Bokt.nl

**Geplaatst:** 29-08-04 18:45

Geplaatst: 29-08-04 18:45

Het is behoorlijk klets dat veulen van een luchtzuiger slecht verkopen. Mijn luchtzuigende merrie heeft drie veulens gehad. Geen van de drie is gaan luchtzuigen. En de eerste twee zijn voor een goede prijs verkocht. De laatste niet, die hou ik namelijk Lachen

En makkelijker een vrucht afstoten heb ik werkelijk nog nooit van gehoord Scheve mond

**Geplaatst:** 29-08-04 19:38

Geplaatst: 29-08-04 19:38

Het veronderstelt dat je het uberhaupt weet van die moeder Sjuim... Hoeveel mensen kopen een veulen?? Ik zie vooral twee en driejarigen verkocht worden. Daar loopt meestal geen moeder meer bij. En mensen vragen daar volgens mij ook niet naar overigens.

Maar goed, ik heb alleen ervaring met de veulens van Lanna. En die twee zijn verkocht met een duidelijk luchtzuigende moeder. Kennelijk zaten die mensen er niet mee.

**Geplaatst:** 30-08-04 10:37

Geplaatst: 30-08-04 10:37

Nou eh... het zal wel.. Heb toch echt heel internet en heel wat universiteiten afgezocht naar kenmerken en onderzoeken van luchtzuigen. Laat mij maar zien waar die veearts die wijsheid vandaan heeft.

Herken het ook niet. Mijn merrie is gruwelijk vruchtbaar zelfs. Alle keren meteen raak en niks afgestoken. Maar 1 merrie is geen voorbeeld. Een luchtzuiger achter stroom in de stal zetten vind ik trouwens vallen onder de categorie "ongelofelijk hoe kun je het een dier aandoen".

**Geplaatst:** 30-08-04 11:56

Geplaatst: 30-08-04 11:56

tja daar ben ik het niet mee eens Lachen

**Geplaatst:** 30-08-04 13:11

Geplaatst: 30-08-04 13:11

Lovely schreef:
Als er geen onderzoek naar gedaan is, dan is er zéker geen wetenschappelijk bewijs voor. Maar als volksstammen mensen iets alsmaar meemaken en weten dat iets waar is, dan is dat niet ineens minder waar bij gebrek aan wetenschappelijk bewijs.

Er is juist veel onderzoek gedaan naar luchtzuigen. Ook door de UVA, waarbij ook praktijkervaringen van mensen zijn meegenomen. Er wordt nog steeds onderzoek gedaan naar luchtzuigen... Wetenschappelijk opgezette studies en onderzoeken zeggen mij meer dan de mening van iemand die wat eigen waarnemingen heeft gedaan, die dan ook nog gekleurd worden door de normatieve oordelen van de betreffende waarnemer.

Volkstammen mensen is wijsgemaakt dat aderlaten een goede remedie tegen ziektes was. Ook toen bewezen was dat dat niet werkte, geloofden volkstammen mensen dit nog. Als er iets is waar ii niet in geloof, dan is het wel collectief nagepraat volksgeloof.

Voor mij nu einde discussie.

**Geplaatst:** 30-08-04 15:06

Geplaatst: 30-08-04 15:06

Onderzoek 1: (over aantallen luchtzuigers, al dan niet overnemen gedrag en stalmanagement) is op te vragen bij de faculteit in Utrecht. Heb ik gewoon gekregen toen ik er naar vroeg.

Onderzoek 2: staat hier:
http://www2.vet.upenn.edu/labs/equinebe ... /mills.htm

Onderzoek 3: (de verkorte op internet gepubliceerde versie)
Recent studies on cribbiting horses

J. Geoffrey Lane

University of Bristol, Depart~nent of Clinical Veterinary Science, Langford House, Langford, Bristol BS18 7DU, U.K

Introduction

There is confusion in the veterinary literature concerning the definition of oral based stereotypies "cribbiting" and "windsucking" in horses and it is a matter of semantics whether horses are "cribbiters" when they grasp fixed objects in the stable or field environment to facilitate the arching of the neck and emission of a characteristic pharyngeal sound, or "windsuckers" when the behaviour is performed without grasping objects between their incisor teeth. For the purposes of this presentation the two terms will be used as if they are synonymous. It has been widely stated that horses which exhibit either of these abnormal behavioural patterns swallow air (aerophagia) and it is also believed that the introduction of large quantities of air into the alimentary tract predisposes horses which cribite to colic and/or to poor bodily condition.

The conditions in force at the leading public auctions of thoroughbred horses in the United Kingdom and Ireland state that the sale of a horse shall be invalidated if "it is a wind sucker, i.e. habitually swallows air whether in association with grasping fixed with its incisor teeth or not, or has been operated upon for the correction of this condition, including cribbiting". Thus, there are important medicolegal reasons for accuracy in the description of the events which occur during the stereotypy.

The purpose of this presentation is to report the results of endoscopic and fluoroscopic studies of the pharyngeal structures of horses during the act of cribbiting/windsucking. The major conclusion has beenthat deglutition does not occur as part of the stereotypy and that "aerophagia" is an inappropriate synonym for this stereotypy.

Normal deglutition

Deglutition is traditionally divided into oraL pharyngeal and oesophageal stages and these are applicable to the horse. The oral phase comprises the prehension, mastication and transfer of food and fluid boluses to the base of the tongue and it is under voluntary control The presence of the bolus at the tongue triggers the complex sequence of reflexes which forms the involuntary transfer of ingesta through the pharynx to the oesophagus and eventually to the stomach. The events which occur during tthe pharyngeal phase include elevation of the soft palate to occlude the nasopharynx, adduction of the arytenoid cartilages and vocal folds, together with retroversion of the apex of the epiglottis to close tthe rime glottidis; contraction of the base of the tongue and constriction of the oro and nasopharoxy by the ciruclar muscles to propel the bolus caudally; and receptive relaxation of the cricopharyngeal sphincter to allow the bolus to enter the upper oesophagus. The oesophageal phase commences with closure of the cricopharynx shich initates a wave of primary oesophageal peristalsis which moves each bolus caudalaly towards the cardia. Secondary oesophageal persitaltic waves are irregular eventsbut result from the stretching of the oesophageal walls by residual material within the lumen.

There are a variety of techniques by which deglutition canbe studies ranging from observations of the movements of the structures of the pharynx and oesophagus by fluoroscopy and endoscopy to electromyographic recording of the electrical activity in the muscles of the region.

Normally, when an endoscope is placed in the nasopharynx via the nasal meatus the structures of the larynx are clearly visible. However, during deglutition the contraction of the pharyngeal walls and dorsal displacement of the soft palate completely obscure the view of the larynx until it has been restored to its intranarial position. Flexible endoscopes can be attached to a headcollar using velcro tape so that endoscopic recordings of pharyngeal activity can be made over a sustained period.

Dynamic fluoroscopic studies of deglutition can be performed during eating be offering the patient food impregnated with contrast medium. In the author's clinic such a technique is regularly used to assess horses showing signs of dsyphagia, and it has been found that a traditional bran mash impregnated with barium sulphate and with the addition of molasses to enhance palatability is an ideal material. Freshly cut or conserved herbage is less suitable, because it tends to produce uneven contrast and less consistent acceptance by the patient. Most horses are starved for 12 to 15 hours before testing to ensure an enthusiasm to participate in the investigation. Occasional patients are deterredby the noises of the radiographicmachinerybutafter one or twoperiods of familiarisationtheyarewilling to eat while the fluoroscopic records are made. The unsedated horses are stood in stocks and offered the mash from a bucket placed between the tube head and image intensifier of a system mounted on an overhead gantry for simultaneous movement.

The positive contrast in the food boluses helps to outline the structures of the oropharynx and oesophagus while the negative contrast provided by air highlights the nasopharynx and larynx. During contrast studies of deglutition the events which can be observed include the gathering of the food bolus at the base of the tongue; contraction of the pharyngeal walls and propulsion of the bolus from the pharynx the pharyngeal "stripping" wave; retroversion of the epiglottis; receptive relaxation of the upper oesophagus as the food bolus passes caudally; primary and secondary oesophageal peristalsis; and restoration of the larynx to its intranarial position.

Videotape recordings are essential for the slow motion analysis of both endoscopic and fluoroscopic images.

Endoscopic and fluoroscopic studies during cribbiting/windsucking

The investigation reported here comprised the study of a group of known cribbiters by making separate fluoroscopic and endoscopic recordings of the pharyngeal region during the performance of the oral based stereotypy. The horses were stood in stocks for both stages of the investigation and a wooden bar covered with coconut matting was placed at the front of the stocks to provide an inducement to cribbite. Complete cubes were also offered from a bucket adjacent to this bar. Fluoroscopic recordings of 6 horses performing a total of 102 stereotypic sequences were made and endoscopic records of 70 similar sequences from 4 horses, three of which had been used in the radiographic study, were also collected for analysis. In advance of the investigations the subjects had been examined by routine endoscopy and palpation to eliminate animals with identifiable structural or functional anomalies of the upper respiratory tract.

Videofluoroscopic findings: Throughout the studies the recorded events were similar for each cribbiting/windsucking sequence in all of the horses used. Initially the upper oesophageal sphincter (the cricopharynx) was closed and there was no air in the oesophagus distally. Immediatelybefore the first stereotypic sequence appetitive behaviour was noted in the form of movements by the base of the tongue and by the soft palate as the horse licked the "cribbing barn. The onset of each stereotypic sequence wa seen as retraction of the larynx caudally and slightly ventrally. Throughout each sequence the distance between the ventral border of the oesophagus and the dorsal margin of the trachea remained constant, the epiglottis remained in a resting position parallel with the tongue and the soft palate was in its normal subepiglottic position maintaining contact with the tongue rostrally. Thus continuity was invariably maintained between the nasopharynx and caudal nasal chambers. Coinciding with the emission of the characteristic noise associated with cribbiting/wind suckinth the proximal oesophagus abruptly filled with air to a maximal dorsoventral diameter approximately 80 % that of tthe diameter of the trachea. This was largely achieved by ballooning of the dorsal oesophageal wall rather than by movement of its ventral margin. The radiographic contrast provided by air in the nasopharynx and proximal oesophagus enabled observations of the palatopharyngeal arch. The caudal pillars of this structure became dorsally displaced as oesophageal distension occurred and the cricopharynx opened. The length of the cricopharynx reduced causing a further increase in the dorsoventral diameter of the rostral oesophageal sphincter. Maximal distensionof the oesophagus coincided with the initial opening fo the crico pharyngeal sphincter. During the process of eflation there was little evidence of primary or secondary oesophageal peristalsis and a ratio of 1 air bolus removed by peristalsis to 12 upper oesophageal distensions was recorded. Thus, it was concluded that the air returned to the pharynx by spontaneous deflation after most stereotypic sequences.

Endoscopic findings: Endoscopy confirmed that during each cribbite the larynx was retracted caudally and that the rime glottidis remained open with no active adduction or abduction by the arytenoid cartilages or vocal folds. The posterior pillars of the palatopharyngeal arch became visible as a curved structure which moved dorsally from its resting position caudal to the apices of the corniculate processes. The ventral border of these pillars was seen to vibrate in synchrony with opening of the oesophageal sphincter and the emission of the characteristic grunt. Again, the rostral margin of the palatopharyngeal arch was seen to remain in a subepiglottic position throughout the stereotypic sequences and there was no constriction by the pharyngeal musculature on any occasion.

Conclusions

1. Deglutition is not a feature of cribbiting/windsucking: the events recorded during the stereotypic sequences did not remotely resemble swallowing.

2. The source of the characteristic noise assoicated with this oral based stereotypy results from an inrush of air into the proximal oesophagus following dilation of the cricopharyngeal sphincter.

3. The movement of air results from pressure gradients created in the soft tissues of the throat rather than by compression of the pharyngeal lumen.

4. Only a small proportion of the air which distends the upper oesophagus is conveyed towards the stomach.

Discussion

Although the invetigation outlined above has clarified some of the events which occur in the pharynx and upper oesophagus during oral based stereotypic sequences, it has not addressed the motivation for the behaviour.Cribbiting, windsucking and grasping all include characteristic arching of the neck accompanied by contraction of the muscles on the ventral aspect of the throat. It seems likely that this muscular effort creates the pressure gradient in the oesophageal lumen and a resultant distension of the cranial oesophagus with or without the emission of a grunt. It is conjectured that is is the di stension of the viscus which is the ultimate objective of this stereotypy and that this is more likely to be the source of gratification than grasping objects between the incisor teeth. This in turn begs the question as to what physiological mechanism might render such a distension a behavioural "needn.

The efficacy of surgical procedures oriented to ablate or denervate the strap muscles in the ventral throatregioncanbe explainedby the suggestionthatitis the contraction of thesemuscleswhichcreates a pressure gradient between the oesophageal lumen and the pharynx.

Observations of cribbiting horses in the study above revealed little primary oesophageal peristalsis and only a smal1 number of air boluses conveyed towards the stomach by secondary peristalsis. In additionin order to perform the studies, cribbiting wasprovokedby offering palatable food and thus, more swallowing may have taken place than during spontaneous demonstrations of the stereotypy. Thus, why is there an accepted association between cribbiting/windsucking and tympanitis colic? One explanation may be that there the diagnosis is incorrect in the first place. In horses with fourth branchial arch defects (tBAD) the cricopharyngeus and thyropharyngeus muscles are frequently absent or vestigial. This congenital defect predisposes afflicted horses to tympanitic colic. Radiographic studies of deglutition in horses with this form of 4BAD shows a continuous column of air from the pharynx to the cervical oesophagus and the caudal propulsion of air by peristalsis is a consistent feature. This constitutes true aerophagia and the attendants of horses afflicted with this congenital disorder frequently believe that they are "windsuckersn because of the eructation noises which they occasionally emit.

Accurate definitions in this area of behaviour are necessary in the context of horse sales and the results reported here confirm that the Conditions of Sale currently in use at public auctions require amendment if unnecessary litigation is to be avoided.

Onderzoek 4
In association with Mark Andrews, BVM&S CertEP MRCVS, of
EQUINE SCIENCE UPDATE
we are pleased to provide the latest veterinary information.

Gastric Ulcers

Equine Gastric Ulcers
Equine gastric ulcer syndrome (EGUS) is the most common disorder of the equine stomach. It affects over 90% of racehorses in training and nearly 60% of other sport horses.(1) No specific cause has been determined, but various factors are thought to play a part, including stabling, ingestion of concentrate foods, intensive exercise and transport.

Normal anatomy of the stomach
Horses are well adapted to eating little and often. They have a relatively small stomach, holding between 8 and 15 litres.

The inside surface of the stomach can be divided into two parts according to the different types of cells that make up the lining (mucosa). The non-glandular part of the stomach is pale pink; the glandular mucosa is darker in colour.

The upper ( non-glandular) part is covered with layers of cells ("stratified squamous epithelium" ). In the adult horse it is usually up to 20 cells thick, although it can be thinner in foals. The outer layers are hardened (cornified) and form a mechanical protective barrier. This part of the stomach has no absorptive or secretory functions.

The lower (glandular ) part is similar to the stomach of other single-stomached animals. The glandular mucosa contains numerous gastric glands which secrete hydrochloric acid . The acid helps in the breakdown of food, providing ideal conditions for the digestive enzymes to work. The gastric glands also secrete pepsinogen. It is activated by the acid conditions, becoming pepsin, the major enzyme involved in protein digestion. There are also cells that secrete a bicarbonate-rich mucus which protects the mucosa from the acidity of the gastric fluid. Chemical messengers known as prostaglandins help to maintain the blood supply to the epithelium and increase mucus secretion from the gastric glandular mucosa.

How do ulcers form?
Ulcers in the non-glandular part of the stomach form when excessive hydrochloric acid and pepsin in gastric secretions overwhelm the protective mechanisms of the gastric mucosa.

The secretion of acid from the gastric glands is stimulated by the vagus nerve, and also by gastrin, a hormone released in response to feeding. Although the amount of acid increases when the horse is eating, secretion continues all the time. Normally the acidity of the stomach contents is buffered by saliva. However, saliva is only produced in significant amounts when the horse is eating. So horses that are grazing most of the time have a constant flow of saliva to neutralise the stomach acid.

The high grain, low roughage diet of horses in training is thought by many to contribute to the development of gastric ulcers. Grain requires less chewing and so stimulates less saliva. It is also more potent at stimulating acid production than is hay.

If a horse is deprived of food for only a couple of hours the stomach contents will rapidly become more acidic (pH2 or lower).Ulcers can appear within 24-48 hours if the horse is prevented from eating.

Others (2) have suggested that a mechanical effect of exercise keeps the stomach acid in contact with the non-glandular mucosa for longer). They suggest that an increase in pressure in the abdomen during intense exercise compresses the stomach, pushing the acidic contents up onto the non-glandular part of the stomach. According to their theory, horses that spend more time training, have acid in contact with the non-glandular part of the stomach for longer, causing more ulcers.

ulcers of the glandular mucosa are commonly caused by overdose/ area common side effect of NSAID treatment.
What factors increase the risk of gastric ulcers?
Various factors are known to increase the risk of gastric ulcers:
· intense physical activity. During physical exertion the blood is diverted from the intestines to the skeletal muscles and skin. Gastric acid secretion increases during hard work As mentioned above, (2) exercise tends to push the acidic stomach contents up onto the non-glandular mucosa.

· diet. Grain and pelleted rations promote higher levels of gastrin in the blood than does hay and so stimulate more acid production..Eating hay stimulates twice as much saliva production as does eating grain.

· stress and illness may cause ulcers by restricting the blood flow to the mucosa
· drug-induced. Non-steroidal anti-inflammatory drugs (NSAID`s - such as phenylbutazone) are thought to exert their effects on the gastric mucosa by inhibiting prostaglandin synthesis, leading to restriction of the blood supply to the glandular mucosa.

What are the signs of gastric ulcers?
Adult horses with gastric ulcers often show no signs. However, they may show non-specific signs such as: weight loss, reduced appetite, poor physical condition, dullness, colic, diarrhoea, poor performance, or change in behaviour. Often the degree of ulceration doesn't relate to the severity of the signs. A horse with mild ulceration may show marked clinical effects; whereas those with extensive ulceration may not appear ill.

Foals usually show more obvious signs of pain. Diarrhoea is the most common sign, other signs include excess salivation, grinding their teeth ( bruxism ) and colic.

Ulcers and crib-biting
Recent work suggests a relationship between gastric ulcers and some stereotypies (previously referred to as vices ). Crib-biting and wind-sucking may be attempts by the horse to stimulate saliva production to neutralise stomach acid.

Professor Christine Nicol and her colleagues have been investigating the relationship between crib-biting and gastric ulceration in foals. They looked at what effect feeding an antacid diet had on both crib-biting behaviour and gastric ulceration.(5) They found that crib-biting foals had more signs of gastric ulceration than did foals that did not crib-bite. Foals that were fed an antacid diet for 14 weeks showed a significant improvement in the condition of the stomach. Although most foals showed a reduction in crib-biting behaviour over the duration of the trial, the reduction was most marked in the foals on the antacid diet. Eleven of twelve foals on the antacid diet showed either an improvement or no change in the gastric ulceration score - (ie they had fewer ulcers at the end of the study.) In contrast, only three foals on the base diet improved or did not change, and four grew worse.

They found that foals that showed the greatest improvement in ulceration score also tended to show the most reduction in crib-biting.

Daniel Mills and Clare MacLeod showed that feeding adult horses an antacid diet led to a reduction in cribbing activity after just one week. Further reductions in cribbing occurred when the antacid diet was fed for another five weeks. They also found that neither age, nor the duration of the cribbing behaviour prior to being fed the antacid diet, affected the effectiveness of the treatment. (6)

How do we diagnose gastric ulcers?
Endoscopic examination of the stomach is used to reach a definitive diagnosis. A long (2-3metre) endoscope is required to inspect the inside of the stomach. The examination is best done after starving the horse for 12-14 hours.

Schemes for grading the severity of ulcers have been developed. For example the Equine Gastric Ulcer Syndrome (EGUS) Council recommends the following system:

Grade 0:The epithelium is intact and there is no hyperaemia of hyperkeratosis - normal
Grade 1: the mucosa is intact but there are areas of reddening and hyperkeratosis (thickening)
Grade2: Small, single or multiple ulcers present
Grade3: Large, single or multiple ulcers or extensive superficial lesions
Grade4: Extensive, deep ulcers

Bleeding is not considered to be a helpful sign in grading ulcers because some small ulcers may bleed while large deep ulcers may not.

However, much debate exists regarding the accuracy of these grading systems. One study carried out in America (3) found that endoscopic examination underestimated the severity of the ulceration.

Many vets do not have access to endoscopes that are long enough to examine horse`s stomachs. Researchers have been investigating other methods for identifying gastric ulcers. One technique that might prove useful as a screening test is to measure the absorption of sucrose across the stomach wall. Normally sucrose is not absorbed in the stomach and is rapidly broken down to fructose and glucose when it reaches the small intestine. However, it can be absorbed across the stomach wall when ulcers are present. The sucrose is then excreted the urine. Researchers have been investigating whether the measurement of sucrose in the urine after oral dosing can be used as a screening test for gastric ulceration. (4)

If endoscopy is not available, a course of empirical therapy that produces an improvement is strong supporting evidence.

Treatment
· stop training. The simplest treatment is pasture grazing. In many cases that is not a practical solution for the type of horses that suffer from EGUS. However in one study , untreated ulcers did not heal spontaneously and tended to get worse while the horses continued in training (7) Conversely, one study showed spontaneous improvement even if no antacid treatment was given provided the horses were taken out of training.(8)

· avoid stress such as box confinement long transportation.
· antacids. These buffer (neutralise) the gastric acids. They usually consist of mixtures of magnesium hydroxide and aluminium hydroxide. They only have a short lived effect. There is some doubt whether horses can be treated often enough to have a significant effect on gastric acidity under practical conditions.

· sucralfate. This is the aluminium hydroxide salt of sucrose. It forms a sticky gel in acid conditions ( pH less than 4), attaches to ulcerated tissue and remains there for six hours or more. Because it requires acid conditions, it will probably not be effective if given at the same time as antacid medication. Sucralfate has not been shown to be effective in treating ulcers of the non-glandular mucosa. It may, however, stimulate mucus production and increase prostaglandin production from the glandular mucosa. So it may be more effective for treating ulcers of the glandular mucosa.

· Histamine H2 receptor antagonists. These are used for treatment of gastric ulcers in humans (eg cimetidine, ranitidine). They block acid secretion by blocking the action of histamine on the H2 receptor of the parietal cell which stimulates acid secretion. There is evidence that they reduce acid production, but their effect on ulcer healing is less certain

· Acid pump inhibitors. These block the action of the final step in the acid secreting pathway. Omeprazole is currently available in USA and should be licensed in the UK by the end of 2003. Recent studies show that a dose of 4mg/kg is most effective, resulting in healing in 77% and improvement in 92%. It exerts its maximum effect on acid secretion in 3-5 days. Ulcers may take 2 - 4 weeks to heal although horses often feel more comfortable within a few days of starting treatment.

References
1 Field survey of the prevalence of gastric ulcers in Thoroughbred racehorses and on response to treatment of affected horses with omeprazole paste. JH Johnson, N Vatistas, L Castro, T Fischer, FS Pipers, D Maye. Equine Vet Educ (2001) 13, (4) 221-224.

2 Is the cause of training-related squamous gastric ulceration primarily a mechanical phenomenon?M Lorenzo-Figueras, JA Burrow, GD Lester, AM Merrit. Proc Seventh Int Colic Research Symp (2002) 80

3 Inability of endoscopic examination to predict gastric ulcer severity in horses. FM Andrews Proc Seventh Int Equine Colic Research Symposium (2002) 83.

4 M O`Connor, A Roussel, J Steiner, J Meddings, N Cohen. Sucrose permeability as a marker for equine gastric ulceration. Proc 7th Equine Colic Research Symposium (2002) p84.

5 Study of crib biting and gastric inflammation and ulceration in young horses. CJ Nicol, HPD Davidson, PA Harris, AJ Waters, AD Wilson. Vet Rec (2002) 151, 658 - 662.

6 Mills DS, MacLeod CA. The response of crib-biting and windsucking in horses to dietary supplementation with an antacid mixture. Ippologia (2002)13, (2) 33 - 41

7 Murray MJ, Schusser GF, Pipers FS, Gross SJ. Factors associated with gastric lesions in thoroughbred racehorses. Equine Vet J (1996) 28, 368-74.

8 Murray MJ, Haven ML, Eichorn ES, Zhang D, Eagleson J, Hickey GJ. Effects of omeprazole on healing of naturally-occurring gastric ulcers in thoroughbred racehorses. Equine Vet J (1997) 29, 425-429

* * * * * *

Ik heb er nog wel een paar, maar dit lijk me voorlopig wel even genoeg.

Laatst bijgewerkt door Anya op 30-08-04 16:15, in het totaal 1 keer bewerkt

**Geplaatst:** 30-08-04 15:20

Geplaatst: 30-08-04 15:20

Volgens mij kun jij niet lezen alabastro Lachen

**Geplaatst:** 30-08-04 15:27

Geplaatst: 30-08-04 15:27

geeft niet hoor... schaar je je toch gewoon onder de mensen die geloven in volksgeloof. Misschien kunnen we aderlaten bij luchtzuigers introduceren. Zou wel kunnen helpen. Je weet nooit Lachen

**Geplaatst:** 30-08-04 15:37

Geplaatst: 30-08-04 15:37

Lovely schreef:
Anya, als het zo lastig voor je is dat andere mensen een andere mening hebben dan jij, dan is het misschien voor jou prettiger om dan niet aan de discussie mee te doen.
Volksgeloof noem jij het als heel veel mensen onafhankelijk van elkaar dezelfde zaken constateren. Dat je nat wordt als het regent, dat hoeft toch niet in een laboratorium onderzocht te worden, neem ik aan??

Tja, ik zou zeggen, lees, vindt het jouwe.
Doe je eigen onderzoek: als Lovely zegt dat het zo is, dan is het zo (net zo onvermijdelijk als regen denk ik). Cool

Je vraag om onderzoek, dat krijg je. Er komt een opmerking van iemand die niet leest.... En ik mag niet meer meediscussieren?

Dat doe ik dan ook maar niet meer.

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