[Rhegmatogenous retinal detachment: Topography of breaks and agreement with lincoff's rules]. / Décollement de rétine rhegmatogène : topographie des déhiscences et conformité aux lois de Lincoff.

PURPOSE: To study the topography of retinal breaks and their agreement with Lincoff's rules. MATERIALS AND METHODS: We performed a retrospective descriptive study of patients with recent rhegmatogenous retinal detachments followed on the ophthalmology service of Abass Ndao Hospital from January 2006 through December 2016. Patients with no prior retinal treatment were included. RESULTS: Over 11 years, we reviewed 97 patients with 107 eyes with retinal detachments. The mean age of our patients was 51.7 years, range 23-79 years. There were 69 male patients, for a male:female ratio of 2.46. Refraction revealed that 38.1% of patients were myopes. Fourteen percent (14%) of patients had experienced trauma to the eye with the detachment. The right eye was involved in 54.6% of patients. The onset was insidious in 54.6% of cases and sudden in 23.7% of cases. All patients had decreased visual acuity, associated with a scotoma in 26.8% of cases. Visual acuity was decreased to light perception through 7/10. In 64.9% of cases, Lincoff's rules were observed. DISCUSSION: Lincoff's rules are still relevant for localization of the breaks in retinal detachments. CONCLUSION: Diagnosis of a retinal detachment is an essential step, since it determines the treatment. Lincoff's rules still have a role in finding the retinal break in retinal detachments.

Oral probiotic treatment of Lactobacillus rhamnosus Lcr35® prevents visceral hypersensitivity to a colonic inflammation and an acute psychological stress.

AIMS: This study evaluated the efficacy of a repeated oral treatment with two active pharmaceutical ingredients (Lcr Lenio® and Lcr Restituo® ) derivated from the probiotic bacterial strain Lactobacillus rhamnosus Lcr35® in two animal models mimicking different features of irritable bowel syndrome (IBS). IBS is characterized by visceral pain associated with alteration of bowel transit. IBS patients present visceral hypersensitivity with peripheral and central origins. METHODS AND RESULTS: The injection of 2,4,6-trinitrobenzenesulfonic acid (TNBS) into the proximal colon as well as an acute partial restraint stress (PRS) produces colonic hypersensitivity measured in conscious rats by a decrease in pain threshold in response to distal colonic distension. Visceral hypersensitivity was produced by injection of TNBS 7 days before colonic distension or by acute PRS on testing day. Treatments were performed once a day during eight consecutive days. CONCLUSIONS: This study indicates that an 8-day probiotic treatment (Lcr Lenio and Lcr Restituo) produces an antihypersensitivity activity in both TNBS and PRS visceral pain models. As this probiotic strain attenuates peripherally and centrally induced visceral hypersensitivity in rats, it may be active in treatment of IBS symptoms. An immunomodulatory effect of the probiotics was highlighted in the TNBS model on the IL-23 secretion, suggesting a mechanism of action involving a regulation of the local IL-23/Th17 immune activation. SIGNIFICANCE AND IMPACT OF THE STUDY: Two formulas of Lcr35® probiotic strain show very encouraging results for the treatment of IBS patients. Further studies are needed to better understand the role and mechanisms of probiotics on the pathogenesis of IBS.

Spin reorientation and magnetic structure of HoCo12B6 ferrimagnetic compound.

The magnetic phase diagram is determined by combining magnetization measurements, ac susceptibility and neutron diffraction. The crystal and magnetic structures are also investigated. The HoCo12B6 compound exhibits ferrimagnetic behavior below TC = 147 K. Two antiferromagnetically coupled sublattices cancel out at the compensation temperature TComp = 46 K. HoCo12B6 undergoes a spin reorientation transition at TSR = 76 K; the easy magnetization axis changes from axial to basal plane upon heating. The magnitude of the magnetic moments and their orientation are described and discussed. It is revealed that HoCo12B6 compound exhibits a commensurate magnetic structure below TSR and an incommensurate one slightly above TSR. Significantly different magnetic moments have been observed on the two Co crystal sites, a very low magnetic moment of 0.14 µB being refined on the Co 18 g position. In addition, the second order crystal electric-field parameter A2(0) at the rare-earth site is determined. This result is discussed and used to explain the observed spin reorientation transition by a competition between the Co and Ho sublattice anisotropy.

Large magnetovolume effects due to transition from the ferromagnetic to antiferromagnetic state in Hf0.825Ta0.175Fe2 intermetallic compound.

Intrinsic magnetic properties and magnetovolume effects have been investigated for the Hf0.825Ta0.175Fe2 itinerant-electron system, which exhibits a temperature-induced first-order transition from the ferromagnetic (FM) to the antiferromagnetic (AFM) state. The spontaneous volume magnetostriction contraction due to this transition from the high-volume FM state to the low-volume AFM state is about 0.66%. Applying a magnetic field increases significantly the FM-AFM transition temperature T(FM-AFM), with a rate of 7.2 K T(-1). At temperatures T > T(FM-AFM) a first-order metamagnetic transition between the AFM and FM states has been observed from isothermal magnetization curves, a result attributed to the itinerant-electron character of the Fe magnetism. This AFM-FM transition is accompanied by a huge field-induced volume magnetostriction. The change in ΔV/V due to the AFM-FM transition is about 0.75%.

Ferrimagnetism in GdCo(12-x)Fe(x)B6.

The effects of iron substitution on the structural and magnetic properties of the GdCo(12-x)Fe(x)B6 (0 ≤ x ≤ 3) series of compounds have been studied. All of the compounds form in the rhombohedral SrNi12B6-type structure and exhibit ferrimagnetic behaviour below room temperature: T(C) decreases from 158 K for x = 0 to 93 K for x = 3. (155)Gd Mössbauer spectroscopy indicates that the easy magnetization axis changes from axial to basal-plane upon substitution of Fe for Co. This observation has been confirmed using neutron powder diffraction. The axial to basal-plane transition is remarkably sensitive to the Fe content and comparison with earlier (57)Fe-doping studies suggests that the boundary lies below x = 0.1.

Interactive involvement of brain derived neurotrophic factor, nerve growth factor, and calcitonin gene related peptide in colonic hypersensitivity in the rat.

BACKGROUND AND AIMS: Neutrophins are involved in somatic and visceral hypersensitivity. The action of nerve growth factor (NGF) on sensory neurones contributes to the development of referred colonic hypersensitivity induced by trinitrobenzene sulfonic acid (TNBS). Based on data on brain derived neurotrophic factor (BDNF) and calcitonin gene related peptide (CGRP) in pain, the aims of the present study were: (1) to investigate the involvement of BDNF and CGRP in this model of referred colonic hypersensitivity, (2) to test the effect of exogenous BDNF and CGRP on the colonic pain threshold, and (3) to investigate the relationship between BDNF, NGF, and CGRP by testing antineurotrophin antibodies or h-CGRP 8-37 (a CGRP antagonist) on bowel hypersensitivity induced by these peptides. METHODS: Colonic sensitivity was assessed using a colonic distension procedure. RESULTS: Anti-BDNF antibody and h-CGRP 8-37 reversed the induced decrease in colonic threshold (33.4 (2.1) and 40.3 (4.1) mm Hg, respectively, compared with a vehicle score of approximately 18 mm Hg; p<0.001). BDNF (1-100 ng/rat intraperitoneally) induced a significant dose dependent decrease in colonic reaction threshold in healthy rats. This effect was reversed by an anti-BDNF antibody and an anti-NGF antibody (33.4 (0.6) v 18.7 (0.7) mm Hg (p<0.001), anti-NGF v vehicle). NGF induced colonic hypersensitivity was reversed by h-CGRP 8-37 but not by the anti-BDNF antibody. Finally, antineurotrophin antibody could not reverse CGRP induced colonic hypersensitivity (at a dose of 1 microg/kg intraperitoneally). CONCLUSION: Systemic BDNF, NGF, and CGRP can induce visceral hypersensitivity alone and interactively. This cascade might be involved in TNBS induced referred colonic hypersensitivity in which each of these peptides is involved.

[Surgical and Orthodontic Treatment of Impacted Canines: A Clinical Report]. / Prise en charge chirurgicale et orthodontique de canines incluses : rapport d'une observation clinique.

Impaction of tooth can be defined as a failure of a tooth to emerge usually due to insufficient space or the presence of a supernumerary tooth blocking its path of eruption. Impaction of the canines deserves particular attention due to their importance regarding occlusal stability and aesthetic. A case of a young girl who presented with an impaction of both upper canines and the lower left canine is reported here. Good therapeutic results have been obtained after 18 month of treatment with a multidisciplinary team involving oral surgeons, periodontists and orthodontists.

Traditional tea drinking in Senegal. A real source of fluoride intake for the population.

Tea drinking after meals is a traditional practice in Senegal where more than 80% of the population from 15 to 60 years old drink tea. According to the tradition, in one session, each tea consumer has to drink 3 cups of decocted tea. The content of a cup is about 30 ml of liquid. Some people drink tea three times daily, that is to say after each meal. Tea plant is rich in fluoride. To determine the effective intake of the Senegalese population from this source, we measured the fluoride concentration not only for each component of the prepared tea but also for each cup of prepared tea. For this study, we used the two main kinds of tea existing locally. The analyses have been done at Rochester, NY Eastman Dental Center, Oral Biology Dept Fluoride Laboratory using the Taves Microdiffusion Method and the fluoride Ion Specific Electrode. The results so that the mean total fluoride concentration of each cup, from the first to the third one, is: 4.0 mg F-/L, 7.436 mg F-/L and 1.230 mg F-/L. It means that on an average in one session, a Senegalese tea consumer has a daily fluoride intake of 1.139 mg F-/L when taking in count the total fluoride and drinking only 90 ml of tea. If we consider the ionic fluoride the amount of daily ingested fluoride for someone who takes only 3 tea-pots of 30 ml each, is 0.830 mg. To conclude, we state that this traditional practice may have a caries preventive effect. Further studies will be grateful for that practice when setting up a caries preventive program in our country. We will also be careful in extending that practice to children less than 8 years old because it might cause dental fluorosis as in Senegal the optimal dose of fluoride is 0.8 mg F-/L.

Involvement of prostaglandins and CGRP-dependent sensory afferents in peritoneal irritation-induced visceral pain.

This study investigates the contribution of prostaglandins (PG) and calcitonin gene-related peptide (CGRP) pathways in visceral pain induced by peritoneal irritation in rats. Peritoneal irritation was produced by i.p. administration of acetic acid (AA: 0.06-1.0%, 10 ml/kg). Visceral pain was scored by counting abdominal contractions. The effect of CGRP (3-100 microg/kg, i.p.) was also evaluated. Like AA, CGRP induced abdominal pain. Neonatal pretreatment with capsaicin reduced abdominal contractions produced by AA (0.6%) and CGRP (20 microg/kg) with 64.6% and 45.6%, respectively. Abdominal contractions induced by AA and CGRP were blocked by two antinociceptive drugs, mu-and kappa-opioid agonists, morphine and (+/-)-U-50,488H, respectively. Indomethacin (3 mg/kg, s.c.) reduced the number of abdominal contractions produced by AA by 78.1%+/-6.4% but did not inhibit abdominal contractions produced by CGRP. The CGRP, receptor antagonist, hCGRP(8-37) (300 microg/kg, i.v.) inhibited AA- and CGRP-induced abdominal contractions with 57.5%+/-12.4% and 51.6%+/-11.3%, respectively. Concomitant i.p. administration of PGE1 and PGE2 (0.3 mg/kg of each) produced abdominal contractions which were inhibited 45.6%+/-9.3% by hCGRP(8-37) (300 microg/kg i.v.). Taken together, these results suggest that peritoneal irritation is likely to trigger the release of prostaglandins, which in turn produces a release of CGRP from primary sensory afferents.

Fedotozine blocks hypersensitive visceral pain in conscious rats: action at peripheral kappa-opioid receptors.

The effect of fedotozine on visceral hypersensitivity was evaluated in conscious rats. One hour after colonic irritation (0.6% acetic acid intracolonically), a 30 mmHg colonic distension was applied for 10 min. Irritation increased the number of abdominal contractions induced by colonic distension (23.4 +/- 4.1 versus 4.8 +/- 1.4 in saline-treated rats, P < 0.001). Facilitation of colonic pain was reversed in a dose-dependent manner by fedotozine ((+)-(-1R1)-1-phenyl-1-[(3,4,5-trimethoxy)benzyloxymethyl]-N ,N-dimethyl-n-propylamine), (+/-)-U-50,488H (trans-(+/-)-3,4-dichloro-N-methyl-N-(2-1-pyrrolidinyl]cyclohexyl)benzen eacetamide) and morphine (respective ED50 values 0.67, 0.51 and 0.23 mg/kg s.c.). The kappa-opioid receptor antagonist, nor-binaltorphimine, abolished the effects of fedotozine and (+/-)-U-50,488H but not those of morphine. Low doses of naloxone (30 microg/kg s.c.) blocked the effect of morphine but not of fedotozine or (+/-)-U-50,488H. After intracerebroventricular administration, morphine was very potent (ED50 1.7 microg/rat), (+/-)-U-50,488H poorly active (58% of antinociception at 300 microg/rat) and fedotozine inactive up to 300 microg/rat. These results show that fedotozine blocks hypersensitive visceral pain by acting on peripheral kappa-opioid receptors in animals.

Antinociceptive effects of morphine and U-50,488H on vaginal distension in the anesthetized rat.

The antinociceptive activity of the kappa- and mu-opioid receptor agonists, (+/-)-U-50,488H and morphine, was examined in a vaginal distension model in anaesthetized female rats. Vaginal distension induced a reproducible cardiovascular response (CVR) which was inhibited in a dose related manner by morphine (0.03-1.0 mg/kg i.v., ED50 = 0.16 mg/kg) and (+/-)-U-50,488H (0.08-1.6 mg/kg i.v., ED50 = 0.49 mg/kg). Morphine (0.3 microg/rat) administered i.c.v. inhibited the CVR by 81.6 +/- 7.9% whereas (+/-)-U-50,488H (30-300 microg/rat) was inactive by this route. A low dose of naloxone (30 microg/kg i.v.) blocked the effect of morphine but not that of (+/-)-U-50,488H. The kappa-opioid antagonist, nor-binaltorphimine (10 mg/kg s.c.) abolished the response to (+/-)-U-50,488H but not that of morphine. This demonstrates that both central and peripheral mu-opioid receptors may be involved in morphine-induced antinociception whereas the kappa-opioid agonist, (+/-)-U-50,488H, blocks vaginal nociception by acting on peripheral kappa-opioid receptors.

Etude comparative du risque traumatique dento-maxillaire en pratique sportive au Senegal : a propos de 600 sportifs

"Les auteurs ont mene une etude comparative de prevalence des traumatismes bucco-dentaires dans la ""lutte avec frappe"" et dans certains sports d'equipe ou individuels comme le football; le basket ball; la boxe anglaise et la lutte libre. L'objectif de cette etude est d'informer; d'eduquer; de communiquer avec le milieu sportif senegalais; mais aussi de prevenir les risques potentiels du sport par le port de gouttieres de protection dento-maxillaires"

Effect of fedotozine on the cardiovascular pain reflex induced by distension of the irritated colon in the anesthetized rat.

The effect of fedotozine was evaluated in a model of colonic hypersensibility to balloon distension in anesthetized rats. Acetic acid (0.6%, intracolonically) significantly enhanced the hypotension reflex response to colonic distension (P < 0.05). At a noxious pain pressure (75 mm Hg), fedotozine ((+)-(-1R)-1-phenyl-1-[(3,4,5- trimethoxy)benzyloxymethyl]-N,N-dimethyl-n-propylamine) had no effect at 0.6 and 1 mg/kg i.v. in saline-treated rats and higher doses were required to produce antinociception (ED50 = 2.57 mg/kg i.v.). By contrast, fedotozine at 0.6 and 1 mg/kg i.v. displayed 38 and 54% antinociception (P < 0.05) respectively, in acetic acid-treated animals, leading to a decrease in its ED50 (1.15 mg/kg i.v.). Similar results were obtained with (+/-)-trans-N-methyl-N-[2-(pyrrolidinyl)-cyclohexyl]benzo[b]-thiophene- 4-acetamide (PD-117,302), a kappa-opioid receptor agonist, while the antinociceptive action of morphine and a kappa-opioid receptor agonist, trans-(+/-)-3,4-dichloro-N-methyl-N-(2-[1- pyrrolidinyl]cyclohexyl)benzenacetamide ((+/-)-U-50,488H), was identical in control and acetic acid-treated animals. Nor-binaltorphimine, a selective kappa-opioid receptor antagonist, reversed the enhanced antinociceptive activity of fedotozine and PD-117,302. It is concluded that acetic acid induces colonic hypersensibility to painful mechanical stimuli and that some but not all kappa-opioid receptor ligands can have enhanced efficacy in this pathological situation.

Peripheral kappa-opioid receptors mediate the antinociceptive effect of fedotozine (correction of fetodozine) on the duodenal pain reflex inrat.

Fedotozine has been shown to act on gastrointestinal sensitivity through peripheral kappa-opioid receptors. The present study investigated the action of fedotozine and reference compounds, morphine and (+/-)-U-50,488H, on duodenal pain in anesthetized rats. The noxious stimulus was produced by duodenal distension (100 mm Hg; 30 s). Fedotozine (1-5 mg/kg i.v.) produced a dose-dependent inhibition of the cardiovascular reflex induced by duodenal distension (ED50 = 1.87 mg/kg) but had no effect at doses up to 300 micrograms/rat by either intracerebroventricular (i.c.v.) or intrathecal routes (i.t.). The mu-opioid receptor agonist, morphine, was active by both i.v. (ED50 = 0.62 mg/kg) and i.c.v. routes (ED50 = 2.17 micrograms/rat) as was the kappa-opioid receptor agonist, (+/-)-U-50,488H (trans-(+/-)-3,4-dichloro-N-methyl-N-(2-[1- pyrrolidinyl]cyclohexyl)benzeneacetamide) (ED50 = 0.25 mg/kg and 149 micrograms/rat for i.v. and i.c.v. routes, respectively). The selective kappa-opioid receptor antagonist, nor-binaltorphimine (10 mg/kg s.c.), abolished the response to fedotozine (5 mg/kg i.v.) and (+/-)-U-50,488H (2 mg/kg i.v.) but not that to morphine (1 mg/kg i.v.). In contrast, naloxone (30 micrograms/kg i.v.) blocked the response to morphine (1 mg/kg i.v.) but not that to fedotozine (5 mg/kg i.v.) or (+/-)-U-50,488H (2 mg/kg i.v.). It is concluded that the antinociceptive effects of fedotozine on duodenal pain are mediated by peripheral kappa-opioid receptors.

Role of vagal afferents in the antinociception produced by morphine and U-50,488H in the colonic pain reflex in rats.

The mechanisms underlying the antinociception induced by morphine or U-50,488H (trans-(+-)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl]- cyclohexyl)benzeneacetamide) against painful colonic distension were examined in anaesthetized rats. The respective ED50 values for morphine and U-50,488H were 0.34 and 0.35 mg/kg for the i.v. route, and 1.68 and 167 micrograms/rat for the i.c.v. route. Morphine was active by the intrathecal route (ED50 = 7.8 micrograms) whereas U-50,488H had no effect at doses up to 100 micrograms/rat. The morphine response was selectively antagonized by naloxone (30 micrograms/kg i.v.) whereas that of U-50,488H was blocked by nor-binaltorphimine (10 mg/kg s.c.). Bilateral vagotomy abolished the response to morphine at 0.35 mg/kg i.v. and reduced by 41.3% that to 1 mg/kg morphine, but had no effect on that to U-50,488H or i.c.v. morphine (10 micrograms/rat). It is concluded that peripheral mu- and kappa-opioid receptors may produce antinociception for colonic pain and that vagal integrity is required for mu-opioid but not kappa-opioid peripheral antinociception.

[Diagnosis and treatment of thyroglossal cysts and fistulae (Sistrunck or Schlange?): reflections on 40 cases]. / Diagnostic et traitement des kystes et fistules thyréoglosses (Sistrunck ou Schlange?): réflexions à propos de 40 cas.

40 cases of cysts and fistulas of the thyroglossal tract duct offer to the authors occasion to review the rare problems of diagnosis raised by this pediatric pathology. They compare the results of surgery obtained by the classic technic of Sistrunck (1920) versus the Schlange's operation (1893) which remove the cyst with the hyoid bone's body only. The average of age is 17 years. A location of a thyroglossal cyst in the submandibular area was noted during operation. Sistrunck's operation was performed in 21 cases (52.5%) and the Schlange's one in 14 cases (35%) without recurrence. 4 cases (10%) recurrences were noted, all after simple cystectomy. Removal of the hyoid bone's body appear to us as the key of success in the surgery of thyroglossal anomalies.

[Test for detection of deafness in newborns at risk. Apropos of 1048 tests]. / Essai de dépistage de la surdité chez le nouveau-né à risque: à propos de 1,048 tests.

It is a prospective study of 1048 newborns incurring the risk of deafness in three hospitals in Dakar from March 14th to January 4th 1989. It comes out of this analysis that the most important causes of suspect cases are neonatal jaundices, congenital malformations, premature birth. The most frequent reactions are noticed in the members of a bilateral way, unlike the general assumption that reactions are noticed in the head. Out of a final population of 846 newborn, 839 were "normal", 7 were "suspect" (less than 1%). This evaluation would be higher for, among the 202 people we ultimately lost sight of (about 19.3%) were "suspect" without any associated pathology). Finally, the authors are then given the opportunity to draw the attention of the public authorities, the medical staff and the populations, on the importance of detecting early the infant's deafness.

Travel stress alters the intestinal migrating myoelectric complex in rats: antagonist effect of trimebutine.

A novel stress model was developed that may closely resemble a real-life situation. Intestinal motility was monitored in rats before and after a 12 hour train voyage (travel stress). Travel stress reduced the duration of phase III of the intestinal MMC by 30% (3.2 +/- 0.3 vs 4.7 +/- 0.6 min; p less than 0.001) while the durations of phase I and II were unaffected. This effect persisted for two days. Phase III duration returned to basal values after 3 days indicating a reversible alteration on intestinal migrating myoelectric complex (MMC). The infusion of trimebutine at a flow rate of 166 micrograms/kg/h during the stress exposure abolished the changes observed in the duration of phase III of the MMC; the infusion of diazepam (16.6 micrograms/kg/h) had no effect. These results indicate that the travel stress model may be similar to common life events that induce alterations of intestinal motility. Furthermore, trimebutine prevented the reduction of phase III duration induced by travel stress suggesting its possible action on mechanisms involved in the mediation of the stress-induced intestinal motility changes.

[Lethal midline granuloma in Senegal. (Apropos of 15 cases)]. / Le granulome médio-facial au Sénégal (A propos de 15 observations).

African authors, other than senegalese, have not paid enough attention to lethal granuloma, a terrible disease. This series is about a series collected between 1975 and 1990. It is particularly high compared to other series in the world. If diagnosis is easy for the clinician, much care must surround the pathological answer. Those diagnosis problems and difficulties of treatment (represented by 11 deaths) are studied.