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Biomedical subjects

T J Corbin

Publications and source records attributed to T J Corbin.

3 recordsLinked to original sources

An analysis of feeding regimens after pyloromyotomy for hypertrophic pyloric stenosis.

We retrospectively reviewed 223 infants who underwent pyloromyotomy for hypertrophic pyloric stenosis (HPS) at our institution from January 1984 to May 1990. Each patient's postoperative feeding regimen was determined by the attending surgeon. The four distinct regimens used were as follows: A (n = 66): NPO overnight (> 10 h) with cautious feeding advancement every 4 hours x 2, then every 2 hours x 2, then every 1 1/2 hours x 8, then ad lib; B (n = 46): NPO until 6 to 8 hours postoperatively with the same cautious feeding advancement as in A; C (n = 42): NPO until 6 hours postoperatively with accelerated feeding advancement every 2 hours x 8, then ad lib; D (n = 69): NPO until 6 hours postoperatively with accelerated feeding advancement every 1 hour x 12, then ad lib. There were no significant differences in age at diagnosis or degree of dehydration among groups. From group A to group D, there was a progressive increase in amount and incidence of postoperative vomiting, both after the first three feedings and in the total postoperative period. However, patients in groups C and D had a shorter postoperative hospital stay and lower charges than did patients in groups A and B. Following discharge, no patient was readmitted for vomiting or dehydration. We conclude that feedings started 6 hours after pyloromyotomy for HPS with accelerated feeding advancement every 2 hours increases the incidence and frequency of postoperative vomiting, but not unacceptably, and results in a significantly shorter postoperative stay.

Analysis of Variance↗

Recombinant human follicle-stimulating hormone is capable of exerting a biological effect in the adult hypophysectomized rat by reducing the numbers of degenerating germ cells.

There is considerable controversy as to whether FSH can, under normal circumstances, exert an effect to promote spermatogenesis in the adult rat. Recombinant human FSH (rhFSH) was used to answer a more limited question relating to whether FSH is capable of exerting a biological effect in promoting adult spermatogenesis. Can a pure preparation of FSH prevent the regressive changes seen after hypophysectomy (Hx) in a short term experiment? To answer this question, five groups of adult rats were used as follows: pituitary-intact animals, 3-day hypophysectomized (Hx), 3-day Hx given 3 mg testosterone propionate (T)/day for 7 days, 3-day Hx given 22 IU rhFSH for 7 days, and 3-day Hx given saline vehicle for 7 days. Testis weight, seminiferous tubule diameter, analysis of four degenerating germ cell types, the relative amount of lipid, and the levels of FSH receptors showed that FSH could, in a significant manner, prevent the regressive changes accompanying Hx. FSH was not as effective as T in doing so, because the FSH values were always intermediate between T-maintained animals and those after long term Hx. The Leydig cell was eliminated as a possible source of FSH-stimulated T promotion of spermatogenesis, given that morphometry and tissue T assays indicated that no additional production of T was elicited by rhFSH. The assay system used to enumerate degenerating germ cells proved a very sensitive indicator of the ability of hormones to maintain cell viability in short term experiments. The data not only show that FSH can exert a biological effect, but that this effect is qualitatively similar to that seen after the administration of T in terms of the maintenance of viability of specific germ cell types. A hypothesis is presented whereby FSH and T, although the former acting by a second messenger system and the latter by binding to nuclear receptors, can stimulate the genome to exert similar qualitative effects promoting the viability of germ cells.

Animals↗

Structural changes in rat Leydig cells posthypophysectomy: a morphometric and endocrine study.

Short and long term responses of the rat Leydig cell were studied posthypophysectomy, at times when germ cell degeneration was first prominent (6 days) and after long term regression of the testis (28 days). In the short term, virtually all structural parameters relating to the volume and surface area of the Leydig cell and its subcellular organelles were significantly lowered compared with those in control animals. Exceptions were the volumes of the nucleolus, heterochromatin, and lysosomes and the surface areas of the nucleus. Structural decreases were generally on the order of 2- to 5-fold in the 6-day period. A statistical analysis of the percent decreases in the short term was performed to determine whether any particular structural features were more sensitive to hypophysectomy than any others. In most instances, no particular organelles were decreased compared to others. However, lipid, although not commonly seen in rat Leydig cells, showed significantly greater percent decreases compared with several other organelles, indicating that the small amount of lipid present is rapidly lost (used) in the short term. After long term hypophysectomy, all structural parameters of the Leydig cell were significantly lowered compared with those in pituitary-intact animals. Only a few parameters (mitochondrial volume, cell surface area, and the surface areas of inner and outer mitochondrial membranes and smooth endoplasmic reticulum) showed more significant decreases in the long term compared with the short term hypophysectomized animals. Most organelle volumes and surface areas correlated positively and significantly with serum and tissue testosterone levels; the exceptions were the volumes of the nucleolus, heterochromatin, lipid, and lysosomes. Compared with the pituitary-intact animal, the content of LH receptors expressed per testis and per Leydig cell was significantly lower in both hypophysectomized groups; however, the number of receptors per given area of individual Leydig cell plasma membrane remained unchanged. Overall, data show that the Leydig cell manifests marked structural changes during early spermatogenic dysfunction.

Animals↗