Colonic tattooing with India ink: benefits, risks, and alternatives.

OBJECTIVE: To provide comprehensive information on key issues concerning colonic tattooing with India ink in reported literature. METHODS: A total of 735 citations on India ink alone were present in the English literature (1966-1995), including 16 on India ink and colonic tattooing. Nine major studies were identified and reviewed for 1) preparation before tattooing (type of ink used, sterilization process, colonic preparation, and antibiotic prophylaxis), 2) the tattooing process (technique and volume injected), 3) success in localization, and 4) complications. RESULTS: A'total of 447 cases of colonic tattooing with India ink have been reported. Major indication was preoperative marking of tumor site. Various India ink preparations were used. Ink was unsterilized in 57% (255/447), autoclaved in 42% (187/447), and gas sterilized in 1% (5/447) of cases. Colonic preparation varied similarly. Prophylactic antibiotics were used in 1% (5/447) of cases. Dilution of India ink varied from undiluted to 1:100 (with 0.9% saline). The volume injected ranged from 0.1 to 2 ml per site injected, commonly with tangential needle insertion and delivery of ink into the submucosa in the majority of the cases. Intraoperative localization was easier with multiple tattoo injections. Five reports of complications have been made. In only one instance did overt clinical complications develop. Risk of a clinical complication with colonic tattooing with India ink is 0.22%. CONCLUSION: Marked variability in technique, as well as potential for reporting bias, limit the quantitative conclusions. In general, colonic tattooing with India ink is a safe, accurate, and inexpensive method for preoperative marking and prospective study of colonic lesions.

Mode of food intake reduction in Lewis rats with indomethacin-induced ulcerative ileitis.

The mechanism of anorexia in inflammatory bowel disease is poorly understood. To gain insight into possible pathophysiologic mechanisms, the feeding indices and food intake were studied in an animal model of Crohn's disease. The anorexia of indomethacin-induced ulcerative ileitis was compared with that of the well-known anorexia of total parenteral nutrition (TPN). Forty-five female Lewis rats were randomized to four groups: Control, Indomethacin, Indomethacin + TPN, and TPN. Feeding indices and food intake were continuously measured using the Automated Computerized Rat Eater Meter. Interleukin-1 alpha (IL-1 alpha), tumor necrosis factor-alpha (TNF-alpha), prostaglandin E2 (PGE2), and leukotriene B4 (LTB4) were assayed in plasma, mononuclear cell culture, or ileum to determine their role in mediating anorexia. In the TPN group, spontaneous food intake (SFI) decreased (52%; p < 0.05), primarily via reduction in meal number (MN, 54%; p < 0.05) and, to a lesser extent, meal size (MZ, 35%; p < 0.05). In comparison, in the Indomethacin group SFI decreased (74%; p < 0.05) primarily via reduction in MZ (67%, p < 0.05); MN also decreased but to a lesser extent (27%; p < 0.05). In the Indomethacin + TPN group, SFI decreased (55%; p > 0.05) primarily via reduction in MN (79%; p < 0.05), whereas MZ decreased slightly (19%; p < 0.05). Only in the Indomethacin group were IL-1 alpha and TNF-alpha detected in the mononuclear cell culture and plasma, respectively. In the Indomethacin group, an inverse correlation existed between MZ and TNF-alpha (p < 0.05). In the Indomethacin group, IL-1 alpha, PGE2, and LTB4 concentrations did not correlate with feeding indices. SFI reduction in this model was mediated primarily via a decrease in MZ. TNF-alpha is proposed to mediate this effect and TPN was shown to overcome the effect on MZ.

Indomethacin fails to induce ulceration in the gastrointestinal tract of newborn and suckling rats.

Little is known about the role of oral prostaglandins and maintenance of intestinal epithelial cell membrane integrity in suckling animals. The presence of prostaglandins in milk suggests that they may have potential cytoprotective effects. Thus, experiments were performed to determine whether indomethacin causes inflammation in the gastrointestinal tract of suckling animals. Rats were treated with daily intraperitoneal injections of indomethacin (10 mg/kg) starting on the 1st day of life. Unlike adult animals which develop intestinal lesions within 72 h, these rats did not develop intestinal ulcerations until weaning started on days 15 to 16. Indomethacin-treated suckling animals prevented from weaning did not develop intestinal lesions until they had access to solid food on day 23. Indomethacin-treated rats had large reductions in jejunal prostaglandin E2 content. In addition, prostaglandin E2 was present in rat milk in relatively large concentration as determined by radioimmunoassay. These studies suggest that exogenous prostaglandins present in milk may protect the intestine of suckling rats from indomethacin-induced inflammation; however, once weaning commences, prostaglandin insufficiency may develop leading to intestinal lesions. We speculate that suckling rats treated with indomethacin did not develop ulcerative lesions, despite a marked reduction in intestinal prostaglandin content, possibly due to prostaglandins present in milk.

Dietary fiber decreases cholesterol and phospholipid synthesis in rat intestine.

The effects of fiber ingestion on the incorporation of oleic acid into triglyceride and lecithin, acetate incorporation into cholesterol, and monosaccharide and amino acid transport were determined in rat intestine. Prolonged pectin (10% by weight) ingestion caused a decrease in jejunal and ileal cholesterol synthesis (33% and 52%, respectively). Pectin ingestion reduced cholesterol synthesis by 60% in ileal crypt cells, but did not affect cholesterol synthesis in the jejunal or ileal villus cells or in jejunal crypt cells. Cholesterol synthesis in isolated crypt cells was markedly less than in isolated villus cells. Prolonged ingestion of a fiber-free diet supplemented with either cellulose or pectin (10% and 5% by weight, respectively) decreased jejunal lecithin glucose and leucine absorption but did not affect jejunal triglyceride synthesis.

Growth and riboflavin status of rats fed different levels of protein and riboflavin.

The relationship between riboflavin and protein utilization was studied in 5-week-old male Sprague-Dawley rats, by using a factorial design with three levels of riboflavin (8, 16 and 24 microgram per rat per day) and protein (1.0, 1.6 and 2.2 g casein per rat per day) in a 9-week experiment. With the lowest level of casein, protein intake was growth limiting, and the level of riboflavin intake had no effect on either weight gain or liver nitrogen retention. With the two higher levels of casein, both weight gain and liver nitrogen retention increased with riboflavin intake, but 24 micrograms riboflavin per day was inadequate for maximal utilization of nitrogen from 2.2 g casein. Neither protein nor riboflavin intake affected the concentration of liver nitrogen per gram of fresh tissue. Increasing the protein intake from 1.0 to 1.6 g increased riboflavin retention in the liver, but additional protein had no further effect. Liver and muscle (gastrocnemius) riboflavin concentrations, as micrograms per gram wet tissue, increased with riboflavin intake. At the two higher intakes of riboflavin, tissue riboflavin levels decreased and the erythrocyte glutathione reductase activity coefficients (EGR-AC) increased with protein intake. These findings are consistent with the view that the effect of protein on riboflavin requirement is related to the rate of growth and not to protein intake, per se.

Veterans Administration cooperative study on aphasia: a comparison of individual and group treatment.

Five Veterans Administration Medical Centers participated in an investigation designed to compare individual with group treatment for aphasic patients who had suffered a left hemisphere cerebral vascular accident. Patients who met selection criteria were assigned randomly to either traditional, individual, stimulus-response type treatment of specific language deficits or group therapy designed to improve communication through group interaction and discussion with no direct treatment of specific language deficits. All patients received eight hours of therapy each week beginning at four weeks postonset and continuing until 48 weeks postonset or until they dropped out of the study. A battery of language measures and a clinical neurologic evaluation were administered at intake and every 11 weeks a patient was in the study. Results show both individually and group-treated patients made significant improvement in language abilities. Individual treatment resulted in significantly better overall performance on the Porch Index of Communicative Ability; however, no significant differences were observed between groups on the other language measures. If the traditional belief is correct that significant spontaneous recovery is complete by three to six months postonset, significant improvement in both groups beyond 26 weeks postonset indicates both individual and group treatment are efficacious methods for managing aphasic patients.

Chronic protracted diarrhea and jejunal atrophy in an infant. Cimetidine-associated stimulation of jejunal mucosal growth.

An infant with 21 months of chronic protracted diarrhea, associated with intestinal mucosal atrophy, decreased crypt mitotic activity, and anti-intestinal antibodies is reported. During a 4-month period, cimetidine was used in an attempt to stimulate mucosal growth. Thirty-minute postprandial serum gastrin levels rose significantly during cimetidine therapy (663 /+- 115 pg/ml, mean /+- SEM). Coincident with the cimetidine therapy, the jejunal mucosa showed progressive histologic improvement and the index of crypt mitotic activity (MI) steadily rose: pretreatment MI = 1.3 (mitoses/100 crypt cells); mid-study, 3.3; end of study, 4.5. There was a direct correlation between 30-min pp serum gastrin and MI (r = 0.989, P less than 0.005). The patient died in renal failure one month after cessation of cimetidine. At autopsy, the small bowel had returned to an atropic state. It is proposed that cimetidine may have influenced jejunal mucosal growth, possibly through meal-stimulated hypergastrinemia.

Effect of insulin on in vitro intestinal fatty acid esterification in the rat.

We have previously shown that glucose metabolism plays an important role in modifying intestinal fatty acid esterification. Because it is well known that glucose metabolism is under insulin regulation, we examined the effect of insulin on intestinal fatty acid esterification. Insulin pretreatment led to a marked decrease in in vitro intestinal fatty acid esterification, but this decrease was abolished by maintaining blood glucose above 80 mg/dl. Addition of insulin to the incubation medium failed to produce any effect on intestinal fatty acid esterification. The decreased fatty acid esterification on hypoglycemic rats was not associated with changes in fatty acid uptake or lipid esterifying enzyme activities. However, there was a significant increase in the production of volatile metabolites of fatty acid. We conclude that 1) insulin itself has no effect on intestinal fatty acid esterification, 2) the effects observed in this study are due to insulin-induced hypoglycemia, 3) hypoglycemia does not alter intestinal fatty acid uptake or intrinsic esterification activity, but leads to preferential oxidation rather than esterification of fatty acid by the small intestine, and 4) the critical blood glucose concentration needed to maintain normal esterification in the rat was approximately at 80 mg/dl.

Phosphatidylcholine synthesis in the developing small intestine.

1. Phosphatidylcholine synthesis in the foetal, newborn and adult small intestine of rats was studied by determination of cytidine diphosphocholine-1,2-diacylglycerocholine phosphotransferase (cholinephosphotransferase) and acyl-CoA-1-acyl-sn-glycerol-3-phosphocholine acyltransferase (lysophosphatidylcholine acyltransferase) activities and the incorporation of [1-14C]oleic acid into phosphatidylcholine. 2. Cholinephosphotransferase activity was low in foetal jejunum and ileum, increased 3-4 fold in the ileum by 6 days of age and by 12 days in the jejunum. Jejunal activity remained constant throughout weaning; ileal activity gradually decreased to values 25% of that of the jejunum. 3. Lysophosphatidylcholine acyltransferase activity was high in foetal jejunum and ileum, decreased 70% immediately after birth in the jejunum and increased to adult values by 12 days of age. Ileal activity decreased by 20% after birth, but decreased more rapidly at weaning to 30% of the activity in jejunum. 4. Initial rates and steady-state incorporation of [1-14C]oleic acid into phosphatidylcholine by jejunal rings of 10 day-old rats exceeded that observed in jejunal rings from adult rats by 2-4-fold. 5. In the postnatal jejunum, neither cholinephosphotransferase and lysophosphatidylcholine acyltransferase activities nor oleic acid incorporation were stimulated by cortisone administration in vivo.

Prognostic value of EEG in acute vascular aphasia: a long term clinical-EEG study of 53 patients.

A group of 53 patients rendered acutely aphasic by occlusive cerebrovascular disease were studied by serial EEG's, repeated neurologic examinations and speech evaluations (Porch Index of Communicative Ability) over a period of eight to twenty-four months, in order to correlate EEG findings with the degree of language disorder and prognosis for language recovery. Normal and mildly abnormal EEG's, posterior slow foci, focal slowing of semirhythmic type and higher alpha frequencies over the intact hemisphere correlated with good language recovery. In the majority of the patients, the curves of "EEG Improvement" and "Language Recovery" closely paralleled each other. These data indicate that the EEG is of prognostic value as to recovery from aphasia in patients suffering from acute occlusive cerebrovascular disease. Despite the advent of newer diagnostic tests, such as CAT scan, which has established its value in evaluation of the anatomy of aphasia, (9) EEG remains to be useful as a tool that could predict the outcome of aphasia in stroke patients.

Uptake of glycine by human kidney cortex.

The transport of glycine was investigated in histologically normal adult human kidney cortical slices. Uptake occurs against a gradient and shows concentration dependence. Kinetic analysis reveals two systems for transport of glycine with apparent transport Km values of 0.511 and 34.2 mM. Glycine transport on the high-Km system is competitively inhibited by 50 mML-proline. Transport inhibition on the low-Km system could not be directly evaluated, but on theoretic grounds appears not to be inhibited by L-proline or hydroxyproline. Alpha-aminoisobutyric acid, valine, and thioproline are also shown to inhibit glycine uptake. Low medium sodium or anaerobic incubation depress the uptake of glycine. These observations are consistent with previous reports of glycine transport in rat kidney and support the proposals for the mechanism of familial iminoglycinuria based on in vivo investigations.

Liquid membrane capsules for treatment of uremia.

The objective of the program is to use ingested liquid membrane capsules (LMC) as gastrointestinal toxin traps as an adjunct to dialysis. Urea has been selected as the model toxic component to study before expanding the technology to other toxins. Transport across the small intestinal mucosa has been indicated to be adequate. There is no indication of reduction of mucosal transport or damage to the intestinal mucosa over short term but repetitive LMC perfusions. Performance of LMC perfused through Thiry Vella small intestinal loops is as good as in vitro performance and can be predicted. Substantial progress has been made toward developing LMC to perform in the more complex environment of the intact gastrointestinal tract. The demonstration of LMC performance in vivo with intact gastrointestinal tracts, and perhaps some increase in rate of toxin removal, will be required before LMC can be considered practical candidates for clinical use.

Metaphyseal chondrodysplasia, neutropenia, and pancreatic insufficiency presenting with respiratory distress in the neonatal period.

Two pairs of brothers suffered respiratory distress in the newborn period because their ribs were abnormally short. The diagnostic radiological features of metaphyseal chondrodysplasia appeared only in the second year. Pancreatic insufficiency and neutropenia were present. One died of overwhelming infection and his brother survived a life-threatening episode of gangrenous proctitis.