Pharmaceutical Co., dissolved in dimethylsul- phoxide; DMSO, Sigma Co.) was injected 1 min before nerve stimulation(FK224 group). To assess plasma exudation, Evans blue dye(20mg/kg,dissolved in saline) was used as a plasma marker and was injected before nerve stimulation. After removal of intravascular dye, the evans blue dye in the tissue was extracted in formamide(37degreesC, 24h) and quantified spectrophotometrically by measuring dye absorbance at 629nm wavelength. Tissue dye content was expressed as ng of dye per mg of wet weight tissue. The amount of plasma extravasation was measured on the part of airways in each groups. RESULTS: 1) Vagus nerve(NANC) stimulation significantly increased plasma leakage in trachea, main bronchus, and peripheral bronchus compared with control group, 14.1 +/-1.6 to 49.7+/-2.5, 17.5 +2.0 to 38.7 +/-2.8, and 12.7+/-2.2 to 19.1 +/-1.6ng of dye per mg of tissue(mean +/- SE), respectively(p0.05) 2) FK224 had significant inhibitory effect upon vagal nerve stimulation-induced airway plasma leakage in any airway tissues of rat,such as trachea, main bronchus, and peripheral bronchus compared with vagus nerve stimulation group, 49%, 58%, and 70%, respectively(p<0.05). Inhibitory effect of FK224 on airway plasma leakage in neurogenic inflammation was revealed the more significant in peripheral bronchus, but no significant in lung parenchyma. CONCLUSION: These results suggest that FK224 is a selective NK receptor antagonist which effectively inhibits airway plasma leakage induced by the endogenous neurotransmitters relased by neurogenic inflammation in rat airway. Tachykinin receptor antagonists may be useful in the treatment of brochial asthma.