[Penile verrucous carcinoma]. / Le cas clinique du mois. Un carcinome verruqueux du penis.

Penile verrucous carcinoma is a rare tumor. Verrucous carcinoma is thought by most to represent a well-differentiated or low-grade squamous-cell carcinoma. The term Buschke-Lowenstein tumor and giant condyloma have also been used to identify this histological lesion. A review of literature points to the role of human papillomavirus infection. The authors report a case of a penile verrucous carcinoma in a circumcised man.

[Urachal adenocarcinoma]. / Adénocarcinome de l'ouraque.

The authors report a case of mucinous adenocarcinoma of the urachus treated with partial cystectomy. The urachal cancer is an uncommon clinicopathologic entity associated with a poor prognosis. Anatomical considerations, clinical features and treatment are discussed.

Dietary oleic acid not used during brain development and in adult in rat, in contrast with sciatic nerve.

In order to determine exactly the effect on the nervous system of concentration of dietary oleic acid on the fatty acid composition of different part of the nervous system, triglycerides were synthesized using chemical and enzymological methods. The dose-effect was determined using an experimental protocol with seven groups of rats who received a diet in which the oleic acid level varied from 0 to 6000 mg per 100 g diet, but the other ingredients were identical (in particular the essential fatty acids, linoleic and alpha-linolenic acid). Rats were fed the diets from two weeks before mating, and their pups were sacrificed aged either 21 or 60 days. When the level of oleic acid in the diet was increased, the main modifications observed in 21-day-old deficient animals were as follows. (i). For 18:1(n-9), in liver, plateau was reached at about 4 g oleic acid per 100 g diet. Below this level, the higher the dose the greater the response. In whole brain, brain myelin, and nerve endings (but not sciatic nerve) the oleic acid level remained optimal and constant whatever the level of oleic acid in the diet. (ii). 16:1(n-7) concentration decreased in liver and in sciatic nerve, but not in nervous tissue. (iii). In 60-day-old animals, results were generally similar to those in 21-day-old animals.

The administration of pig brain phospholipids versus soybean phospholipids in the diet during the period of brain development in the rat results in greater increments of brain docosahexaenoic acid.

Dietary porcine brain phospholipids are much more efficient than soybean phospholipids for ensuring a normal (optimal obtained with lab chow diet) level of docosahexaenoic acid (DHA) in tissues and brain subcellular fractions (brain myelin and nerve endings). Two weeks before mating, rats were divided into two groups (one group was subdivided into subgroups, fed with varying amounts of porcine brain phospholipids; the other group was divided into subgroups fed varying amounts of soybean phospholipids). Pups were killed when 21 days old. DHA (22:6(n-3)) increased up to normal levels in parallel with increasing amounts of (n-3) fatty acids (omega-3 fatty acids) in the diet, up to 60 mg with dietary porcine brain phospholipids and up to 200 mg with soybean phospholipids. Thus a smaller amount of dietary brain phospholipids resulted in the same level of DHA in tissues as a larger amount of dietary soybean phospholipids. In contrast, 22:5(n-6) declined when (n-3) fatty acids in the diet increased. It stabilized at 60 mg of (n-3) fatty acids/100 g diet with brain phospholipids, and approximately 200 mg/100 g diet with soybean phospholipids. As 22:5(n-6) replaced DHA in tissue when (n-3) fatty acids were not sufficient in the diet, this result shows that the recovery of a normal (and minimal) amount of 22:5(n-6) was obtained with lower dietary levels of brain phospholipids compared with soybean phospholipids.

[Prospective randomized single-blind trial comparing oral sodium phosphate with polyethylene glycol for colonoscopy preparation]. / Etude prospective randomisée en simple aveugle comparant phosphate de sodium oral et polyéthylène glycol pour la préparation à la coloscopie.

AIM AND METHODS: The aim of this prospective, randomized, study performed in 60 outpatients was to compare 2 precolonoscopy bowel preparations: oral sodium phosphate (NaP) versus standard polyethylene glycol-based lavage solution (PEG). None of the patients met any of NaP exclusion criteria. All patients were prepared on the day prior to colonoscopy. A patient-questionnaire and measure of serum electrolytes (calcium, phosphate, sodium, potassium), pulse and blood pressure were used to assess tolerance and acceptability of the preparation. The quality of colon cleansing was judged by blinded endoscopists. RESULTS: Patient's tolerance to NaP was superior to PEG: NaP preparation was easier to drink and feelings of abdominal plenitude occurred in a smaller proportion of patients. A potassium decrease, a sodium increase and hyperphosphatemia were observed in the NaP group but without clinical events. PEG preparation seemed to allow a better cleansing ability compared with NaP but this difference was not statistically significant. CONCLUSIONS: NaP solution was better tolerated and accepted by patients. Colonic preparation quality compared to PEG is still to be discussed depending on the intake schedule. A biochemical data check seems necessary on account of significant serum electrolytes changes induced by NaP preparation.

Vitamin E deficiency has different effects on brain and liver phospholipid hydroperoxide glutathione peroxidase activities in the rat.

The effect of vitamin E deficiency on glutathione peroxidase activity (GPX) and on the activity of a selenoenzyme (phospholipid hydroperoxide glutathione peroxidase (PHGPX) was measured in rat brain and liver. In brain, the activity of both enzymes was in the same range in homogenate and in microsomes. In contrast, in liver homogenate, PHGPX activity was approximately 20 times lower than that of GPX. Very interestingly, PHGPX activity was significantly decreased in brain microsomes by vitamin E deficiency, but slightly significantly increased in liver microsomes. In contrast, GPX activity was not affected in brain by vitamin E deficiency, but was significantly lower in liver homogenate and microsomes. Thus, PHGPX activity is partially controlled by vitamin E in membranes, and PHGPX is probably an enzyme different from GPX.

Possible role of the choroid plexus in the supply of brain tissue with polyunsaturated fatty acids.

Delta-6 desaturase was measured in rat brain microvessels and choroid plexus by incubation in the presence of radioactive linoleic acid. Under our conditions, in 21-day-old animals, delta-6 desaturase was not detected in brain microvessels. In contrast, it was present in choroid plexus (about 21 pmol/min per mg protein). In comparison, the activity in brain was much lower (about 1 pmol/min per mg protein) and higher in liver (about 55 pmol/min per mg protein). Interestingly, during development the activity in choroid plexus peaked at day 6 after birth and declined slightly thereafter. The pattern of incorporation of linoleic acid radioactivity was not the same in choroid plexus and microvessels. These results show that delta-6 desaturase was not detected in brain microvessels but was present in choroid plexus.

Endogenous synthesis cannot compensate for absence of dietary oleic acid in rats.

It is important to know whether an organism is able to synthesize all the oleic acid it needs. To determine this, it is sufficient to feed animals a diet containing essential fatty acids but totally lacking oleic acid, and then determine whether tissue concentrations of fatty acids of the (n-9) series are altered due to insufficient endogenous synthesis of oleic acid from stearic acid. In fact, the effects of a total oleic acid deficiency have not previously been studied because all the vegetable oils used in human and animal nutrition contain this fatty acid in variable amounts. Thus, we fed rats semipurified diets whose lipids (triglycerides) were synthesized chemically. Female rats were fed the diets for 3 wk before mating, and their pups (fed the same diets) were killed when 21 and 60 d old. Generally speaking, oleic acid deficiency resulted in a lower level of this acid in the various organs examined (liver, kidney, testes, heart, muscle and sciatic nerve in 21-d-old rats and liver, kidney, heart, muscle and sciatic nerve in 60-d-old rats). Brain, myelin and nerve endings were not affected at either age. This lower level was accompanied by a higher level of 16:1(n-7) and, to a lesser extent, 18:1(n-7). Dietary supplementation with oleic acid (1666 mg/100 g diet) for up to 21 d resulted in normal levels of this fatty acid in some organs (liver, heart, sciatic nerve) but not in others (kidney, muscle, testes) and a decrease in 16:1(n-7), which returned to about the same levels as in the control group in all organs except liver. Adding small or large amounts of stearic acid to the oleic acid-deficient diet had little or no effect on oleic acid levels in the tissues. We conclude that rats (particularly in liver) do not have sufficient synthesizing potential to guarantee the normal fatty acid composition of certain organs if oleic acid is totally absent in the diet.

Does an increase in dietary linoleic acid modify tissue concentrations of cervonic acid and consequently alter alpha-linolenic requirements? Minimal requirement of linoleic acid in adult rats.

Rats were fed a control diet containing both linoleic and alpha-linolenic acid. When 60-days-old they were divided into 8 groups, each receiving the same amount of alpha-linolenic acid, but varying amounts of linoleic acid. When the (n-6)/(n-3) ratio in the diet varied from 2 to 32 (with a constant amount of 150 mg alpha-linolenic acid per 100 g diet), tissue levels of the (n-3) series fatty acids were not significantly modified, except in the liver, heart and testes. In all organs studied, the saturated and monounsaturated fatty acids were practically unchanged. For the (n-6) series fatty acids, arachidonic acid was not significantly affected, in muscle, kidney, brain, myelin, nerve-endings or sciatic nerve, whatever the quantity of linoleic acid in the diet. In liver, arachidonic acid plateaued at 2400 mg linoleic acid/100 g diet and at 400 mg/100 g diet in heart. Results for 22:5(n-6) showed a marked increase in heart, a moderate increase in liver and kidney, and no effect in muscle, testes, brain, myelin, nerve-endings or sciatic nerve. This experiment defined the minimum amount of linoleic acid required in the diet to maintain fatty acids of the linoleic family in the young adult rat. For the first time it was demonstrated that 1200 mg/100 g diet are sufficient for the liver, as evidenced by maintenance of the arachidonic acid concentration. For the other organs, there is either a very marked preservation of this acid, or the dietary level is less than 300 mg/100 g diet. For the essential fatty acid precursors (i.e. linoleic and alpha-linolenic acids), the optimal (n-6)/(n-3) ratio required in the diet is about 8.

[Mid-term failure of balloon dilatation treatment of antral stenosis induced by caustics]. / Echec à moyen terme du traitement d'une sténose antrale caustique par dilatation au ballonnet.

We report the case of an antral stricture following lye ingestion. The patient was treated by 3 dilations using a through-the-scope balloon dilator, initially with good results. One year later, the recurrence of the symptoms led to 2 other sessions of dilation without success and a partial gastrectomy was performed. The intensity of the gastric wall fibrosis on the surgical specimen, probably responsible for major motor impairment, accounts for the discordance between the good endoscopic result and the clinical failure. Endoscopic dilation of lye-induced gastric strictures could be a temporary alternative to surgical resection because the gastric wall fibrosis blemishes the long-term functional result.

Comparison of recovery of previously depressed hepatic delta 6 desaturase activity in adult and old rats.

The ability to recover hepatic delta 6 desaturase (delta 6D) activity with linoleic acid as substrate was compared in adult and old rats. Male rats fed a diet deficient in alpha-linolenic acid were used either at 6 or 21 months. From these two ages onward, animals were fed a diet containing 10% fish oil for 3 months to reduce delta 6D activity. After this period, some of the animals were killed. The other animals were returned to the original diet deficient in alpha-linolenic acid. Fatty acid composition in liver and brain and hepatic delta 6D activity were analysed 3 and 7 days after the change in diet. When rats were fed the diet containing 10% fish oil, delta 6D activity was lower than in those fed the diet deficient in alpha-linolenic acid. The liver fatty acid composition was altered with disappearance of 22:5 n-6 and a decrease in 18:2 n-6, 20:4 n-6 and 22:4 n-6 accompanied by an increase in 20:5 n-3, 22:5 n-3 and 22:6 n-3. When rats were re-fed the original diet, delta 6D activity returned after 3 days to its initial level in the 9-month-old rats; in 24-month-old animals, recuperation was incomplete. The level of 20:4 n-6 and 18:2 n-6 increased in the liver concurrently with a decrease in levels of 20:5 n-3, 22:5 n-3 and 22:6 n-3. In both age groups, the brain fatty acid profile remained unchanged 7 days after returning to the diet deficient in alpha-linolenic acid.

Comparison of liver microsome enzyme and fatty acid composition recovery in adult and old rats deficient in 18:3n-3 refed a diet containing 18:3n-3.

The effect of dietary n-3 deficiency on liver microsome enzymes activities and fatty acid composition was studied in adult (3 months old) and old rats (18 months old). At these two ages, deficient animals were refed with 18:3n-3 diet for 1 or 2 months and the recovery of these parameters was investigated. Cytochrome P 450 level was decreased by n-3 PUFA (Polyunsaturated fatty acid) deficiency. After refeeding, it returned to control values after 1 month. NADH-cytochrome b5 reductase activity was decreased, the activities of NADPH cytochrome c reductase, aminopyrine demethylase, aniline hydroxylase were also decreased, but in old rats they were increased by refeeding. N-3 PUFA deficiency caused a decrease of 18:2n-6 and 22:6n-3 and an increase in 20:4n-6, 22:5n-6 and 18:1n-9. After refeeding, in adult rats, the PUFA level remained lower; in old rats, the MUFA (Monounsaturated fatty acid) and PUFA levels returned to control values. Liver microsomal enzyme activities depend on the degree of unsaturation of fatty acids rather than the specific species of polyunsaturated fatty acids.

Incorporation of trans long-chain n-3 polyunsaturated fatty acids in rat brain structures and retina.

During heat treatment, polyunsaturated fatty acids and specifically 18:3n-3 can undergo geometrical isomerization. In rat tissues, 18:3 delta 9c,12c,15t, one of the trans isomers of linolenic acid, can be desaturated and elongated to give trans isomers of eicosapentaenoic and docosahexaenoic acids. The present study was undertaken to determine whether such compounds are incorporated into brain structures that are rich in n-3 long-chain polyunsaturated fatty acids. Two fractions enriched in trans isomers of alpha-linolenic acid were prepared and fed to female adult rats during gestation and lactation. The pups were killed at weaning. Synaptosomes, brain microvessels and retina were shown to contain the highest levels (about 0.5% of total fatty acids) of the trans isomer of docosahexaenoic acid (22:6 delta 4c,7c,10c,13c,16c,19t). This compound was also observed in myelin and sciatic nerve, but to a lesser extent (0.1% of total fatty acids). However, the ratios of 22:6 trans to 22:6 cis were similar in all the tissues studied. When the diet was deficient in alpha-linolenic acid, the incorporation of trans isomers was apparently doubled. However, comparison of the ratios of trans 18:3n-3 to cis 18:3n-3 in the diet revealed that the cis n-3 fatty acids were more easily desaturated and elongated to 22:6n-3 than the corresponding trans n-3 fatty acids. An increase in 22:5n-6 was thus observed, as has previously been described in n-3 fatty acid deficiency. These results encourage further studies to determine whether or not incorporations of such trans isomers into tissues may have physiological implications.

Dietary alpha-linolenic acid at 1.3 g/kg maintains maximal docosahexaenoic acid concentration in brain, heart and liver of adult rats.

We have previously determined the dietary alpha-linolenic requirement for membrane synthesis in the developing animal. This study measures the dietary requirement for maintaining normal membrane composition in adult rats, as determined by 22:6(n-3) (docosahexaenoic acid) concentration. Sixty-day-old rats, previously fed a diet containing both linoleic and alpha-linolenic acid, were divided into nine groups, each receiving different quantities of alpha-linolenic acid but the same amount of linoleic acid. They were killed 4 wk after initiation of the new diet to determine the minimum quantity of alpha-linolenic acid required in the diet for maintaining the 22:6(n-3) tissue concentration in brain (whole tissue, myelin and nerve endings), liver and heart. The minimal amount of dietary alpha-linolenic acid that maintained the maximal 22:6(n-3) level and minimal 22:5(n-6) level in tissues was considered to be the dietary requirement. The quantity was found to be 1.30 g/kg diet (0.26% of dietary energy). It was lower than that found for the developing animal (0.4% of energy). At lower quantities of dietary alpha-linolenic acid, 22:6(n-3) was replaced by 22:5(n-6) in the organs examined, except in nervous tissue, in which 22:6(n-3) was highly preserved.

Brain phospholipids as dietary source of (n-3) polyunsaturated fatty acids for nervous tissue in the rat.

In a previous work, we calculated the dietary alpha-linolenic requirements (from vegetable oil triglycerides) for obtaining and maintaining a physiological level of (n-3) fatty acids in developing animal membranes as determined by the cervonic acid content [22:6(n-3), docosahexaenoic acid]. The aim of the present study was to measure the phospholipid requirement, as these compounds directly provide the very long polyunsaturated fatty acids found in membranes. Two weeks before mating, eight groups of female rats (previously fed peanut oil deficient in alpha-linolenic acid) were fed different semisynthetic diets containing 6% African peanut oil supplemented with different quantities of phospholipids obtained from bovine brain lipid extract, so as to add (n-3) polyunsaturated fatty acids to the diet. An additional group was fed peanut oil with rapeseed oil, and served as control. Pups were fed the same diet as their respective mothers, and were killed at weaning. Forebrain, sciatic nerve, retina, nerve endings, myelin, and liver were analyzed. We conclude that during the combined maternal and perinatal period, the (n-3) fatty acid requirement for adequate deposition of (n-3) polyunsaturated fatty acids in the nervous tissue (and in liver) of pups is lower if animals are fed (n-3) very long chain polyunsaturated fatty acids found in brain phospholipids [this study, approximately 60 mg of (n-3) fatty acids/100 g of diet, i.e., approximately 130 mg/1,000 kcal] rather than alpha-linolenic acid from vegetable oil triglycerides [200 mg of (n-3) fatty acids/100 g of diet, i.e., approximately 440 mg/1,000 kcal].

Function of dietary polyunsaturated fatty acids in the nervous system.

The brain is the organ with the second greatest concentration of lipids; they are directly involved in the functioning of membranes. Brain development is genetically programmed; it is therefore necessary to ensure that nerve cells receive an adequate supply of lipids during their differentiation and multiplication. Indeed the effects of polyunsaturated fatty acid (PUFA) deficiency have been extensively studied; prolonged deficiency leads to death in animals. Linoleic acid (LA) is now universally recognized to be an essential nutrient. On the other hand, alpha-linolenic acid (ALNA) was considered non-essential until recently, and its role needs further studies. In our experiments, feeding animals with oils that have a low alpha-linolenic content results in all brain cells and organelles and various organs in reduced amounts of 22:6(n-3), compensated by an increase in 22:5(n-6). The speed of recuperation from these anomalies is extremely slow for brain cells, organelles and microvessels, in contrast with other organs. A decrease in alpha-linolenic series acids in the membranes results in a 40% reduction in the Na-K-ATPase of nerve terminals and a 20% reduction in 5'-nucleotidase. Some other enzymatic activities are not affected, although membrane fluidity is altered. A diet low in ALNA induces alterations in the electroretinogram which disappear with age: motor function and activity are little affected but learning behaviour is markedly altered. The presence of ALNA in the diet confers a greater resistance to certain neurotoxic agents, i.e. triethyl-lead. We have shown that during the period of cerebral development, there is a linear relationship between brain content of (n-3) acids and the (n-3) content of the diet up to the point where alpha-linolenic levels reach 200 mg for 100 g food intake. Beyond that level there is a plateau. For the other organs, such as the liver, the relationship is also linear up to 200 mg/100 g, but then there is merely an abrupt change in slope and not a plateau. By varying the dietary 18:2(n-6) content, it was noted that 20:4(n-6) optimum values were obtained at 150 mg/100 g for all nerve structures, at 300 mg for testicle and muscle, 800 mg for the kidney, and 1200 mg for the liver, lung and heart. A deficiency in ALNA or an excess of LA has the same main effect: an increase in 22:5(n-6) levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Dietary alpha-linolenic acid deficiency in adult rats for 7 months does not alter brain docosahexaenoic acid content, in contrast to liver, heart and testes.

In adult rats, 22:6(n - 3) dietary deficiency does not affect brain membranes, but has a significant effect on some other visceral organs. 60-day-old male rats fed a diet containing sufficient amounts of both linoleic and alpha-linolenic acid were divided into three groups. One group continued the same diet; the second was fed a diet containing 2% sunflower oil, the third was fed 10% sunflower oil (sunflower oil contains linoleic acid, but trace amount of alpha-linolenic acid). Animals were killed different times after receiving the new diets (1 to 31 weeks). For animals fed the diets containing only sunflower oil, deficiency in cervonic acid content (DHA, docosahexaenoic acid, 22:6(n - 3)) was not detected in whole brain, myelin or nerve endings within 31 weeks. In contrast, this acid progressively declined in liver, heart and testes up to 3 weeks and remained nearly stable thereafter. In parallel to the reduction of cervonic acid content, 22:5(n - 6) content increased in liver and heart, but not in testes. It also increased in brain, nerve endings and myelin from week 3, 6 and, 9 respectively. These results suggest that brain cervonic acid is highly preserved or is maintained at the expense of other organs.

Structural and functional importance of dietary polyunsaturated fatty acids in the nervous system.

The nervous system is the organ with the second greatest concentration of lipids. These lipids participate directly in membrane functioning. Brain development is genetically programmed. It is therefore necessary to ensure that nerve cells receive an adequate supply of nutrients, especially of lipids, during their differentiation and multiplication, and throughout their lives. The effects of polyunsaturated fatty acid deficiency have been extensively studied; prolonged deficiency leads to death in animals. Linoleic acid is now universally recognized to be an essential nutrient. Until recently, however, alpha-linolenic acid was considered non-essential. Feeding animals with oils that have a low alpha-linolenic content results in all brain cells and organelles and various organs having reduced amounts of 22:6n-3, which is compensated for by an increase in 22:5n-6. The speed of recuperation from these anomalies is extremely slow for brain cells, organelles, and microvessels, in contrast to other organs. A decrease in alpha-linolenic series acids in the membranes results in a 40% reduction in the Na(+)-K(+)-ATPase of nerve terminals and a 20% reduction in 5'-nucleotidase. Some other enzymatic activities are not affected, although membrane fluidity is altered. A diet low in alpha-linolenic acid induces alterations in the electroretinogram which disappear with age; motor function and activity are little affected, but learning behavior is markedly altered. The presence of alpha-linolenic acid in the diet confers a greater resistance to certain neurotoxic agents (triethyl-lead). During the period of cerebral development, there is a linear relationship between brain content of n-3 acids and the n-3 content of the diet up to the point where alpha-linolenic levels reach 200 mg for 100 g of food intake. Beyond that level there is a plateau. For other organs, such as the liver, the relationship is also linear up to 200 mg/100 g, but then there is merely an abrupt change in slope and not a plateau. When dietary 18:2n-6 content was varied, it was noted that 20:4n-6 optimum values were obtained at 150 mg/100 g for all nerve structures, 300 mg for testicle and muscle, 800 mg for kidney, and 1200 mg for liver, lung and heart. A deficiency in alpha-linolenic acid and an excess of linoleic acid have the same main effect: an increase in 22:5n-6 levels.(ABSTRACT TRUNCATED AT 400 WORDS)