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PubMed1994

Concomitant activation of Cl- and K+ currents by secretory stimulation in human epithelial cells.

1. Whole-cell currents were investigated in the model salt-secreting epithelium, human T84 cell line, by means of the perforated patch-clamp technique. In the control extracellular medium containing Cl-, depolarizing voltage ramps evoked current responses which peaked at 5.43 +/- 0.81 pA pF-1 at +60 mV and had a reversal potential (Erev) of -38.4 +/- 2.5 mV (n = 23). 2. Activation of the cAMP pathway with forskolin increased the current at +60 mV from 3.81 +/- 0.61 to 20.79 +/- 5.08 pA pF-1 (n = 18). In thirteen cells, Erev was initially shifted towards positive potentials (Erev of the cAMP-activated initial current was -18.2 +/- 1.2 mV) and subsequently shifted towards more negative potentials, consistent with the activation of both Cl- and K+ currents during cAMP stimulation. 3. Increasing the intracellular Ca2+ concentration, [Ca2+]i, with ionomycin (1 microM) or with acetylcholine (1 microM), increased the current at +60 mV from 7.79 +/- 1.57 to 57.50 +/- 12.10 pA pF-1 (n = 6) and from 6.36 to 34.13 pA pF-1 (n = 4), respectively. With both agonists, Erev was shifted either towards the reversal potential for potassium, EK, or towards the reversal potential for chloride, ECl, depending on the cell. 4. In the absence of chloride ions (gluconate substituted), stimulation of the Ca2+ pathway activated a time-independent outward current of large amplitude. This current exhibited inward rectification at positive voltages, reverted at -89.5 +/- 0.2 mV and was markedly reduced by charybdotoxin (10 nM), a specific blocker of Ca(2+)-activated K+ channels. When a voltage step protocol was used, increased [Ca2+]i also activated an outward current at potentials more positive than -40 mV which slowly relaxed during depolarizing steps. 5. The activation of both (i) a time-dependent inwardly rectifying charybdotoxin-sensitive K+ current, and (ii) a time-dependent slowly inactivating current was also produced by cAMP stimulation. 6. We concluded that (i) in the T84 epithelial cells, both Cl- and K+ currents are concomitantly increased by secretagogue stimulation, and (ii) two different types of K+ conductances are activated by either the cAMP or the intracellular Ca2+ secreting pathways.

Acetylcholine↗
PubMed1997

[A case of left subclavian artery occlusion with transient ischemic attacks probably in the internal carotid artery system].

The subclavian steal syndrome is known to steal blood flow from the vertebrobasilar system. However, we experienced a case of subclavian artery occlusion presenting transient ischemic attacks in left internal carotid system. A left handed 41-year-old man developed transient dysarthria and right hemiparesis including face several times when he physically used his arms. He had no symptoms of the vertebrobasilar system. A brain MRI revealed an old cerebral lacuna at the left putamen supplied by perforating arteries of the middle cerebral artery. The angiography demonstrated a complete occlusion of the proximal portion of the left subclavian artery without a reverse flow from the vertebral artery. Instead, descending cervical branches and deep cervical branches of the ipsilateral external carotid artery supplied collateral pathways to the occluded subclavian artery. On the basis of above observations, we speculated that he developed symptoms of the internal carotid system due to the steal through the collateral network of the cervical arteries directed to the subclavian artery. We should consider not only the vertebrobasilar system but also the internal carotid system, especially its cervical artery network, when exploring collateral pathways for the subclavian steal syndrome.

Adult↗
PubMed2000

Two distinct Ca(2+)-dependent signaling pathways regulate the motor output of cochlear outer hair cells.

The outer hair cells (OHCs) of the cochlea have an electromotility mechanism, based on conformational changes of voltage-sensitive "motor" proteins in the lateral plasma membrane. The translocation of electrical charges across the membrane that accompanies electromotility imparts a voltage dependency to the membrane capacitance. We used capacitance measurements to investigate whether electromotility may be influenced by different manipulations known to affect intracellular Ca(2+) or Ca(2+)-dependent protein phosphorylation. Application of acetylcholine (ACh) to the synaptic pole of isolated OHCs evoked a Ca(2+)-activated apamin-sensitive outward K(+) current. It also enhanced electromotility, probably because of a phosphorylation-dependent decrease of the cell's axial stiffness. However, ACh did not change the voltage-dependent capacitance either in conventional whole-cell experiments or under perforated-patch conditions. The effects produced by the Ca(2+) ionophore ionomycin mimicked those produced by ACh. Hyperpolarizing shifts of the voltage dependence of capacitance and electromotility were induced by okadaic acid, a promoter of protein phosphorylation, whereas trifluoperazine and W-7, antagonists of calmodulin, caused opposite depolarizing shifts. Components of the protein phosphorylation cascade-IP(3) receptors and calmodulin-dependent protein kinase type IV-were immunolocalized to the lateral wall of the OHC. Our results suggest that two different Ca(2+)-dependent pathways may control the OHC motor output. The first pathway modulates cytoskeletal stiffness and can be activated by ACh. The second pathway shifts the voltage sensitivity of the OHC electromotile mechanism and may be activated by the release of Ca(2+) from intracellular stores located in the proximity of the lateral plasma membrane.

Acetylcholine↗
PubMed2000

Haloperidol reverses the changes in striatal glutamatergic immunolabeling following a 6-OHDA lesion.

We reported previously that 3 months following a unilateral lesion of the nigrostriatal pathway with 6-hydroxydopamine (6-OHDA), there was a decrease in the extracellular level of striatal glutamate as determined by in vivo microdialysis. This resulted in an accumulation or increase in the density of nerve terminal glutamate immunolabeling (Meshul et al., 1999). We also reported on blockade of dopamine D-2 receptors with haloperidol resulting in ultrastructural changes within the striatum consistent with increased functioning of the glutamatergic corticostriatal pathway (Meshul and Tan 1994). We hypothesized that administration of haloperidol to 6-OHDA-lesioned rats may be capable of activating the corticostriatal pathway and thereby counteracting the effects of the unilateral nigrostriatal lesion. Striatal glutamatergic function was evaluated using electron microscopy and quantitative glutamate immunocytochemistry. Starting 1 month after a unilateral lesion of the nigrostriatal pathway with 6-OHDA, haloperidol (0.5 mg/kg/d) was administered for the next 2 months. Within the dorsolateral caudate nucleus, the main area of innervation from the motor cortex, haloperidol blocked the 6-OHDA-induced increase in the density of nerve terminal glutamate immunolabeling. Within all three experimental groups (6-OHDA, haloperidol, 6-OHDA/haloperidol) there was an increase in the mean percentage of striatal asymmetrical synapses containing a perforated postsynaptic density. In addition, haloperidol treatment resulted in a reduction in the number of apomorphine-induced contralateral rotations in unilaterally 6-OHDA lesioned rats. The data suggests that the decrease in striatal glutamatergic function 3 months following a unilateral 6-OHDA lesion can be reversed by daily haloperidol treatment. This finding is discussed in terms of current therapy for Parkinson's disease. Synapse 36:129-142, 2000. Published 2000 Wiley-Liss, Inc.

Animals↗
PubMed1988

Perforant path activation of the hippocampus: spatial distribution, effects of urethane and atropine.

Spatial distribution of field responses evoked by perforant path stimulation were studied in the hippocampus of both anaesthetized and drug-free rats. Simultaneous recordings with an array of 4 electrodes allowed us to construct a 2-dimensional map of the evoked field potentials. In addition, we examined the effects of atropine-SO4 and urethane on the amplitude of the dentate response. Trisynaptic activation of the CA1 region occurred regularly in the drug-free rat while CA1 population spikes were rarely seen in the anaesthetized animal. The latency of the CA1 population spike was shortest at the fimbrial side and increased gradually towards the subicular side. In the dentate gyrus atropine increased the amplitude of the population spike. We suggest that atropine may interfere with the septo-hippocampal feed-forward inhibition, and urethane may decrease the effectiveness of the perforant path-granule cell synapse, as well as the intrahippocampal excitatory circuit.

Animals↗
PubMed1995

Role of calmodulin in the activation of carbachol-activated cationic current in guinea-pig gastric antral myocytes.

In mammalian gastrointestinal myocytes, it is known that muscarinic stimulation activates nonselective cation channels through a G-protein and a Ca2+-dependent pathway. We recorded inward cationic currents following application of carbachol (ICCh) to guinea-pig gastric myocytes, which were held at -20 mV using the whole-cell patch-clamp method. ICCh was suppressed by nicardipine or removal of Ca2+ from the bath solution. The peak value of inward current induced by repetitive applications of carbachol (CCh) decreased progressively (run-down phenomenon). This run-down was significantly alleviated by the addition of calmodulin to the pipette solution (0.15 mg/ml) or by using the perforated-patch whole-cell voltage-clamp technique. Moreover, W-7[N-6(aminohexyl)-5-chloro-1-naphthalenesulphonamide], a calmodulin antagonist, was a reversible inhibitor of ICCh. However, @-7 had only a weak inhibitory effect on the same cationic current which was induced by guanosine 5'-O-(3-thiotriphosphate) (GTP¿gammaS] 0.2 mM) in the pipette solution. This GTP[gammaS]-induced cationic current was still markedly suppressed by the Ca2+-free bath solution. W-7 itself had a weak inhibitory effect on voltage-operated Ca2+ channels as well as the effects on ICCh. These data suggest that multiple Ca2+-dependent pathways are involved in the activation of CCh-gated cation channels in guinea-pig antral myocytes and a Ca2+/calmodulin-dependent pathway would be one of them.

Animals↗
PubMed1991

Focal stimulation of specific pathways in the rat hippocampus causes a reduction in radioligand binding to the haloperidol-sensitive sigma receptor.

Focal electrical stimulation of selected excitatory pathways in the hippocampal slice caused a decrease in the binding of [3H]-1,3-di(2-tolyl)guanidine (DTG) or [3H]-(+)-3-[hydroxyphenyl]-N-(1-propyl)piperidine [( 3H )-(+)3-PPP) to haloperidol-sensitive sigma binding sites in the slice. Activation of the mossy fibers or perforant path by high frequency electrical stimulation caused the reduction in [3H]-DTG binding; whereas activation of fibers in the strata radiatum, lacunosum-moleculare, alveus, or oriens did not affect [3H]-DTG binding. The decrease in binding observed was calcium-dependent and tetrodotoxin sensitive and varied with the frequency, intensity, and duration of stimulation. Although haloperidol-sensitive [3H]-DTG binding sites are distributed throughout the hippocampus, stimulation of the perforant path or mossy fibers resulted in a significant reduction in binding only in the dentate region of the slice. The decrease in binding following perforant path stimulation was blocked by the glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX); whereas the decrease in binding caused by mossy fiber stimulation was not affected by CNQX or DL-APV. The results obtained support the hypothesis that activation of the granule cells in the hippocampal slice caused the release of an endogenous ligand which acts at the haloperidol-sensitive sigma binding site in the dentate gyrus.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2006

Neurotransmitter mechanisms mediating low-glucose signalling in cocultures and fresh tissue slices of rat carotid body.

The mammalian carotid body (CB) is a polymodal chemosensor which can detect low blood glucose (hypoglycaemia), leading to increased afferent discharge and activation of counter-regulatory autonomic pathways. The underlying neurotransmitter mechanisms are unknown and controversy surrounds whether the action of low glucose is direct or indirect. To address this, we used a coculture model containing functional chemosensory units of rat CB receptor (type I) cell clusters and afferent petrosal neurones (PN). During perforated-patch, whole-cell recordings, low glucose (0-2 mM) stimulated sensory discharge in cocultured PN. When the background P(O2) was lowered to levels typical of arterial blood (approximately 90 mmHg), robust PN chemoexcitation could be induced by physiological hypoglycaemia (3.3-4 mM glucose). These sensory responses were reversibly inhibited by a combination of purinergic (suramin, 50 microM) and nicotinic (mecamylamine, 1 microM) receptor blockers, suggesting that transmission depended on corelease of ATP and ACh. Hypoglycaemic responses were additive with those evoked by hypoxia or hypercapnia; further, they could be potentiated by the GABAB receptor blocker (CGP 55845) and inhibited by 5-HT2A receptor blockers (ketanserin or ritanserin). During paired simultaneous recordings from a PN and a type I cell in an adjacent cluster, the afferent PN response coincided with type I cell depolarization, which was associated with a decrease in input resistance. In fresh tissue slices of rat CB, low glucose stimulated ATP secretion as determined by the luciferin-luciferase assay; this secretion was cadmium sensitive, potentiated by CGP 55845, and inhibited by ketanserin. Taken together these data indicate that CB receptors act as direct glucosensors, and that processing of hypoglycaemia utilizes similar neurotransmitter and neuromodulatory mechanisms as hypoxia.

Acetylcholine↗
PubMed1977

The development of olfactory and hippocampal pathways in the brain of the rat.

The temporal order of development of olfactory, hippocampal and thalamocortical connections has been determined by light microscopy. Scalpel lesions were made to interrupt these connections and the resulting terminal degeneration was stained by Eager's method (1970). A post-operative survival time of one to four days was used. Evidence of the development of these connections was first obtained at the following ages: Olfactory mucosa to olfactory bulb: axon fascicles by 16 days of gestation and terminals in glomeruli at birth; Olfactory bulb to prepyriform cortex at birth; Prepyriform to entorhinal cortex at 13 days after birth; Entorhinal cortex to hippocampus (the perforant path) at 9 days; Hippocampal dentate-Ammonic mossy fibres at 9 days; Hippocampal efferent projection to the septum at birth; Subicular projections to the anterior thalamus at birth and to the mammillary body at 6 days; Hippocampal commissural connections at birth; Corticothalamic and thalamocortical connections by 2 days. These results are discussed in relation to the question of how the development of brain connections is programmed.

Animals↗
PubMed2005

Impact of COX-2 inhibitors in common clinical practice a gastroenterologist's perspective.

Non-selective NSAIDs enhance the risk of serious ulcer complications (bleeding, perforation, obstruction), hospitalization and death about 3-10-fold. The gastrointestinal side effects of NSAIDs have a considerable economical burden, since they are responsible for 5-10 billion dollars in hospitalization charges and lost work time. NSAIDs cause gastrointestinal damage by both topical and systemic effects. COX-1-mediated inhibition of prostaglandin synthesis is probably the most relevant mechanism, but NSAIDs can cause gastrointestinal injury also by COX-independent pathways. COX-2-selective inhibitors (Coxibs) such as celecoxib, rofecoxib or valdecoxib have been developed to achieve an equal relief of pain and inflammation as classical NSAIDs but without their risk of gastrointestinal side effects. Within the first three months, celecoxib became the fastest selling drug in history. The gastrointestinal safety of classical NSAIDs and Coxibs has been compared in a variety of endoscopic investigations, meta-analyses and outcome studies. In conclusion, these studies have clearly shown, that Coxibs are associated with significantly less dyspeptic symptoms, erosions, ulcers and ulcer complications. In contrast, Coxibs seem to delay gastric ulcer healing to the same extent as traditional NSAIDs. Besides their effects on the upper gastrointestinal tract, NSAIDs can cause small intestinal inflammation, ulcers of the small and large intestine, ileal dysfunction, intestinal strictures, colitis and NSAID enteropathy. In addition, NSAIDs increase the risk of lower gastrointestinal complications including bleeding, perforation and obstruction. Current data suggest, that Coxibs are associated with a significantly lower risk of serious lower GI events than traditional NSAIDs. It is now under debate, who should receive COX-2-selective inhibitors instead of classical NSAIDs, since Coxibs are much more expensive. Data from cost-effectiveness studies suggest, that Coxibs should currently be used only in patients with high risks of GI complications.

Animals↗
PubMed1985

A selective loss of hippocampal mossy fiber Timm stain accompanies granule cell seizure activity induced by perforant path stimulation.

Perforant path stimulation for 24 h evoked hippocampal granule cell spikes and epileptiform discharges throughout the stimulation period. After stimulation, hippocampal neurons that receive granule cell output were irreversibly damaged and the stimulated hippocampus of each rat revealed a selective loss of Timm stain in the mossy fiber pathway. These results provide evidence in vivo for a role for synaptic zinc in neurotransmission and/or seizure mechanisms.

Animals↗
PubMed1988

Exploratory behavior and reaction to novelty in rats with hippocampal perforant path systems disrupted.

In this article, exploratory behavior and reaction to novelty were investigated in rats with either disruption of the total hippocampal perforant path projection (TPP), the medial perforant path (MPP), or lateral perforant path (LPP). All three experimental groups displayed increased locomotor activity, and the LPP group was even more active than the TPP and MPP groups. The TPP and LPP animals made more rearings than the control rats. The MPP and LPP groups exhibited less exploration of familiar objects than the TPP and control groups. TPP animals appeared unable to recognize novelty, LPP rats showed decreased preference for novelty, and MPP rats had only a slight deficit in recognition of novelty. It is suggested that perforant path disruptions reduce the hippocampal formation's access to sensory information of neocortical origin.

Animals↗
PubMed1994

Surgical Prevention and Treatment of Late Normal Tissue Injury.

There is a definite increase in combined-modality treatment of malignancies. Surgery, radiation therapy and/or chemotherapy often are combined. A disadvantage is the increased risk for short- and long-term complications, especially radiation-induced damage to normal healthy tissue such as intestine and bone. Brachytherapy and intraoperative radiotherapy are new radiation techniques with the potential to increase the radiation dose to the tumor while reducing the radiation dose to surrounding normal tissues. The surgical transposition of organs outside the pathway of the ionizing beam is a new surgical technique often used in the pelvis. Radiation damage to the gastrointestinal tract is often mentioned. Fibrosis and obstruction may occur as a result of stricture formation or fibrinous adhesions. Ischemic necrosis of the bowel wall may lead either to perforation or fistulae. Mucosal damage and lymphatic obstruction can cause malabsorption. These complications are difficult to manage and should be treated in specialized centers.

Journal Article↗
PubMed1983

Effects of baclofen on synaptically-induced cell firing in the rat hippocampal slice.

The effects of baclofen on the synaptically-induced firing of pyramidal and granule cell populations were tested in the rat hippocampal slice. Population spikes were evoked by stimulating excitatory pathways in the presence and absence of bath-applied drug. (+/-)-Baclofen (20 microM) completely blocked the firing of CA1 or CA3 hippocampal pyramidal cells subsequent to stimulation of projections that originate in area CA3. In contrast, the firing of dentate granule cells evoked by stimulation of the perforant path fibres was depressed by only 46% and baclofen did not affect the monosynaptic firing of CA3 pyramidal cells evoked by mossy fibre stimulation. These results are consistent with the effects of baclofen on the corresponding extracellularly-recorded excitatory postsynaptic potentials (e.p.s.ps). The Schaffer collateral-commissural population spike in area CA1 was depressed by (-)-baclofen (EC50 = 2.8 microM), GABA (EC50 = 2.2 mM) and 3-aminopropanesulphonic acid (3-APS) (EC50 = 0.34 mM). (-)-Baclofen was 180 times as potent as (+)-baclofen. Bicuculline methiodide (100 microM) did not reverse the depressant action of (-)-baclofen. GABA-induced depressions were antagonized to only a small degree, whilst the effect of 3-APS was readily reversed. Raising the concentration of bicuculline from 100 microM to 500 microM did not further reverse the action of GABA. The effects of (-)-baclofen and 3-APS on the relationship between extracellular e.p.s.p. and population spike were tested by stimulation of the Schaffer collateral-commissural fibres in area CA1. (-)-Baclofen shifted the 'input/output' curve to the right at a concentration of 1 microM, but less or not at all at 3 microM. In contrast, increasing the concentration of 3-APS shifted this curve farther to the right.

Animals↗
PubMed1986

Correlation between long-term potentiation and release of endogenous amino acids from dentate gyrus of anaesthetized rats.

The relationship between long-term potentiation (l.t.p.) and the release of endogenous amino acid transmitters has been investigated in the dentate gyrus of rats anaesthetized with urethane. The molecular layer was perfused with artificial cerebrospinal fluid using a push-pull cannula. The perfusate was collected and analysed for glutamate, aspartate, glycine, glutamine and gamma-aminobutyric acid (GABA) using high-performance liquid chromatography (h.p.l.c.) with fluorometric detection. Recording electrodes were attached to the cannula to enable responses evoked by test stimuli to the perforant path to be monitored in the molecular and cell body layers. Perfusion was continued for 3 h while test stimuli were delivered to the perforant path at 30 s intervals. In the control group (n = 8), no further stimulation was given. In a second group (n = 8), a single high-frequency train (250 Hz for 200 ms) was delivered at the end of the first hour to induce l.t.p. The average potentiation of the slope of the excitatory post-synaptic potential (e.p.s.p.) 2 h later was 15%. In a third group (n = 8), the train to the perforant path was paired with a train to the commissural input to the dentate gyrus, a procedure which blocks the induction of l.t.p. In the potentiated group, there was an increase in the concentrations of glutamate and aspartate following the induction of l.t.p., relative to the decline seen in corresponding periods of the control group. This increase remained statistically significant for 1.5 h in the case of glutamate and for 45 min in the case of aspartate. There were no l.t.p.-associated changes in the release of glutamine or glycine; there was an indication that l.t.p. may be associated with a decrease in the release of GABA. Increasing the frequency and intensity of perforant path activation resulted in enhanced concentrations of glutamate and aspartate in the perfusate; no such changes occurred when granule cells were activated antidromically. We discuss the origin of the relative increases in the concentration of glutamate and aspartate which are found in the perfusate following the induction of l.t.p. and conclude that the most likely source is a sustained increase in activity-dependent release of these amino acids from perforant path terminals.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2006

Autophosphorylation of alphaCaMKII is not a general requirement for NMDA receptor-dependent LTP in the adult mouse.

Autophosphorylation of alpha-Ca2+/calmodulin kinase II (alphaCaMKII) at Thr286 is thought to be a general effector mechanism for sustaining transcription-independent long-term potentiation (LTP) at pathways where LTP is NMDA receptor-dependent. We have compared LTP at two such hippocampal pathways in mutant mice with a disabling point mutation at the Thr286 autophosphorylation site. We find that autophosphorylation of alphaCaMKII is essential for induction of LTP at Schaffer commissural-CA1 synapses in vivo, but is not required for LTP that can be sustained over days at medial perforant path-granule cell synapses in awake mice. At these latter synapses LTP is supported by cyclic AMP-dependent signalling in the absence of alphaCaMKII signalling. Thus, the autophosphorylation of alphaCaMKII is not a general requirement for NMDA receptor-dependent LTP in the adult mouse.

Action Potentials↗
PubMed1976

Microsurgical anatomy of the anterior cerebral-anterior communicating-recurrent artery complex.

The microvascular relationships important to surgery of aneurysms in the anterior communicating region were defined in 50 cadaver brains. The recurrent artery of Heubner was frequently exposed before the A-1 segment in defining the neck on anterior cerebral aneurysms because it commonly courses anterior to A-1. It arose from the A-2 segment of the anterior cerebral artery (ACA) in 78% and most commonly terminated in the area of the anterior perforated substance, and lateral to it in the Sylvian fissure. The anterior communicating artery (ACoA) frequently gave rise to perforating arteries which terminated in the superior surface of the optic chiasm and above the chiasm in the anterior hypothalamus. This finding contrasts with previous reports that no perforating branches arise from the communicating artery. The proximal half of the A=1 segment was a richer source of perforating arteries than the distal half. The A-1 branches most commonly terminated in the anterior perforated substance, the optic chiasm, and the region of the optic tract. The ACoA increased in size as the difference in the diameter between the right and left A-1 segments increased. Frequent variants such as double or triple ACoA's, triple A-2 segments, and duplication of the A-1 segments were encountered. The clinical consequences of occlusion of the recurrent artery and of the perforators from the ACoA and medial and lateral segment of A-1 are reviewed.

Arteries↗
PubMedDate not supplied

[Values of white blood cell count in the diagnosis of acute appendicitis].

BACKGROUND: The diagnosis of acute appendicitis remains a critical challenge for paediatric surgeons. White Blood Cell (WBC) count, once considered a basic exam, is still routinely performed in most institutions, despite its lack of accuracy. Aim of this study is to assess the additional value of WBC count in the diagnosis of acute appendicitis. METHODS: We retrospectively reviewed the charts of children who underwent appendectomy for acute appendicitis in the last two years at our institution. In the patients treated in 1999 (Group A), WBC count was assessed routinely after admission. The surgeons relied on leukocytosis as well as on clinical findings and on ultrasound abdominal scan for the diagnosis of acute appendicitis. In the patients treated in 2000 (Group B), blood cell count was not tested or deliberately ignored by the surgeons. RESULTS: There were 65 children in Group A and 70 in Group B; the two groups of patients were similar in terms of gender (p = 0.989) and age (p = 0.758). Criteria for operation were similar in the two groups (p = 0.222). No differences were found in the number of perforated (p = 0.989) and normal (p = 0.217) appendixes in the two groups as well as in the duration of hospital stay after surgery (p = 0.849). CONCLUSIONS: WBC count at admission has no proven additional value in the diagnosis of acute appendicitis and can be omitted without modifying diagnostic pathway and without affecting diagnostic accuracy.

Acute Disease↗